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17,057
|
<blockquote>
<p>Also, transplants from one identical twin to another are <strong>almost never</strong> rejected.<br />
<sub>[ Source: <a href="http://www.nlm.nih.gov/medlineplus/ency/article/000815.htm" rel="nofollow noreferrer">Medline Plus</a> ]</sub></p>
</blockquote>
<p>Why can a tissue from an <em>identical</em> twin be rejected ?</p>
|
[
{
"answer_id": 17068,
"pm_score": 2,
"text": "<p>MattDMo, I think you're right on. Also remember the <a href=\"http://en.wikipedia.org/wiki/Thymus\" rel=\"nofollow\">thymus</a> is where T-cell recombination and maturation occurs during fetal development, and rates are highest during neonatal period through pre-adolescent childhood - long after sharing a womb.</p>\n\n<p>The immune system keeps developing during childhood. It's the immune system that's responsible for tissue rejection in transplant.</p>\n\n<p>In our immune system, T cells attack and kill foreign cells in the body. They're supposed \nto ignore cells that carry molecules belonging to their own body.\nT cells go through selection in the thymus during these years to eliminate the T cells that attack their own molecules;the rest of the T cells that recognize foreign molecules are allowed to live.</p>\n\n<p>Next, consider that environmentally-induced <a href=\"http://en.wikipedia.org/wiki/Epigenetics\" rel=\"nofollow\">epigenetics</a> influence the expression of proteins and other products. Even twins have different experiences and exposures, so there may be a difference in protein components in their bodies. </p>\n\n<p>Also, this is conjecture, but the same concepts involved in autoimmune disorders (which are another topic entirely) might also be involved in some of these situations as well.</p>\n"
}
] |
[
{
"answer_id": 17059,
"pm_score": 2,
"text": "<p>This was too long for a comment, but I have absolutely no evidence for what I'm about to say :)</p>\n\n<p>It looks like that sentence was a little bit of hand-waving, as the author didn't want to categorically state that identical twin tissue would <strong>never</strong> be rejected. I suspect that in the early days there may have been reports of organ failure (esp. kidneys) in the recipient that were incorrectly identified as rejection episodes. I suppose there's also the slight possibility that one twin could have a mutation event very shortly after the separation of the twins <em>in utero</em> (when all the cells are still pluripotent) that could somehow change or (more likely) silence one or more of the HLA or other surface antigens involved in transplant rejection. This would almost certainly have to happen when the separated twin was a single cell. The mutated twin would therefore not express an antigen the non-mutated twin did, and if the non-mutated twin donated a kidney or other organ to the mutated one, its immune system wouldn't recognize the silenced antigen and could potentially result in rejection.</p>\n\n<p>Like I said earlier, all pure conjecture :) </p>\n"
}
] |
17,065
|
<p>In math, there are special numbers, like Pi (3.14159...) and e (2.71828...). In chemistry, there's numbers like avogadro's number (6.0221413e+23). For example a circle can be defined in terms of 2 * Pi.</p>
<p><strong>Are there any significant constant numbers in biology that define the shape of an organism</strong> (ex: mammal)? I'm talking about stuff like shoulder to hip ratio or length of an organism, etc? </p>
<p>Here's an example that came to mind - different fetuses developing into different organisms. Is there any constant that is the same for these at some stage of development? Like the ratio of head to tail?</p>
<p><img src="https://i.stack.imgur.com/Zc2Lj.gif" alt="enter image description here"></p>
|
[
{
"answer_id": 17067,
"pm_score": 4,
"text": "<p>I don't know if this is what you mean, but take a look at <a href=\"http://bionumbers.hms.harvard.edu/\" rel=\"nofollow\">BioNumbers</a>.</p>\n\n<p>Also, mathematical constants like pi are different from physical constants. Mathematical constants are true in a mathematical (logic) sense, and do not need to be related to any physical quantity. They are derived by <strong>logic</strong>. Physical constants, on the other hand, typically describe an observed relation between two types of quantities. They are derived by <strong>measurement</strong>.</p>\n"
}
] |
[
{
"answer_id": 17088,
"pm_score": 2,
"text": "<p>I think you have the direction of causality reversed. Due to either physical, chemical or dynamical properties of cells and organisms, it would certainly be possible to see patterns of constants emerge when making some measurements. I don't think you can say that the mathematical constants define any aspect of an organism. The Golden Ratio, or phi, was brought up as a recurring pattern in nature (e.g., the spiral pattern of snail. shells and sunflower seeds) but these are emergent properties of a physical system bound by physical constraints, and it so happens some pattern is used because it is efficient (in whatever sense that may mean).</p>\n"
}
] |
17,081
|
<p>In his song <a href="https://www.youtube.com/watch?v=ESFANzZTdYM" rel="nofollow">Lullaby</a>, Tim Minchin <a href="https://www.youtube.com/watch?v=ESFANzZTdYM?t=57s" rel="nofollow">sings</a>:</p>
<blockquote>
<p>Your nappy is dry and your tummy is full<br>
Of enough antihistamine to chill out a bull<br>
Yet still all this gringing</p>
</blockquote>
<p>According to Wikipedia, antihistamines are used against allergies.</p>
<p>So, why is there antihistamine in his baby's tummy and why is it supposed to make her sleepy?</p>
|
[
{
"answer_id": 17083,
"pm_score": 4,
"text": "<p>This song most likely refers to an <strong>off-label</strong> (<em>and usually <strong>inappropriate</em></strong>) use for certain antihistamines like <strong>Benadryl</strong>. They are sometimes used by parents to <strong>sedate their children</strong>, functioning through the exact physiological mechanisms @Chris describes. Parents use it <strong>inappropriately</strong> as a means of <strong>behavioral control</strong> for active or upset children to make them more docile or sleepy, such as for airplane rides, etc. <a href=\"https://www.rnzcgp.org.nz/assets/documents/Publications/JPHC/June-2013/JPHCNuggetsJune2013.pdf\"><strong>It's not recommended by most pediatricians</strong></a>, because even though adverse (bad) side effects are usually rare, it is an actual medication with another primary mechanism of action having effects on many body functions, not a medication designed as a sedative. </p>\n"
}
] |
[
{
"answer_id": 17082,
"pm_score": 2,
"text": "<p>This is not only happening in babies...\nIn short (I will look for some references later and edit the post) the antihistamines are effective in the whole body and block the histamines there. The antihistamines which cross the blood-brain barrier do the same in the brain and hinder the small amounts of histamines which stimulate the nerve cells there from doing so. This results in the typical sleepyness.</p>\n"
}
] |
17,104
|
<p>I recently read about an experiment where they removed the dendrites and axons from rat neurons and placed them on a grid. After a while they started reconnecting and were able to learn things.</p>
<p>Since I'm trying to create a model simulating this, I'd like to know (as much as is needed to make it look at least a little bit realistic) how they reconnected. As far as I know some molecules are secreted attracting or repelling axon growth cones.</p>
<p>I think I can model that part, but the problem is that the axons can easily grow back to where they came from, so how do the axons in a brain 'know' they are not growing back to the neuron they originated from.</p>
|
[
{
"answer_id": 17291,
"pm_score": 4,
"text": "<p>I think I can partially answer you question. As far as I'm aware, there are many surface receptor molecules such as ephrins that are responsible for axonal guidance and dendritic repulsion in developing organisms such as flies (Drosophila). As you can tell this is extremely crucial since its important for neurons to spread their dendrites and axons as far as possible, evenly spaced out with axons bifurcating (separating) correctly and not sticking together. This is for example important in the Drosophila brain for axonal projections into different lobes.</p>\n\n<p>One such surface receptor, which helps achieving the above is Dscam (Down syndrome cell adhesion molecule) (schmucker et al 2000 Cell). Dscam gene is expressed in over 38000 isoforms (through complex alternative splicing of Dscam mRNA) in flies. It is the homophilic binding and subsequent repulsion of Dscam protein isoforms that enables an intrinsic self-recognition for repulsion of same-cell axon. As far as I understand it, if a number of similar Dscam isoforms are present on axons or dendrites of a neuron, this is self recognised and the dendrites and axons get repelled from one another. This is the molecular pathway that ensures sister dendrites are not adhered together or become concentrated in one area.</p>\n\n<p>In the absence of Dscam or when Dscam protein isoform diversity is removed flies die during larval stages and the early embryonic axonal patterning of the fly nervous system is clearly disrupted. In the absence of Dscam protein, Bolwig's axons exhibit frequent axon pathfinding errors at a specific intermediate target. Most of these processes are conserved in mammals.</p>\n\n<p>For further information please look at Schmucker & chen, 2009 Genes and Dev</p>\n"
}
] |
[
{
"answer_id": 17302,
"pm_score": 3,
"text": "<p>In cases of severe head injury where a large portion of neurons and their connections get shredded. I don't think a neuron would be very choosy when presented with quite a few axons and lots of intracellular fluid </p>\n\n<p>There are coup and the contra coup (p silent) brain injuries that occur because the brain bounces back and forth in the skull. The contra coup, other side contusion (bruise) is usually worse. A lot of axonal injury occurs in the brain stem and since the basics of life (breathing centers) a severe injury to the brain stem can cause not surviving the injury.</p>\n\n<p>Probably speed of healing I is the priority. I forgot which journal it was in but those with a college education were 60% more likely to have a good recovery while those with just a high school diploma have only 10-20% chance of having a good recovery. It's a similar ranking when it comes to neuronal connections. </p>\n\n<p>Thank you for answering my curiosities on how indeed does one heal from Diffuse Axonal Injury (DAI) on a molecular basis. I was a 1sr yr. radiology resident when I had a severe TBI or Traumatic Brain Injury. TBI is the fancy way of saying brain damaged. But now we know victims of severe head injury can recover and even grow new neurons until old age.</p>\n"
}
] |
17,159
|
<p>What is the difference between transformation and transfection? How do both of these methods work?</p>
|
[
{
"answer_id": 17161,
"pm_score": 4,
"text": "<p>If you are interested in the history of molecular biology this is an interesting question. </p>\n\n<p>Basically transformation came to be used to describe experiments in which the phenotype of an organism was changed by the uptake of DNA, and because of the way this developed in bacterial systems this DNA was usually a plasmid. Then it became possible to use purified phage DNA to infect cells, whereupon the 'transformed' cells produced phage particles - for obvious reasons this was called transfection. </p>\n\n<p>When efforts turned to getting the same techniques working with cultured animal cells many of the vectors were based on viral genomes (e.g. SV40) and these workers referred to this as transfection. At this point the distinction between the two terms became meaningless, and usage tends to be for historical reasons. Interestingly in molecular manipulations of yeast, where there are no viruses, the transfection word is rarely used.</p>\n"
}
] |
[
{
"answer_id": 17160,
"pm_score": 2,
"text": "<p>As far as I know (and I haven't found no evidence against it) this is mostly a semantic difference. Both processes describe the addition of genetic material into cells using various techniques. </p>\n\n<p>Transformation is here mostly used for bacterial work (transforming plasmids for example), while transfection is almost exclusively used for eukaryotic cells. The reason may be, that the term transformation is used in eukaryotic cells as well to describe the progresion of cells into cancer cells.</p>\n\n<p>The techniques are not very different and there are a lot of them. Transfections often use transfection agents, which form pores in the cell membrane through which the DNA can enter the cell. This can also be done by using a short electropulse. A lot of transformations are done using \"chemically treated\" cells, where the cells are brought into a state in which they take up DNA which adheres to their outside. </p>\n\n<p>The Wikipedia articles on <a href=\"http://en.wikipedia.org/wiki/Transfection\" rel=\"nofollow\">Transfection</a> and <a href=\"http://en.wikipedia.org/wiki/Transformation_%28genetics%29\" rel=\"nofollow\">Transformation</a> gives you more details on the methods.</p>\n"
}
] |
17,170
|
<p>I am trying to determine the "translated" meanings (not seeking the common names) of different insects, (presently some bees and wasps). Does anyone know of a printed or internet resource that defines the various names. I have one for plants, but not for animals. Knowing the (English) meaning of the Latin / Greek/ etc. is often very informative -- IF I can find it. </p>
<p>I can give more specifics if you want.</p>
<p>Thanks.</p>
<p>Glen B
Olympia WA, USA</p>
|
[
{
"answer_id": 17161,
"pm_score": 4,
"text": "<p>If you are interested in the history of molecular biology this is an interesting question. </p>\n\n<p>Basically transformation came to be used to describe experiments in which the phenotype of an organism was changed by the uptake of DNA, and because of the way this developed in bacterial systems this DNA was usually a plasmid. Then it became possible to use purified phage DNA to infect cells, whereupon the 'transformed' cells produced phage particles - for obvious reasons this was called transfection. </p>\n\n<p>When efforts turned to getting the same techniques working with cultured animal cells many of the vectors were based on viral genomes (e.g. SV40) and these workers referred to this as transfection. At this point the distinction between the two terms became meaningless, and usage tends to be for historical reasons. Interestingly in molecular manipulations of yeast, where there are no viruses, the transfection word is rarely used.</p>\n"
}
] |
[
{
"answer_id": 17160,
"pm_score": 2,
"text": "<p>As far as I know (and I haven't found no evidence against it) this is mostly a semantic difference. Both processes describe the addition of genetic material into cells using various techniques. </p>\n\n<p>Transformation is here mostly used for bacterial work (transforming plasmids for example), while transfection is almost exclusively used for eukaryotic cells. The reason may be, that the term transformation is used in eukaryotic cells as well to describe the progresion of cells into cancer cells.</p>\n\n<p>The techniques are not very different and there are a lot of them. Transfections often use transfection agents, which form pores in the cell membrane through which the DNA can enter the cell. This can also be done by using a short electropulse. A lot of transformations are done using \"chemically treated\" cells, where the cells are brought into a state in which they take up DNA which adheres to their outside. </p>\n\n<p>The Wikipedia articles on <a href=\"http://en.wikipedia.org/wiki/Transfection\" rel=\"nofollow\">Transfection</a> and <a href=\"http://en.wikipedia.org/wiki/Transformation_%28genetics%29\" rel=\"nofollow\">Transformation</a> gives you more details on the methods.</p>\n"
}
] |
17,185
|
<p>I need to draw simple, phylogenetic tree for kids lecture. </p>
<p>I am looking for an online tool where I can enter organisms (e.g., human, wasp, fungus) and get figure of a phylogenetic tree. Tree should be based on how close those organisms are (I don't need genome alignments).</p>
<p>Similar figure producing tool would be perfect.
<img src="https://i.stack.imgur.com/rSi0A.jpg" alt="## Heading ##"></p>
|
[
{
"answer_id": 20273,
"pm_score": 4,
"text": "<p>As per your requirements I will suggest:</p>\n\n<p><a href=\"http://www.onezoom.org/\" rel=\"nofollow noreferrer\">http://www.onezoom.org/</a></p>\n\n<p><img src=\"https://i.stack.imgur.com/4IXP7.jpg\" alt=\"\"></p>\n"
}
] |
[
{
"answer_id": 20271,
"pm_score": 2,
"text": "<p>I don't know what background you have given the kids or what level, but here's something we do in a non-majors freshman level biology course that could easily be adjusted. First, to get them thinking about trees and relationships, give them a simple family genealogy (use only 1 parent for simplicity). I use my family tree going back to my grandmother. With cousins, aunts, and siblings, they begin to understand how to interpret family trees. You can substitute the family names with organism names to make it a basic phylogenetic tree.</p>\n\n<p>We teach tree construction simply. We give students a list of six species (fake birds) with DNA sequences that are only 20 nucleotides long. Students have to calculate the number of base pair differences between each pair of sequences which, in our case, range from 2-10 nucleotides. </p>\n\n<p>They then use the pairwise differences to construct their tree, with the understanding that fewer nucleotide differences between organisms means they are more closely related.</p>\n\n<p>You can do this type of activity over a couple of days (depending on time). Then, you can begin to show them trees that become gradually more complex. Because the kids will have constructed a tree and now <em>how</em> it is constructed, they will have a much easier time interpreting larger trees.</p>\n"
}
] |
17,186
|
<p>What are the functions of disulphide bonds between amino acids in proteins or peptides?</p>
|
[
{
"answer_id": 20273,
"pm_score": 4,
"text": "<p>As per your requirements I will suggest:</p>\n\n<p><a href=\"http://www.onezoom.org/\" rel=\"nofollow noreferrer\">http://www.onezoom.org/</a></p>\n\n<p><img src=\"https://i.stack.imgur.com/4IXP7.jpg\" alt=\"\"></p>\n"
}
] |
[
{
"answer_id": 20271,
"pm_score": 2,
"text": "<p>I don't know what background you have given the kids or what level, but here's something we do in a non-majors freshman level biology course that could easily be adjusted. First, to get them thinking about trees and relationships, give them a simple family genealogy (use only 1 parent for simplicity). I use my family tree going back to my grandmother. With cousins, aunts, and siblings, they begin to understand how to interpret family trees. You can substitute the family names with organism names to make it a basic phylogenetic tree.</p>\n\n<p>We teach tree construction simply. We give students a list of six species (fake birds) with DNA sequences that are only 20 nucleotides long. Students have to calculate the number of base pair differences between each pair of sequences which, in our case, range from 2-10 nucleotides. </p>\n\n<p>They then use the pairwise differences to construct their tree, with the understanding that fewer nucleotide differences between organisms means they are more closely related.</p>\n\n<p>You can do this type of activity over a couple of days (depending on time). Then, you can begin to show them trees that become gradually more complex. Because the kids will have constructed a tree and now <em>how</em> it is constructed, they will have a much easier time interpreting larger trees.</p>\n"
}
] |
17,207
|
<p>I was at the park lying on the grass and its the third time I have seen them, I used to think they were parasites when I was like 7. It is the very small brown worm on the green leaf. It moves by squiggling. It comes in different colors but same size.</p>
<p><a href="http://postimg.org/image/ea3x2nw95/" rel="nofollow">http://postimg.org/image/ea3x2nw95/</a>
<a href="http://postimg.org/image/zfawh9pr1/" rel="nofollow">http://postimg.org/image/zfawh9pr1/</a></p>
|
[
{
"answer_id": 35153,
"pm_score": 2,
"text": "<p>For me it looks like an <a href=\"http://en.wikipedia.org/wiki/Geometer_moth\" rel=\"nofollow noreferrer\">inchworms</a> which are the larvae of geometer moth or Geometridae.</p>\n\n<p>By your picture it is almost impossible to see of which type it is.</p>\n\n<p>I took picture of one in Switzerland (but likely not the same as yours).</p>\n\n<p><img src=\"https://i.stack.imgur.com/h7hZz.jpg\" alt=\"caterpillar-geometer\"></p>\n\n<p>Full resolution here: <a href=\"https://flic.kr/p/utFsiU\" rel=\"nofollow noreferrer\">https://flic.kr/p/utFsiU</a></p>\n"
}
] |
[
{
"answer_id": 17379,
"pm_score": 2,
"text": "<p>Is this what you mean? </p>\n\n<p><img src=\"https://i.stack.imgur.com/popbq.png\" alt=\"wireworm\"></p>\n\n<p>It's pretty hard to tell from this photo, and I'm no entemologist, but to me, it looks like it may be a <strong>wireworm</strong>, a larvae of a <a href=\"http://en.wikipedia.org/wiki/Click_beetle\" rel=\"nofollow noreferrer\"><strong>click beetle</strong></a>. This is a diverse group, so I think it would be pretty difficult to give a specific identification. (<a href=\"https://www.google.com/search?q=Wireworms&tbm=isch\" rel=\"nofollow noreferrer\">More images</a>)</p>\n"
}
] |
17,213
|
<p>There's undoubtedly more than one way to do this, but if a DIY biologist were to attempt to detect food fraud (e.g. as done by students from <a href="http://conservationmagazine.org/2008/09/impostor-fish/" rel="nofollow">Stanford University</a> and <a href="http://www.nytimes.com/2008/08/22/science/22fish.html?_r=0" rel="nofollow">Trinity School, Manhattan</a> with respect to fish samples from markets and sushi restaurants), then what would be the minimum steps and equipment?</p>
<p><em>(I know barely anything about molecular genetics, but have been reading about DremelFuge, OpenPCR, and Blue Transilluminator, and wondered whether they - or things like them - might get such an investigator some of the way towards the goal above; and what else would be required.)</em></p>
|
[
{
"answer_id": 17221,
"pm_score": 4,
"text": "<p>There are several ways you could go about identifying species through DNA. If you want to do everything yourself, the simplest option in terms of equipment needed consists of evaluating fragment lengths observed during gel electrophoresis after amplifying specific DNA sequences using PCR.</p>\n\n<p>If you are content with some outsourcing, you can also send DNA samples to a commercial company for sequence analysis.</p>\n\n<p>A compromise between these options in terms of information obtained, is to do study <a href=\"http://en.wikipedia.org/wiki/Restriction_fragment_length_polymorphism\" rel=\"nofollow\">Restriction Fragment Length Polymorphism</a> (RFLP) by amplifying DNA fragments and using restriction enzymes to cut the fragments, before analyzing the fragmentation pattern using gel electrophoresis. To perform RFLP analysis, you would need to obtain restriction enzymes in addition to the chemicals mentioned below, and they can be a bit pricey.</p>\n\n<p>The minimum equipment would consist of a PCR machine, one or more pipettes with matching pipette tips, a gel electrophoresis tray with power supply and a transilluminator (preferably blue-light/non-UV). A centrifuge is not strictly necessary, but can be useful for processing/filtering your DNA source. </p>\n\n<p>Some chemicals will also be needed: Polymerase and dNTPs for the PCR reaction (or a pre-made \"master mix\" containing both), electrophoresis-grade agarose and running buffer for the electrophoresis, along with a DNA dye specific to the type of transilluminator (Usually UV or blue light). For a blue-light transilluminator, GelGreen is a suitable DNA dye. You will also want to use a \"loading dye\" to mix in your DNA sample before applying it to the electrophoresis gel. This can either be purchased or prepared yourself by mixing sugar and food coloring in water.</p>\n\n<p>You need some form of heating to dissolve the agarose - a microwave oven is convenient for this, but take care to avoid over-heating, glass explosions or flash boiling. It is convenient but not strictly necessary to have some lab glassware. Preferably use a screw-top bottle to mix your agarose solution. Always leave the top off when heating bottles.</p>\n\n<p>Photographic equipment can be also useful for documenting results of gel electrophoresis.</p>\n\n<p>Finally, you will need single-stranded DNA oligomers (primers) specific to the DNA regions you want to amplify. DNA primers can be bought from a number of companies, but it varies how easy it is for non-affiliated individuals to order and make payments. <a href=\"http://www.macrogen.com/eng/\" rel=\"nofollow\">Macrogen</a> has been my choice: They both deliver DNA primers and perform DNA sequencing.</p>\n\n<p>You may be interested in the following thread on the DIY Bio e-mail group: <a href=\"https://groups.google.com/forum/#!topic/diybio/cPzfEuiZH58\" rel=\"nofollow\">https://groups.google.com/forum/#!topic/diybio/cPzfEuiZH58</a></p>\n\n<p>I have collected some of the primer sequences mentioned in the thread on a page on OpenWetware: <a href=\"http://openwetware.org/wiki/User%3aJarle_Pahr/Meat\" rel=\"nofollow\">http://openwetware.org/wiki/User:Jarle_Pahr/Meat</a></p>\n"
}
] |
[
{
"answer_id": 17267,
"pm_score": 1,
"text": "<p>This can in principle be done at least partly with DIY methods, by using PCR followed by gel electrophoresis. The DremelFuge, OpenPCR, and Blue Transilluminator would be the primary tools, along with pipettes, test tubes, autoclave (or equivalent), etc.</p>\n\n<p>For a clear video demonstration of using PCR to amplify DNA from various samples, as well as a PDF containing the details of the protocol used, see <a href=\"http://www.dnabarcoding101.org/\" rel=\"nofollow\">www.dnabarcoding101.org</a>. That procedure would be followed by using gel electrophoresis on a small portion of the amplified product, to check that the product appears to be of <a href=\"http://www.biotechlearn.org.nz/themes/dna_lab/video_clips/using_gel_electrophoresis_to_check_a_pcr_reaction_v0036\" rel=\"nofollow\">adequate quality for sequencing</a>. If so, then the remaining portion of the product can be sent to a lab for sequencing.</p>\n\n<p>Alternatively, by using a suitable primer for each species one wishes to test for, one could check for the presence of that species using <a href=\"http://journals.tubitak.gov.tr/veterinary/issues/vet-07-31-3/vet-31-3-3-0601-30.pdf\" rel=\"nofollow\">PCR and gel electrophoresis alone</a>.</p>\n"
}
] |
17,245
|
<p>If a person's head was cleanly and rapidly decapitated by a sharp blade slicing through the neck, such as would happen on the guillotine, could that person remain conscious? If so for how long? Long enough to be aware of (the head) falling down and hitting the ground? </p>
<p>Obviously it would be brief due to lack of blood supply, but it seems plausible that it could be a few seconds.</p>
<p>Or is there some inherent neurological shock due to the severing the top of the spinal cord that would cause near instantaneous loss of conciousness?</p>
<p>Could Marie Antoinette have seen her own severed neck from the basket below the blade?</p>
|
[
{
"answer_id": 17247,
"pm_score": 4,
"text": "<p>According to <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3029360/\">this</a>, in rats it takes about 17 seconds after decapitation for the EEG to become iso-electric. But there is no known correlation between EEG and consciousness. Also at 50-80 seconds after decapitation, EEG being iso-electric, a very slow, late wave appears on the EEG record.</p>\n\n<p><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3029360/\">The same article</a> concludes that it takes about 3-4 seconds after decapitation for the animal to lose conscience and perceive no stress and pain.</p>\n\n<p>Also, dr. Harold Hilman states in <a href=\"http://books.google.com/books?id=pKU5MXqo4UYC\"><em>An unnatural way to die</em></a> article from october 1983 issue of <em>New Scientist</em>, page 277 that:</p>\n\n<blockquote>\n <p>Consciousness is probably lost within 2-3 seconds, due to a rapid fall of intracranial perfusion of blood.</p>\n</blockquote>\n"
}
] |
[
{
"answer_id": 17263,
"pm_score": 0,
"text": "<p>I remember reading that during the French Revolution Antoine Lavoisier arranged with his assistant condemned to death to blink after the cut off if he still had conscience (Lavoisier was to call his name first to limit automatisms). He reported a possibility that the assistant did hear him (the blinking was apparently not that obvious) </p>\n"
}
] |
17,246
|
<p>It is obviously very onerous to generate heat at all, although it has advantages. We don't have to lie on the sun like a crocodile to get warmer. And we avoid the freezing of our body water by out own means. But wouldn't just a little of heat be enough? </p>
<p>Why do humans go as far as 37 C? Couldn't we just have a temperature of 10 C to avoid freezing but stay at it?</p>
|
[
{
"answer_id": 17247,
"pm_score": 4,
"text": "<p>According to <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3029360/\">this</a>, in rats it takes about 17 seconds after decapitation for the EEG to become iso-electric. But there is no known correlation between EEG and consciousness. Also at 50-80 seconds after decapitation, EEG being iso-electric, a very slow, late wave appears on the EEG record.</p>\n\n<p><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3029360/\">The same article</a> concludes that it takes about 3-4 seconds after decapitation for the animal to lose conscience and perceive no stress and pain.</p>\n\n<p>Also, dr. Harold Hilman states in <a href=\"http://books.google.com/books?id=pKU5MXqo4UYC\"><em>An unnatural way to die</em></a> article from october 1983 issue of <em>New Scientist</em>, page 277 that:</p>\n\n<blockquote>\n <p>Consciousness is probably lost within 2-3 seconds, due to a rapid fall of intracranial perfusion of blood.</p>\n</blockquote>\n"
}
] |
[
{
"answer_id": 17263,
"pm_score": 0,
"text": "<p>I remember reading that during the French Revolution Antoine Lavoisier arranged with his assistant condemned to death to blink after the cut off if he still had conscience (Lavoisier was to call his name first to limit automatisms). He reported a possibility that the assistant did hear him (the blinking was apparently not that obvious) </p>\n"
}
] |
17,264
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<p>I couldn't seem to find one elsewhere, at least not with a scientific source.</p>
<p>It would seem as it's quite a striking feature there would be an advantage it would infer.</p>
|
[
{
"answer_id": 17287,
"pm_score": 4,
"text": "<p>As your commenters have suggested, no.</p>\n\n<p>In order for an explanation to be a <strong>good</strong> evolutionary explanation, it needs to have a testable hypothesis and a mechanism to test it. </p>\n\n<p>The most common mechanism for testing the crypsis (camouflage) hypothesis is to take a large number of closely-related species, and see if their coloration differences are correlated to a particular habitat. Since pandas have few black-and-white relatives, there is no statistical power in this analysis. </p>\n\n<p>Another option is to take a large number of pandas, create a treatment and control group and bleach the treatment group (or their eyespots) white, and compare survival or visual acuity. Unsurprisingly, this has not been done. </p>\n\n<p>Here's a nice article to animal coloration for those that have access: </p>\n\n<p>Caro, T. I. M. (2005). The adaptive significance of coloration in mammals. Bioscience, 55(2), 125-136.</p>\n"
}
] |
[
{
"answer_id": 17417,
"pm_score": 0,
"text": "<p>I quite like the explanation I found on the website of \"Exploring the BioEdge\". Robin and Honeybadger explain the black and white colouration as follows: To minimize the risk of being attacked by the tiger, the colouration of the giant panda is aposematic, warning would-be predators of its vice-like hug and bite. This warning signal, visible even in poor light, consists of a black-and-white contrast on the face (ears and eyes) as well as the body as a whole.”</p>\n\n<p><a href=\"http://explorebioedge.com/bio-bullets/item/43-warning-colouration-in-the-giant-panda.html\" rel=\"nofollow\">http://explorebioedge.com/bio-bullets/item/43-warning-colouration-in-the-giant-panda.html</a></p>\n"
}
] |
17,276
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<p>There are two different cell lines but we do not know that these cell lines have Gs or Gi proteins, associated with their G-protein coupled receptors. If we wants to know about this. Can we design a experiment through which we would be able to identify specific Gs or Gi proteins in cell lines?</p>
|
[
{
"answer_id": 17414,
"pm_score": 3,
"text": "<p>Bez experiments are too difficult and costly you don't need to do that.</p>\n\n<p>Take, label samples then apply ligands and sustenance. The inhibitory will have have a slower rate of <strong><em>growth</em></strong> not death and use a control with replicates. Also if you have the money buy an epac FRET to measure cAMP. Find someone to do the FRET if you can't. It will take a longer than a day but you avoid the whole I gave it too much it was going to die anyways. If you did not initially separate your cell lines by proteins and have a mix of Gs Gi within the cell lines and you need to find which ligand causes a dominant response then you will have to do individuals of these test. There are companies that specialize in growth response. </p>\n\n<p>If not FRET. Find some business with an <a href=\"http://allseq.com/knowledgebank/sequencing-platforms/life-technologies-ion-torrent\" rel=\"nofollow\">ION torrent</a> and sequence the <strong><em>genome</em></strong> its really really cheap. If your proteins have known homology to Gs or Gi this will give the best results quickest. If you're proteins function is novel add ligands and the Gi will have less PCR amp than the Gs. Don't do your own NA extraction just let them. I've seen so many samples go bad in delivery because people tried to save a buck. </p>\n\n<p>Also since you had trouble designing this experiment find a company which will run the whole of the experiment for you. Most places with ION torrents have the whole lab setup to run such an experiment and do so on a weekly basis. </p>\n"
}
] |
[
{
"answer_id": 17337,
"pm_score": 2,
"text": "<p>EDITED ANSWER</p>\n\n<p>Based on comments and responses my original answer to this question received I have decided to edit the answer and respond to some questions.</p>\n\n<p>Since I work on proteins, I tend to favour protein based approaches specially when wondering about the presence of a protein. This is simply the case because protein is what is important functionally (purely talking about protein based problems/questions here and not talking about RNAi stuff here) so what I have experienced editors require for majority of papers, they want to see some sort of protein work. Now I'm aware that is not always possible since the antibody (Ab) might not be very specific or sensitive specially for low expressing proteins. If a protein is highly transient that makes the problem even worse, which is why many people resort to mRNA expression to make deductive reasoning for the presence of proteins although that makes a number of assumptions about how the mRNA is processed and whether the relationship between mRNA expression and protein expression level is linear but thats another discussion. So all I'm trying to say is that it's important check for the presence of a protein using Ab based techniques, which are immunohistochemistry (IHC) and western-blot (WB).</p>\n\n<p>So my primary recommendation is to use Gi and Gs species specific (non-cross reactive) antibodies to check for the presence of your proteins of interest and always use Ab heavy chain control for IHC and a negative control for your WB using a sample that you know doesn't express your proteins of interest, if thats available. IHC also tells you some spatial information and whether Gs and Gi are both present in the same cell line or not and if they co-localise etc etc! Obviously check for Ab availability and if its compatible for IHC or WB procedures.</p>\n\n<p>The other method that is feasible is if you know your two different cells express only one of the Gs or Gi exclusively, you can look at their specific inhibitors and add it to some of your cells and the chances are if the dose is high enough it will cause the cells to die since Gs or Gi are crucial for cell function. You can probably get away with an experiment like this using wells in a 24 well dish so you don't have to use that much media or drugs. But with stuff like this it might not work and you might get off-target effects so just do this as a complementary test. For your drug test always do a DMSO control since the chances are that's what the drugs are dissolved in and if not just use whatever solvent the drugs are dissolved in and add them to your cells in your control experiments.</p>\n\n<p>Now the other possible and commonly used method to check for the gene expression of protein and subsequently infer its presence as a protein is to use a reverse transcription based PCR, such as RT-PCR although it doesn't have to be real-time as correctly mentioned in the comments. Please note that I'm not at all an expert in this and do check my answer in this section since I haven't personally done reverse transcription based PCR. As far as I'm aware, the basic procedure is to extract cellular mRNA, which can be performed using kits such as RNeasy or a similar product (I'm not promoting any products here and these are just what I have came across!). The protocols come with the kits and available online, and tells you exactly what min/max cell number/RNA levels should be present and how your cells should be (pelleted) before processing. Another method for RNA extraction is CsCl but thats pretty messy and complicated and requires high expertise to get it right but I know its inevitable for certain situations but for cell processing, a kit will do. At least RNeasy protocol states it enriches for mRNA and selectively exclude other types of RNA. Once you have your cellular mRNA you can proceed to reverse transcription using the appropriately designed primers for your gene of interest using a thermocycler. Again I'm not sure what tools to use for designing the primers for making cDNA from mRNA and what to look for (apart from the fact that make sure your primers are specific) as I only do regular PCR but would welcome any edits! Once you get from mRNA to cDNA, you can then run them on your (Ethidium Bromide or whatever DNA staining based) agarose gel and see if your amplicon is present and is the correct size (again based on the primers you have chosen you would know what the correct size is) and hence whether your gene is expressed or not. At least RNeasy kit says you do not need to use DNase digestion to get rid of any DNA before reverse transcribing your mRNA as most of it gets cleaned up when using the kit but you have that option. Now regarding the next-generation RNA sequencing I do not know anything about them so would again welcome any edits but seems unnecessary since you only want to know if the gene of interest is expressed so don't need any sequence info but thats an option too (although I imagine a little expensive?). Just to mention something very obvious, it's important that the species, which your lines have been generated from are sequenced or you have good sequence information about the Gs and Gi genes in your lines otherwise designing primers would be guess work. Its always best to see if anyone has done what you are trying to do and ask for their primers as most people are happy to share reagents.</p>\n\n<p>Now you have probably noticed so far that my methods are quite biased towards molecular biology approaches and that's simply because that's what I know more about, however a great suggestion was to use cAMP levels as an indicator for Gs or Gi expression. Again I'm not an expert in this since I haven't ever analysed small molecules but I imagine that involves something like a HPLC, which you need to discuss with a chemist/biochemist how to extract and clean up your cells from everything and leave only the cAMP. There is probably a procedure/kit/biosensor for it but I will avoid getting into it as I know virtually nothing about this. However I have a note of caution for these types of indirect experiments. I have no idea what your cell lines are and how well they are characterised but since lines have all sorts of mutations and deletions and insertions in them, it's not a good idea to make inferences from cAMP levels. Since considering cAMP presence is quite important for cellular function, their absolute levels in a cell line is not necessarily a good indicator of whether one cAMP production regulator is present or not and I'm sure if you do something like this you open yourself to major criticism by any journal editor/referee. What will be a good idea though in any future experiments you do with these cells is to over express Gs or Gi and see their effects on cAMP production but I just don't recommend using cAMP levels as a sole indicator as to whether Gs or Gi is expressed or not.</p>\n\n<p>If everything else fails and you got tired and wanted to wash your hands off this identification task, you can always lyse your cells and send them for mass spectrometry (MS) if there is such a facility at your institute. It's crucial that the species, which your lines originate from are characterised in terms of their global protein sequences since programs such as Mascot query the raw spectral data against databases such as UniProt to get protein coverage and subsequently protein hits. Also before you go ahead with you MS experiments, just speak to the facility manager and ask for guidance as to what lysis buffer is best to lyse your cells in and what components should not be in your lysis buffer and how sensitive their machines are and how likely you are to get detection and what your protein concentration should be. I think the best machine to use is Orbitrap and as a general rule, the higher the protein amount, the more likely you are to detect it. Since cell lysate is pretty messy and the MS machine columns can get saturated by abundant proteins such as actin, it would be best to run your lysates on an SDS-PAGE gel under reducing conditions (you can even do multiple loads by running your samples in the gel, switching off the WB machine, loading more samples and running them in the gel and continue doing this a few times. It works, I have done it myself but for pulled down samples which are a bit cleaner (less contaminants/unwanted proteins) in general). Once your gel runs through just cut the region of the gel corresponding to the molecular weights of Gs and Gi and send that for MS identification. This method (running your lysate through SDS-PAGE gel) gets rid of unwanted proteins that can interfere with the identification process. But MS is very expensive!</p>\n\n<p>Again I would highly welcome any edits to my own edited reply! I'm here to help and learn.</p>\n"
}
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17,320
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<p>I thought that the definition of a definitive host was that the parasite had to sexually reproduce in that particular host. </p>
<p>I've been told that mosquitoes are the definitive host for the plasmodium parasite, but I thought that the fertilization (and thus the sexual reproduction) takes place in the human?</p>
|
[
{
"answer_id": 17321,
"pm_score": 4,
"text": "<p><em>Plasmodium falciparum</em> (the main causative agent of malaria) and other <em>Plasmodium</em> species have a very complex life cycle, with stages in the female host <a href=\"http://en.wikipedia.org/wiki/Anopheles\" rel=\"nofollow noreferrer\"><em>Anopheles</em></a> mosquito, in the human liver, and in the human circulatory system, where it primarily resides in the <a href=\"http://en.wikipedia.org/wiki/Erythrocyte\" rel=\"nofollow noreferrer\">erythrocytes</a> (red blood cells, or RBCs):</p>\n\n<p><img src=\"https://www.cdc.gov/dpdx/images/malaria/malaria_LifeCycle.gif\" alt=\"Plasmodium spp. life cycle\"></p>\n\n<p>During a blood meal, a malaria-infected mosquito injects sporozoites in its saliva into the human host (<strong><em>1</em></strong>). Sporozoites travel through the circulatory system and first infect <a href=\"http://en.wikipedia.org/wiki/Hepatocyte\" rel=\"nofollow noreferrer\">hepatocytes</a> (liver cells) (<strong><em>2</em></strong>, stage <strong><em>A</em></strong>) and mature into schizonts (<strong><em>3</em></strong>), which rupture and release merozoites (<strong><em>4</em></strong>). After this initial replication in the liver (exo-erythrocytic schizogony (<strong><em>A</em></strong>), which can last a minimum of 5.5 days), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony (stage <strong><em>B</em></strong>)). Merozoites leave the liver and enter the circulatory system where they infect red blood cells (<strong><em>5</em></strong>). The ring stage trophozoites mature into schizonts, which rupture releasing more merozoites, which continue the cycle of infection of RBCs (<strong><em>6</em></strong>). Some immature trophozoites, in the so-called \"ring stage,\" differentiate into sexual erythrocytic stages (gametocytes) (<strong><em>7</em></strong>). Blood stage parasites are responsible for the clinical manifestations of the disease. </p>\n\n<p>It is important to note here (in answer to your question) that while the male and female gametocytes are formed at this stage in the human (the equivalent of meiosis), sexual reproduction does not occur until the micro and macrogametocytes are taken up by a mosquito.</p>\n\n<p>The male (microgametocytes) and female (macrogametocytes) gametocytes are ingested by a female <em>Anopheles</em> mosquito during a blood meal (<strong><em>8</em></strong>) - only female mosquitoes (of pretty much any species) drink blood. The parasites' multiplication in the mosquito is known as the sporogonic cycle (stage <strong><em>C</em></strong>). While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes (<strong><em>9</em></strong>). The zygotes in turn become motile and elongated (ookinetes) (<strong><em>10</em></strong>) which invade the midgut wall of the mosquito where they develop into oocysts (<strong><em>11</em></strong>). The oocysts grow, rupture, and release sporozoites (<strong><em>12</em></strong>), which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle (<strong><em>1</em></strong>).</p>\n\n<h3>Sources</h3>\n\n<ol>\n<li><p>The Centers for Disease Control and Prevention: <a href=\"https://www.cdc.gov/dpdx/malaria/\" rel=\"nofollow noreferrer\">Malaria</a></p></li>\n<li><p>Wikipedia: <a href=\"http://en.wikipedia.org/wiki/Plasmodium_falciparum_biology\" rel=\"nofollow noreferrer\"><em>Plasmodium falciparum</em> biology</a></p></li>\n</ol>\n"
}
] |
[
{
"answer_id": 56874,
"pm_score": 0,
"text": "<p>The answer contains a lot of information, some incorrect, and does not answer the question.</p>\n\n<p>The mosquito is the definite host of plasmodium, despite the humanocentric way this parasite is always looked at.</p>\n\n<p>What happens in the human is the generation of the gammonts (named gametocytes). In the mosquito, these develop into the gametes (microgametes and macrogamete) and sexual reproduction takes place. In the then formed zygote, meiosis occurs, but is not immediately followed by cytokinesis.</p>\n\n<p>As Plasmodium is haploid, the occurrence of meiosis relative to the formation of gametes is shifted in time, but this does not effect the definition of when sexual reproduction takes place (anyway both occurs within the mosquito). </p>\n\n<p>Mirko Singer</p>\n"
}
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17,370
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<p>An <a href="https://pets.stackexchange.com/questions/3159/what-is-an-acceptable-flea-treatment-for-kittens/3176#3176">answer at Pets</a> suggested using dawn dish soap to kill fleas. I did a little looking around, and found several references supporting the idea. Most of what I found was in 'selfhelp' and 'save a dime' type books and web sites. So while it seems to be a popular idea, I am unsure if it is an effective idea.</p>
<p>Is there any reliable science supporting the use of dish soap to kill fleas and/or ticks? If so what points in the life cycle would it be effective? If it does work, how often would I need to use it to be relatively sure all the fleas/ticks have been through the appropriate life cycle and are dead?</p>
|
[
{
"answer_id": 17477,
"pm_score": 5,
"text": "<p>First part of the answer - Yes fleas (Siphonaptera) can be drowned. But not as easily as the internet would lead you to believe.</p>\n\n<p>There are many claims on the internet (and printed works) expounding on how simple it is to drown fleas. The best science I found so far on the topic is in <a href=\"http://books.google.com/books?id=c4FNatmAE48C&pg=PT101&dq=drown+Siphonaptera&hl=en&sa=X&ei=Az93U66IKMjRsASn8IDwBQ&ved=0CEwQ6AEwBg#v=onepage&q=drown%20Siphonaptera&f=false\" rel=\"nofollow noreferrer\">Forensic Entomology: An Introduction By Dorothy Gennard; John Wiley & Sons, Apr 30, 2013; section 4.3</a> which reflects a 1985 work by Simpson K. (<em>Journal of the New York Entomological Society 76: 253-265, not finding this online</em>). Gennard is using the fleas present on a human body at death to determine how long the body had been submerged. Findings - </p>\n\n<ul>\n<li>A flea submerged for up to 12 hours will appear to dead, but can revive in about 60 minutes after being removed from the water</li>\n<li>A flea submerged for 18 - 20 hours will appear to dead, but can revive in 4- 5 hours after being removed from the water</li>\n<li>It takes 24 hours of full submersion to fatally drown a flea \n\n<ul>\n<li>Side note; lice (Phthiraptera) can be fatally drowned in about 12 hours.</li>\n</ul></li>\n</ul>\n\n<p>Second part of the answer - Yes soap can facilitate the death of fleas in bathing</p>\n\n<p>So far the best I have is <a href=\"http://books.google.com/books?id=T8CWvVGwKhoC&pg=PT404&dq=drown+flea&hl=en&sa=X&ei=oz13U9OoE8uosQSZ_ID4Cw&ved=0CEkQ6AEwAg#v=onepage&q=drown%20flea&f=false\" rel=\"nofollow noreferrer\">Medical and Veterinary Entomology by Gary R. Mullen, Lance A. Durden Academic Press, Apr 22, 2009</a> </p>\n\n<ul>\n<li>This work suggests the process of washing the flea (and the pet) removes integumental waxes on the fleas body and they die from desiccation (dehydration).</li>\n</ul>\n\n<p>More Research</p>\n\n<p>I have been unable to find solid research specific to fleas (Siphonaptera) and soap (surfactants), so I had to reach in to the general insect works for answers. There are a number of pesticides which include surfactants in their make up to increase effectiveness but these seem to be to an aid in the delivery of the pesticide not because the surfactant has any additional killing power.</p>\n\n<blockquote>\n <p>a surfactant may affect the efficacy of an insecticide by its influence on wetting, spreading and run-off rather than by its influence on cuticular penetration</p>\n</blockquote>\n\n<p><a href=\"http://books.google.com/books?id=_AUQ_wntE8gC&pg=PA335&dq=surfactant+insects&hl=en&sa=X&ei=xup_U9XQA_DNsQTlr4E4&ved=0CDIQ6AEwAQ#v=onepage&q=surfactant%20insects&f=false\" rel=\"nofollow noreferrer\">The Physiology of Insecta, Volume 6 edited by Morris Rockstein</a></p>\n\n<p>There is some science suggesting soaps can help break down cell membranes but they seem to be most effective on soft bodied insects (which fleas are not)</p>\n\n<blockquote>\n <p>Soaps... kill insects by disrupting the exoskeleton and breaking down cell membranes. Soaps generally work best against small soft bodied insects such as aphids, scale crawlers, meatybugs, and young caterpillars as well as spider mites.</p>\n</blockquote>\n\n<p><a href=\"http://books.google.com/books?id=zMJ4MSKG9-AC&pg=PA67&dq=surfactant+insects&hl=en&sa=X&ei=iOt_U42uAtDIsAST-4DgBg&ved=0CCoQ6AEwADgU#v=onepage&q=surfactant%20insects&f=false\" rel=\"nofollow noreferrer\">Destructive Turfgrass Insects: Biology, Diagnosis, and Control By Daniel A. Potter</a></p>\n\n<p><strong>Summary</strong></p>\n\n<p>There are multiple online reports of \"drowning fleas\" and killing them with soapy water. After looking for the science there does not seem to be much support for these fatal claims. There is little doubt that giving your pet a soapy bath in the tub will help remove the fleas, they may even appear dead. But in all likelihood these fleas are just waiting to dry out and be revived, hopefully in the city sewer. If you bath your pet in the yard, and than let the dry pet in the yard again the next day the clean pet and clean revived fleas will likely reunite. Soapy water is more likely to facilitate removal of the comatose flea from the pet and carry it down the drain. So it is reasonable to have noticeable decrease in the flea population after a bath. But <a href=\"https://pets.stackexchange.com/questions/196/\">excessive bathing has it's own risks</a> and given the <a href=\"https://en.wikipedia.org/wiki/Flea#Life_cycle_and_habitat\" rel=\"nofollow noreferrer\">life cycle of a flea</a> soapy baths alone are unlikely to be a final solution.</p>\n"
}
] |
[
{
"answer_id": 37134,
"pm_score": 2,
"text": "<p>You have to use Lemon Dawn specifically because they have <a href=\"https://en.m.wikipedia.org/wiki/Limonene\" rel=\"nofollow noreferrer\">Limonene</a> and <a href=\"https://en.m.wikipedia.org/wiki/Linalool\" rel=\"nofollow noreferrer\">Linalool</a> from Lemon essential oil. There are actually registered patents on these compounds for use in killing and repelling fleas and other insects.</p>\n<ul>\n<li>Limonene: <a href=\"http://www.google.com/patents/US4379168\" rel=\"nofollow noreferrer\">http://www.google.com/patents/US4379168</a></li>\n<li>Linalool: <a href=\"https://www.google.com/patents/US4933371\" rel=\"nofollow noreferrer\">https://www.google.com/patents/US4933371</a></li>\n</ul>\n<p>Lemon oil paralyses and can kill the fleas. After the bath you have to comb the dog with a flea comb to remove the fleas, eggs and larva. Do this once a week and your dog should be flea free. Lemon also repels fleas, so it prevents re-infestation.</p>\n<blockquote>\n<p>D-limonene, a citrus peel extract, is toxic to adult fleas; products with D-limonene plus linalool control both adults and larvae. <strong>DO NOT USE THESE PRODUCTS ON CATS, AS SOME CATS HAVE ADVERSE REACTIONS.</strong> Only use products on pets that are labeled for use on the animal\n<a href=\"http://idl.entomology.cornell.edu/files/2013/11/Fleas-2bc2ok5.pdf\" rel=\"nofollow noreferrer\">source(<em>idl.entomology.cornell.edu</em>)</a></p>\n</blockquote>\n"
}
] |
17,441
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<p>It is said that genes define how we look physically and psychologically; so for example if a male human sperm carries a certain number of genes, say x, and a female carries y, then mathematically there would be m genes from the male and n from the female, and a finite total available. Could there be people identical in appearance if the same genetic combinations recur?</p>
<p>Also we find similar-looking people with perhaps similar behaviour accross diferent geographic locations; does this means that they have similar genetic make-up, up to some percentage?</p>
<p>Please correct my biology and share the possiblity of having genetically identical people across different geographic locations.</p>
|
[
{
"answer_id": 17478,
"pm_score": 3,
"text": "<p>For ease of explanation let me first tell you that the \"genetic makeup\" is called \"genotype\" and that \"how we look physically and psychologically\" is known as \"phenotype\". These are not complete definitions of the terms but this should help you understand what we're talking about. I also apologise for the lack of detail or inaccuracies which many fellow contributors may find aggravating, but the question calls for keeping things down to the most important aspects :)</p>\n\n<p><strong>Do genes define how we look?</strong></p>\n\n<p>Genotype defines <em>to some extent</em> the human phenotype, but we don't know exactly to what extent regarding most aspects of the phenotype. This is called the \"nature vs. nurture\" debate and is concerned with the effects of genotype itself on phenotype vs. the effects of non-genetic influences after fertilisation (such as chemical surroundings during embryonal growth, experiences at young age etc).</p>\n\n<p><strong>Numbers of genes from males and females</strong></p>\n\n<p>Another misunderstanding is that a sperm carries a certain number of genes which it combines with a number of genes from the egg. While this is strictly true, the number isn't what matters because <strong>we all carry the same number of genes</strong> (*). The genotype doesn't depend on the <em>number</em> of genes, but rather, almost all genes exist in several <em>variants</em> within the human population. So the genotype is actually about which variants an individual carries, not about the number of genes. In biology, we use the term \"allele\" to refer to variants in this context. So in other words, each gene can have different alleles.</p>\n\n<p><strong>People with identical appearance</strong> </p>\n\n<p>If two people have identical alleles for all genes (i.e. identical genotype), then they can indeed look almost identical. However, because of the vast number of genes and alleles present in the human population, it is practically impossible for the same alleles to come together in two humans. With only one exception: if two individuals result from the same combination of sperm and egg cell, they will be identical, and this is exactly what happens in monozygotic twins.</p>\n\n<p><strong>Similarities by geographical region</strong></p>\n\n<p>However, the total number of genes and alleles is limited (**). This concept is what people call the \"gene pool\" and is the reason why humans are still always humans and share certain similarities. In particular, for most of human history our geographical movement has been limited (most of the time), creating geographical \"sub-gene pools\" (to keep it simple). This is why people from the same geographical region are more likely to look similar; they have a higher chance to share the same alleles of genes that determine appearance. In terms of behaviour - to whatever degree genotype influences behaviour, peopel from the same geographical region will be more likely to be similar in these regards than people from different geographical regions. However, you can now hopefully understand why this \"degree of similarity\" is next to impossible to quantify (lack of knowledge: which genes determine what, how many alleles exist of them, how many people have which allele, how much and how far do people travel,...).</p>\n\n<hr>\n\n<p>(*) Ok, not quite - it is possible for an individual to have the odd gene actually completely missing, but for the sake of simplicity we all have the same number.</p>\n\n<p>(**) Again, not strictly, because new alleles and possibly even entire genes can result from mutation, but this is relatively rare and on the large scale you can work on the assumption that they are limited in number.</p>\n"
}
] |
[
{
"answer_id": 17475,
"pm_score": 1,
"text": "<blockquote>\n <p>It is said that genes define how we look physically and psychologically</p>\n</blockquote>\n\n<p>I would be skeptical of anyone saying this. Nature vs. nurture is far from settled, especially in psychology. The trend seems to be that many behavioral traits have a large heritable component, but are far from being determined only by heritable traits.</p>\n\n<blockquote>\n <p>if a male human sperm carries a certain number of genes, say x, and a female carries y, then mathematically there would be m genes from the male and n from the female</p>\n</blockquote>\n\n<p>I think you are confused. If a sperm carries $x$ genes and an egg carries $y$ genes, the resulting zygote will have $x+y$ genes. If the male had $m$ and the female had $n$ genes, $x+y\\approx m+n$ and $m \\approx 2x$, $n \\approx 2y$.</p>\n\n<blockquote>\n <p>Could there be people identical in appearance if they end up with identical combinations of genes?</p>\n</blockquote>\n\n<p>Yes, we call these people identical twins. It could also occur by chance in unrelated individuals (well, everyone is somewhat related...) but this is extremely rare. There is just that too much variation in the human genome. There are literally tens of millions of points in the genome where some people have one version and others have another, and this person would have to happen to have the exact same version at each one as you do. This is an order of $10^{-8}$, if we consider humanity completely homogenous (and it isn't, so the probability is even lower).</p>\n\n<blockquote>\n <p>we find similar-looking people with perhaps similar behaviour accross diferent geographic locations; does this means that they have similar genetic make-up, up to some percentage?</p>\n</blockquote>\n\n<p>The genes may be different and still lead to the same phenotype. Say one person has the set of genes that result in red hair, another one has the set that results in brown hair. They are both albinos. They'd look the same, but have different genes.</p>\n\n<p>Also, genes are not the only thing that determines how people look or behave.</p>\n\n<p>So the fact that two people are phenotypically identical does not imply they are genetically identical. You can come up with a Bayesian probability that says they are more likely to have similar genes if they look similar, but how do you calculate the priors? Worse, how are you even going to measure how \"similar\" people look, or behave?</p>\n"
}
] |
17,498
|
<p>I am wondering exactly what a-fib is (causes and symptoms).
<p>
I would really appreciate having a sample of an EKG with it (because in my limited research, I have found it nearly impossible to find just a sample piece of an EKG that has a-fib on it) with your answer, so I can actually get an idea of what it looks like. With the sample EKG, I would love to have a normal one beside it so I can kind of analyze the differences between the two.</p>
<p><strong>Note:</strong> This is not and never was a homework question! </p>
|
[
{
"answer_id": 17555,
"pm_score": 4,
"text": "<p>A human heart can be viewed as 2 hearts, the left and the right heart, each consisting of an atrium and a ventricle. The atrium's function is to fill the ventricle with as much blood as it can and the ventricle then pump the blood away. Also there is a system of valves to control blood flow on each side. Basically this is how our heart works.</p>\n\n<p>Now, to make this system work we need to have a coordinated movement of atrium and ventricle, that is, first atrium is filled, then it pumps blood into ventricle, valve closes and then ventricle compresses. \nThe movement of heart muscle causes currents that can be measured (this is the ECG pronounced EKG). These currents are representative of the movements of atrium and ventricles are expressed respectively as p waves (for atria) and qrs (for ventricles). </p>\n\n<p>It is the case that atria are not very important and sometimes they can stop working properly. They now longer have coherent movement and stop helping to pump blood into the ventricles, but they still move. This event is called atrial fibrillation. </p>\n\n<p>From this explanation one can expect that no longer p waves will be identifiable in the ecg, but instead a random noise overlapping with \"normal\" qrs representing normal ventricular movement. The movement is actually not exactly normal, because the ventricular contraction due to atrial fibrillation now occurs at random times, that is qrs complexes occur with random spaces between them. The explanation for this is rather more complex: there are bundles of specialized cardiomyocites with different frequencies of depolarization. The fastest ones are on SAN and basically guide the whole heart rhythm through specialized bundles. When you have atrial fibrillation, the depolarization signals no longer come from these preferential bundles, but from any part of the atria at random. This causes the ventricles to initiate motion at irregularly spaced intervals.\nI've included a photo of a normal rhythm and a atrial fibrillation side by side, but I hope you can use this explanation to find better ones by yourself in the web.</p>\n\n<p>Note: don't confuse atrial fibrillation with atrial flutter. Flutter is a faster paced regular (therefore organized) atrial movement. It will appear as a saw-tooth shaped wave with regularly spaced qrs complexes.</p>\n\n<p><img src=\"https://i.stack.imgur.com/cUhHR.jpg\" alt=\"a-fib\"></p>\n\n<p>Hope this helps.</p>\n\n<p>Causes of atrial fibrillation are numerous, bur mainly high blood pressure, vascular disease, heart and lung disease among others. It can be asymptomatic in most cases or presenting with the symptoms of its underlying cause.</p>\n\n<p>Please refer to <a href=\"http://www.webmd.com/heart-disease/atrial-fibrillation/heart-disease-atrial-fibrillation-basics\" rel=\"nofollow noreferrer\">http://www.webmd.com/heart-disease/atrial-fibrillation/heart-disease-atrial-fibrillation-basics</a> for a quick overview.</p>\n"
}
] |
[
{
"answer_id": 27565,
"pm_score": 2,
"text": "<p>Remember that except for the concluding pathway through the A-V bundle, the atrial muscle mass is separated from the ventricular muscle mass by fibrous tissue. Therefore, ventricular fibrillation.</p>\n\n<p>The mechanism of atrial fibrillation, except that the process occurs only in atrial muscle mass instead of the ventricular mass. A frequent cause of atrial fibrillation is atrial enlargement resulting from heart valve lesions that prevent the atria from emptying adequately into the ventricles, or from ventricular failure with excess damming of blood in the atria. the dilated atrial walls provide ideal conditions of along conductive pathway as well as slow conduction, both of which predispose to atrial fibrillation.\nFor the same reasons that the ventricle will not pump blood during ventricle fibrillation. Neither do the atria pump blood in atrial fibrillation. therefore, the atria become useless as primer pumps for the ventricles. Even so, blood flow passively through the atria into the ventricles, and the efficiency of ventricular pumping is decreased only 20-30 percent. Therefore, in contrast to the lethality of ventricular fibrillation, a person can live for months or even years with atrial fibrillation, although at reduced efficiency of overall heart pumping.</p>\n\n<p>numerous small depolarization waves spread in all directions through the atria during atrial fibrillation. Because the waves are weak and many of them are opposite polarity at any given time, they usually almost completely electrically neutralize one another. Therefore, in the electrocardiography, one can see either no P waves from the atria or only a fine, high-frequently, very low voltage wavy record. conversely, the QRS-T complexes are normal unless there is some pathology of the ventricles, but their timing is irregular.</p>\n\n<p><img src=\"https://i.stack.imgur.com/seiZX.jpg\" alt=\"enter image description here\"></p>\n\n<p><img src=\"https://i.stack.imgur.com/9nxVD.gif\" alt=\"enter image description here\"></p>\n"
}
] |
17,532
|
<p>The Price equation describes mathematically the evolution of a population of units from one generation to the next. </p>
<blockquote>
<p>$\bar{w}\Delta \bar{z}$ = $Cov (w_i,z_i) $+$ E(w_i\Delta z_i)$</p>
</blockquote>
<p>I would like to know how to actually employ the equation to some data. Perhaps a simple online "walk-through" type guide of the Price equation would help. It should simply show the calculation of the Price equation using numbers from an example population. For example, I'd like to see how the Price equation is applied to the following scenario:</p>
<blockquote>
<p>A population, $P$, of 5 individuals reproduces to produce population
$P'$. </p>
<p>The trait value of the $i^{th}$ individual is $z_{i}$ where $z_1$,
$z_2$ and $z_3$ all = 1 and where $z_4$ and $z_5$ both = 2 and $\bar{z}$ = 1.4. </p>
<p>Absolute fitness is $w_i$ for the $i^{th}$ individual where $w_1$,
$w_2$ and $w_3$ all = 1, and $w_4$ and $w_5$ both = 5. </p>
<p>Relative fitnesses, $\omega_i$, are $\omega_{z=1}$ = 0.077, and $\omega_{z=2}$ = 0.385.</p>
<p>Thus the population $P'$ has $n$ = 13, with 3 individuals where $z$ = 1
and 10 individuals where $z$ = 2 and $\bar{z}'$ = 1.769. </p>
<p>$\Delta z $ is the transmission bias and is equal to 0 in this case
(perfect transmission of the trait score $z$)</p>
<p>The value $\Delta \bar{z}$ = $Cov (w,z)/ \bar{w}$ = ....</p>
</blockquote>
<p>Here's an R script to create the above information:</p>
<pre><code># Define two trait values:
z1 = 1
z2 = 2
# Define two fitness values:
w1 = 1
w2 = 5
# Set number of units possesing each trait in P population:
n1 = 3
n2 = 2
# Create data
df = data.frame(c(rep(z1,n1),rep(z2,n2)),c(rep(w1,n1),rep(w2,n2)))
colnames(df) = c("z","w")
df$omega = df$w / sum(df$w)
n_P = length(df$z)
n_O = sum(df$w)
z_P_bar = mean(df$z)
z_O_bar = sum(df$w*df$z) / sum(df$w)
omega_z1 = mean(df$omega[df$z==z1])
omega_z2 = mean(df$omega[df$z==z2])
# Parental population size:
n_P
# Offspring population size:
n_O
# Parental mean trait:
z_P_bar
# Offspring mean trait:
z_O_bar
# Realtive fitnesses:
omega_z1
omega_z2
</code></pre>
|
[
{
"answer_id": 17560,
"pm_score": 3,
"text": "<p>Here is a simple example using your data in which both terms of the Price equation are needed, since the value of the character for $z_2 $ changes in the second generation. I used your suggested change $z_2'=(9\\cdot 2 + 1\\cdot 3)/10 = 2.1$. </p>\n\n<p>The Price equation or theorem is:\n$$(1)\\hspace{10mm}w\\cdot \\Delta z = \\text{cov}(z_i,w_i) + E(w_i\\Delta z_i) $$</p>\n\n<p>While the idea here is just to give a credible calculation using both terms in the right side of the equation, and while the intuition behind the equation is essentially mathematical (or is it? $^1$), Steven Franks' paper, 'George Price's Contribution to Evolutionary Genetics', J. Theor. Biol. 175 (1995), 373-88, is a good introduction. His characterization of the right side may be the best one can do: </p>\n\n<blockquote>\n <p>\"The two terms may be thought of as changes due to selection and transmission, respectively. The covariance between fitness and character value gives the change in the character caused by differential reproductive success. The expectation term is a fitness weighted measure of the change in character values between ancestor and descendant. The full equation describes both selective changes within a generation and the response to selection...\" p. 376. </p>\n</blockquote>\n\n<p>We work with reference to the following data and will define variables below. </p>\n\n<p>$$\\begin{array}{c | c | c | } n_i & 3 & 2 \\\\ \\hline\nz_i &1 & 2 \\\\ \\hline\nw_i &1& 5 \\\\ \\hline\nn_i' & 3 & 10 \\\\ \\hline \nz_i' & 1 & 2.1 \\\\ \\hline \\end{array}$$</p>\n\n<p>All cites WK are to the Wiki page on the <a href=\"http://en.wikipedia.org/wiki/Price_equation\" rel=\"nofollow\">Price equation</a>: </p>\n\n<hr>\n\n<p><strong>(1) We can write</strong> $\\text{cov} (w_i, z_i)$ as $E(w_iz_i) - wz.\\hspace{10mm}$ WK eq. (7).</p>\n\n<p>Explicitly: </p>\n\n<p>$$ \\text{Cov}(w_i,z_i) = E(w_iz_i)- wz = \\frac{ w_1z_1n_1 + w_2z_2n_2}{n_1+n_2} - wz $$</p>\n\n<p>$$ = \\frac{1\\cdot1\\cdot3 + 5\\cdot2\\cdot2}{3+2} - (2.6)(1.4) =\\frac{23}{5} - (2.6)(1.4)= 0.96$$</p>\n\n<hr>\n\n<p><strong>(2) We can write</strong> $E(w_i\\Delta z_i) = E(w_i z_i') - E(w_i z_i).\\hspace{10mm}$ WK eq. (8).</p>\n\n<p>Now $E(w_i z_i') = \\frac{1}{n}\\sum w_iz_i'n_i\\hspace{40mm} $ WK eq. (9a). </p>\n\n<p>$ = \\frac{1}{2 + 3}(1\\cdot 1\\cdot 3 + 5\\cdot(2.1)\\cdot 2) = 24/5.$</p>\n\n<p>$E(w_iz_i) = 23/5$ from (1) above.</p>\n\n<p>So $ E(w_i z_i') - E(w_i z_i) = \\frac{24}{5} - \\frac{23}{5} = 1/5$</p>\n\n<hr>\n\n<p><strong>(3) Finally</strong> we have $\\Delta z = z' - z = \\frac{2.1(10) + 3(1)}{13}-\\frac{3\\cdot 1+2\\cdot 2}{5} = \\frac{29}{65} $</p>\n\n<p>and $w = \\frac{3\\cdot 1+ 2\\cdot 5}{3+2} = \\frac{13}{5} = 2.6$</p>\n\n<p>So $$w \\Delta z = (2.6) \\frac{29}{65} = 1.16 $$</p>\n\n<p>$$= \\text{cov}(z_i,w_i) + E(w_i \\Delta z_i) = 0.96 + .2 = 1.16 $$</p>\n\n<blockquote>\n <p>$n_i$ is the number of elements in group $i.$ </p>\n \n <p>$n_i'$ is the same for the filial generation.</p>\n \n <p>$z_i$ is the value of a character for group $i.$</p>\n \n <p>$z_i'$ is the same for offspring of $z_i.$</p>\n \n <p>$w_i$ is a fitness weight, often the number of offspring an element $z_i$ will have. </p>\n \n <p>$w$ is the average fitness for the parental generation.</p>\n \n <p>$z$ is the average value of z for parental generation;</p>\n \n <p>$z'$ is the average of z for the filial generation.</p>\n \n <p>$z_2' - z_2$ (for example) is the average value of $z_2$ in the second filial \n generation minus the average of $z_2$ in the parent's generation. </p>\n</blockquote>\n\n<p>$^1$ This <a href=\"http://evolutionandgames.nl/wiki/index.php?title=Price_3.0\" rel=\"nofollow\">site</a> condenses some critical discussion of the Price equation. I have not worked through it yet but it addresses some lingering doubts I have about just what this equation means. Strongly recommended. </p>\n"
}
] |
[
{
"answer_id": 17533,
"pm_score": 2,
"text": "<p>This is a nice numerical walk-through and explanation, see this <a href=\"http://www.tedpavlic.com/post_price_equation.php\" rel=\"nofollow noreferrer\">webpage</a>.</p>\n<p>As requested I've sketched out a solution to the specific case above.</p>\n<p>A nicer way for caclulations is to rewrite the price equation as:</p>\n<p><span class=\"math-container\">$$ \\Delta z = Cov(w_i/\\bar{w}, z_i) +E(w_i/\\bar{w}, \\Delta z_i) $$</span></p>\n<p>So lets draw out some important terms.</p>\n<p>In the current population average for <span class=\"math-container\">$z$</span>, the average trait value in the second generation <span class=\"math-container\">$z'$</span> and, the average relative fitness of the parents <span class=\"math-container\">$\\bar{w}$</span> are:</p>\n<p><span class=\"math-container\">$\\bar{z} = 1.4$</span></p>\n<p><span class=\"math-container\">$z' = 1.769$</span></p>\n<p><span class=\"math-container\">$\\bar{w} = 0.2002$</span></p>\n<p>So we an brute force the <span class=\"math-container\">$\\Delta z$</span> by doing <span class=\"math-container\">$1.769-1.4 = 0.369$</span>. However we shall also show this using the price equation (note for sample data the correction is <span class=\"math-container\">$n-1$</span> not <span class=\"math-container\">$n$</span> as shown below).</p>\n<p><span class=\"math-container\">$Cov(x,y) = ((x_1 - \\bar{x})*(y_2 - \\bar{y})+(x_2 - \\bar{x})*(y_1 - \\bar{y})+ ... (x_n - \\bar{x})*(y_n - \\bar{y}))/n$</span></p>\n<p>Using the data provided we can say:</p>\n<p><span class=\"math-container\">$Cov(w_i/\\bar{w}, z_i)= ((3 * (0.077 - 0.2002)*(1-1.769)) + (2 * (0.385-0.2002)*(2-1.769)))/5 = 0.07392 $</span></p>\n<p>This is a per capita change. <span class=\"math-container\">$0.07392 * 5 = 0.3696$</span> (rounding error).</p>\n<h1>Expectation</h1>\n<p>So the OP identifies a situation where transmission effects are non zero. Lets just consider that the mutation that causes z=2 is a super-synergistic and causes its offspring to be z=4. The expectation term in this case is:</p>\n<p><span class=\"math-container\">$E(w_i/\\bar{w}, \\Delta z_i)= ((w_4/\\bar{w})*(z'_4-z_4) + (w_5/\\bar{w})*(z'_5-z_5)) /5$</span></p>\n<p>I've ignored the first 3 individuals because the transmission effect will make their terms 0 (1-1=0).</p>\n"
}
] |
17,539
|
<p>I fail to see how natural selection can build any kind of new functionality.</p>
<p>New functionality in a design requires sacrificing a complex series of meanwhile useless steps before the new functionality works and becomes advantageous.</p>
<p>For example, if I want to upgrade a stationary chair to a wheelchair, there are many intermediate steps that must be done (which are not advantageous) before the added functionality becomes advantageous.</p>
<p>If a human being sits there and tries to intelligently assemble the wheelchair in such a way that it will be advantageous at each step, he will not be able to do it. it just doesn't work like this.</p>
<p>Can someone fill me in as to how this works and whether there have been experiments that demonstrate this, for example, having someone assemble a simple functional design with the limitation that every few step adds advantageous functionality.</p>
|
[
{
"answer_id": 17560,
"pm_score": 3,
"text": "<p>Here is a simple example using your data in which both terms of the Price equation are needed, since the value of the character for $z_2 $ changes in the second generation. I used your suggested change $z_2'=(9\\cdot 2 + 1\\cdot 3)/10 = 2.1$. </p>\n\n<p>The Price equation or theorem is:\n$$(1)\\hspace{10mm}w\\cdot \\Delta z = \\text{cov}(z_i,w_i) + E(w_i\\Delta z_i) $$</p>\n\n<p>While the idea here is just to give a credible calculation using both terms in the right side of the equation, and while the intuition behind the equation is essentially mathematical (or is it? $^1$), Steven Franks' paper, 'George Price's Contribution to Evolutionary Genetics', J. Theor. Biol. 175 (1995), 373-88, is a good introduction. His characterization of the right side may be the best one can do: </p>\n\n<blockquote>\n <p>\"The two terms may be thought of as changes due to selection and transmission, respectively. The covariance between fitness and character value gives the change in the character caused by differential reproductive success. The expectation term is a fitness weighted measure of the change in character values between ancestor and descendant. The full equation describes both selective changes within a generation and the response to selection...\" p. 376. </p>\n</blockquote>\n\n<p>We work with reference to the following data and will define variables below. </p>\n\n<p>$$\\begin{array}{c | c | c | } n_i & 3 & 2 \\\\ \\hline\nz_i &1 & 2 \\\\ \\hline\nw_i &1& 5 \\\\ \\hline\nn_i' & 3 & 10 \\\\ \\hline \nz_i' & 1 & 2.1 \\\\ \\hline \\end{array}$$</p>\n\n<p>All cites WK are to the Wiki page on the <a href=\"http://en.wikipedia.org/wiki/Price_equation\" rel=\"nofollow\">Price equation</a>: </p>\n\n<hr>\n\n<p><strong>(1) We can write</strong> $\\text{cov} (w_i, z_i)$ as $E(w_iz_i) - wz.\\hspace{10mm}$ WK eq. (7).</p>\n\n<p>Explicitly: </p>\n\n<p>$$ \\text{Cov}(w_i,z_i) = E(w_iz_i)- wz = \\frac{ w_1z_1n_1 + w_2z_2n_2}{n_1+n_2} - wz $$</p>\n\n<p>$$ = \\frac{1\\cdot1\\cdot3 + 5\\cdot2\\cdot2}{3+2} - (2.6)(1.4) =\\frac{23}{5} - (2.6)(1.4)= 0.96$$</p>\n\n<hr>\n\n<p><strong>(2) We can write</strong> $E(w_i\\Delta z_i) = E(w_i z_i') - E(w_i z_i).\\hspace{10mm}$ WK eq. (8).</p>\n\n<p>Now $E(w_i z_i') = \\frac{1}{n}\\sum w_iz_i'n_i\\hspace{40mm} $ WK eq. (9a). </p>\n\n<p>$ = \\frac{1}{2 + 3}(1\\cdot 1\\cdot 3 + 5\\cdot(2.1)\\cdot 2) = 24/5.$</p>\n\n<p>$E(w_iz_i) = 23/5$ from (1) above.</p>\n\n<p>So $ E(w_i z_i') - E(w_i z_i) = \\frac{24}{5} - \\frac{23}{5} = 1/5$</p>\n\n<hr>\n\n<p><strong>(3) Finally</strong> we have $\\Delta z = z' - z = \\frac{2.1(10) + 3(1)}{13}-\\frac{3\\cdot 1+2\\cdot 2}{5} = \\frac{29}{65} $</p>\n\n<p>and $w = \\frac{3\\cdot 1+ 2\\cdot 5}{3+2} = \\frac{13}{5} = 2.6$</p>\n\n<p>So $$w \\Delta z = (2.6) \\frac{29}{65} = 1.16 $$</p>\n\n<p>$$= \\text{cov}(z_i,w_i) + E(w_i \\Delta z_i) = 0.96 + .2 = 1.16 $$</p>\n\n<blockquote>\n <p>$n_i$ is the number of elements in group $i.$ </p>\n \n <p>$n_i'$ is the same for the filial generation.</p>\n \n <p>$z_i$ is the value of a character for group $i.$</p>\n \n <p>$z_i'$ is the same for offspring of $z_i.$</p>\n \n <p>$w_i$ is a fitness weight, often the number of offspring an element $z_i$ will have. </p>\n \n <p>$w$ is the average fitness for the parental generation.</p>\n \n <p>$z$ is the average value of z for parental generation;</p>\n \n <p>$z'$ is the average of z for the filial generation.</p>\n \n <p>$z_2' - z_2$ (for example) is the average value of $z_2$ in the second filial \n generation minus the average of $z_2$ in the parent's generation. </p>\n</blockquote>\n\n<p>$^1$ This <a href=\"http://evolutionandgames.nl/wiki/index.php?title=Price_3.0\" rel=\"nofollow\">site</a> condenses some critical discussion of the Price equation. I have not worked through it yet but it addresses some lingering doubts I have about just what this equation means. Strongly recommended. </p>\n"
}
] |
[
{
"answer_id": 17533,
"pm_score": 2,
"text": "<p>This is a nice numerical walk-through and explanation, see this <a href=\"http://www.tedpavlic.com/post_price_equation.php\" rel=\"nofollow noreferrer\">webpage</a>.</p>\n<p>As requested I've sketched out a solution to the specific case above.</p>\n<p>A nicer way for caclulations is to rewrite the price equation as:</p>\n<p><span class=\"math-container\">$$ \\Delta z = Cov(w_i/\\bar{w}, z_i) +E(w_i/\\bar{w}, \\Delta z_i) $$</span></p>\n<p>So lets draw out some important terms.</p>\n<p>In the current population average for <span class=\"math-container\">$z$</span>, the average trait value in the second generation <span class=\"math-container\">$z'$</span> and, the average relative fitness of the parents <span class=\"math-container\">$\\bar{w}$</span> are:</p>\n<p><span class=\"math-container\">$\\bar{z} = 1.4$</span></p>\n<p><span class=\"math-container\">$z' = 1.769$</span></p>\n<p><span class=\"math-container\">$\\bar{w} = 0.2002$</span></p>\n<p>So we an brute force the <span class=\"math-container\">$\\Delta z$</span> by doing <span class=\"math-container\">$1.769-1.4 = 0.369$</span>. However we shall also show this using the price equation (note for sample data the correction is <span class=\"math-container\">$n-1$</span> not <span class=\"math-container\">$n$</span> as shown below).</p>\n<p><span class=\"math-container\">$Cov(x,y) = ((x_1 - \\bar{x})*(y_2 - \\bar{y})+(x_2 - \\bar{x})*(y_1 - \\bar{y})+ ... (x_n - \\bar{x})*(y_n - \\bar{y}))/n$</span></p>\n<p>Using the data provided we can say:</p>\n<p><span class=\"math-container\">$Cov(w_i/\\bar{w}, z_i)= ((3 * (0.077 - 0.2002)*(1-1.769)) + (2 * (0.385-0.2002)*(2-1.769)))/5 = 0.07392 $</span></p>\n<p>This is a per capita change. <span class=\"math-container\">$0.07392 * 5 = 0.3696$</span> (rounding error).</p>\n<h1>Expectation</h1>\n<p>So the OP identifies a situation where transmission effects are non zero. Lets just consider that the mutation that causes z=2 is a super-synergistic and causes its offspring to be z=4. The expectation term in this case is:</p>\n<p><span class=\"math-container\">$E(w_i/\\bar{w}, \\Delta z_i)= ((w_4/\\bar{w})*(z'_4-z_4) + (w_5/\\bar{w})*(z'_5-z_5)) /5$</span></p>\n<p>I've ignored the first 3 individuals because the transmission effect will make their terms 0 (1-1=0).</p>\n"
}
] |
17,541
|
<p>I'm planning to scale up a PCR reaction, and I'm wondering if filling the PCR tubes to the maximum volume of 200 ul would be a problem. It would mean a lot less pipetting as I would only need 1/4 of the tubes.</p>
<p>The typical protocols I've seen always use 50 ul for a PCR reaction, I'm wondering if there are any issues with larger volumes, e.g. differences in heat transfer, that could cause issues if I scale up the volume in one tube.</p>
<p>Is scaling up the volume problematic? Any specific aspects I should consider?</p>
|
[
{
"answer_id": 17560,
"pm_score": 3,
"text": "<p>Here is a simple example using your data in which both terms of the Price equation are needed, since the value of the character for $z_2 $ changes in the second generation. I used your suggested change $z_2'=(9\\cdot 2 + 1\\cdot 3)/10 = 2.1$. </p>\n\n<p>The Price equation or theorem is:\n$$(1)\\hspace{10mm}w\\cdot \\Delta z = \\text{cov}(z_i,w_i) + E(w_i\\Delta z_i) $$</p>\n\n<p>While the idea here is just to give a credible calculation using both terms in the right side of the equation, and while the intuition behind the equation is essentially mathematical (or is it? $^1$), Steven Franks' paper, 'George Price's Contribution to Evolutionary Genetics', J. Theor. Biol. 175 (1995), 373-88, is a good introduction. His characterization of the right side may be the best one can do: </p>\n\n<blockquote>\n <p>\"The two terms may be thought of as changes due to selection and transmission, respectively. The covariance between fitness and character value gives the change in the character caused by differential reproductive success. The expectation term is a fitness weighted measure of the change in character values between ancestor and descendant. The full equation describes both selective changes within a generation and the response to selection...\" p. 376. </p>\n</blockquote>\n\n<p>We work with reference to the following data and will define variables below. </p>\n\n<p>$$\\begin{array}{c | c | c | } n_i & 3 & 2 \\\\ \\hline\nz_i &1 & 2 \\\\ \\hline\nw_i &1& 5 \\\\ \\hline\nn_i' & 3 & 10 \\\\ \\hline \nz_i' & 1 & 2.1 \\\\ \\hline \\end{array}$$</p>\n\n<p>All cites WK are to the Wiki page on the <a href=\"http://en.wikipedia.org/wiki/Price_equation\" rel=\"nofollow\">Price equation</a>: </p>\n\n<hr>\n\n<p><strong>(1) We can write</strong> $\\text{cov} (w_i, z_i)$ as $E(w_iz_i) - wz.\\hspace{10mm}$ WK eq. (7).</p>\n\n<p>Explicitly: </p>\n\n<p>$$ \\text{Cov}(w_i,z_i) = E(w_iz_i)- wz = \\frac{ w_1z_1n_1 + w_2z_2n_2}{n_1+n_2} - wz $$</p>\n\n<p>$$ = \\frac{1\\cdot1\\cdot3 + 5\\cdot2\\cdot2}{3+2} - (2.6)(1.4) =\\frac{23}{5} - (2.6)(1.4)= 0.96$$</p>\n\n<hr>\n\n<p><strong>(2) We can write</strong> $E(w_i\\Delta z_i) = E(w_i z_i') - E(w_i z_i).\\hspace{10mm}$ WK eq. (8).</p>\n\n<p>Now $E(w_i z_i') = \\frac{1}{n}\\sum w_iz_i'n_i\\hspace{40mm} $ WK eq. (9a). </p>\n\n<p>$ = \\frac{1}{2 + 3}(1\\cdot 1\\cdot 3 + 5\\cdot(2.1)\\cdot 2) = 24/5.$</p>\n\n<p>$E(w_iz_i) = 23/5$ from (1) above.</p>\n\n<p>So $ E(w_i z_i') - E(w_i z_i) = \\frac{24}{5} - \\frac{23}{5} = 1/5$</p>\n\n<hr>\n\n<p><strong>(3) Finally</strong> we have $\\Delta z = z' - z = \\frac{2.1(10) + 3(1)}{13}-\\frac{3\\cdot 1+2\\cdot 2}{5} = \\frac{29}{65} $</p>\n\n<p>and $w = \\frac{3\\cdot 1+ 2\\cdot 5}{3+2} = \\frac{13}{5} = 2.6$</p>\n\n<p>So $$w \\Delta z = (2.6) \\frac{29}{65} = 1.16 $$</p>\n\n<p>$$= \\text{cov}(z_i,w_i) + E(w_i \\Delta z_i) = 0.96 + .2 = 1.16 $$</p>\n\n<blockquote>\n <p>$n_i$ is the number of elements in group $i.$ </p>\n \n <p>$n_i'$ is the same for the filial generation.</p>\n \n <p>$z_i$ is the value of a character for group $i.$</p>\n \n <p>$z_i'$ is the same for offspring of $z_i.$</p>\n \n <p>$w_i$ is a fitness weight, often the number of offspring an element $z_i$ will have. </p>\n \n <p>$w$ is the average fitness for the parental generation.</p>\n \n <p>$z$ is the average value of z for parental generation;</p>\n \n <p>$z'$ is the average of z for the filial generation.</p>\n \n <p>$z_2' - z_2$ (for example) is the average value of $z_2$ in the second filial \n generation minus the average of $z_2$ in the parent's generation. </p>\n</blockquote>\n\n<p>$^1$ This <a href=\"http://evolutionandgames.nl/wiki/index.php?title=Price_3.0\" rel=\"nofollow\">site</a> condenses some critical discussion of the Price equation. I have not worked through it yet but it addresses some lingering doubts I have about just what this equation means. Strongly recommended. </p>\n"
}
] |
[
{
"answer_id": 17533,
"pm_score": 2,
"text": "<p>This is a nice numerical walk-through and explanation, see this <a href=\"http://www.tedpavlic.com/post_price_equation.php\" rel=\"nofollow noreferrer\">webpage</a>.</p>\n<p>As requested I've sketched out a solution to the specific case above.</p>\n<p>A nicer way for caclulations is to rewrite the price equation as:</p>\n<p><span class=\"math-container\">$$ \\Delta z = Cov(w_i/\\bar{w}, z_i) +E(w_i/\\bar{w}, \\Delta z_i) $$</span></p>\n<p>So lets draw out some important terms.</p>\n<p>In the current population average for <span class=\"math-container\">$z$</span>, the average trait value in the second generation <span class=\"math-container\">$z'$</span> and, the average relative fitness of the parents <span class=\"math-container\">$\\bar{w}$</span> are:</p>\n<p><span class=\"math-container\">$\\bar{z} = 1.4$</span></p>\n<p><span class=\"math-container\">$z' = 1.769$</span></p>\n<p><span class=\"math-container\">$\\bar{w} = 0.2002$</span></p>\n<p>So we an brute force the <span class=\"math-container\">$\\Delta z$</span> by doing <span class=\"math-container\">$1.769-1.4 = 0.369$</span>. However we shall also show this using the price equation (note for sample data the correction is <span class=\"math-container\">$n-1$</span> not <span class=\"math-container\">$n$</span> as shown below).</p>\n<p><span class=\"math-container\">$Cov(x,y) = ((x_1 - \\bar{x})*(y_2 - \\bar{y})+(x_2 - \\bar{x})*(y_1 - \\bar{y})+ ... (x_n - \\bar{x})*(y_n - \\bar{y}))/n$</span></p>\n<p>Using the data provided we can say:</p>\n<p><span class=\"math-container\">$Cov(w_i/\\bar{w}, z_i)= ((3 * (0.077 - 0.2002)*(1-1.769)) + (2 * (0.385-0.2002)*(2-1.769)))/5 = 0.07392 $</span></p>\n<p>This is a per capita change. <span class=\"math-container\">$0.07392 * 5 = 0.3696$</span> (rounding error).</p>\n<h1>Expectation</h1>\n<p>So the OP identifies a situation where transmission effects are non zero. Lets just consider that the mutation that causes z=2 is a super-synergistic and causes its offspring to be z=4. The expectation term in this case is:</p>\n<p><span class=\"math-container\">$E(w_i/\\bar{w}, \\Delta z_i)= ((w_4/\\bar{w})*(z'_4-z_4) + (w_5/\\bar{w})*(z'_5-z_5)) /5$</span></p>\n<p>I've ignored the first 3 individuals because the transmission effect will make their terms 0 (1-1=0).</p>\n"
}
] |
17,565
|
<p>I am a bit confused with the notion that "<strong>walking after meals helps you in digestion</strong> ", </p>
<p>Some say that it helps, whereas others oppose it. Can someone come up with a valid explanation for this?</p>
|
[
{
"answer_id": 17566,
"pm_score": 4,
"text": "<p>apparently walking helps in the movement of food into the stomach and improves digestion. Also helps in decreasing blood sugar after meals, which decreases cardiovascular risk and potential signal diabetes by helping muscles absorb glucose in the blood. Here is <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/18392240\">the link</a> to a study done comparing the results of walking after food and after a drink. Also a study <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/19560716\">was conducted</a> where when people with Type 2 diabetes took a 20 minute walk just 15 minutes after eating, their post-meal blood sugar levels were lower than if they had walked before dinner or not walked at all. Here is <a href=\"http://care.diabetesjournals.org/content/early/2013/06/03/dc13-0084.abstract\">the link</a> to another similar study.</p>\n"
}
] |
[
{
"answer_id": 35432,
"pm_score": 2,
"text": "<p>Well it depends what you mean by helping digestion. </p>\n\n<p>This <a href=\"https://skeptics.stackexchange.com/posts/11169/edit\">answer</a> in skeptics may shade some light:</p>\n\n<blockquote>\n <p><b>a walk after my lunch [is] a healthy habit that helps with digestion.</b></p>\n</blockquote>\n\n<p>Walking may be a healthy habit but it does not specifically assist digestion. </p>\n\n<blockquote>\n <p>Digestion is a process which takes place in resting conditions. Exercise is characterised by a shift in blood flow away from the gastrointestinal (GI) tract towards the active muscle and the lungs.</p>\n</blockquote>\n\n<p>From: <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/8460288\" rel=\"nofollow noreferrer\">Is the gut an athletic organ? Digestion, absorption, and exercise. [Sports Med. 1993] - PubMed - NCBI</a></p>\n\n<p>So it's seems walking help sugar level (but this is independent to having eaten just before) but seems to not be beneficial to the digestion (in particular stomach contractions ― nutrient absorption will only start in general two hours after your meal, once the food leave the stomac) </p>\n"
}
] |
17,568
|
<p>To what extent do brains (e.g. of humans) contain <a href="http://en.wikipedia.org/wiki/Recurrent_neural_network">recurrent </a> connections? </p>
<p>I am studying artificial neuronal networks and frequently encountered the statement, that recurrent neural networks are closer to biological neuronal networks than for example <a href="http://en.wikipedia.org/wiki/Feedforward_neural_networks">feed forward networks</a>. But I didn't find information on the question if feed forward or recurrent architectures dominate the brain architecture.</p>
|
[
{
"answer_id": 17569,
"pm_score": 4,
"text": "<p>The recurrent patterns of connections in a network are known as network motifs.</p>\n\n<p>You can check <a href=\"http://www.sciencemag.org/content/298/5594/824.full\">this</a> paper out. They have identified common network motifs in different types of real networks including neural networks (of C.elegans though). </p>\n\n<p>Apart from feed forward loops, bi-fan is also a common network motif in neural networks.</p>\n\n<p>Perhaps the <a href=\"http://www.humanconnectomeproject.org/\">connectome project</a> has data for human brain which you can analyze for identifying network motifs. You would have to request for the data, though.</p>\n"
}
] |
[
{
"answer_id": 20766,
"pm_score": 2,
"text": "<p>Ok, let's talk about mammalian neocortex rather than about the entire central nervous system.</p>\n\n<p>The vast majority of synapses within the cortex are formed between neurons within the same cortical area (<a href=\"http://dx.doi.org/10.1523/JNEUROSCI.1400-04.2004\" rel=\"nofollow\">Binzegger et al 2004</a>). Although most of these synapses will not be self-connections (from a single neuron back to itself), they are <em>recurrent</em> in the sense that there is a high degree of interconnectivity within a cortical area. In visual cortex, connections within the superficial layers of cortex (layer 2/3 <-> layer 2/3) make up around <strong>70% of all</strong> excitatory synapses in visual cortex!</p>\n\n<p>In contrast, the \"feed-forward\" pathway into visual cortex makes up <strong>less than 1%</strong> of the excitatory synapses in visual cortex (<a href=\"http://dx.doi.org/10.1002/cne.22133\" rel=\"nofollow\">Costa & Martin 2011</a>).</p>\n\n<p>If you change your scope to look only at inter-cortical-regional projections, then there is comparatively less recurrence (i.e. strong bi-directional connections between two cortical areas), although it still exists. Connections between cortical areas seem to be correlated with physical distance across the cortex (<a href=\"http://dx.doi.org/10.1177/1073858404268478\" rel=\"nofollow\">Vezoli et al. 2004</a>). Connections between adjacent areas (V1 and V2, for example) are strong in both directions, and appear to project to similar cortical laminae in both directions. In contrast, projections over longer distances are comparatively weaker, and target different cortical laminae in either direction.</p>\n"
}
] |
17,591
|
<p>If the squamous (top) layer of epidermis, or skin, is burned or damaged in another way, will it then be replaced by the next layer of below?</p>
<p>Also, from where does the basal membrane originate? Does it regenerate from a different layer of cells? </p>
|
[
{
"answer_id": 17654,
"pm_score": 3,
"text": "<p>The epidermis is a four- or five-layered epithelium. The top layers are squamous whereas the bottom ones are more columnar (<a href=\"http://en.wikipedia.org/wiki/Epidermis_(skin)\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/wiki/Epidermis_(skin)</a>). The lowest layer is separated from the dermis by the basal membrane (a.k.a. basal lamina, basement membrane).</p>\n\n<p>The process of wound healing in skin is extremely complex and obviously depends on the individual wound and how many layers are destroyed. There is a lot of detail on Wikipedia: <a href=\"http://en.wikipedia.org/wiki/Wound_healing\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/wiki/Wound_healing</a>.</p>\n\n<p>If the basement membrane is not disrupted, there are two main components as a rule of thumb: 1) outwards-inwards migration, i.e. cells surrounding a wound will migrate into the wound. 2) bottom-upwards differentiation, i.e. the bottom-most layer contains replicating cells which will differentiate and squamify to regenerate upper layers.</p>\n\n<p>Something like this (picture modified from Wikipedia): <img src=\"https://i.stack.imgur.com/Xvd2W.jpg\" alt=\"enter image description here\"></p>\n\n<p>If the wound is bleeding, this means the basement membrane is disrupted and the dermis underneath is also wounded (the epidermis itself contains no blood vessels). In this case, the dermis needs to regenerate first, in a process which is probably similar as described above. Simultaneously, the bottom-most epidermal cell layer will proliferate to close the gap, and then deposit new basement membrane. Remember that the basement membrane is a mesh of proteins, not an actual cell layer.</p>\n"
}
] |
[
{
"answer_id": 17655,
"pm_score": 2,
"text": "<p>It would first be good to look at the <a href=\"http://www.webmd.com/skin-problems-and-treatments/picture-of-the-skin\" rel=\"nofollow noreferrer\">different layers within the skin </a> as you mentioned in your question. </p>\n\n<blockquote>\n <p>The skin is made up of:</p>\n \n <ul>\n <li>Epidermis: the outermost layer of skin, provides a waterproof barrier and creates our skin tone</li>\n <li>Dermis: beneath the epidermis, contains tough connective tissue, hair follicles, and sweat glands</li>\n <li>Hypodermis: deeper subcutaneous tissue is made of fat and connective tissue</li>\n </ul>\n</blockquote>\n\n<p><img src=\"https://i.stack.imgur.com/WUs0I.jpg\" alt=\"enter image description here\"></p>\n\n<p>Different kinds of damage can occur to the skin, including <strong>burns</strong>, which have different degrees based on what layer of skin is damaged and how far down the burn goes. Therefore, it is <a href=\"https://umm.edu/health/medical/altmed/condition/burns\" rel=\"nofollow noreferrer\">not as simple as</a> the epidermis itself getting burned, it could also be much worse and the healing process may be hindered if too much damage occurs.</p>\n\n<blockquote>\n <p>Burns can happen when the skin is exposed to heat (from fire or hot liquids), electricity, corrosive chemicals, or radiation (UV rays from the sun or tanning beds, or radiation treatments). </p>\n \n <p>Burns are classified as follows, according to the severity of tissue damage:</p>\n \n <ul>\n <li>First degree burns: affect only the outer layer of the skin (epidermis), causing pain and redness. The prototype is mild sunburn</li>\n <li>Second degree burns: extend to the second layer of the skin (the dermis), causing pain, redness, and blisters that may ooze; deep second degree burns may progress to third degree burns over the course of several days</li>\n <li>Third degree burns: involve both layers of the skin and may also damage the underlying bones, muscles, and tendons; the burn site appears pale, charred, or leathery; there is generally no pain in the area because the nerve endings are destroyed.</li>\n <li>Fourth degree burns: extend through the skin and subcutaneous fat into the underlying muscle and bone; are stiff and charred</li>\n </ul>\n</blockquote>\n\n<p>Depending on the type of burn, different skin generation occurs. If it is a really terrible burn, then a <strong>skin graft</strong> from another area of the body may be needed, as it <a href=\"http://faculty.stcc.edu/AandP/AP/AP1pages/Units1to4/skin/repairof.htm\" rel=\"nofollow noreferrer\">cannot regenerate the epidermis layer</a> due to the excessive damage.</p>\n\n<blockquote>\n <p>First degree burns are the easiest from which to recover [...] the dermis remains intact and can support the regeneration of the epidermis. It may happen that the skin will get inflamed (due to responses in the underlying dermis) during this time; the inflammation is to encourage clean-up cells (macrophages) and nutrients to reach the damaged area.</p>\n</blockquote>\n\n<p>It appears as though the dermis itself will help with the regeneration of the epidermal cells.</p>\n\n<blockquote>\n <p>In a second degree burn, the dermis is also affected, at least partially. But, with a second-degree burn, most (or at least some) skin accessory organs typically remain in tact. Remember, these accessory organs (like glands and hairs) are built from invaginations of the epidermis, creating the epithelium of the glands or hair follicles. If these organs survive the burn, the epithelial cells that remain will begin to divide to regenerate a new epidermis.</p>\n \n <p>Third-degree burns are the worst. In these, even the accessory organs are destroyed. How can we recover from this? Skin grafts are about the best way, but they cannot really be done across one's entire body, so a very widespread third-degree burn is not usually something that a person can recover from.</p>\n</blockquote>\n\n<p><strong>AND</strong> although this is a separate question and topic, the basal membrane is thought to be of epithelial origin, but this is very complex and still not completely known. There is more information about it in <a href=\"http://onlinelibrary.wiley.com/doi/10.1002/aja.1001970404/pdf\" rel=\"nofollow noreferrer\">this article</a>; <em>Cellular origin of the dermal-epidermal basement membrane</em> (Marinkovich et al. 1993). It is a dated article but has some interesting information.</p>\n"
}
] |
17,597
|
<p>Quoting from : Scientific American July 1975 <em>The Manipulation of genes</em> by Stanley Cohen :</p>
<blockquote>
<p>Restriction endonucleases (and modification methylases) are widespread
in microorganisms; genes for <strong>making</strong> them were found on <strong>viral
chromosomes</strong> and extrachromosomal plasmid DNA as well as on many
bacterial chromosomes.</p>
</blockquote>
<p>Why would the genes for making RE be found on viral chromosomes ? Also, could you give some examples where they are found on plasmids ?</p>
|
[
{
"answer_id": 17654,
"pm_score": 3,
"text": "<p>The epidermis is a four- or five-layered epithelium. The top layers are squamous whereas the bottom ones are more columnar (<a href=\"http://en.wikipedia.org/wiki/Epidermis_(skin)\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/wiki/Epidermis_(skin)</a>). The lowest layer is separated from the dermis by the basal membrane (a.k.a. basal lamina, basement membrane).</p>\n\n<p>The process of wound healing in skin is extremely complex and obviously depends on the individual wound and how many layers are destroyed. There is a lot of detail on Wikipedia: <a href=\"http://en.wikipedia.org/wiki/Wound_healing\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/wiki/Wound_healing</a>.</p>\n\n<p>If the basement membrane is not disrupted, there are two main components as a rule of thumb: 1) outwards-inwards migration, i.e. cells surrounding a wound will migrate into the wound. 2) bottom-upwards differentiation, i.e. the bottom-most layer contains replicating cells which will differentiate and squamify to regenerate upper layers.</p>\n\n<p>Something like this (picture modified from Wikipedia): <img src=\"https://i.stack.imgur.com/Xvd2W.jpg\" alt=\"enter image description here\"></p>\n\n<p>If the wound is bleeding, this means the basement membrane is disrupted and the dermis underneath is also wounded (the epidermis itself contains no blood vessels). In this case, the dermis needs to regenerate first, in a process which is probably similar as described above. Simultaneously, the bottom-most epidermal cell layer will proliferate to close the gap, and then deposit new basement membrane. Remember that the basement membrane is a mesh of proteins, not an actual cell layer.</p>\n"
}
] |
[
{
"answer_id": 17655,
"pm_score": 2,
"text": "<p>It would first be good to look at the <a href=\"http://www.webmd.com/skin-problems-and-treatments/picture-of-the-skin\" rel=\"nofollow noreferrer\">different layers within the skin </a> as you mentioned in your question. </p>\n\n<blockquote>\n <p>The skin is made up of:</p>\n \n <ul>\n <li>Epidermis: the outermost layer of skin, provides a waterproof barrier and creates our skin tone</li>\n <li>Dermis: beneath the epidermis, contains tough connective tissue, hair follicles, and sweat glands</li>\n <li>Hypodermis: deeper subcutaneous tissue is made of fat and connective tissue</li>\n </ul>\n</blockquote>\n\n<p><img src=\"https://i.stack.imgur.com/WUs0I.jpg\" alt=\"enter image description here\"></p>\n\n<p>Different kinds of damage can occur to the skin, including <strong>burns</strong>, which have different degrees based on what layer of skin is damaged and how far down the burn goes. Therefore, it is <a href=\"https://umm.edu/health/medical/altmed/condition/burns\" rel=\"nofollow noreferrer\">not as simple as</a> the epidermis itself getting burned, it could also be much worse and the healing process may be hindered if too much damage occurs.</p>\n\n<blockquote>\n <p>Burns can happen when the skin is exposed to heat (from fire or hot liquids), electricity, corrosive chemicals, or radiation (UV rays from the sun or tanning beds, or radiation treatments). </p>\n \n <p>Burns are classified as follows, according to the severity of tissue damage:</p>\n \n <ul>\n <li>First degree burns: affect only the outer layer of the skin (epidermis), causing pain and redness. The prototype is mild sunburn</li>\n <li>Second degree burns: extend to the second layer of the skin (the dermis), causing pain, redness, and blisters that may ooze; deep second degree burns may progress to third degree burns over the course of several days</li>\n <li>Third degree burns: involve both layers of the skin and may also damage the underlying bones, muscles, and tendons; the burn site appears pale, charred, or leathery; there is generally no pain in the area because the nerve endings are destroyed.</li>\n <li>Fourth degree burns: extend through the skin and subcutaneous fat into the underlying muscle and bone; are stiff and charred</li>\n </ul>\n</blockquote>\n\n<p>Depending on the type of burn, different skin generation occurs. If it is a really terrible burn, then a <strong>skin graft</strong> from another area of the body may be needed, as it <a href=\"http://faculty.stcc.edu/AandP/AP/AP1pages/Units1to4/skin/repairof.htm\" rel=\"nofollow noreferrer\">cannot regenerate the epidermis layer</a> due to the excessive damage.</p>\n\n<blockquote>\n <p>First degree burns are the easiest from which to recover [...] the dermis remains intact and can support the regeneration of the epidermis. It may happen that the skin will get inflamed (due to responses in the underlying dermis) during this time; the inflammation is to encourage clean-up cells (macrophages) and nutrients to reach the damaged area.</p>\n</blockquote>\n\n<p>It appears as though the dermis itself will help with the regeneration of the epidermal cells.</p>\n\n<blockquote>\n <p>In a second degree burn, the dermis is also affected, at least partially. But, with a second-degree burn, most (or at least some) skin accessory organs typically remain in tact. Remember, these accessory organs (like glands and hairs) are built from invaginations of the epidermis, creating the epithelium of the glands or hair follicles. If these organs survive the burn, the epithelial cells that remain will begin to divide to regenerate a new epidermis.</p>\n \n <p>Third-degree burns are the worst. In these, even the accessory organs are destroyed. How can we recover from this? Skin grafts are about the best way, but they cannot really be done across one's entire body, so a very widespread third-degree burn is not usually something that a person can recover from.</p>\n</blockquote>\n\n<p><strong>AND</strong> although this is a separate question and topic, the basal membrane is thought to be of epithelial origin, but this is very complex and still not completely known. There is more information about it in <a href=\"http://onlinelibrary.wiley.com/doi/10.1002/aja.1001970404/pdf\" rel=\"nofollow noreferrer\">this article</a>; <em>Cellular origin of the dermal-epidermal basement membrane</em> (Marinkovich et al. 1993). It is a dated article but has some interesting information.</p>\n"
}
] |
17,599
|
<p>I'd appreciate some help identifying these three corvids I photographed in Austria during the Summer:</p>
<p><a href="https://i.stack.imgur.com/AIyuO.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/AIyuO.jpg" alt="corvids"></a></p>
<p>I know identifying corvids can be difficult and I'm not an ornithologist -- just an amateur bird watcher. After looking through many images of various crow species and their hybrids, I've tentatively identified these as:</p>
<ol>
<li>Carrion crow (<em>Corvus corone</em>)</li>
<li>Carrion crow × Hooded crow (<em>Corvus corone × Corvus cornix</em>)</li>
<li>Carrion crow × Hooded crow (<em>Corvus corone × Corvus cornix</em>)<br>
I initially believed this to be a Hooded crow (<em>Corvus cornix</em>), but the broken coloration on the wings made me think it might actually be a hybrid as well.</li>
</ol>
<p>Can someone here either confirm my identification or provide a more informed identification?</p>
|
[
{
"answer_id": 60503,
"pm_score": 4,
"text": "<h1>1. <strong>Carrion crow</strong> (<a href=\"https://en.wikipedia.org/wiki/Carrion_crow\" rel=\"noreferrer\"><em><strong>Corvus corone</strong></em></a>)</h1>\n<p><a href=\"https://i.stack.imgur.com/fl9tJm.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/fl9tJm.jpg\" alt=\"enter image description here\" /></a></p>\n<blockquote>\n<p>The plumage of carrion crow is black with a green or purple sheen, much greener than the gloss of the rook. The bill, legs and feet are also black. It can be distinguished from the common raven by its size (48–52 cm or 19 to 20 inches in length as compared to an average of 63 centimetres (25 inches) for ravens) and from the hooded crow by its black plumage</p>\n</blockquote>\n<h1>3. <strong>Hooded crow</strong> (<a href=\"https://en.wikipedia.org/wiki/Hooded_crow\" rel=\"noreferrer\"><em><strong>Corvus cornix</strong></em></a>)</h1>\n<p><a href=\"https://i.stack.imgur.com/Umr0nm.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/Umr0nm.jpg\" alt=\"enter image description here\" /></a></p>\n<blockquote>\n<p>ashy grey bird with black head, throat, wings, tail, and thigh feathers, as well as a black bill, eyes, and feet.</p>\n</blockquote>\n<h1>2. This one is a bit more difficult, but I think it is also a hooded crow or possibly a hybrid Carrion crow × Hooded crow (<em>Corvus corone × Corvus cornix</em>).</h1>\n<p><a href=\"https://i.stack.imgur.com/ZYn1wm.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/ZYn1wm.jpg\" alt=\"enter image description here\" /></a></p>\n<p><sup> <a href=\"http://www.surfbirds.com/gallery/search2.php?species=Hooded%20Crow&photographer=&location=&country=&start=21\" rel=\"noreferrer\">Hybrid</a> </sup></p>\n<p>At first glance, #2 looked somewhat like a Western jackdaw (<a href=\"https://en.wikipedia.org/wiki/Western_jackdaw\" rel=\"noreferrer\"><em>Corvus monedula</em></a>) because the grey feathers travel fairly high up on its neck and because the bird appears to be somewhat smaller.</p>\n<blockquote>\n<p>Measuring 34–39 centimetres (13–15 in) in length, the western jackdaw is the second smallest member of the genus Corvus...<strong>The cheeks, nape and neck are light grey to greyish-silver, and the underparts are slate-grey</strong>. The legs are black, as is the short stout bill.</p>\n</blockquote>\n<p>However, <em>C. monedula</em> has fairly conspicuous grey eyes and its feathers travel up the neck/head almost as far superiorly/anteriorly as the eyes. Neither appear to be the case in your specimen.</p>\n<p><a href=\"https://i.stack.imgur.com/iSYt3.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/iSYt3.jpg\" alt=\"enter image description here\" /></a></p>\n<p>All three species are common in Europe.</p>\n"
}
] |
[
{
"answer_id": 21355,
"pm_score": 3,
"text": "<p>The first 2 are correct.\nThe third one is actually a hooded crow. The different color of the wing depends on the generation of feathers. Feathers of different generations (changed during different time) are abraded (used) in a different way. The wing feathers of this guy are older than the rest.</p>\n\n<p>Cheers and good luck birding :)</p>\n"
}
] |
17,629
|
<p>For maggot therapy, how are maggots disinfected? I'd imagine there's a limited scope of measurements that can be taken to sterilize the maggots - i.e. we don't want to sterilize them and kill them too. </p>
|
[
{
"answer_id": 17793,
"pm_score": 5,
"text": "<p><strong>History</strong></p>\n<p><a href=\"http://en.wikipedia.org/wiki/Ambroise_Par%C3%A9\" rel=\"noreferrer\">Ambroise Paré</a> is credited with being the first to note his observations on <a href=\"http://en.wikipedia.org/wiki/Maggot_therapy\" rel=\"noreferrer\">Maggot Debridement Therapy</a> (MDT) in the 1500 though it is a technology that has been used for centuries (<a href=\"http://medent.usyd.edu.au/projects/maggott.htm\" rel=\"noreferrer\">reference</a>). It wasn't until the 1920's that therapeutic experimentation with maggots was instigated by William Baer, a clinical professor in orthopaedic surgery at the Johns Hopkins University in Baltimore, Maryland, whose unorthodox methods were successful in the treatment of osteomyelitis and pyogenic wounds. He is also considered the father of modern MDT since he was the first to devise a way to sterilize maggots (<a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3048269/\" rel=\"noreferrer\">reference</a>).</p>\n<p><strong>Procedure</strong></p>\n<p>In addition to removing necrotic tissue from the wound (a procedure known as debridement) maggots have also been proven to disinfect wounds, promote healing, and inhibit a pesky substance known as biofilm from forming on the wound bed. Maggots are nature’s cleansers, showing up to remove dead tissue and promote healing (<a href=\"http://www.thewca.com/blog/201401/%E2%80%9Coh-maggot-where-art-thou%E2%80%9D-quick-history-and-update-maggot-therapy\" rel=\"noreferrer\">reference</a>).</p>\n<p>Currently <em>Lucilia sericata</em>, or the greenbottle blowfly larvae is preferred for MDT because</p>\n<blockquote>\n<p>Firstly, larvae have been shown to debride wounds with extremely low\nprobability of <a href=\"http://en.wikipedia.org/wiki/Myiasis\" rel=\"noreferrer\">myiasis</a> upon clinical application. Larval secretions\nhave been shown to help in tissue regeneration. <em>L. sericata</em> have also\nbeen shown to lower bacteremia levels in patients infected with <a href=\"http://en.wikipedia.org/wiki/Methicillin-resistant_Staphylococcus_aureus\" rel=\"noreferrer\">MRSA</a> (<a href=\"http://en.wikipedia.org/wiki/Common_green_bottle_fly#Medical_importance\" rel=\"noreferrer\">reference</a>).</p>\n</blockquote>\n<p><strong>Sterilizing maggots</strong></p>\n<p>In early applications, sterilizing the larvae was a major problem. Doctors had to first bathe the eggs in bleach and then soak them in mercuric chloride or formaldehyde. The bandages, gaudy and cumbersome for the patients, were held in place with either surgical tape or Unna’s paste—made of zinc oxide, gelatin, glycerine, and water. Other problems that doctors faced included the maggots escaping during the application process and the leakage of toxic waste secreted by the maggots into the wound, which led to infections such as tetanus. Today, commercial and research laboratories produce sterile larvae. And instead of the bulky gauze bandage, a form-fitting cast with a nylon net to corral the larvae is placed over the wound. An absorbent pad put on top of the netting soaks up the larvae’s toxic waste products. The number of larvae used has also changed. Early prescriptions ranged from 5–6 maggots for a fingertip injury to 500–600 for a more serious wound. Today, the scientific standard of 10 larvae/cm<sup>2</sup> is used (<a href=\"http://pubs.acs.org/subscribe/archive/mdd/v04/i10/html/10health.html\" rel=\"noreferrer\">reference</a>).</p>\n<p>William Baer proposed a method to produce sterilized maggots and it is understood that sterilization has to start from the egg stage in itself (<a href=\"http://jbjs.org/content/16/3/572\" rel=\"noreferrer\">reference</a>). The sterilization solution that he proposed was.</p>\n<blockquote>\n<p>Stock Solution of bichloride of mercury, strength one in 1,000 parts.\nStock Solution of fifty per cent. ethyl alcohol. Take equal volume of\neach Solution, mix, and add one-half of one per cent. chemically pure\nhydrochloric acid. The final Solution will contain bichloride of\nmercury, strength one in 2,000 parts, twenty-five per cent. alcohol,\nand one-half of one per cent. hydrochloric acid.</p>\n</blockquote>\n<p>He did not sterilize the maggots as such but took care to feed it sterile food. His work can be read <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3048276/\" rel=\"noreferrer\">here</a>. Another solution used for sterilization was 5 per cent solution of formalin plus 1 per cent sodium hydroxide (<a href=\"http://www.sciencedirect.com/science/article/pii/S0002961034901471\" rel=\"noreferrer\">reference</a>). Sterilization of maggot larvae in itself was found to be hard with some success being reported (<a href=\"http://www.sciencedirect.com/science/article/pii/S0002961033904614\" rel=\"noreferrer\">reference</a>). Current maggot sterilization techniques include.</p>\n<blockquote>\n<p>UV Sterilization</p>\n<p>Rapid washer sterilization</p>\n<p>Egg to maggot sterilization (<a href=\"http://www.researchgate.net/publication/259438977_Development_of_sterilizing_techniques_for_the_production_of_sterile_maggots_used_in_therapy_of_intractable_wounds\" rel=\"noreferrer\">reference</a>)</p>\n</blockquote>\n<p>There is no first generation that has been detailed as such. Mostly sterilization starts from the egg stage. As far as bacteria in the gut is concerned, if sterilization is carried out well, it has been found that there is a significant decrease in any harmful bacteria present (<a href=\"http://www.bioone.org/doi/abs/10.1603/0022-2585-38.2.161\" rel=\"noreferrer\">reference</a>). Most details of sterilizing maggot larvae is given in <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/16883286\" rel=\"noreferrer\">this paper</a>. Consider reading <a href=\"http://www.hkmj.org/article_pdfs/hkm0710p382.pdf\" rel=\"noreferrer\">this paper</a> as well.</p>\n"
}
] |
[
{
"answer_id": 17792,
"pm_score": 3,
"text": "<p>There is an interesting and authoritative paper on rearing of larvae of blue bottle flies for debridement purposes, cited below. </p>\n\n<blockquote>\n <p>Essentially the eggs are disinfected (rinsed) using .25 % chloramine solution (NH2Cl), then the larvae are hatched and reared in aseptic conditions and fed sterilized food. There are some additional controls after initial disinfection (eggs are placed in agar and the resulting growth is compared to non-disinfected eggs). The procedure is detailed on page 127-128.</p>\n</blockquote>\n\n<p>Whether the eggs are perfectly germ-free may be somewhat moot. Historically this was done without disinfecting the eggs (or anything else). Secondary infections were probably not uncommon but the advantages of the technique far outweighed the disadvantages until the advent of antibiotics. Apparently these things are great at debridement of wounds (but shouldn't be used too close to organs or blood vessels). </p>\n\n<p><em>See</em> Wolff and Hansson, Rearing Larvae of <em>Lucilia sericata</em> for Chronic Ulcer Treatment--An Improved Method, Acta Derm. Venereol. (2005) 85: 126-131. </p>\n"
}
] |
17,631
|
<p>I have been wondering why would insects in general, not be scared when important changes happen on your monitor where they have landed...</p>
<p>If you move even just a finger, they are <em>scared to death</em> and fly away, but anything on my monitor and they remain completely placid.</p>
|
[
{
"answer_id": 28251,
"pm_score": 5,
"text": "<p>Flies see motion. When the monitor screen changes, the visible spectrum of the pixel is changing and nothing is moving.</p>\n\n<blockquote>\n <p>Flies have limited color vision. Each color has its own wave frequency, but flies have only two kinds of color receptor cells. This means they have trouble distinguishing between colors, for instance discerning between yellow and white. Insects cannot see the color red, which is the lowest color frequency humans can see. However, houseflies have the ability to see polarized light, but humans cannot differentiate between polarized and unpolarized light. Polarized light is light in which the waves travel only in one plane. <a href=\"http://animals.pawnation.com/flies-see-out-compound-eye-5361.html\">[1]</a></p>\n</blockquote>\n\n<p>Monitors have polarized film on them so you could test the color hypothesis by taking an old monitor you are willing to sacrifice and removing the polarized film. Then you could test if the flies jump when the screen changes. See <a href=\"http://www.instructables.com/id/Privacy-monitor-made-from-an-old-LCD-Monitor/\">here</a> for removing the polarized film on the monitor, or if you have access, this article on <a href=\"http://link.springer.com/article/10.1007/BF00189764#page-1\">A behavioural study of polarization vision in the fly, Musca domestica</a> may hold the answer without needing to ruining a monitor.</p>\n"
}
] |
[
{
"answer_id": 50671,
"pm_score": 1,
"text": "<p>Flies monitor the space above them:</p>\n\n<p>Flies have a very strong innervation of the back of the head, which contacts the surface ( <a href=\"http://flybase.org/reports/FBim0000875.html\" rel=\"nofollow\">http://flybase.org/reports/FBim0000875.html</a> ). While working in a fly lab, which studied behavior, I was told that these nerves sense changes in the light intensity above a fly - and it is this \"third eye\", which usually triggers the escape response of flies.</p>\n"
}
] |
17,741
|
<p>Wikipedia says Caliciviridae Family.
My notes say that Norovirus includes the following</p>
<p>Noroviruses</p>
<ul>
<li>Norwalk-like viruses</li>
<li>Caliciviruses</li>
<li>Astroviruses and some small gastroenteroviruses</li>
</ul>
<p>which is a larger definition including at least two families than the Wikipedia definition.
I think </p>
<ul>
<li>Caliciviruses $\subset$ Caliciviridae </li>
<li>Astroviruses and some small gastroenteroviruses $\subset$ astroviridae</li>
</ul>
<p>so the note is taking subsets among different families and classifying them into abstract class called <strong>Noroviruses</strong>.</p>
<p><strong>Extension based by Chris' excellent <a href="https://biology.stackexchange.com/a/17744/86">answer</a>.</strong></p>
<p>Criteria of Noroviruses</p>
<ul>
<li>(+)sense ssRNA viruses</li>
<li>Structure and replication:
<ul>
<li>1) only (+)sense ssRNA, </li>
<li>2) simple nucleocapsid viruses, </li>
<li>3) only viruses transmitted by fecal-oral route, </li>
<li>4) size about 30 nm in diameter. </li>
</ul></li>
</ul>
<p>and then final classification of Noroviruses by these criteria</p>
<p>Noroviruses</p>
<ul>
<li><strong>Noroviruses</strong> $\subset$ Norwalk-like viruses ($\subset$ F. Caliciviruses)</li>
<li>Some Astroviruses ($\subset$ F. astroviridae) and some small gastroenteroviruses (what?)</li>
</ul>
<p>which, however, does not make sense since Caliciviridae $\not\subset$ Astroviridae.
I do not understand what is the point of referring to the viruses by the sentence</p>
<blockquote>
<p>Astroviruses and some other round/small gastroenteris viruses</p>
</blockquote>
<p>which are not part of Astroviridae.</p>
<p><strong>Which viruses of Caliciviridae are similar to <em>Astroviruses that are apparently round and small gastroenteritis viruses</em>?</strong></p>
|
[
{
"answer_id": 17744,
"pm_score": 4,
"text": "<p>You are mixing different things here: Virus are grouped based on their genetic material (dsDNA, ssDNA ssRNA and so on) into several groups (see <a href=\"http://en.wikipedia.org/wiki/Virus_classification\">here</a> for details), then grouped into families, subgrouped into a genus and then into species. </p>\n\n<p>So it is: Group > Family > Genus > Species.</p>\n\n<p>What you have here are are different positions in this classification.\nThe names you mention belong all to the same tree:</p>\n\n<p>Group: IV (<a href=\"http://en.wikipedia.org/wiki/Positive-sense_ssRNA_virus#Group_IV.E2.80.94positive-sense_ssRNA_viruses\">(+)ssRNA-Viruses</a>) > Family (<a href=\"http://en.wikipedia.org/wiki/Caliciviridae\">Caliciviridae</a>) > Genus (<a href=\"http://en.wikipedia.org/wiki/Norovirus\">Norovirus</a>) > Species (<a href=\"http://en.wikipedia.org/wiki/Norwalk_virus\">Norwalk Virus</a>).</p>\n\n<p>The <a href=\"http://en.wikipedia.org/wiki/Astrovirus\">Astrovirus</a> belongs into the same group, but then form an own family.\nTo answer your question: No, since the Norovirus forms its own genus in the caliciviridae family.</p>\n"
}
] |
[
{
"answer_id": 17752,
"pm_score": 1,
"text": "<p>I take <a href=\"http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi\" rel=\"nofollow\">NCBI's taxonomy</a> any day over what wikipedia says. According to NCBI Caliciviridae includes Lagovirus, Nebovirus, Norovirus, Recovirus, Sapovirus, Vesivirus, Secalivirus, etc. For example:</p>\n\n<p>Viruses; ssRNA viruses; ssRNA positive-strand viruses, no DNA stage; Caliciviridae; Norovirus; Norwalk virus; Chiba virus</p>\n\n<p>Anyway, due to the absence of universal phylogenetic marker genes, viral taxonomy is mostly based on capsid shape and isn't thus very accurate..</p>\n"
}
] |
17,742
|
<p>Digesting (trypsin or whatever other proteolytic enzyme) proteins generates multiple peptides so the degree of complexity of the sample, at the peptide level, increases a lot. In addition there is the problem of infering the original protein from its constituent peptides.
Why is this digestion step needed when you have to go back to protein level ? Is it just technological limitation? </p>
|
[
{
"answer_id": 19139,
"pm_score": 1,
"text": "<p>I found the answer to my own question\nIt was formulated in a Nature publication by Mathias Mann (Title: The ABC's (and XYZ's) of peptide sequencing), a pope in Proteomics:</p>\n<blockquote>\n<p>Why are peptides, and not proteins, sequenced?</p>\n<p>After protein purification, the first step is to convert proteins to a\nset of peptides using a sequence-specific protease. Even though mass\nspectrometers can measure the mass of intact proteins, there are a\nnumber of reasons why peptides, and not proteins, are analysed in\nproteomics. Proteins can be difficult to handle and might not all be\nsoluble under the same conditions (it should be noted here that many\ndetergents interfere with MS, because they ionize well and are in a\nhuge excess relative to the proteins). In addition, the sensitivity of\nthe mass spectrometer for proteins is much lower than for peptides,\nand the protein might be processed and modified such that the\ncombinatorial effect makes determining the masses of the numerous\nresulting isoforms impossible. Furthermore, it is not easy to predict\nfrom the sequence what the mass of a mature, correctly modified\nprotein will be or, conversely, which protein might have given rise to\na measured protein mass. Most importantly, if the purpose is to\nidentify the protein, sequence information is needed and the mass\nspectrometer is most efficient at obtaining sequence information from\npeptides that are up to approx20 residues long, rather than from whole\nproteins. Nevertheless, with very specialized equipment, it is\nbecoming possible to derive partial sequence information from intact\nproteins, which can then be used for identification purposes or the\nanalysis of protein modifications in an approach called 'top-down'\nprotein sequencing</p>\n</blockquote>\n"
}
] |
[
{
"answer_id": 17743,
"pm_score": 2,
"text": "<p>This is going to be a very long answer but to give a short response.</p>\n\n<p>You have to consider that MS for peptide detection works on the bases/principle of mass to charge (m/z) to detect an AA molecule, which is then normalised and analysed etc etc (<a href=\"http://en.wikipedia.org/wiki/Mass_spectrometry\" rel=\"nofollow\">http://en.wikipedia.org/wiki/Mass_spectrometry</a>). Once you have the amino acids, then you just look at the order in which they get through and then you have your peptide sequence. Please read about the B, A and Y-type ions although this page is slightly technical (<a href=\"http://www.matrixscience.com/help/fragmentation_help.html\" rel=\"nofollow\">http://www.matrixscience.com/help/fragmentation_help.html</a>). If the proteins was not digested then it would be far too big to be analysed since it would be read as one massive blob of m/z, which could be anything! So once you have your spectra from a peptide, you need to compare it to a model spectra, and based on that you predict what the sequence is as fragmentations peaks can be anything. Look at SEQUEST (<a href=\"http://en.wikipedia.org/wiki/List_of_mass_spectrometry_software\" rel=\"nofollow\">http://en.wikipedia.org/wiki/List_of_mass_spectrometry_software</a>). Now there are tons of correction algorithms that are applied, which you can look up.</p>\n\n<p>Now RP-LC is carried out before MS to prevent all the sample rushing into the MS machine all at once as the machine can not cope if too much sample is inserted hence the flow rate is controlled. What I think you are thinking in terms of the set machine limit, is the (digested) peptide fragment that enters the machine, before undergoing electrospray. Now the experts that run the MS machines do set a peptide mass upper and lower limit, for what size/mass of fragment to accept and what size/mass to ignore. Look at this theoretical digest example (<a href=\"http://prospector.ucsf.edu/prospector/cgi-bin/msform.cgi?form=msdigest\" rel=\"nofollow\">http://prospector.ucsf.edu/prospector/cgi-bin/msform.cgi?form=msdigest</a>). This happens frequently with trypsin digest as it recognises specific AA before cleavage (<a href=\"http://en.wikipedia.org/wiki/Trypsin\" rel=\"nofollow\">http://en.wikipedia.org/wiki/Trypsin</a>). Now a days, MS has advanced so much that we have machines such as Orbitrap (<a href=\"http://en.wikipedia.org/wiki/Orbitrap\" rel=\"nofollow\">http://en.wikipedia.org/wiki/Orbitrap</a>), which can cope with peptides, digested with elastase, which cleaves non specifically, which means you are less likely to get peptides that are far too big for analysis, hence increasing the protein coverage.</p>\n\n<p>Hope this helps!</p>\n"
}
] |
17,799
|
<p><strong>Background</strong></p>
<p>The standard definition of species refers to the concept of <a href="http://simple.wikipedia.org/wiki/Reproductive_isolation" rel="nofollow noreferrer">reproductive isolation</a>. If two lineages are found to be reproductively isolated, then we consider these two lineages to belong to different species. My question concerns evolved reproductive isolation in Drosophila sp. following labs due to experimental evolution.</p>
<p><strong>Question</strong></p>
<p>Have we ever demonstrated that two Drosophila sp. lineages that could initially interbreed (in nature or in labs) evolved through artificial selection (and drift and mutations) in labs to finally not be able to interbreed anymore either due pre- or post- zygotic isolation (see <a href="http://en.wikipedia.org/wiki/Reproductive_isolation" rel="nofollow noreferrer">wiki</a>)? Or, in other words, have we ever demonstrated that two drosophila lineages evolved to become different species (reproductive isolation definition) in labs experiments?</p>
<p>If not, have we ever observed some partial reproductive isolation such as inbreeding depression for example?</p>
<hr>
<p>Note: This question is motivated by @LotusBiology that could not receive the answers she/he was waiting for because he/she failed to ask questions that are possibly answerable! So I wanted to ask this question that somehow addresses <a href="https://biology.stackexchange.com/questions/17736/if-evolution-is-true-how-would-you-explain-the-fruit-fly-experimentations">this</a> question he/she asked (now on-hold)</p>
<p>For more information about the concept of species, please have a look at <a href="https://biology.stackexchange.com/questions/39664/how-could-humans-have-interbred-with-neanderthals-if-were-a-different-species">How could humans have interbred with Neanderthals if we're a different species?</a></p>
|
[
{
"answer_id": 17801,
"pm_score": 5,
"text": "<p>Rice and Salt$^1$ bred fruit flies for 35 generations and from one line of flies created two groups that were isolated from each other reproductively. They could not interbreed because they no longer bred in the same environment. Depending on one's definition of 'species' this could be a case of artificial speciation.</p>\n\n<p>$^1$Rice WR, Salt GW (1988), Speciation via disruptive selection on habitat preference: experimental evidence\". The American Naturalist 131 (6): 911–917.</p>\n"
}
] |
[
{
"answer_id": 17819,
"pm_score": 3,
"text": "<p>Diane Dodd's experiments on Drosophila pseudoobscura would be another example of lab-based speciation. </p>\n\n<p><a href=\"http://www.jstor.org/stable/2409365?__redirected\" rel=\"noreferrer\">http://www.jstor.org/stable/2409365?__redirected</a></p>\n\n<p>To summarise - four populations each adapted to feeding on a starch-based diet and a maltose-based diet were evolved in the lab to test effects on mating preferences; compared to what is expected by random, using chi-squared tests, 11 of 16 combinations showed greater isolation than expected by chance - strong evidence for assortative mating.</p>\n\n<p>An alternate link to the PDF of the paper is here <a href=\"http://www.sulfide-life.info/mtobler/images/stories/readings/dodd%201989%20evolution.pdf\" rel=\"noreferrer\">http://www.sulfide-life.info/mtobler/images/stories/readings/dodd%201989%20evolution.pdf</a> </p>\n\n<hr>\n\n<p><strong>Reference:</strong></p>\n\n<p>Dodd, Diane M. B. (September 1989). \"Reproductive isolation as a consequence of adaptive divergence in <em>Drosophila pseudoobscura</em>\". <em>Evolution</em> <strong>43</strong> (6): 1308–1311. doi:<a href=\"https://dx.doi.org/10.2307%2F2409365\" rel=\"noreferrer\">10.2307/2409365</a>.</p>\n"
}
] |
17,823
|
<p>I read about this <a href="http://www.instructables.com/id/Mosquito-trap-mosquito-abortion-clinic-or-source-t/">idea for a mosquito trap</a> (with a rather tactless name) where the idea seems to be that because the water available for the mosquito eggs is so shallow, they will die somehow or not be viable. Mosquitos are pretty small though, wouldn't they not need much water for the eggs to hatch?</p>
|
[
{
"answer_id": 17824,
"pm_score": 4,
"text": "<p>Many mosquitoes, such as Culex quinquefasciatus, lay their eggs on the surface of fresh or stagnant water. The water may be in tin cans, barrels, horse troughs, ornamental ponds, swimming pools, puddles, creeks, ditches, catch basins or marshy areas. Mosquitoes prefer water sheltered from the wind by grass and weeds (<a href=\"http://www.mosquito.org/biology\">reference</a>). There are mosquitoes like Aedes taeniorhyncus (floodwater mosquitoes) which can even lay eggs in moist soil (because the eggs need to dry out before they can hatch) which then waits for the rainy season for hatching. These eggs are capable of surviving through summer, winter and spring to find the right time to hatch (<a href=\"http://mosquito.ifas.ufl.edu/Mosquito_Habitats.htm\">reference</a>). Water is necessary during the life cycle of a mosquito but how much is never an issue. Even the top of some mushrooms can be a place for mosquitoes to lay eggs (<a href=\"http://www.clarku.edu/~tlivdahl/back/index.html\">reference</a>).</p>\n"
}
] |
[
{
"answer_id": 77062,
"pm_score": 0,
"text": "<p>I have them in my property breeding in my containers all the time. From a few inches gets the best results (more mosquitoes) but I’ve gotten colonies in water up to 2-3’ deep. </p>\n"
}
] |
17,840
|
<p>In the resting membrane potential of neurons the inside of membrane is kept negative and outside of membrane is kept positive by the utilization of energy through Na-K Atpase pump, While during action membrane potential through the opening of specific gated ion channels inside of membrane is made positive while outside is made negative, What is the significance of specific charges across the membrane, does these specific charges across the membrane play any role in the passage of neurotransmitters ? or these charges are just arbitrary ?does this can happen that during resting membrane potential the inside will become positive and outside will become negative and vice versa, I want to know that what is the significance of these specific charges across the membrane ..?</p>
|
[
{
"answer_id": 17824,
"pm_score": 4,
"text": "<p>Many mosquitoes, such as Culex quinquefasciatus, lay their eggs on the surface of fresh or stagnant water. The water may be in tin cans, barrels, horse troughs, ornamental ponds, swimming pools, puddles, creeks, ditches, catch basins or marshy areas. Mosquitoes prefer water sheltered from the wind by grass and weeds (<a href=\"http://www.mosquito.org/biology\">reference</a>). There are mosquitoes like Aedes taeniorhyncus (floodwater mosquitoes) which can even lay eggs in moist soil (because the eggs need to dry out before they can hatch) which then waits for the rainy season for hatching. These eggs are capable of surviving through summer, winter and spring to find the right time to hatch (<a href=\"http://mosquito.ifas.ufl.edu/Mosquito_Habitats.htm\">reference</a>). Water is necessary during the life cycle of a mosquito but how much is never an issue. Even the top of some mushrooms can be a place for mosquitoes to lay eggs (<a href=\"http://www.clarku.edu/~tlivdahl/back/index.html\">reference</a>).</p>\n"
}
] |
[
{
"answer_id": 77062,
"pm_score": 0,
"text": "<p>I have them in my property breeding in my containers all the time. From a few inches gets the best results (more mosquitoes) but I’ve gotten colonies in water up to 2-3’ deep. </p>\n"
}
] |
17,845
|
<p>There are many combination vaccines available but I've noticed that there don't seem to be any with both live and non-live components, e.g. DTaP/IPV/MMR. Such combinations could be useful in some cases, since most developed countries give a second dose of MMR (or MMRV) at the same time as DTaP/IPV. Is there a biological reason that this is difficult?</p>
|
[
{
"answer_id": 20110,
"pm_score": 4,
"text": "<p>First let me point out that for the US, I'm not knowledgeable enough to speak for the rest of the world, you are correct.</p>\n\n<hr>\n\n<p><strong>There are no approved live attenuated vaccines mixed with componet/subunit/inactivated vaccines.</strong></p>\n\n<hr>\n\n<h2>Background:</h2>\n\n<p>Before we go into why that's true, let's work a little to show that's true. The FDA publishes a <a href=\"http://www.fda.gov/biologicsbloodvaccines/vaccines/approvedproducts/ucm093833.htm\" rel=\"noreferrer\">wonderful list</a> of every approved vaccine for use in the US. Of the 78 vaccines listed (and there is a lot of redundancy due to different manufacturers etc), only 16 are live attenuated (or about 20%).</p>\n\n<p>Another thing to notice is that we have vaccines to both <a href=\"http://en.wikipedia.org/wiki/Virus\" rel=\"noreferrer\">viruses</a> and <a href=\"http://en.wikipedia.org/wiki/Bacteria\" rel=\"noreferrer\">bacteria</a>. Technically, some of the vaccines are to bacterial toxins, not bacteria themselves, but for the sake of simplicity, we're going to group all bacterial <a href=\"http://www.vaccinesafety.edu/components.htm\" rel=\"noreferrer\">component, subunit, and inactivated vaccine preparations</a> together in one group.</p>\n\n<p>First you will note that there is only one live attenuated vaccine for bacteria, <a href=\"https://en.wikipedia.org/wiki/Mycobacterium_bovis\" rel=\"noreferrer\">Mycobacterium bovis</a> (more on this exception later). There are several reasons for this, but as a general rule, you don't want to put a foreign object capable of self replication inside a person. Viruses cannot self replicate, they are <a href=\"http://en.wikipedia.org/wiki/Obligate_parasite\" rel=\"noreferrer\">obligate parasites</a> by definition, so they don't fall under this rule. One could, however engineer bacteria that were sufficiently deficient in replication that this might not be an issue. Another safety concern with live attenuated bacteria is <a href=\"http://en.wikipedia.org/wiki/Sepsis\" rel=\"noreferrer\">sepsis</a>. Again by choosing a delivery route that doesn't involve injections, you might be able to mitigate this risk.</p>\n\n<p>I also want to be clear that I think live attenuated bacterial/fungal (yeast mostly) vaccines can work more broadly, and are likely to be used in <a href=\"http://dx.doi.org/10.1016/j.vaccine.2013.07.029\" rel=\"noreferrer\">innovative vaccine strategies</a>. </p>\n\n<p>The main obstacle to a live attenuated bacteria vaccine is that the component and subunit vaccines <strong>work</strong>. Sometimes they work even better by only supply the part of an organism that is known to provide <a href=\"http://en.wikipedia.org/wiki/Neutralizing_antibody#Broadly-neutralizing_antibodies\" rel=\"noreferrer\">broad neutralization</a> (getting rid of) of the pathogen. And if you know that you can provide protection with out the risk of putting the live organism in a person, why would you take that risk?</p>\n\n<p>Quite simply you don't. Back to <em>M. bovis</em>. For the most part, humans are not vaccinated with <em>M. bovis</em> (BCG) to prevent <em>M. Bovis</em> infection (though <a href=\"https://en.wikipedia.org/wiki/Zoonosis\" rel=\"noreferrer\">zoonotic</a> infections can <a href=\"http://whqlibdoc.who.int/hq/1996/WHO_EMC_ZOO_96.4.pdf\" rel=\"noreferrer\">occur</a>). Instead it is to prevent <em><a href=\"https://en.wikipedia.org/wiki/Mycobacterium_tuberculosis\" rel=\"noreferrer\">M. tuberculosis</a></em> (MTB) infection. <a href=\"https://en.wikipedia.org/wiki/Attenuated_vaccine\" rel=\"noreferrer\">Attenuation</a> of MTB is <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3544749/\" rel=\"noreferrer\">difficult</a>, and <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC23125/\" rel=\"noreferrer\">not complete</a>. Indeed we don't have a subunit or component vaccine that has worked for MTB, and an inactivated MTB has <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3515764/\" rel=\"noreferrer\">more safety concerns</a> than BCG. Thus we choose a related organism, <em>M. Bovis</em>, which naturally doesn't cause disease in humans (or rarely), but can provide some protection against TB. Even the <a href=\"http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM202934.pdf\" rel=\"noreferrer\">product insert</a> admits that efficacy of the vaccine is in question.</p>\n\n<p>The same pattern of necessity holds true for viral live attenuated vaccines. They are used when you need a more <a href=\"https://en.wikipedia.org/wiki/Immunogenicity\" rel=\"noreferrer\">immunogenic</a> vaccine, and where we haven't been able to make safe and effective, inactivated, subunit, or <a href=\"https://en.wikipedia.org/wiki/Virus-like_particle\" rel=\"noreferrer\">VLP</a> vaccines. Thus when you need a live attenuated vaccine, you really do need it to be alive for it work.</p>\n\n<hr>\n\n<h2>Answering the core question:</h2>\n\n<p>As @MattDMo pointed out, the storage conditions are very different for live attenuated vaccines. Not only that, but most of the <a href=\"http://cellculturedish.com/2011/10/recombinant-albumin-enhances-stability-of-attenuated-vaccines/\" rel=\"noreferrer\">preservatives</a> used in many inactivated vaccines cause <a href=\"https://en.wikipedia.org/wiki/Titer\" rel=\"noreferrer\">titer</a> loss (though there is <a href=\"http://dx.doi.org/10.1016%2Fj.vaccine.2011.07.054\" rel=\"noreferrer\">work</a> to find alternatives). </p>\n\n<p>On the theory that a picture is worth a thousand words, I did a little experiment just for this post (and also I was cleaning out an -80). I took a high titer stock of measles virus that has a protein tag on one of the proteins so we can easily detect it (F is Flag tagged). Then I spiked 3 different tubes of virus in ether <a href=\"https://en.wikipedia.org/wiki/Phosphate_buffered_saline\" rel=\"noreferrer\">PBS</a> (saline) or <a href=\"http://www.nlm.nih.gov/medlineplus/ency/article/002021.htm\" rel=\"noreferrer\">DTaP</a> (an actual dose, just past expiration), and left them in the refrigerator (4oC) for 8h. Note that <a href=\"https://www.merckvaccines.com/Products/Mmr/Pages/storageandhandling\" rel=\"noreferrer\">Merk thinks</a> you should toss the measles vaccine if you don't use it within 8/hours (also note their comment on preservatives). Then I infected some cells that grow up measles, and harvested the cells in a total cell lysate. Finally I ran equal amounts of total protein form each preparation on a gel for a <a href=\"https://en.wikipedia.org/wiki/Western_blot\" rel=\"noreferrer\">western blot</a>:</p>\n\n<p><img src=\"https://i.stack.imgur.com/Y1J8S.png\" alt=\"Western of 3 measles replicates\"></p>\n\n<p>You should notice the three pairs of bands, in each case the lighter band (indicating less protein) belongs to the DTaP group. That is to say less measles F protein (something you want to make antibodies to) came from the samples that were put into the DTaP vaccine compared to PBS.</p>\n\n<h2>Another serious problem is <a href=\"https://en.wikipedia.org/wiki/Cold_chain\" rel=\"noreferrer\">cold chain</a>:</h2>\n\n<p>Again we need the virus to be \"alive\" when we give a person a vaccine. This almost always means that we have to keep it frozen or at least refrigerated from the manufacturer, all the way up until moments before it goes into a person's arm. There are <a href=\"http://dx.doi.org/10.1016/j.biologicals.2014.05.007\" rel=\"noreferrer\">many good</a> reviews on cold chain to be found. Quite simply, inactivated and component vaccines do not have the thermo-stability requirements that live vaccines do. It would be a waste of energy in most cases to chill all of the vaccines which could be left at room temperature, and it would remove one of their clear advantages.</p>\n\n<p>As far as the immunology is concerned, there is probably not a real limit on what the body can react to. Indeed, as you point out, they are often administered at the same time in developed countries. It is merely a question of how you can keep live-attenuated vaccines \"alive\" in the same preparation. It is certainly possible that there is a solution to this, and vaccine stability is an active field of research. Hopefully in 10-20 years we will be able to adjust this answer to say that such a vaccine has been made, and that it's safe enough for approval.</p>\n"
}
] |
[
{
"answer_id": 20059,
"pm_score": 3,
"text": "<p>The major reason for this are differences in the preparation methods. <a href=\"http://en.wikipedia.org/wiki/Attenuated_vaccine\">Live (attenuated) vaccines</a> need permanent cooling, which makes their use in third world countries difficult. </p>\n\n<p><a href=\"http://en.wikipedia.org/wiki/Inactivated_vaccine\">Inactivated vaccines</a> are inactivated either by heat, radiation of chemicals and are often freeze-dried after purification (removal of chemicals used for killing). In this condition, they have a very long shelf-life and need no cooling. Before use they are dissolved in water and then administered.</p>\n\n<p>There is another problem with mixing these vaccines: Live vaccines can not be given to anybody, people which have a weakened immune system (because of an infection like HIV, chemotherapy or the adimistration of drugs, which downregulate the immune system after an organ transplantation) are not able to receive them. The attenuated pathogen which replicates usually only slowly would still be a possible danger for these people. So they can still be vaccinated with inactivated vaccines to provide at least some protection.</p>\n\n<p>For more information on this topic see the chapter on immunization in \"<a href=\"http://pathmicro.med.sc.edu/ghaffar/immunization-ver2.htm\">Microbiology and Immunology online</a>\" and this information from the <a href=\"http://www.niaid.nih.gov/topics/vaccines/understanding/pages/typesvaccines.aspx\">National Institute of Health</a>.</p>\n"
}
] |
17,899
|
<p>Some <em>Aspergillus</em> species appear to like walnuts. My question concerns the association of <em>Penicillium</em> and <em>Aspergillus</em>. No sooner does <em>Aspergillus</em> colonize a walnut (or some other challenging carbon source) than <em>Penicillium</em> seems to move in, eventually killing the <em>Aspergillus</em> colony.</p>
<p>A totally unscientific guess is that <em>Aspergillus</em> is a good colonizer and <em>Penicillium</em> a good opportunist and that this is a common pattern with these two species. Is there any science in this direction? I do recall a sort of well-known picture from an old text in which <em>Penicillium</em> is shown more or less strangling a species of <em>Aspergillus</em>. I didn't think about it much at the time. </p>
<p>The image attached is not very incriminating but the theme is the same. <em>Penicillium</em> are the green hand-like structures strewn about the clover-like <em>Aspergillus.</em> Foot-cell of the latter cropped. </p>
<p>This seems like a simple question but a quick search doesn't reveal a lot, I think in part because this would generally come up as a contamination issue. </p>
<p><img src="https://i.stack.imgur.com/hJwq7.jpg" alt="enter image description here"></p>
|
[
{
"answer_id": 17901,
"pm_score": 4,
"text": "<p>It is hard to find any articles on the <em>association</em> between <em>Penicillium</em> and <em>Aspergillus</em> species, although they are both considered <a href=\"http://www.jiaci.org/issues/vol18issue3/2.pdf\" rel=\"noreferrer\">two of the most common mold species</a> found indoors.</p>\n\n<blockquote>\n <p>In this study, the most prevalent spore types detected in both the indoor and outdoor air samples were generally from the <em>Penicillium</em>/<em>Aspergillus</em> group [...] these findings are qualitatively similar to those observed in other geographical locations, confirming the ubiquitous nature of these fungi.</p>\n</blockquote>\n\n<p>Although these genera seem to be found commonly, it also has to do with environmental factors, and the relative humidity of the area as well.</p>\n\n<blockquote>\n <p>Geographical location, climate, and short-term meteorological \n conditions are responsible for outdoor types and levels of fungal \n spores.</p>\n</blockquote>\n\n<p>As for the association and apparently colonization/opportunistic behaviour of the genera, it seems like there are not any associations between the two, unless perhaps <a href=\"http://www.mycologia.org/content/97/1/202.full\" rel=\"noreferrer\">environmental conditions are subject to changing</a>, and different mold species have different moisture/temperature thresholds, although again these mold groups tend to be generalists and do well at a wider range of environmental conditions than other fungi.</p>\n\n<blockquote>\n <p>A laboratory procedure was developed in which viable peanut seeds were wounded and inoculated with field soil containing natural populations of fungi, then incubated under different conditions of seed water activity and temperature. [...] <em>A. parasiticus</em> colonized peanut seeds at lower temperatures than <em>A. flavus</em>, and cool soil temperatures relative to temperatures of aerial crop fruits might explain why <em>A. parasiticus</em> is found mostly in peanuts. </p>\n \n <p>Other fungi, dominated by the genera <strong><em>Penicillium</em></strong>, <em>Fusarium</em> and <em>Clonostachys</em>, colonized seeds primarily at water activities and temperatures suboptimal for section <em>Flavi</em> species and <em>A. niger</em>. </p>\n \n <p><em>Eupenicillium ochrosalmoneum</em> frequently sporulated on the conidial heads of section Flavi species and showed specificity for these fungi. The inoculation of wounded viable peanut seeds with soil containing natural populations of fungi provides a model system for studying the infection process, the interactions among fungi and those factors important in aflatoxin formation.</p>\n</blockquote>\n\n<p>Any associations with different fungi species and <a href=\"http://www.mycologia.org/content/100/1/12.full\" rel=\"noreferrer\">their different structures</a>, including, for example, with the conidial heads of <em>Aspergillus</em> seem to be currently under study:</p>\n\n<blockquote>\n <p>The genus <em>Penicillium</em> comprises species that mostly colonize plant matter. However early reports suggest that several species are capable of parasitizing <em>Aspergillus</em> and sporulating on the conidial heads of the host. More recently <em>Eupenicillium ochrosalmoneum</em> and <em>E. cinnamopurpureum</em>, [...] have been observed sporulating on the heads of <em>Aspergillus</em> species belonging to section <em>Flavi</em> during the colonization of peanut seeds.</p>\n</blockquote>\n\n<p><img src=\"https://i.stack.imgur.com/JmuYD.gif\" alt=\"*Eupenicillium* and *Penicillium* species sporulating on heads of *Aspergillus*.\"></p>\n\n<blockquote>\n <p><strong>Little is known about the host specificity underlying these <em>Aspergillus</em>-<em>Penicillium</em> associations</strong>. [...] all species spread across Aspergillus colonies by means of aerial hyphae that grew from head to head. Additional studies are required to clarify whether <em>Eupenicillium</em> and <em>Penicillium</em> species are parasitic or simply epibiotic on their hosts.</p>\n</blockquote>\n"
}
] |
[
{
"answer_id": 40652,
"pm_score": 2,
"text": "<p>A year after the fact I found a short passage in Thom and Raper's 1945 text, <em>Manual of the Aspergilli.</em> At page 59 the authors relate that <em>Aspergillus niger</em> colonies are commonly overrun with <em>Penicillium rugulosum</em> which \"winds its hyphae within and about the conidiophores, and fruits in a radiating series of short-stalked penicilli surrounding the heads and upper halves of the conidiophores.\" There is a photo illustrating this on p. 60. </p>\n"
}
] |
17,902
|
<p>Some peppers, such as the <a href="https://en.wikipedia.org/wiki/Habanero_chili">habanero</a> or <a href="https://en.wikipedia.org/wiki/Carolina_Reaper">Carolina reaper</a> are extremely spicy, and when eaten in larger amounts than one is accustomed to, can cause some discomfort.</p>
<p>I've also heard anecdotes claiming that pepper spray, if applied with sufficient intensity, can cause death.</p>
<p>What if you were to eat as many spicy peppers as possible, despite the noxious taste? Is it possible to commit suicide in this way (and what would the cause of death)? Would you faint from excessive mouth pain? Would uncontrollable vomiting prevent you from consuming further peppers?</p>
|
[
{
"answer_id": 17903,
"pm_score": 5,
"text": "<p>The more "dangerous" properties of spicy peppers are chiefly due to capsaicin.</p>\n<p>Sigma-Aldrich sells <a href=\"http://www.sigmaaldrich.com/catalog/product/sigma/m2028?lang=en&region=US\" rel=\"noreferrer\">purified capsaicin</a>, for which they provide safety information, including an MSDS. Most of it is the usual, unsurprising set of warnings about irritation to eyes and the respiratory system. However, there are LD50 numbers:</p>\n<blockquote>\n<p>LD50 Oral - rat - male - 161.2 mg/kg</p>\n<p>LD50 Oral - rat - female - 148.1 mg/kg</p>\n<p>LD50 Dermal - mouse - >512 mg/kg</p>\n</blockquote>\n<p>From this, we can conclude that one would have to eat quite a bit of capsaicin to die. If lethality in humans is exactly the same as rat (which it probably isn't), a 70 kg human would need to consume about 11 g of capsaicin to reach similar levels of lethality.</p>\n<p>The Carolina Reaper, one of the hottest known peppers, averages about <a href=\"https://en.wikipedia.org/wiki/Carolina_Reaper\" rel=\"noreferrer\">1.6 million</a> on the Scoville scale. Capsaicin amount is related to <a href=\"https://en.wikipedia.org/wiki/Scoville_scale#High-performance_liquid_chromatography\" rel=\"noreferrer\">Scoville heat units</a>, so we can make an imprecise conversion from one to the other.</p>\n<p>Using values given in 2 publications (<a href=\"http://www.sciencepub.net/newyork/ny0309/03_3176ny0309_17_21.pdf\" rel=\"noreferrer\">Nwokem 2010</a> and <a href=\"http://www.mdpi.com/1420-3049/16/10/8919\" rel=\"noreferrer\">Al Othman 2011</a>) we can observe the following trend:</p>\n<p><img src=\"https://i.stack.imgur.com/jaTOQ.png\" alt=\"enter image description here\" /></p>\n<p>So on average, about <span class=\"math-container\">$6.25 \\cdot 10^{-5}$</span> mg/g capsaicin per SHU. With this, we get <span class=\"math-container\">$(1.6 \\cdot 10^5) \\cdot (6.25 \\cdot 10^{-5}) = 10$</span> mg/g, or 1% capsaicin for dry Carolina Reapers. To eat the equivalent of 11 g of capsaicin in peppers, you would have to eat 1.1 kg of dry peppers - which should be a couple of dozen.</p>\n<p>So, I think we can conclude that it is relatively "feasible" to consume a dangerously large amount of capsaicin by eating very spicy peppers. However, there are numerous caveats with my reasoning:</p>\n<ul>\n<li>Human LD50 and rat LD50 are not necessarily the same.</li>\n<li>Toxicity is not necessarily linearly related to body weight.</li>\n<li>Peppers have compounds besides capsaicin that contribute to hotness.</li>\n<li>It would be very difficult to eat such a large amount of spicy peppers, and various involuntary reflexes would interfere. Even if one were force fed the peppers, I imagine the body would attempt to vomit it up - which brings up the question of how the toxicologists even managed to feed several milligrams of capsaicin to rats to measure the LD50.</li>\n</ul>\n"
}
] |
[
{
"answer_id": 17910,
"pm_score": -1,
"text": "<p>If you have cardiovascular problems, then it should be quite possible for the pain cause by spicy peppers to trigger a heart attack via a spike in blood pressure. A similar scenario might occur with respiratory diseases. And of course an anaphylactic shock, if you are allergic.</p>\n\n<p>Apart from such special circumstances, I imagine that it would be nearly impossible to overcome the debilitating effects of capsaicin long enough to consume a lethal dose.</p>\n"
}
] |
17,924
|
<p>I have a question about cancer cure statistics. Many of the cancer literature or databases I have come across speak about 5 year or 10 year survival rates. In this case survival means that the patient with cancer is still alive 5 or 10 years after diagnosis. I am in need of references about the statistics which explain what is the percentage of people in these groups who are in progression-free survival group and disease-free survival group. That is for instance among the cancer patients which survive for some X years, who are completely cured of cancer (which means that the cancer is completely cured and has not reoccured with in this X years). </p>
<p>Update: USA data is preferred</p>
<p>Thanks</p>
|
[
{
"answer_id": 17903,
"pm_score": 5,
"text": "<p>The more "dangerous" properties of spicy peppers are chiefly due to capsaicin.</p>\n<p>Sigma-Aldrich sells <a href=\"http://www.sigmaaldrich.com/catalog/product/sigma/m2028?lang=en&region=US\" rel=\"noreferrer\">purified capsaicin</a>, for which they provide safety information, including an MSDS. Most of it is the usual, unsurprising set of warnings about irritation to eyes and the respiratory system. However, there are LD50 numbers:</p>\n<blockquote>\n<p>LD50 Oral - rat - male - 161.2 mg/kg</p>\n<p>LD50 Oral - rat - female - 148.1 mg/kg</p>\n<p>LD50 Dermal - mouse - >512 mg/kg</p>\n</blockquote>\n<p>From this, we can conclude that one would have to eat quite a bit of capsaicin to die. If lethality in humans is exactly the same as rat (which it probably isn't), a 70 kg human would need to consume about 11 g of capsaicin to reach similar levels of lethality.</p>\n<p>The Carolina Reaper, one of the hottest known peppers, averages about <a href=\"https://en.wikipedia.org/wiki/Carolina_Reaper\" rel=\"noreferrer\">1.6 million</a> on the Scoville scale. Capsaicin amount is related to <a href=\"https://en.wikipedia.org/wiki/Scoville_scale#High-performance_liquid_chromatography\" rel=\"noreferrer\">Scoville heat units</a>, so we can make an imprecise conversion from one to the other.</p>\n<p>Using values given in 2 publications (<a href=\"http://www.sciencepub.net/newyork/ny0309/03_3176ny0309_17_21.pdf\" rel=\"noreferrer\">Nwokem 2010</a> and <a href=\"http://www.mdpi.com/1420-3049/16/10/8919\" rel=\"noreferrer\">Al Othman 2011</a>) we can observe the following trend:</p>\n<p><img src=\"https://i.stack.imgur.com/jaTOQ.png\" alt=\"enter image description here\" /></p>\n<p>So on average, about <span class=\"math-container\">$6.25 \\cdot 10^{-5}$</span> mg/g capsaicin per SHU. With this, we get <span class=\"math-container\">$(1.6 \\cdot 10^5) \\cdot (6.25 \\cdot 10^{-5}) = 10$</span> mg/g, or 1% capsaicin for dry Carolina Reapers. To eat the equivalent of 11 g of capsaicin in peppers, you would have to eat 1.1 kg of dry peppers - which should be a couple of dozen.</p>\n<p>So, I think we can conclude that it is relatively "feasible" to consume a dangerously large amount of capsaicin by eating very spicy peppers. However, there are numerous caveats with my reasoning:</p>\n<ul>\n<li>Human LD50 and rat LD50 are not necessarily the same.</li>\n<li>Toxicity is not necessarily linearly related to body weight.</li>\n<li>Peppers have compounds besides capsaicin that contribute to hotness.</li>\n<li>It would be very difficult to eat such a large amount of spicy peppers, and various involuntary reflexes would interfere. Even if one were force fed the peppers, I imagine the body would attempt to vomit it up - which brings up the question of how the toxicologists even managed to feed several milligrams of capsaicin to rats to measure the LD50.</li>\n</ul>\n"
}
] |
[
{
"answer_id": 17910,
"pm_score": -1,
"text": "<p>If you have cardiovascular problems, then it should be quite possible for the pain cause by spicy peppers to trigger a heart attack via a spike in blood pressure. A similar scenario might occur with respiratory diseases. And of course an anaphylactic shock, if you are allergic.</p>\n\n<p>Apart from such special circumstances, I imagine that it would be nearly impossible to overcome the debilitating effects of capsaicin long enough to consume a lethal dose.</p>\n"
}
] |
17,926
|
<p>I received a gift that is a jug of Pure Mexican Vanilla. Having never dealt with large quantities of vanilla, it made me curious as to what would happen if a person had too much vanilla.</p>
<p>I understand that the alcohol has a higher toxicity rate and is probably more fatal than the actual vanilla itself, but I'm curious as to what ratio of mass of pure vanilla to mass of the human would be considered fatal.</p>
<p>Also, what is the physiological effect of a vanilla overdose as it pertains to inhibiting critical bodily functions? That is -- specifically what about a vanilla overdose would cause fatality?</p>
|
[
{
"answer_id": 17928,
"pm_score": 5,
"text": "<p>Vanillin is the chemical that gives vanilla its flavour and smell <sup>[1]</sup>.</p>\n\n<blockquote>\n <p>Vanillin is pharmacologically active, causing depressed blood pressure, increased respiratory rate & death due to cardiovascular collapse <sup>[3]</sup>.</p>\n \n <p>Non-Human Toxicity Values <sup>[4]</sup></p>\n \n <ul>\n <li>LD50 Rat oral 1580 mg/kg</li>\n <li>LD50 Rat ip 1160 mg/kg</li>\n <li>LD50 Rat sc 1500 mg/kg</li>\n <li>LD50 Mouse ip 475 mg/kg</li>\n <li>LD50 Guinea pig oral 1400 mg/kg</li>\n <li>LD50 Guinea pig ip 1190 mg/kg</li>\n <li>LD50 Rat oral 2.8 g/kg</li>\n <li>LD50 Guinea pig oral 1.40 g/kg</li>\n <li>LD50 Mouse ip 0.78 g/kg</li>\n <li>LD50 Rat sc 1.8 g/kg</li>\n <li>LD50 Dog iv 1.32 g/kg slow in fusion.</li>\n </ul>\n</blockquote>\n\n<hr>\n\n<p>References:</p>\n\n<ol>\n<li><p>Wikipedia contributors, \"Vanillin,\" Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Vanillin&oldid=613429267\" rel=\"noreferrer\">http://en.wikipedia.org/w/index.php?title=Vanillin&oldid=613429267</a> (accessed June 26, 2014).</p></li>\n<li><p>PATTY F. A. 1963. <em>Industrial Hygiene and Toxicology. Volume II Toxicity</em>, page 1696 (referenced from <a href=\"http://toxnet.nlm.nih.gov/cgi-bin/sis/search2/r?dbs+hsdb%3a@term+@rn+@rel+121-33-5\" rel=\"noreferrer\">TOXNET, <em>Vanillin</em></a> - Human Toxicity Excerpts)</p></li>\n<li>TOXNET. <a href=\"http://toxnet.nlm.nih.gov/cgi-bin/sis/search2/r?dbs+hsdb%3a@term+@rn+@rel+121-33-5\" rel=\"noreferrer\"><em>Vanillin</em></a></li>\n</ol>\n"
}
] |
[
{
"answer_id": 17927,
"pm_score": 2,
"text": "<p>Out of interest, I've had a look around a bit and it seems like the most dangerous part of that bottle might be the alcohol.</p>\n\n<p>According to the <a href=\"http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=169.3\" rel=\"nofollow\">FDA</a>...</p>\n\n<blockquote>\n <p>The term unit of vanilla constituent means the total sapid and odorous principles extractable from one unit weight of vanilla beans, as defined in paragraph (b) of this section, by an aqueous alcohol solution in which the content of <strong>ethyl alcohol by volume amounts to not less than 35 percent</strong>.</p>\n</blockquote>\n\n<p>(Emphasis mine.)</p>\n"
}
] |
17,980
|
<p>In a documentary on fitness I saw it was stated that women can't get big like men because of their low concentration of testosterone. If it is true that women have testosterone, where is it made? Why do some women, especially later in life, develop facial hair (though obviously not as much as men)? Do men also have "female" hormones in their body? </p>
|
[
{
"answer_id": 17981,
"pm_score": 5,
"text": "<p>Yes, they do. The ovaries produce both testosterone and estrogen. Relatively small quantities of testosterone are released into your bloodstream by the ovaries and adrenal glands. Sex hormones are involved in the growth, maintenance, and repair of reproductive tissues <sup>[1]</sup>.</p>\n\n<p>The serum testosterone level in women with no acne, hirsutism, or menstrual dysfunction is 14.1 +/- 0.9 ng/dL (nanograms per decilitre) <sup>[2]</sup>. An average adult man has 270-1,070 ng/dL serum testosterone <sup>[3]</sup>.</p>\n\n<p>Men have female sex hormones too. For a prepubescent male, estrogen levels are expected to be between 1 and 3.7 ng/dL. During puberty, normal levels fall between 2.3 and 8.4 ng/dL. Levels for an adult male should be between 2.5 and 5 ng/dL <sup>[4]</sup>.</p>\n\n<hr>\n\n<p>References:</p>\n\n<ol>\n<li>WebMD, LLC. <a href=\"http://www.webmd.com/women/guide/normal-testosterone-and-estrogen-levels-in-women\" rel=\"nofollow\"><em>Normal Testosterone and Estrogen Levels in Women.</em></a></li>\n<li>Ayala C, Steinberger E, Smith KD, Rodriguez-Rigau LJ, Petak SM. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/15251653\" rel=\"nofollow\"><em>Serum testosterone levels and reference ranges in reproductive-age women.</em></a></li>\n<li>Alexia Severson. <em><a href=\"http://www.healthline.com/health/low-testosterone/testosterone-levels-by-age\" rel=\"nofollow\">Testosterone Levels by Age.</a></em> Healthline Networks, Inc.</li>\n<li>wiseGEEK.com. <a href=\"http://www.wisegeek.com/what-are-normal-estrogen-levels-in-men.htm\" rel=\"nofollow\"><em>What Are Normal Estrogen Levels in Men?</em></a> (Measurements cited in picograms per millilitre, converted to ng/dL)</li>\n</ol>\n"
}
] |
[
{
"answer_id": 19328,
"pm_score": 1,
"text": "<p>Healthy young males have estradiol levels in the area of 20-30 pg/ml.\nAlso, estrogen is a group of hormones, including estradiol and estrone for example. You shouldn't think of any hormones as women hormones or men hormones really, as both genders have them all, albeit in different proportions, and generated often through different pathways/organs.</p>\n\n<p>this link is the best i could find within a few seconds of a google search:\n<a href=\"http://emedicine.medscape.com/article/273153-overview\" rel=\"nofollow\">http://emedicine.medscape.com/article/273153-overview</a>\nit will really describe where and what hormones are created where and in what quantities, as well as how and where they can convert within the body into more potent steroids.</p>\n"
}
] |
18,987
|
<p>Guanidium salts like (G-isothiocyanate) disrupt the hydrophobic interactions inside a protein or nucleic acid and denature it. What happens when hydrophobic interactions in DNA are broken? (I don't think it should get ssDNA because guanidium doesn't break hydrogen bonds within molecules)</p>
|
[
{
"answer_id": 18989,
"pm_score": 3,
"text": "<p>Guanidium is a chaotrope i.e it increases the entropy in the solution. It doesn't <em>disrupt</em> hydrophobic interactions. Guanidium and urea act by forming hydrogen bonds. They can bond with both the dissolved macromolecule and water. The water molecules are arranged as a shell around the hydrophobic regions so as to <em>contain</em> it, which leads to the reduction of entropy. This containment causes hydrophobic regions to come together and give rise to a pseudo-interaction (hydrophobic interaction. See the figure below). Guanidium interacts with the water shell and disorders it, thereby reducing the hydrophobic effect.\nGuanidium can also interact with macromolecules directly, by forming hydrogen bonds. In this process they can disrupt the normal H-bonds in the macromolecule. </p>\n\n<p><img src=\"https://i.stack.imgur.com/rasQY.jpg\" alt=\"enter image description here\"></p>\n"
}
] |
[
{
"answer_id": 18990,
"pm_score": 2,
"text": "<p>It is important to realize that the hydrophobic effect is largely due to the exclusion of water from non-polar surfaces, which increases entropy. This effect is a major contributor to the helical structure of DNA, which effectively brings the bases closer together and excludes water from contacting their hydrophobic rings. Chaotropic agents like guanidine thiocyanate increase water entropy by disrupting its hydrogen bonding network (decreasing it's order) and this makes it more favourable for hydrophobic surfaces to be exposed to water, thus denaturation can occur. Implicit in that process is that GITC is a hydrogen bond competitor, which is also evident when looking at its structure. So, in fact, GITC can disrupt the hydrogen bonds between base pairs and denature dsDNA at high enough concentrations. </p>\n\n<p>That all said, we're ignoring a major component of aqueous solutions that can also form hydrogen bonds with the bases: water itself! So we must ask ourselves that if a compound capable of hydrogen bonding (water) is present, what exactly is it that holds helical DNA together? While base pairing certainly does contribute, the major factors are the hydrophobic and base stacking interactions.</p>\n"
}
] |
19,002
|
<p>Is there any academic reference that shows α-tubulin is around 50-55 kDa? The only thing I found is some data sheets from companies. I need the real reference.</p>
|
[
{
"answer_id": 19003,
"pm_score": 3,
"text": "<p>The paper titled <a href=\"http://jcs.biologists.org/content/119/5/858.full\" rel=\"nofollow\">Identification of α-tubulin as a granzyme B substrate during CTL-mediated apoptosis</a> mentions it as 51KDa and the paper titled <a href=\"http://www.nature.com/nature/journal/v282/n5737/abs/282423a0.html\" rel=\"nofollow\">Carboxy-terminal amino acid sequence of α-tubulin from porcine brain</a> mentions it as 55,000 Da. Hope that suffices. </p>\n"
}
] |
[
{
"answer_id": 19004,
"pm_score": 2,
"text": "<p>This is not so easy to answer, since alpha-tubulin has at 10 known genes in this family (data from <a href=\"http://www.ensembl.org/Homo_sapiens/Gene/Family/Genes?cdb=compara;db=core;family=ENSFM00250000000217;g=ENSG00000167552;r=12:49578579-49583107\" rel=\"nofollow\">Ensembl</a>):</p>\n\n<ul>\n<li>TUBA1A tubulin, alpha 1a</li>\n<li>TUBA1B tubulin, alpha 1b</li>\n<li>TUBA3E tubulin, alpha 3e</li>\n<li>TUBA3D tubulin, alpha 3d</li>\n<li>TUBA4A tubulin, alpha 4a</li>\n<li>TUBAL3 tubulin, alpha-like 3</li>\n<li>TUBA1C tubulin, alpha 1c</li>\n<li>TUBA3C tubulin, alpha 3c</li>\n<li>TUBA8 tubulin, alpha 8</li>\n<li>TUBAL3 tubulin, alpha-like 3</li>\n</ul>\n\n<p>You can go on the site linked above and choose any of the proteins. I checked <a href=\"http://www.ensembl.org/Homo_sapiens/Transcript/ProteinSummary?db=core;g=ENSG00000167552;r=12:49578579-49583107;t=ENST00000301071\" rel=\"nofollow\">TUBA1A</a>, and get a length of 451 amino acids and a weight of approximately 50,1 kDa.</p>\n"
}
] |
19,013
|
<p>Why are some neurons tetraploid, and how does this result from it's ancestor cell ?</p>
|
[
{
"answer_id": 19015,
"pm_score": 3,
"text": "<p>Neurons are tetraploid in pathological situations like Alzheimer disease:</p>\n<blockquote>\n<p>Neurons that duplicate their DNA are rarely observed to undergo mitosis, and they remain for long time as tetraploid cells, in accordance with the chronic course of the disease. We have recently shown that cell cycle re-entry and somatic tetraploidization occurs during normal development in a subpopulation of RGCs (retinal ganglion cells), giving rise to enlarged neurons with extensive dendritic trees. Tetraploization in these neurons occurs in response to the activation of the neurotrophin receptor p75NTR by an endogenous source of NGF (nerve growth factor).</p>\n</blockquote>\n<p><em><strong>Source:</strong></em> Frade JM, López-Sánchez N. A novel hypothesis for Alzheimer disease based on neuronal tetraploidy induced by p75NTR. Cell Cycle 2010; 9:1934 - 1941; PMID: 20436277; <a href=\"http://dx.doi.org/10.4161/cc.9.10.11582\" rel=\"nofollow noreferrer\">http://dx.doi.org/10.4161/cc.9.10.11582</a></p>\n<blockquote>\n<p>These neurons are generated in response to nerve growth factor (NGF) acting through the neurotrophin receptor p75 (p75NTR), which induces E2F1 activity and cell cycle re-entry in migrating RGC neuroblasts lacking retinoblastoma (Rb) protein. We have also showed that brain-derived neurotrophic factor (BDNF) prevents G2/M transition in the tetraploid RGCs, thus being crucial for the maintenance of the tetraploid status as well as the survival of these neurons. The realization that tetraploid neurons can be readily observed in the vertebrate nervous system has important physiological consequences.</p>\n<p>Several eukaryotes are known to undergo endoreduplicative cycles leading to somatic polyploidy, thus increasing cell size in specific tissues. Examples of polyploidy in neurons are known in some invertebrates.</p>\n</blockquote>\n<p><em><strong>Source:</strong></em> José María Frade. <em><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2889987\" rel=\"nofollow noreferrer\">Somatic tetraploidy in vertebrate neurons - Implications in physiology and pathology.</a></em> Commun Integr Biol. 2010 Mar-Apr; 3(2): 201–203. PMCID: PMC2889987</p>\n"
}
] |
[
{
"answer_id": 73131,
"pm_score": 0,
"text": "<p>It's not all pathological. From the same second article cited:</p>\n\n<blockquote>\n <p>Modern techniques such as flow cytometry, fluorescent in situ\n hybridization (FISH), slide-based cytometry (SBC) and quantitative PCR\n analysis of DNA from isolated nuclei can all reliably quantify the\n amount of nuclear DNA in neurons.11 By using SBC, flow cytometry and\n FISH, <strong>we have recently demonstrated that tetraploid neurons exist in\n the normal vertebrate retina</strong>, representing a subpopulation of RGCs\n that, in the chick, innervate lamina F in the\n stratum-griseum-et-fibrosum-superficiale of the tectal cortex.12 These\n neurons are generated during the early stages of retinal development,\n soon after they acquire neuronal markers. Indeed, a subset of\n migrating RGCs expressing the transcription factor E2F1, and lacking\n Rb protein, was observed to undergo S-phase and remain in a permanent\n G2-like state. Therefore, endoreduplication, but not alternative\n mechanisms such as aneuploidy or cell fusion,13,14 represents the\n mechanism generating tetraploid RGCs in the vertebrate nervous system.</p>\n</blockquote>\n"
}
] |
19,020
|
<p>I have been reading about Maltose Binding Proteins. Mutant forms of the molecule seem to be named MalE_ where the _ represents a number, for example MalE36 or MalE50.</p>
<p>Please can someone explain the naming convention for this? i.e. what does the 'E' stand for? Does the number refer to the amino acid that has changed?</p>
|
[
{
"answer_id": 19015,
"pm_score": 3,
"text": "<p>Neurons are tetraploid in pathological situations like Alzheimer disease:</p>\n<blockquote>\n<p>Neurons that duplicate their DNA are rarely observed to undergo mitosis, and they remain for long time as tetraploid cells, in accordance with the chronic course of the disease. We have recently shown that cell cycle re-entry and somatic tetraploidization occurs during normal development in a subpopulation of RGCs (retinal ganglion cells), giving rise to enlarged neurons with extensive dendritic trees. Tetraploization in these neurons occurs in response to the activation of the neurotrophin receptor p75NTR by an endogenous source of NGF (nerve growth factor).</p>\n</blockquote>\n<p><em><strong>Source:</strong></em> Frade JM, López-Sánchez N. A novel hypothesis for Alzheimer disease based on neuronal tetraploidy induced by p75NTR. Cell Cycle 2010; 9:1934 - 1941; PMID: 20436277; <a href=\"http://dx.doi.org/10.4161/cc.9.10.11582\" rel=\"nofollow noreferrer\">http://dx.doi.org/10.4161/cc.9.10.11582</a></p>\n<blockquote>\n<p>These neurons are generated in response to nerve growth factor (NGF) acting through the neurotrophin receptor p75 (p75NTR), which induces E2F1 activity and cell cycle re-entry in migrating RGC neuroblasts lacking retinoblastoma (Rb) protein. We have also showed that brain-derived neurotrophic factor (BDNF) prevents G2/M transition in the tetraploid RGCs, thus being crucial for the maintenance of the tetraploid status as well as the survival of these neurons. The realization that tetraploid neurons can be readily observed in the vertebrate nervous system has important physiological consequences.</p>\n<p>Several eukaryotes are known to undergo endoreduplicative cycles leading to somatic polyploidy, thus increasing cell size in specific tissues. Examples of polyploidy in neurons are known in some invertebrates.</p>\n</blockquote>\n<p><em><strong>Source:</strong></em> José María Frade. <em><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2889987\" rel=\"nofollow noreferrer\">Somatic tetraploidy in vertebrate neurons - Implications in physiology and pathology.</a></em> Commun Integr Biol. 2010 Mar-Apr; 3(2): 201–203. PMCID: PMC2889987</p>\n"
}
] |
[
{
"answer_id": 73131,
"pm_score": 0,
"text": "<p>It's not all pathological. From the same second article cited:</p>\n\n<blockquote>\n <p>Modern techniques such as flow cytometry, fluorescent in situ\n hybridization (FISH), slide-based cytometry (SBC) and quantitative PCR\n analysis of DNA from isolated nuclei can all reliably quantify the\n amount of nuclear DNA in neurons.11 By using SBC, flow cytometry and\n FISH, <strong>we have recently demonstrated that tetraploid neurons exist in\n the normal vertebrate retina</strong>, representing a subpopulation of RGCs\n that, in the chick, innervate lamina F in the\n stratum-griseum-et-fibrosum-superficiale of the tectal cortex.12 These\n neurons are generated during the early stages of retinal development,\n soon after they acquire neuronal markers. Indeed, a subset of\n migrating RGCs expressing the transcription factor E2F1, and lacking\n Rb protein, was observed to undergo S-phase and remain in a permanent\n G2-like state. Therefore, endoreduplication, but not alternative\n mechanisms such as aneuploidy or cell fusion,13,14 represents the\n mechanism generating tetraploid RGCs in the vertebrate nervous system.</p>\n</blockquote>\n"
}
] |
19,051
|
<p><a href="https://en.wikipedia.org/wiki/Botulinum_toxin" rel="nofollow noreferrer">Botulinum toxin</a> is the neurotoxin protein created when botulism spores grow. The requirements for growth and/or for keeping the toxin from denaturing would seem to be very difficult to create in bale of hay.</p>
<p>There are well documented <a href="http://www.omafra.gov.on.ca/english/livestock/horses/facts/info_botulism.htm" rel="nofollow noreferrer">incidents of botulism in horses</a> who are eating hay, all the references I found were centered around hay in large plastic wrapped bales. </p>
<p>I have been <a href="https://pets.stackexchange.com/questions/4407">involved in an event</a> where the presumed DX is botulism secondary to ingestion from hay from last year. In this case the hay is second cutting timothy hay (making it 6 plus months old), in rectangular 50 pound (22 kg) bales that are not wrapped, have been barn kept, and when purchased from the vendor where stacked in rows 4 feet wide, by 6 feet (2 meters) high. The bale then spent more then a week on an shelf (chrome platted heavy wire) with good air circulation. </p>
<p>Three pet <a href="http://rabbit.org/" rel="nofollow noreferrer">house rabbits</a> appear to have been effected. with 2 dead and one recovering from a case of descending paralysis. Several tests are underway, but my understanding is that it may be difficult to conclusively show either the botulism in the rabbits, or significant presence of 'botulinum toxin' or 'clostridium botulinum' in the hay (samples from the mangers of effected animals are being tested).</p>
<p>Is it possible to logically conclude that Botulinum toxin could, or could not, be created and/or survive in a bale of hay meeting the above criteria? </p>
<p><strong>Note</strong> </p>
<p>If there is an awareness of a plant based neurotoxin that would cause similar symptoms that may be growing in the hay field please offer that in an answer at <a href="https://gardening.stackexchange.com/questions/11007">Gardnening</a>. </p>
|
[
{
"answer_id": 19130,
"pm_score": 4,
"text": "<p>As an addendum to Spinorial's answer, and after some research, the Center for Food Security and Public Health <em>specifically</em> lists hay / grass / <strong>decaying vegetable matter</strong> as a potential source for <em>C. botulinum</em> growth in their (very informative) <a href=\"http://www.cfsph.iastate.edu/Factsheets/pdfs/botulism.pdf\" rel=\"nofollow\">Botulism PDF</a>.</p>\n\n<blockquote>\n <p>All species of Clostridium can produce spores, dormant \n forms of the organism that are highly resistant to \n disinfectants, heat and environmental conditions that kill \n vegetative cells. These spores can survive for many years \n until favorable conditions allow them to germinate and \n grow. C. botulinum spores are common in the environment...<br>\n ...\n Different strains or groups of C. botulinum may have \n somewhat different requirements. For instance, the acidity \n necessary to inhibit C. botulinum type C strains is reported \n to be pH 5.1 to 5.6, but other organisms can survive a lower \n pH. Each group also has an optimal, minimal and maximal \n temperature for growth. For example, some group II \n organisms may be able to grow in foods at refrigeration \n temperatures (3-4°C/ 37-39°F), but group I organisms and \n type C toxin-producing strains are inhibited. Because C. \n botulinum does not compete well with other \n microorganisms, growth is more likely to occur if other \n bacteria and molds have been killed or inhibited. C. \n botulinum spores can survive cooking and some food-\n processing conditions that kill vegetative cells, then \n germinate and grow in the cooked food. </p>\n</blockquote>\n\n<p>As for your question...</p>\n\n<blockquote>\n <p>Is it possible to logically conclude that Botulinum toxin could, or could not, be created and/or survive in a bale of hay meeting the above criteria? </p>\n</blockquote>\n\n<p>Could the toxin survive? Probably. The toxin itself isn't particularly hearty, <strong>BUT</strong>...</p>\n\n<p>Could the <em>spores</em> survive (and go on to create the toxin)? <strong>Definitely</strong>. The spores survive direct heating/boiling, very low pH environments, and desiccation. For instance, botulism from canned foods <em>can</em> occur from eating the food (and toxin) directly - but you're supposed to throw it out if it look suspicious because even if you cook it and inactivate the toxin, the spores are still present after cooking. The spores can find anaerobic environments inside the body and germinate, then produce toxin afterwards.</p>\n"
}
] |
[
{
"answer_id": 19129,
"pm_score": 3,
"text": "<p>Clostridium botulinum toxin is present ubiquitously in soil. As such it is more than plausible that hay bails, which come into contact with soil can and I should expect almost probably will be infected with these bacteria. However it is not the mere presence of the bacteria itself which causes poisoning, it is the toxins they produce when the appropriate conditions are met. These toxins are produced as a consequence of spore formation. </p>\n\n<p>Traditionally in human cases, the presence of toxins has been linked to home canned foods, where there is an anaerobic environment with a ph < 4.5 (<a href=\"http://cid.oxfordjournals.org/content/41/8/1167.full\" rel=\"nofollow\">http://cid.oxfordjournals.org/content/41/8/1167.full</a>). It is conceivable that such an anaerobic environment exists within a hay bail (even if not wrapped). The following site from the ontario minestry agriculture and food (<a href=\"http://www.omafra.gov.on.ca/english/livestock/horses/facts/info_haylage.htm\" rel=\"nofollow\">http://www.omafra.gov.on.ca/english/livestock/horses/facts/info_haylage.htm</a>) suggest that the pH certain methods of hay bailing have pH < 5. This would seemingly confirm hay as potential source for botulinum toxins.</p>\n\n<p>With regards to testing the hay for C. botulinum I would expect there to be a very high chance of finding this, due to soil contamination, however this does not imply this was a definite source for poisoning. A more conclusive test would be for the toxin. So in summary it is logical to suggest that hay could be the toxin source, but this does not mean it was the source. </p>\n"
}
] |
19,081
|
<p>It is a cliche of freshman biology labs to point out that "every cycle of PCR doubles the DNA, so the yield will be $2^{cycles}$ times the template amount". However, if this were true, 1 ng of template would generate about 35 billion ng after 35 cycles, or 35 <em>grams</em> of DNA. This is clearly absurd and not the case.</p>
<p>Of course, the power-of-2 claim is a gross oversimplification (if anything, it is an <em>upper bound</em> - but even so, a very uninformative one), and in practice, yields will fall far short of it because:</p>
<ul>
<li>Every single duplex of DNA does not denature at each cycle</li>
<li>Primers do not bind to every single molecule of DNA at each cycle</li>
<li>Not every DNA strand gets bound by a polymerase at every cycle</li>
<li>Not every polymerase that binds manages to complete the entire product in time in every cycle</li>
<li>The reaction inhibits itself by depleting dNTPs</li>
<li>The heat denatures the reaction by degrading enzyme</li>
</ul>
<p>In fact, cursory examination of qPCR output often follows saturation kinetics:</p>
<p><img src="https://i.stack.imgur.com/JlTkp.png" alt="enter image description here"></p>
<p>Mathematical methods for modeling qPCR are obviously well developed.</p>
<p>My question is about ordinary PCR: Is it possible get a reasonable expectation of nanogram yield for an ordinary PCR done in a tabletop cycler, with typical PCR reagents?</p>
<p>For instance, when amplifying from a plasmid, I would like to calculate how many cycles to do, how much template to use, and how much product to load on the agarose gel to ensure that I will be able to clearly distinguish exponential amplification (both primers anneal), linear amplification (only one primer anneals), and no amplification (neither primer can anneal or the reaction did not work).</p>
|
[
{
"answer_id": 42267,
"pm_score": 4,
"text": "<p><strong>An expected efficiency for a typical PCR is 80%, meaning each cycle multiplies the copy number of the targeted DNA sequence 1.58 times.</strong></p>\n\n<p>Firstly, it makes more sense to refer to the amount of DNA in a polymerase chain reaction in terms of <em>copy number</em> or in terms of <em>moles</em>; the <em>number of DNA molecules</em> of interest is what the reaction is operating on, and the mass of product generated is a function of the length of the product (and, to a lesser degree, on the composition of the product).</p>\n\n<p>The following discussion is sourced from this URL: <a href=\"https://www.csun.edu/~hcbio027/biotechnology/lec3/pcr/p.htm\" rel=\"nofollow noreferrer\">https://www.csun.edu/~hcbio027/biotechnology/lec3/pcr/p.htm</a></p>\n\n<p>According to Perkin-Elemer, copy-number <strong>amplification of 100,000 fold</strong> of the targeted sequence of DNA can be expected from a PCR with 0.1 ng of Lambda phage DNA (a well-characterized and standard DNA isolate) in a 100 µL reaction with > 25 cycles of denaturation, annealing, and extension.</p>\n\n<p>In the above 100,000-fold amplification example, if the targeted amplicon were to be 500 bp in length, the estimated molecular-weight of duplex DNA of 500bp is 325,000 g/mol (based an average base-pair having a molecular mass of 650 g/mol).</p>\n\n<p>The Lamdba Phage genome is 42,502 base-pairs in length.\n42,502 bp × 650 grams/mol/bp = 2.762×10^7 grams/mol.</p>\n\n<p>0.1 ng Lambda DNA -> 0.1×10^-9 grams.\n0.1×10^-9 g ÷ 2.762×10^7 g/mol = 3.619 × 10^-18 moles.\n3.619 × 10^-18 moles × NA (Avogradro's Number) = 2.179×10^6 copies, or 2,179,000 copies.</p>\n\n<p>2.179×10^6 copies × 100,000 = 2.179×10^11 copies.\n2.179×10^11 copies ÷ NA × 325,000 g/mol = 1.176×10^-7 grams of sequence.\n1.176×10^-7 grams is equal to 0.117 µg or 117 ng.</p>\n\n<p>An amplification yield of 100,000x after 25 cycles would mean at each cycle 1 template would yield 1.58 templates for the next round of synthesis.</p>\n\n<p>How was this calculated? If c is the number of copies made per round of synthesis, then:</p>\n\n<pre><code>c^25 = 100,000 = 10^5\nso c^5 = 10\nand so 5(log c) = log 10 = 1\nso log c = 0.2 and c = 1.58 (approximately)\n\n(Or you could calculate the 25th root of 100,000 on a calculator, if you prefer.) \n</code></pre>\n\n<p>If we obtain 1.58 copies instead of the theoretical maximum of 2 copies, then the efficiency of the reaction could be said to be 79% (because 1.58/2.00 = 0.79).</p>\n\n<p>One reason this calculation is important is that a slight loss of efficiency is magnified through the amplification. A reaction may appear to have not worked if the efficiency drops (in each cycle) by just a few percent. Optimization is critically important in the polymerase chain reaction.</p>\n"
}
] |
[
{
"answer_id": 19094,
"pm_score": 1,
"text": "<p>The equation is correct, but there's an additional asymptotic limit to a maximum concentration of product depending on the starting concentration of NTPs, template and primer pairs in solution too. </p>\n"
}
] |
19,095
|
<p>For example, what's a $dt^{sz}$ hamster? (<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1144494/" rel="nofollow">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1144494/</a>). </p>
<p>What's a Rgs9-Cre/+;gtROSA/+ mouse? (<a href="http://www.sciencedirect.com/science/article/pii/S2212877813000719" rel="nofollow">http://www.sciencedirect.com/science/article/pii/S2212877813000719</a>)</p>
|
[
{
"answer_id": 19097,
"pm_score": 4,
"text": "<p>Those describe the genotype of an animal (or plant, virus etc.).</p>\n\n<p>The nomenclature can be very varied and domain-specific, but for those two examples:</p>\n\n<p>$dt^{sz}$ is a Syrian golden hamster model with a spontaneous mutation (i.e. occurred during breeding, without specific human intervention) which gives predisposition to seizures.<br>\nThey are described in this paper:</p>\n\n<p><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/1270790\" rel=\"nofollow\">Spontaneous seizures: a new mutation in Syrian golden hamsters. - Yoon et al. - J Hered 1976</a></p>\n\n<blockquote>\n <p>SPONTANEOUS motor seizures with tonic muscle spasms and severe paralytic states have been observed in inbred line BIO® 86.93 of Syrian hamsters\n (Mesocricetus auratus auratus). These animals had been inbred for 23 generations and maintained by Bio-Research Consultants. The seizures, which last from 2 to 5 hours, can be precipitated by mild stress, and occur in\n animals between the ages of 30 days and 60 days. Breeding tests have shown that the condition is transmitted as a simple recessive; accordingly, the gene symbol\n sz is proposed for this condition.</p>\n</blockquote>\n\n<p>The lowercase indicates that the mutation is recessive that is, you need to have two copies of the mutation to see its effect (its phenotype).</p>\n\n<p>dt comes from dystopia, another symptom of the mutation.</p>\n\n<p>As for Rgs9-Cre/+;gtROSA/+ mouse, the genotype is a bit more complex.</p>\n\n<p>Whenever you see /+ it means that the animal is heterozygous, that is, it only carries one copy of that specific gene.</p>\n\n<p>For instance these are transgenic animals producing the bacterial protein Cre under the Rgs9 promoter. A promoter is a sequence of DNA that controls the expression of a certain gene. In this case the DNA sequence for the promoter of the gene Rgs9 was attached to the DNA sequence for Cre. This new construct was then inserted into the genome of the mouse.\nThe result is a mouse in which the cells that normally transcribe the Rgs9 gene also produce Cre.</p>\n\n<p>This mouse line was then crossed with a reporter mouse line called gtROSA26, which expresses a certain protein called $\\beta$-galactosidase in a Cre-dependent manner. </p>\n\n<p>The gene for the galactosidase is present in all the cells, but only where Cre is present (in our case the Rgs9 positive cells) it will be transcribed.\nEventually the crossing leads to the expression of $\\beta$-galactosidase in Rgs9 positive cells. \n$\\beta$-galactosidase has the nice property that it can change the colour of certain chemicals to blue, which allows to easily visualize the cells that produce it. This can help you answer questions like: \"where is the Rgs9 gene transcribed?\".</p>\n\n<p>Wikipedia has a neat <a href=\"http://en.wikipedia.org/wiki/Gene_nomenclature\" rel=\"nofollow\">page on Gene nomenclature</a> with lots of links to nomenclature guidelines. </p>\n"
}
] |
[
{
"answer_id": 19096,
"pm_score": 3,
"text": "<p>These strings are specific genotypes of these animals. They often denominate mutations or transgenes. \nFor the hamster $dt^{sz}$ stands for dystopic, the sz comes from the first denomination of this symptoms as seizure. See <a href=\"http://books.google.de/books?id=Qq0SfGR_R_QC&pg=PA459&lpg=PA459&dq=dtsz%20hamster%20seizure&source=bl&ots=HY1P3hOl8V&sig=cDs_cxe1zti-1UYD69fGk4aj01U&hl=de&sa=X&ei=G16bU8eBFobXPeGEgPgE&ved=0CCMQ6AEwAA#v=onepage&q=dtsz%20hamster%20seizure&f=false\">here</a> for a brief explanation.</p>\n\n<p>For the mouse you have both alleles named: Rgs9-cre is a transgene, + in this context always stands for the wildtype. So this mouse has one allele of the transgene Rgs9-cre while the other allele is wildtype for it. Transgene constructs with the cre-recombinase can be inserted into the genome upon induction, which is a useful tool to modify genes. This needs to be done in mice which harbour the gtROSA transgene, which denominates a specific genetic background for the mice.\nSee here for more details: </p>\n\n<ul>\n<li>\"<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/1653172\">Promoter traps in embryonic stem cells: a genetic screen to\nidentify and mutate developmental genes in mice.</a>\"</li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/18037879\">Identification and targeting of the ROSA26 locus in human embryonic\nstem cells.</a></li>\n</ul>\n"
}
] |
19,115
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<p>Why isn't DNA like RNA; why isn't RNA like DNA, that is, helical? Why are RNA chains straight?</p>
|
[
{
"answer_id": 19118,
"pm_score": 4,
"text": "<p>The helix shape of DNA molecule is a consequence of its secondary structure. This refers to the bases contained in the molecule which pair, thus determining tertiary structure [1].</p>\n<p>Basepairing also occurs in RNA, so it can form a double helix. In fact, RNA is composed of short helices packed together [2]. Base pairs maintain DNA's helical structure no matter the nucleotide sequence [3].</p>\n<p>A nucleic acid strand is composed of nucleotides joined together by covalent bonds between the sugar of one nucleotide and the phosphate of the next. Adenine pairs with thymine and cytosine pairs with guanine by hydrogen bonds and form the double-stranded structure [3]. Because covalent bonds are stronger than hydrogen bonds, the double helical structure of DNA is easily broken by heat [4], but the nucleotides remain bonded together.</p>\n<p>Here is the tRNA molecule (you can see it has short helices):</p>\n<p><a href=\"https://commons.wikimedia.org/wiki/File:TRNA-Phe_yeast_1ehz.png#mediaviewer/File:TRNA-Phe_yeast_1ehz.png\" rel=\"nofollow noreferrer\"><img src=\"https://upload.wikimedia.org/wikipedia/commons/b/ba/TRNA-Phe_yeast_1ehz.png\" alt=\"TRNA-Phe yeast 1ehz.png\"></a><br>\"<a href=\"https://commons.wikimedia.org/wiki/File:TRNA-Phe_yeast_1ehz.png#mediaviewer/File:TRNA-Phe_yeast_1ehz.png\" rel=\"nofollow noreferrer\">TRNA-Phe yeast 1ehz</a>\" by <a href=\"//commons.wikimedia.org/wiki/User:Yikrazuul\" rel=\"nofollow noreferrer\" title=\"User:Yikrazuul\">Yikrazuul</a> - Own work. Licensed under <a href=\"https://creativecommons.org/licenses/by-sa/3.0/\" rel=\"nofollow noreferrer\" title=\"Creative Commons Attribution-Share Alike 3.0\">CC BY-SA 3.0</a> via <a href=\"https://commons.wikimedia.org/wiki/Main_Page\" rel=\"nofollow noreferrer\">Wikimedia Commons</a>.</p>\n<p>Here is the DNA structure:</p>\n<p><a href=\"https://commons.wikimedia.org/wiki/File:ADN_animation.gif#mediaviewer/File:ADN_animation.gif\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/J3Umv.gif\" alt=\"ADN animation.gif\"></a><br/><sub>(source: <a href=\"https://upload.wikimedia.org/wikipedia/commons/8/81/ADN_animation.gif\" rel=\"nofollow noreferrer\">wikimedia.org</a>)</sub><br/><br>\"<a href=\"https://commons.wikimedia.org/wiki/File:ADN_animation.gif#mediaviewer/File:ADN_animation.gif\" rel=\"nofollow noreferrer\">ADN animation</a>\" by brian0918™ - Own work. Licensed under Public domain via <a href=\"https://commons.wikimedia.org/wiki/Main_Page\" rel=\"nofollow noreferrer\">Wikimedia Commons</a>.</p>\n<hr />\n<p>References:</p>\n<ol>\n<li><p>Wikipedia contributors, "Nucleic acid double helix," Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Nucleic_acid_double_helix&oldid=609435163\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/w/index.php?title=Nucleic_acid_double_helix&oldid=609435163</a> (accessed June 26, 2014).</p>\n</li>\n<li><p>Wikipedia contributors, "RNA," Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=RNA&oldid=612056511\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/w/index.php?title=RNA&oldid=612056511</a> (accessed June 26, 2014).</p>\n</li>\n<li><p>Wikipedia contributors, "DNA," Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=DNA&oldid=611891356\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/w/index.php?title=DNA&oldid=611891356</a> (accessed June 26, 2014).</p>\n</li>\n<li><p>Wikipedia contributors, "Nucleic acid thermodynamics," Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Nucleic_acid_thermodynamics&oldid=606379256\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/w/index.php?title=Nucleic_acid_thermodynamics&oldid=606379256</a> (accessed June 26, 2014).</p>\n</li>\n</ol>\n"
}
] |
[
{
"answer_id": 19119,
"pm_score": 3,
"text": "<p>RNA (single or double stranded) actually can and does form a helix in the absence of certain complex 3D structures. The RNA helix is typically A-form, as opposed to B-form for typical DNA. The A-form helix is right-handed like the B-form but is more compact (2.6 Å rise versus 3.4 Å) and wider (26 Å diameter vs 20 Å). The differing helices arise from the 2'-OH present in RNA which sterically hinders the formation of a B-form helix (by constricting the ribose to C-3' endo pucker).</p>\n\n<hr>\n\n<p><img src=\"https://i.stack.imgur.com/X84s7.jpg\" alt=\"enter image description here\"></p>\n\n<p>[From Wikipedia. Double stranded DNA helices. A-form is on the left, B-form in the middle and Z-form on the right. There are other forms not illustrated here.]</p>\n\n<hr>\n\n<p><img src=\"https://upload.wikimedia.org/wikipedia/commons/a/a4/Pre-mRNA-1ysv-tubes.png\" height=\"500\" /></p>\n\n<p>[From Wikipedia. A hairpin loop (the result of intrastrand base pairing in a single RNA molecule) that has adopted an A-form helix.]</p>\n\n<hr>\n\n<p><img src=\"https://i.stack.imgur.com/UGljc.jpg\" alt=\"enter image description here\"></p>\n\n<p>[Just emphasizing that a single strand nucleic acid, even without secondary structure, also forms helices.]</p>\n\n<hr>\n\n<p>The helices of both DNA and RNA form in aqueous solution because of the hydrophobic and aromatic (which also implies planar) nature of the bases themselves. By forming a helix, the bases within one strand come closer together which is thermodynamically more favourable because of stacking interactions between the conjugated ring systems as well as the exclusion of water from their hydrophobic surfaces (which thus increases entropy). </p>\n"
}
] |
19,162
|
<p>Once, as a child, I found a spider in my parents' garden. I remember catching it in a jar because I thought it looked unusual, but I never figured out what kind of spider it was and unfortunately didn't get any pictures. I've been looking for it in books and on the Internet since, based on memory, with no luck.</p>
<p>This was twenty years ago now, and I realize my memory of it may not be good enough to identify it now, but here's trying.</p>
<p>What I remember best was its abdomen, which was a dark metallic blue and sort of rectangular in shape. Its body was probably about 1.5 cm long, without the legs, and maybe 1 cm wide or a little less (I was a child, things look bigger when you're small.) It was found in a garden in the suburbs of Copenhagen, Denmark, sitting on a bed sheet drying in the sun. It left only a few strings of web, almost like a bridge, from the bottom of the jar to the lid where it had escaped during the night because the lid wasn't sealed. I never found it again or saw another spider like it.</p>
|
[
{
"answer_id": 19698,
"pm_score": 3,
"text": "<p>This may be what you are searching for:</p>\n\n<p><img src=\"https://i.stack.imgur.com/dDlkk.jpg\" alt=\"enter image description here\"></p>\n\n<p>It's actually a <strong>male purseweb spider</strong> (Atypus affinis), the color fades to black, eventually.</p>\n\n<p>Source: <a href=\"http://www.spiderzrule.com/purseweb2.htm\" rel=\"nofollow noreferrer\">http://www.spiderzrule.com/purseweb2.htm</a></p>\n"
}
] |
[
{
"answer_id": 97043,
"pm_score": 0,
"text": "<p>Was it this? This is another purseweb spider species.</p>\n<p><a href=\"https://i.stack.imgur.com/r9Gtv.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/r9Gtv.jpg\" alt=\"enter image description here\" /></a></p>\n"
}
] |
19,204
|
<p>Say you have a needle, and you poke a very specific area on your left thumb.
A signal gets sent from that nerve up your spine and into your brain.</p>
<p>How does the brain know exactly where this signal has come from to such accuracy?</p>
<ul>
<li>Does each nerve in every conceivable part of the body have a unique path that goes up the spine and into the brain, so that's how the brain knows where it came from?</li>
<li>Or does the nerve encode the signal as data which travels up a generic nerve, and the brain decodes the information, which contains the "address" of the particular spot that was stimulated? If this is the case, how are the data encoded? Binary?</li>
</ul>
|
[
{
"answer_id": 19209,
"pm_score": 3,
"text": "<p>In addition to what Spinoral has said, and in response to your comment above, I will add a bit more about the mechanisms.</p>\n\n<p>Essentially, in some form or another it's receptive fields all the way up.</p>\n\n<p>A brief outline of the anatomy:\nThe cells from the spinal cord are <a href=\"http://en.wikipedia.org/wiki/Pseudounipolar_neuron\" rel=\"nofollow\">pseudounipolar</a> and have their cell bodies in the dorsal root ganglia in the spinal cord. The other \"leg\" of the <a href=\"http://blog.ketyov.com/2012/05/what-is-longest-axon.html\" rel=\"nofollow\">sensory neuron</a> projects to the medulla, which has cell bodies which send axons to the <a href=\"http://en.wikipedia.org/wiki/Ventral_posterolateral_nucleus\" rel=\"nofollow\">VPL thalamus</a>, which then has cell bodies that project to the primary somatosensory cortex. There are points of decussation (crossing over the midline), but I'll ignore those for now. </p>\n\n<p>The receptive fields:</p>\n\n<blockquote>\n <p>The receptive fields of somatosensory neurons share much in common with the receptive fields of visual neurons. As for visual neurons, the somatosensory receptive fields comprise a restricted 2-dimensional region of space where a stimulus can evoke a neuronal response. In somatosensory neurons, however, space refers to a region of the body and the stimulus can be touch, vibration, temperature or pain</p>\n</blockquote>\n\n<p>(from <a href=\"http://www.scholarpedia.org/article/Receptive_field#Somatosensory_receptive_fields\" rel=\"nofollow\">Scholarpedia</a>)</p>\n\n<p>Essentially, the somatosensory input is \"filtered\" at all of those stops along the way and refined in terms of things such as whether the sensation came from the center or the edges of the receptive field, etc. </p>\n\n<p>Cells in the cortex (the waypoint for the sensory information) are organized in <a href=\"http://en.wikipedia.org/wiki/Cortical_minicolumn\" rel=\"nofollow\">microcolumns</a>, which are representative of a particular location on the body (and arranged topographically into the \"homunculus\", as the other answer mentions).</p>\n\n<p>All of this follows what is called the <a href=\"http://www.d.umn.edu/~jfitzake/Lectures/DMED/SensoryPhysiology/GeneralPrinciples/CodingTheories.html\" rel=\"nofollow\">\"labeled line\"</a> theory, which is getting a bit outmoded due to new knowledge about ensemble coding in neurons, but for purposes of the somatosensory system it still holds up pretty well. </p>\n"
}
] |
[
{
"answer_id": 19206,
"pm_score": 3,
"text": "<p>The accuracy of sensation is actually quite variable depending on the region of our body. Highly innervated areas such as our fingers have a higher degree of accuracy than sparsely innervated areas such as our legs.</p>\n\n<p>There is a simple experiment you can do to illustrate this. Close your eyes and then get a friend to lightly and slowly run their finger from your wrist, up towards the bend in your elbow on the inside of your arm. Try to guess at what point the reach the joint of your elbow. </p>\n\n<p>In terms of how the brain knows where it came from, there is part of your brain called the sensory cortex. This sensory cortex has a pattern that corresponds to areas of the body. This pattern is known as a the sensory homunculus (google images will find this). As signals pass up the various different spinal pathways and into the brain they are sent up to this sensory area and the appropriate region of the homunculus is stimulated thereby giving the sensation in the appropriate body area. </p>\n\n<p>Interestingly in some brain surgery a patient may be kept conscious so that these areas can be directly stimulated by electric current and the patient will experience sensations. </p>\n\n<p>There is also a matching area, called the motor cortex, which corresponds to movement rather than sensation. </p>\n\n<p>The above is a simplified version of what goes on and there is lots more detail which would be covered in neuroanatomy books</p>\n"
}
] |
19,210
|
<p><strong>Background:</strong> I'm currently performing research in mathematical biology,
specifically on the treatment dynamics of HIV and TB co-infection.</p>
<p><strong>Question:</strong> Can a person infected with TB disease, who are undergoing treatment for it, infect a person with no history of TB bacteria in their body? </p>
<p><strong>Reformulation:</strong> In other words, is there a similar analogue for TB as for HIV, wherein an HIV+ person undergoing treatment for HIV will have a lowered viral load and thus have negligible chances of infecting a person with no history of HIV?</p>
<p>Please note that my model does not incorporate latent TB because it would become too complicated to analyze. I am focusing only on TB disease because <strong>only it</strong> is infectious.</p>
<p>Thanks for any help.</p>
|
[
{
"answer_id": 19211,
"pm_score": 4,
"text": "<p>First there is one major difference between HIV and TB: As long as the TB bacteria are still susceptible to treatment (which is developing into a major problem in some regions of the world) there is a effective treatment which can eradicate the infection. For HIV this is not possible. Here we can only lower the viral load (sometimes under the detection limit), but when the treatment is stopped, the virus will return.</p>\n\n<p>Then it seems that patients under treatment of a drug susceptible TB are infectious for a longer time than previously thought. Until now they have been isolated at the beginning of the treatment (typically around the first two weeks) until three consecutive sputum samples had been negative. Then they were released from isolation and thought to be non-infectious. At this point they are not cured, the treatment has to go on for several weeks.</p>\n\n<p>Now there is newer research indicating that patients can still be infectious although they are under treatment <em>and</em> have negative sputum samples. It seems here that the currently used detection method is not sensitive enough. See these references for more information:</p>\n\n<ul>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/23224098\">How Many Sputum Culture Results Do We Need To Monitor\nMultidrug-Resistant-Tuberculosis (MDR-TB) Patients during Treatment?</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/24278293\">High incidence of tuberculosis, low sensitivity of current diagnostic\nscheme and prolonged culture positivity in four colombian prisons. A\ncohort study.</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/20624064\">Prolonged infectiousness of tuberculosis patients in a directly\nobserved therapy short-course program with standardized therapy.</a></li>\n</ul>\n"
}
] |
[
{
"answer_id": 19217,
"pm_score": 2,
"text": "<p>I think its a bit difficult to compare HIV and TB this way because TB is transmitted mainly through respiratory droplets whilst HIV is mainly through contamination of blood products/sex, etc but not via the respiratory route. As far as I know, there's still a likelihood of TB transmission from a treated patient to an untreated patient. TB is quite complex, treated patients can still undergo reactivation later in life and still infect other people-the mechanisms are not fully understood. Treated patients can also develop drug resistance and then relapse which will make them again highly infectious. </p>\n"
}
] |
19,303
|
<p>I bought a blood pressure monitor (A&D UA-851) which has the option to measure irregular heartbeat. I do understand what 'irregular' means, but why do irregular heartbeats happen and what are it's implications short and long term? </p>
|
[
{
"answer_id": 19306,
"pm_score": 5,
"text": "<p>The normal cardiac cycle is comprised of two distinct phases: <strong>the systolic phase</strong> in which the heart contracts, ejecting the blood, followed by the <strong>the diastolic phase</strong> when the cardiac muscle relaxes, refilling the heart with blood.</p>\n\n<p>This cycle is assured by specialised cardiomyocytes (Cardiac muscle cells) that conduct electrical impulses through the heart. When there's interference in this electric activity, the cycle becomes irregular or arrhythmic.</p>\n\n<p>Arrhythmias can be divided by their place of origin: </p>\n\n<ul>\n<li>Atrial (atria are the upper chambers of the heart)</li>\n<li>Ventricular (ventricles are lower chambers of the heart)</li>\n<li>Junctional (the junction between the two)</li>\n<li>Heart blocks (caused by a blockade in the conductivity of the electrical specialised cardiomyocytes)</li>\n</ul>\n\n<p>Some arrhythmias are physiological, such as the Respiratory sinus arrhythmia, a naturally occurring variation in heart rate that occurs during a breathing cycle. Also, in healthy individuals, some extra sistoles might occur without being the translation of a subjacent heart condition and have benign prognosis in individuals without other conditions. </p>\n\n<p>However, some arrhythmias can have a wide range of health implications, from asymptomatic, to a mild intolerance to exercise, to Cerebrovascular Accident (CVA or stroke) or even sudden death due to cardiac arrest.</p>\n\n<p>Therapeutic varies with the underlying cause but can be medical (with drugs such as Na+, K+ and Ca+ channel blockers, beta-blockers and Digoxin) or surgical (ie: Artificial pacemaker).</p>\n"
}
] |
[
{
"answer_id": 27472,
"pm_score": 3,
"text": "<p>Very simply putting, irregular heat beat means that the pulse is not regular. It can be diagnosed by checking your pulse clinically. </p>\n\n<p>Irregularities are further classified as: </p>\n\n<ol>\n<li><p>Regularly Irregular: this occurs in heart blocks where every second or third beat is skipped regularly causing a pattern. Usually as time progresses the degree of block worsens and result in the final form which is complete block (fourth degree heart block)</p></li>\n<li><p>Irregularly Irregular: this occurs in arrhythmia where there is total dissociation between atria and ventricles and the ventricles beat very irregularly with no pattern. The ventricles don't follow intrinsic rhythm because every SA nodal impulse that occurs at the end of latency of AV node will get conducted. Thus the heart rate is very high without any pattern. (Here heart rate means ventricular rate)</p></li>\n</ol>\n"
}
] |
19,310
|
<p>Not all carcinogens are mutagens. Alcohol and estrogen, for example, does not damage DNA.</p>
<p>It's one of the assumptions of the Ames test that mutagenicity implies carcinogenicity, but is this <em>always</em> the case? I assumed that it was, but then I <a href="https://biology.stackexchange.com/questions/14399/carcinogens-how-do-they-work?rq=1">saw one of the comments here</a>. I did some more research but the internet seems to be reluctant to be definitive on the subject. <a href="https://answers.yahoo.com/question/index?qid=20120324145935AAa36mO" rel="nofollow noreferrer">This guy</a> claims 'no', but I'd prefer sources or at least a response that handles counterexamples like HPV. <a href="http://carcin.oxfordjournals.org/content/25/3/299.abstract" rel="nofollow noreferrer">This paper</a> claims 'yes', but doesn't list any specific examples. Some mutagens might be more specific to genes involved in cell cycle regulation, so I could see how a weak mutagen is a powerful carcinogen.</p>
<p>My question is, can you go the other way? Are there mutagens that just do not cause cancer? If they do not exist or are not known to exist, are they even possible?</p>
|
[
{
"answer_id": 19331,
"pm_score": 5,
"text": "<h3>Short answer</h3>\n<p>All mutagens are potential carcinogens unless the mutagen is highly specific to a site. As noted in the question, carcinogens need not be mutagenic.</p>\n<hr />\n<p>HPV causes oncogenic transformation of a cell because of certain proteins that it expresses. HPV is considered a carcinogen by the <a href=\"https://monographs.iarc.fr/list-of-classifications-volumes/\" rel=\"nofollow noreferrer\">IARC</a>. Some retroviruses are oncogenic: they might carry an oncogene or insert randomly near an endogenous proto-oncogene and cause oncogenic transformation; this phenomenon is called insertional mutagenesis (<a href=\"https://www.ncbi.nlm.nih.gov/books/NBK19409/\" rel=\"nofollow noreferrer\">Coffin JM, Hughes SH, Varmus HE, editors. <em>Retroviruses</em></a>). They can also integrate within a gene and knock it out. Many of these viruses are considered carcinogens by <a href=\"https://monographs.iarc.fr/list-of-classifications-volumes/\" rel=\"nofollow noreferrer\">IARC</a>.</p>\n<p>Hepatitis viruses (B & C) can also induce carcinogenesis but insertional mutagenesis is not the sole mechanism (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/16461228\" rel=\"nofollow noreferrer\">Cougot et al., 2005</a>; <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/19874379\" rel=\"nofollow noreferrer\">Fung et al., 2009</a>; <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422399/\" rel=\"nofollow noreferrer\">Lemon & McGivern, 2012</a>). Hepatitis viruses are considered carcinogens by IARC.</p>\n<p>Ethanol in alcoholic beverages is considered carcinogenic by IARC. There are many substances listed as carcinogens by IARC but they are not mutagenic. The general mechanism of carcinogenesis by these substances may be prolonged inflammation or ROS generation.</p>\n<p>Loss of function of the tumour suppressor gene p53 leads to cancerous progression (<a href=\"https://doi.org/10.1038/onc.2016.396\" rel=\"nofollow noreferrer\">Chiche et al., 2016</a>; <a href=\"https://doi.org/10.1007/978-1-59259-100-8_14\" rel=\"nofollow noreferrer\">Venkatachalam et al.</a> ISBN:978-1-59259-100-8). So an siRNA that targets p53 should be called a carcinogen. It would however not cause any mutations and is hence not a mutagen.</p>\n<p>If you consider the tools developed for genome editing, such as ZFN, CRISPR-Cas and TALEN as mutagens then they are not carcinogenic. However the term <em>mutagen</em> is not used for these molecules. Mutagen almost always refers to a molecule that causes random mutagenesis thereby making it a potential carcinogen.</p>\n"
}
] |
[
{
"answer_id": 19311,
"pm_score": 1,
"text": "<p>I'm no expert on the matter, but just quoting from <a href=\"http://en.wikipedia.org/wiki/Mutagen\" rel=\"nofollow noreferrer\">Wikipedia</a>:</p>\n<blockquote>\n<p>Mutagens are not necessarily carcinogens, and vice versa. Sodium Azide for example may be mutagenic (and highly toxic), but it has not been shown to be carcinogenic.</p>\n</blockquote>\n<p>It cites <a href=\"http://ntp.niehs.nih.gov/ntp/htdocs/lt_rpts/tr389.pdf\" rel=\"nofollow noreferrer\">Toxicology And Carcinogenesis Studies Of Sodium Azide</a>.</p>\n<p>So it would appear the answer is <strong>no</strong>. Not all mutagens are carcinogens.</p>\n"
}
] |
19,312
|
<p>I am not comparing a cat with leopard.</p>
<p>I am just saying that we humans are all one type of creature and we are diverse (I am not saying we are class of mammals and phylum of etc and kingdom etc, because my religion doesn't believe in it).</p>
<p>So consider the class of cats they are one type of species so why aren't they diverse in phenotype like us? </p>
<p>Why do other animals, plants, unicellular organisms not have diversity in their phenotype and how they can recognize each other, like a bird always brings food to his offspring and it can't make mistake by giving it to other offspring of its own species? </p>
<p>So can I say they aren't diverse because of in their meiosis division their chromosomes don't cross over and random assort (alignment)? </p>
|
[
{
"answer_id": 19313,
"pm_score": 5,
"text": "<p>In your question, your assumption that animal species are less diverse phenotypically than humans is wrong. I am sure you will appreciate @terdon's answer to <a href=\"https://biology.stackexchange.com/questions/14414/do-humans-have-enough-biological-differences-to-be-grouped-into-races-or-subspec/\">this post</a> and @rg255 answer to <a href=\"https://biology.stackexchange.com/questions/16385/why-do-different-humans-look-different\">this post</a>.</p>\n\n<p>Don't forget that we are good at detecting differences among humans (because we evolved for this purpose). We are doing much worse at telling apart animals from other species just because we have not evolved for this purpose. This is the reason why we tend to see human faces when looking at clouds but we rarely see sheep faces! Several studies (<a href=\"http://www.nature.com/nature/journal/v414/n6860/full/414165a0.html\" rel=\"nofollow noreferrer\">here</a> and <a href=\"http://rstb.royalsocietypublishing.org/content/361/1476/2155.long\" rel=\"nofollow noreferrer\">here</a>) showed that sheep are able to recognize each other (and we even know the number of neurones needed to remember one face). They are probably better at telling two sheep apart than telling two human apart.</p>\n\n<p>Another interesting fact is the so-called <a href=\"http://en.wikipedia.org/wiki/Cross-race_effect\" rel=\"nofollow noreferrer\">cross-race effect</a>. We, humans, are better at recognizing faces of people from our own ethnic group than faces of people from other ethnic groups. For example, a Japanese is very good at Japanese faces recognition but not good at recognizing European faces. Same is true the other way around.</p>\n\n<p>As @user568459 said in the comments: some people are not able to recognize faces. This is due to a cognitive disease called <a href=\"http://en.wikipedia.org/wiki/Prosopagnosia\" rel=\"nofollow noreferrer\">Prosopagnosia</a> (also called face blindness). Those suffering from this disease are not better at recognizing sheep faces than human faces.</p>\n\n<hr>\n\n<blockquote>\n <p>So consider the class of cats they are one type of species so why aren't they diverse in phenotype like us?</p>\n</blockquote>\n\n<p>There is no good definition I think of what is phenotypic diversity (no accurate and objective index to measure it) but at first sight I would tend to think that cats are more diverse than humans. One of the main features one would probably raise when talking about human diversity is skin color. And in terms of color, cats are much more diverse than humans. You may think of an extraordinary diversity when thinking of Norwegian that are taller than Indonesian (I may not have chosen the two extremes) by several centimeters on average but think about cats! The average cat weight 4 to 5 kg but some cats weight less than 2 kg and some other (like the <a href=\"http://en.wikipedia.org/wiki/Maine_Coon\" rel=\"nofollow noreferrer\">coon cat</a>) weight more than 10 kg (<a href=\"http://www.cat-world.com.au/cat-world-records\" rel=\"nofollow noreferrer\">World Record</a>: 21.3 kg). Imagine a human ethnic group that would on average weight 5 times more than another ethnic group! And think also about cats' hair length or tail shape! Humans vary in terms of facial feature (lips size, nose shape, etc.) so do cats. Some look like their face was smashed against a wall while others have a long muffle. Again I welcome you to have a look to <a href=\"https://biology.stackexchange.com/questions/14414/do-humans-have-enough-biological-differences-to-be-grouped-into-races-or-subspec/\">this post</a>.</p>\n\n<blockquote>\n <p>how they can know each like a bird always brings food to his offspring and it can't make mistake by giving it to other offspring of it's own species?</p>\n</blockquote>\n\n<p>As I said above humans evolved to recognize their own. Many species also evolved in order to recognize their own. In some species individuals use smell rather than visual features in order to recognize each other (odor is also a kind of phenotypic variation). But still some species are poor to recognize each other. For a bird, it seems rather easy to not feed the wrong individual as all their offspring are usually together in the same nest. However you might be interested the lifestyle of the <a href=\"http://en.wikipedia.org/wiki/Common_cuckoo\" rel=\"nofollow noreferrer\">cuckoo</a> who parasites nests of other bird species. Cuckoos' babies and particularly the inner beak resemble to the babies of the species they parasite and often the parents (often the mother only is involved in feeding the young) get fooled and feed the cuckoo.</p>\n\n<blockquote>\n <p>So can i say they aren't diverse because of in their meiosis division their chromosomes don't cross over and random assort (alignment)?</p>\n</blockquote>\n\n<p>No, you can't say that! Because they are diverse and because for many of the species you may think about, cross-over does occur. Their genetic diversity as well as their phenotypic diversity is as high than in humans. There is nothing extraordinary about humans (except their brain and the related fact that we predigest our food by cooking it) compare to other lineages. And there is nothing extraordinary to have one extraordinary feature (such as a big brain) that you can't find in other lineages! Many lineages are extraordinary in some sense.</p>\n"
}
] |
[
{
"answer_id": 19315,
"pm_score": 3,
"text": "<p>I'd like to add that the variations in individuals within a species are a fundamental observation upon which modern biology is standing. Darwin wrote at least <a href=\"http://www.markhannam.com/essays/essay5a.htm\" rel=\"nofollow noreferrer\">2 chapters of Origin of Species demonstrating how animals and plants have a lot of individual variations</a>:</p>\n\n<blockquote>\n <p>Darwin's argument involved four steps. First, he noted the wide variation between many types of living organisms: between species of plant, fish, bird and mammal; and also between different family groups within the same species; and also between different exemplars within the same family. Wherever we look - and during his five-year voyage on The Beagle in his early twenties, there were few places on earth where Darwin had not looked - we see differences between organisms: different sizes, different colours, different features, different behaviours and, of course, different survival rates. The theory of natural selection takes variation of species and within species as its starting point. </p>\n</blockquote>\n\n<p>Before that era (he was not the only one who made this argument) pretty much everyone believed that all animals of a given species were the same. </p>\n\n<p>It took quite a while before everyone was convinced, but an entire generation of scientists was won over. </p>\n\n<p>If you need a modern confirmation of this, look into cattle breeding. <a href=\"http://www.theatlantic.com/technology/archive/2012/05/the-perfect-milk-machine-how-big-data-transformed-the-dairy-industry/256423/\" rel=\"nofollow noreferrer\">Individual phenotypes make some bulls worth many thousands of dollars/euros</a>. Others nothing. Lastly, now that we understand that the basis of inheritance is in the DNA, we can quantitate the specific mutation rates in various genes and segments of DNA and show that <a href=\"http://rd.springer.com/article/10.1007%2FBF00393984#page-1\" rel=\"nofollow noreferrer\">they are comparable from species to species</a>. <a href=\"http://en.wikipedia.org/wiki/Mutation_rate#Variation_in_mutation_rates\" rel=\"nofollow noreferrer\">These vary somewhat, but humans are not exceptional</a>.</p>\n"
}
] |
19,381
|
<p>I visited a bird enclosure close to where I live in Australia. The enclosure had several different species. The birds that stood out most were these doves sitting right along the fence railing, making a deep "Wo-wo-wo-woo" sound. That and also I thought they looked and sounded similar to Spotted Doves.</p>
<p><img src="https://i.stack.imgur.com/X6Jxl.jpg" alt="enter image description here">
<img src="https://i.stack.imgur.com/cgtAi.jpg" alt="enter image description here"></p>
<p>Does anyone know what the species of this birds may be?</p>
|
[
{
"answer_id": 19382,
"pm_score": 3,
"text": "<p>I think this is a Barbary dove (or Ringneck dove). See this image (from the <a href=\"http://nzbirdsonline.org.nz/species/barbary-dove\" rel=\"nofollow noreferrer\">here</a>):</p>\n\n<p><img src=\"https://i.stack.imgur.com/dFbDY.jpg\" alt=\"enter image description here\"></p>\n\n<p>More information can be found <a href=\"http://en.wikipedia.org/wiki/Barbary_dove\" rel=\"nofollow noreferrer\">here</a> and <a href=\"http://nzbirdsonline.org.nz/species/barbary-dove\" rel=\"nofollow noreferrer\">here</a>. The second pages shows also images of different color variations.</p>\n"
}
] |
[
{
"answer_id": 19383,
"pm_score": 1,
"text": "<p>it is symi bird and more over it is commonly called as collared dove its a resident of symi and would have brought to australia by other means\n<img src=\"https://i.stack.imgur.com/dX223.jpg\" alt=\"enter image description here\">\nyou can find a list off all the symi birds <a href=\"http://symifloraandfauna.jigsy.com/symibirdlist\" rel=\"nofollow noreferrer\">here</a></p>\n"
}
] |
19,411
|
<p>I got this doubt when I was studying about <a href="http://en.wikipedia.org/wiki/Hematocrit" rel="nofollow">haematocrit</a> value. According to my NCERT textbook males have greater number of RBCs than females. But who will have more RBCs when comparing a normal male and a female who lives at a higher altitude?</p>
<p>*edit</p>
<p>the magnitude of altitude would be less than <a href="http://en.wikipedia.org/wiki/Kangchenjunga" rel="nofollow">8,586 m (28,169 ft</a>) as the woman I know is not exactly at the top summit of <a href="http://en.wikipedia.org/wiki/Kangchenjunga" rel="nofollow">Kanchenjunga</a> so what would be the answer then?</p>
|
[
{
"answer_id": 19413,
"pm_score": 3,
"text": "<p>Currently impossible to give a definite answer... It depends what altitude you look at. </p>\n\n<p>Going from @Alan_boyd's answer the normal range is 40-50% for males and 36-44% for females. If the altitude at which a person is acclimatized to correlates well with red blood cell count (RBCC), and this effect is not gender specific (i.e. both sexes are affected similarly), then an average woman from high altitude should have a higher RBCC than an average from low altitude. But whether or not the high altitude female RBCC exceeds that of the male depends on the altitude of the two measured.</p>\n\n<p>This rough graph, <em><a href=\"http://en.wikipedia.org/wiki/Altitude_training\" rel=\"nofollow noreferrer\">assuming RBCC and altitude correlate</a> and that <a href=\"http://www.nlm.nih.gov/medlineplus/ency/article/003646.htm\" rel=\"nofollow noreferrer\">male RBCC is higher than female RBCC</a></em>, shows the problem. Female (red dashed line) A is from a higher altitude than the selected male (blue dashed line) and has lower RBCC. Female (red dashed line) B is from a higher altitude than the selected male (blue dashed line) and has higher RBCC. </p>\n\n<p><img src=\"https://i.stack.imgur.com/oLScX.png\" alt=\"enter image description here\"></p>\n\n<p><strong>Define altitudes and the question may be answerable.</strong></p>\n"
}
] |
[
{
"answer_id": 19412,
"pm_score": 2,
"text": "<p>According to the <a href=\"http://www.nlm.nih.gov/medlineplus/ency/article/003646.htm\" rel=\"nofollow\">MedlinePlus site</a> these are the normal ranges for haematocrit:</p>\n\n<p>Male: 40.7 - 50.3%</p>\n\n<p>Female: 36.1 - 44.3%</p>\n\n<p>Unfortunately it isn't clear if these ranges are for people living at low altitude, but since most people in the USA do, I think this is a safe inference. So clearly there is already some overlap.</p>\n\n<p>The paper accessible <a href=\"http://www.jpp.krakow.pl/journal/archive/11_07_s5/pdf/811_11_07_s5_article.pdf\" rel=\"nofollow\">here</a> reports various changes in haematocrit due to moving between different altitudes. Broadly speaking these changes are in the range of 10 - 15 percentage points (e.g. a change from 39% to 49%).</p>\n\n<p>So yes, a female who has moved to a high altitude is likely to experience an erythrocytosis (or polycythaemia) which would mean that her haematocrit would exceed that of many males. </p>\n"
}
] |
19,416
|
<p>FRET only works for interactions between 1nm to 20nm.</p>
<p>How can you be sure that the interaction that you want to study isn't less than 1 nm/greater than 20nm apart?</p>
|
[
{
"answer_id": 19413,
"pm_score": 3,
"text": "<p>Currently impossible to give a definite answer... It depends what altitude you look at. </p>\n\n<p>Going from @Alan_boyd's answer the normal range is 40-50% for males and 36-44% for females. If the altitude at which a person is acclimatized to correlates well with red blood cell count (RBCC), and this effect is not gender specific (i.e. both sexes are affected similarly), then an average woman from high altitude should have a higher RBCC than an average from low altitude. But whether or not the high altitude female RBCC exceeds that of the male depends on the altitude of the two measured.</p>\n\n<p>This rough graph, <em><a href=\"http://en.wikipedia.org/wiki/Altitude_training\" rel=\"nofollow noreferrer\">assuming RBCC and altitude correlate</a> and that <a href=\"http://www.nlm.nih.gov/medlineplus/ency/article/003646.htm\" rel=\"nofollow noreferrer\">male RBCC is higher than female RBCC</a></em>, shows the problem. Female (red dashed line) A is from a higher altitude than the selected male (blue dashed line) and has lower RBCC. Female (red dashed line) B is from a higher altitude than the selected male (blue dashed line) and has higher RBCC. </p>\n\n<p><img src=\"https://i.stack.imgur.com/oLScX.png\" alt=\"enter image description here\"></p>\n\n<p><strong>Define altitudes and the question may be answerable.</strong></p>\n"
}
] |
[
{
"answer_id": 19412,
"pm_score": 2,
"text": "<p>According to the <a href=\"http://www.nlm.nih.gov/medlineplus/ency/article/003646.htm\" rel=\"nofollow\">MedlinePlus site</a> these are the normal ranges for haematocrit:</p>\n\n<p>Male: 40.7 - 50.3%</p>\n\n<p>Female: 36.1 - 44.3%</p>\n\n<p>Unfortunately it isn't clear if these ranges are for people living at low altitude, but since most people in the USA do, I think this is a safe inference. So clearly there is already some overlap.</p>\n\n<p>The paper accessible <a href=\"http://www.jpp.krakow.pl/journal/archive/11_07_s5/pdf/811_11_07_s5_article.pdf\" rel=\"nofollow\">here</a> reports various changes in haematocrit due to moving between different altitudes. Broadly speaking these changes are in the range of 10 - 15 percentage points (e.g. a change from 39% to 49%).</p>\n\n<p>So yes, a female who has moved to a high altitude is likely to experience an erythrocytosis (or polycythaemia) which would mean that her haematocrit would exceed that of many males. </p>\n"
}
] |
19,442
|
<p>I am impressed by the illustrations for the Protein Data Bank ‘Molecule of the month’, e.g. the gorgeous image of <a href="http://www.rcsb.org/pdb/101/motm.do?momID=168" rel="nofollow noreferrer">DNA Helicase</a> below. Does anyone know how they were made or how one might create something similar?</p>
<p><a href="https://i.stack.imgur.com/GDfyn.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/GDfyn.jpg" alt="DNA Helicase" /></a><br />
<sub>(source: <a href="http://www.rcsb.org/pdb/education_discussion/molecule_of_the_month/images/168-DNAHelicase_4esv.jpg" rel="nofollow noreferrer">rcsb.org</a>)</sub></p>
|
[
{
"answer_id": 19447,
"pm_score": 4,
"text": "<p>Those (really cool) pictures are created by David Goodsell using custom-written software.</p>\n<p>From an <a href=\"http://www.rcsb.org/pdb/static.do?p=education_discussion/molecule_of_the_month/about.html\" rel=\"noreferrer\">interview to the artist</a>:</p>\n<blockquote>\n<p><em>PDB</em>: How do you create the illustrations?</p>\n<p><em>Goodsell</em>: Most of the pictures are created with a computer program that I developed back when I was doing postdoctoral work with Dr. Art Olson here at The Scripps Research Institute. I've been using this style of illustration--with flat colors and black outlines--for about 10 years now. I like the way that this style simplifies the molecule, giving a feeling for the overall shape and form of the molecule, but at the same time you can still see all the individual atoms. On the last page of each Molecule of the Month--"Exploring the Structure"--I always use RasMol, to give visitors an idea of the kinds of pictures that they can create themselves with off-the-shelf software.</p>\n</blockquote>\n<p>There are good tools around if you want to replicate that look. Although it may take a bit of tweaking (and possibly programming) I would surely give <a href=\"http://www.pymol.org/\" rel=\"noreferrer\">PyMOL</a> and <a href=\"http://www.bioblender.eu/\" rel=\"noreferrer\">Bioblender</a> a try.</p>\n"
}
] |
[
{
"answer_id": 81545,
"pm_score": 2,
"text": "<p>I don’t actually consider these pictures either “gorgeous” or “cool” — they are not to my taste — and I’m not really sure that the question is about biology, but as it has resurfaced after almost 5 years I thought I’d give an answer which explained how one might create something similar, rather than how they were actually made.</p>\n\n<p>The original 3D-graphics program used was <em>RasMol</em>, but as that only runs on Windows, hasn’t been updated for years, and has no viable web version, I would suggest using <em>JMol/JSMol</em> instead. You can either download the application and work with it as described in my answer to a previous question. Alternatively you can just find a web page with a JSMol window (such as a page used in <a href=\"https://www.mvls.gla.ac.uk/Teaching/SLS-GMC/prstr.html\" rel=\"nofollow noreferrer\">my own teaching material</a>) and use that with the Console available from the JSMol logo. So what I do is:</p>\n\n<ol>\n<li>Get the PDB file I want to work with from the Protein Data Bank.</li>\n<li>Drag it into the JMol window when the molecule loads in wireframe mode as in (A), below.</li>\n<li>Give a series of commands such as the following to get a spacefilling image (B) in colours other than CPK (you can specify the colours of the chains if you wish) and without the shiny light patches, which are fine for standard images, but will cause problems. The beauty of JMol is you can generate high resolution images which you can drag back into a JMol window and work on again later (as long as you haven’t edited them).</li>\n</ol>\n\n<pre>\n restrict protein\n wireframe off\n select protein\n spacefill on\n colour chains\n set specular off\n write pngj 2000 2000 \"my.png\"\n</pre>\n\n<ol start=\"4\">\n<li><p>Next you need access to decent bitmap graphics application. If you are in a University someone will have a copy of Photoshop (old versions are fine), but otherwise you will have to make do with what you can find. I am almost certain that the original artist would have developed the style he uses with Photoshop. He says he wrote a program himself to automate it, but he could just have well used a Photoshop script (Action) in my opinion. Any, for occasional use, just do it interactively.</p></li>\n<li><p>The first thing to do is to get the outlines on the spheres and make the the colours flat. The former is done with a filter that finds the edges, and the latter by posterizing (reducing the number of colours in the image). I used a filter called ‘Poster Edges’ to produce C. There are sliders which allow you to change the intensity of the edges and degree of posterizing.</p></li>\n<li><p>Finally to reproduce the rather washed out feel of the colours I used the ‘Exposure’ tool (Image > Adjustments > Exposure), but I could have used curves (Image > Adjustments > Curves) or, no doubt, other options.</p></li>\n</ol>\n\n<p><a href=\"https://i.stack.imgur.com/zp3TE.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/zp3TE.png\" alt=\"Stages in "Molecule of the Month preparation"\"></a> </p>\n\n<p>And there you have the final image in D. It doesn't have quite the same posterization as the DNA Helicase illustrated in the question, but if you really wanted that you could experiment.</p>\n"
}
] |
19,455
|
<p>I have a list of gene name in a file </p>
<pre><code>CHRNB2
EGR2
GCK
KRT14
LMNA
FGF3
TK2
ABCC8
</code></pre>
<p>How can I map them to uniprot ID ? <br>
<strong>P.S</strong> I tried Uniprot "ID mapping" (from-"GENEID" to-"UNIPROTKB AC"), but it couldn't map.<br>
Please suggest me what to do.</p>
|
[
{
"answer_id": 19471,
"pm_score": 1,
"text": "<p>for biomart goto below link<br>\n<a href=\"http://central.biomart.org/converter/#!/ID_converter/gene_ensembl_config_2\" rel=\"nofollow\">http://central.biomart.org/converter/#!/ID_converter/gene_ensembl_config_2</a></p>\n\n<p>Also there is one more converter which i found pretty useful<br>\n<a href=\"http://biodbnet.abcc.ncifcrf.gov/db/db2db.php#biodb\" rel=\"nofollow\">http://biodbnet.abcc.ncifcrf.gov/db/db2db.php#biodb</a></p>\n"
}
] |
[
{
"answer_id": 48427,
"pm_score": 2,
"text": "<h1>ID mapping</h1>\n<p>This is called ID mapping. It used to be a headache as programmatic access was the only real way, but it is pretty trivial these days.</p>\n<p>As mentioned in the comments, by far the most popular and easy method is to use <strong>Uniprot's</strong> <a href=\"http://www.uniprot.org/mapping/\" rel=\"nofollow noreferrer\">list uploader for mapping</a>. The corresponding publication can be found <a href=\"http://bioinformatics.oxfordjournals.org/content/27/8/1190.full\" rel=\"nofollow noreferrer\">here</a>. You must convert from Gene name to Uniprot KB ID</p>\n<h2>Programmatic access</h2>\n<p>The <a href=\"http://www.uniprot.org/uploadlists/\" rel=\"nofollow noreferrer\">Uniprot web user interface</a> will work for thousands of IDs, but is like to result in errors for queries exceeding 10,000 IDs. In that case, programmatic queries are probably better. I've slightly modified this from <a href=\"http://www.uniprot.org/help/programmatic_access\" rel=\"nofollow noreferrer\">the Uniprot docs</a> so that the IDs are queried 1 at a time to avoid any errors in exceeding query size. The python code would be:</p>\n<pre><code>import urllib,urllib2\n\nlist_to_convert = ["CHRNB2", "EGR2", "GCK", "KRT14", "LMNA", "FGF3", "TK2", "ABCC8"]\nurl = 'http://www.uniprot.org/mapping/'\n\nprint "From To"\nfor i in list_to_convert:\n params = {\n 'from':'GENENAME',\n 'to':'ACC',\n 'format':'tab',\n 'query':i\n }\n\n data = urllib.urlencode(params)\n request = urllib2.Request(url, data)\n contact = "" # Please set your email address here.\n request.add_header('User-Agent', 'Python %s' % contact)\n response = urllib2.urlopen(request)\n page = response.read(200000)\n print page.splitlines()[1] #Ignores the header line returned by uniprot\n</code></pre>\n<p>The output from this looks like:</p>\n<pre><code>From To\nCHRNB2 A0A096MXS8\nEGR2 A0A096P554\nGCK A0A021WXA1\nKRT14 A0A024R1X6\nLMNA A0A096MQV4\nFGF3 A0A096NXI3\nTK2 A0A096NJ58\nABCC8 A0A088S7J5\n</code></pre>\n"
}
] |
19,472
|
<p>Last night I laid on my bed and tried to go to sleep with the light off.
I closed my eyes (but hadn't gone to sleep). My younger brother touched the wireless mouse (which had laser) for the laptop. He wiggled the mouse and it's laser contacted my closed eye . I knew some light was thrown on my face, and it's color was red. The laser on the mouse was actually red. So my question is, when my eyes are not functioning (not seeing, closed) how did I come to know that there was a light aimed at my eyes, and it was red? </p>
|
[
{
"answer_id": 19474,
"pm_score": 5,
"text": "<p>There are two reasons for light to appear red through the eyelids.</p>\n\n<ol>\n<li><p>Eyelids get a rich supply of blood which contains iron (in hemoglobin). The iron in blood absorbs all colors of light but reflects red light. (<a href=\"http://www.chemistry.wustl.edu/~edudev/LabTutorials/Hemoglobin/MetalComplexinBlood.html\" rel=\"noreferrer\">reference</a>)</p></li>\n<li><p>Our tissue transmits red wavelengths of light very well, but it doesn't transmit blue or wavelengths of light towards the blue end of the spectrum very well. So, the blue light is absorbed by the skin, while the red light travels through. When this light hits our eye through our eyelids, it is mostly red. (<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/8719122\" rel=\"noreferrer\">reference</a>).</p></li>\n</ol>\n\n<p>Also, as Rickard Sjogren said, the eyelid is a thin membrane and allows light to pass through. </p>\n"
}
] |
[
{
"answer_id": 19473,
"pm_score": 5,
"text": "<p>Short answer, your eyelids does not block all light. Since they are only a thin layer of skin, the light is able to pass through although not completely obviously. Since the eyes are still completely functional when you close them, only covered by the eyelids, you are able to see when light strikes your face. </p>\n"
}
] |
19,495
|
<p>How does a woodpecker go about smacking it's head into a tree without killing itself?</p>
|
[
{
"answer_id": 19496,
"pm_score": 5,
"text": "<p>Various features of brain,skull and beak anatomy help to achieve protection.</p>\n<p>A paper was published in PLoSOne in 2011 on this very topic:</p>\n<p><a href=\"http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0026490\" rel=\"noreferrer\">Why do woodpeckers resist head impact injury: a biomechanical investigation</a></p>\n<p><a href=\"http://www.bbc.com/news/science-environment-15458633\" rel=\"noreferrer\">There is also a very readable summary on the BBC website.</a> I advise that you read the whole article, but here is a quotation which lists the main findings:</p>\n<blockquote>\n<p>The team's simulations showed that three factors were at work in sparing the birds injury.</p>\n<p>Firstly, the hyoid bone's looping structure around the whole skull was found to act as a "safety belt", especially after the initial impact.</p>\n<p>The team also found that the upper and lower halves of the birds' beaks were uneven, and as force was transmitted from the tip of the beak into the bone, this asymmetry lowered the load that made it as far as the brain.</p>\n<p>Lastly, plate-like bones with a "spongy" structure at different points in the skull helped distribute the incoming force, thereby protecting the brain.</p>\n<p>The team stresses that it is the combination of the three, rather than any one feature, that keeps woodpeckers pecking without injury.</p>\n</blockquote>\n"
}
] |
[
{
"answer_id": 19497,
"pm_score": 3,
"text": "<p>Gibson (2006) identified three characteristics that help woodpeckers avoid brain injury:</p>\n<blockquote>\n<p>their small size, which reduces the stress on the brain for a given acceleration</p>\n<p>the short duration of the impact, which increases the tolerable acceleration</p>\n<p>the orientation of the brain within the skull, which increases the area of contact between the brain and the skull.</p>\n</blockquote>\n<p>Combined with <a href=\"http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0026490\" rel=\"noreferrer\">Wang et al.'s findings</a>, maybe that makes six features.</p>\n<p><a href=\"http://onlinelibrary.wiley.com/doi/10.1111/j.1469-7998.2006.00166.x/abstract\" rel=\"noreferrer\">Gibson, LJ. 2006. Woodpecker pecking: how woodpeckers avoid brain injury. Journal of Zoology 270: 462-465</a></p>\n"
}
] |
19,508
|
<p>I have observed that frequently when people are hungry; they tend to get angry more easily on pointless issues. Does this mean that our fight or flight response is more active when a person is hungry? What is a possible reason for this? Is this phenomenon linked with our cell signaling pathways? If it is, then what would be the pathway that leads to the aggressive behavior?
<p>
To summarize the question: </p>
<p><strong>When a person is hungry and they get angry, is it due to a cell signaling pathway? If so, what pathway?</strong></p>
|
[
{
"answer_id": 19511,
"pm_score": 4,
"text": "<p>Brain's main energy source is glucose. It uses about 20% of total glucose [1]. Brain hypoglycemia causes depressive-like behaviors in mice through adrenergic pathways [2].</p>\n<p>When it comes to humans, here is a study that claims low glucose leads to increased aggression in married couples (see <a href=\"http://o.canada.com/health/hunger-in-the-form-of-low-blood-sugar-leads-to-greater-aggression-and-anger-in-married-couples-study-finds\" rel=\"noreferrer\">this</a> too):</p>\n<blockquote>\n<p>Self-control requires energy, part of which is provided by glucose. For 21 days, glucose levels were measured in 107 married couples. To measure aggressive impulses, each evening participants stuck between 0 and 51 pins into a voodoo doll that represented their spouse, depending how angry they were with their spouse. ... As expected, the lower the level of glucose in the blood, the greater number of pins participants stuck into the voodoo doll, and the higher intensity and longer duration of noise participants set for their spouse [3].</p>\n</blockquote>\n<p>However, the conclusion is disputed:</p>\n<blockquote>\n<p>Bushman et al.'s study does not demonstrate that fluctuations in blood glucose affect individuals' self-control abilities. As an important consequence, there is no reason to assume that giving couples a sugary “boost to their self-control energy” (p. 3) will reduce intimate partner violence. Because the glucose model of self-control lacks empirical foundation, it does not qualify as a framework for scientifically based intervention strategies [4].</p>\n</blockquote>\n<p>What is sure, is that hypoglycemia activates sympathetic nervous system:</p>\n<blockquote>\n<p>... the neurogenic symptoms of hypoglycemia are largely the result of sympathetic neural, rather than adrenomedullary, activation [5].</p>\n<p>Hypoglycemia increases plasma levels of both epinephrine and norepinephrine. These catechols are released primarily from the adrenal medulla. However, it is well documented that hypoglycemic increases muscle sympathetic nerve activity, and that both alpha and beta adrenergic activity increase [6].</p>\n</blockquote>\n<p>And this leads to behavioral changes (at least in animals):</p>\n<blockquote>\n<p>Noradrenaline is involved in many different functions, which all are known to affect behaviour profoundly. ... Part of these effects may arise in indirect ways that are by no means specific to aggressive behaviour, however, they are functionally relevant to it. Other effects may affect brain mechanisms specifically involved in aggression. Hormonal catecholamines (adrenaline and noradrenaline) appear to be involved in metabolic preparations for the prospective fight; the sympathetic system ensures appropriate cardiovascular reaction, while the CNS noradrenergic system prepares the animal for the prospective fight. ... It appears that neurons bearing postsynaptic alpha2-adrenoceptors are responsible for the start and maintenance of aggression, while a situation-dependent fine-tuning is realised through neurons equipped with beta-adrenoceptors [7].</p>\n</blockquote>\n<hr />\n<p>References:</p>\n<ol>\n<li>Wikipedia contributors, "Human brain," Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Human_brain&oldid=615456836\" rel=\"noreferrer\">http://en.wikipedia.org/w/index.php?title=Human_brain&oldid=615456836</a> (accessed July 6, 2014).</li>\n<li>Park MJ, Yoo SW, Choe BS, Dantzer R, Freund GG. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/21820138\" rel=\"noreferrer\">Acute hypoglycemia causes depressive-like behaviors in mice.</a> Metab. Clin. Exp. 2012 Feb;61(2):229-36. doi: <a href=\"http://dx.doi.org/10.1016/j.metabol.2011.06.013\" rel=\"noreferrer\">10.1016/j.metabol.2011.06.013</a>. PubMed PMID: 21820138.</li>\n<li>Bushman BJ, Dewall CN, Pond RS, Hanus MD. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/24733932\" rel=\"noreferrer\">Low glucose relates to greater aggression in married couples.</a> Proc. Natl. Acad. Sci. U.S.A. 2014 Apr 29;111(17):6254-7. doi: <a href=\"http://dx.doi.org/10.1073/pnas.1400619111\" rel=\"noreferrer\">10.1073/pnas.1400619111</a>. PubMed PMID: 24733932.</li>\n<li>Lange F and Kurzban R (2014) Sugar levels relate to aggression in couples without supporting the glucose model of self-control. Front. Psychol. 5:572. doi: 10.3389/fpsyg.2014.00572</li>\n<li>DeRosa MA, Cryer PE. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/14970007\" rel=\"noreferrer\">Hypoglycemia and the sympathoadrenal system: neurogenic symptoms are largely the result of sympathetic neural, rather than adrenomedullary, activation.</a> Am. J. Physiol. Endocrinol. Metab. 2004 Jul;287(1):E32-41. doi: <a href=\"http://dx.doi.org/10.1152/ajpendo.00539.2003\" rel=\"noreferrer\">10.1152/ajpendo.00539.2003</a>. PubMed PMID: 14970007.</li>\n<li>Hoffman RP. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/18220670\" rel=\"noreferrer\">Sympathetic mechanisms of hypoglycemic counterregulation.</a> Curr Diabetes Rev. 2007 Aug;3(3):185-93. PubMed PMID: 18220670.</li>\n<li>Haller J, Makara GB, Kruk MR. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/9491941\" rel=\"noreferrer\">Catecholaminergic involvement in the control of aggression: hormones, the peripheral sympathetic, and central noradrenergic systems.</a> Neurosci Biobehav Rev. 1998;22(1):85-97. PubMed PMID: 9491941.</li>\n</ol>\n"
}
] |
[
{
"answer_id": 19615,
"pm_score": 2,
"text": "<p><em>This is a short review about the issue and not complete.\nThis and the earlier answer are not proofs of the link between the two proceses.</em></p>\n\n<p>To investigate this better, I think it would be much easier first to narrow the case to </p>\n\n<ul>\n<li>testosterone and energy homeostasis (Embryology; or better formulated research case)</li>\n<li>catabolism and anger</li>\n<li>anger and aggressive behaviour.</li>\n</ul>\n\n<p>Then, think about specific cases. \nThink genes which are associated with aggressive behaviour and violence in catabolism (criminal studies). </p>\n\n<p>Terms</p>\n\n<ul>\n<li>Satiety</li>\n<li>Appetite</li>\n<li>Hunger </li>\n</ul>\n\n<p>I was not sure in which specific area you are particularly interested. \nAt this stage, we cannot provide a proof between hunger and aggressive behaviour. \nIt depends so much on the individual (life style; genomics) what is the end result.\nHere follows little general pieces of information:</p>\n\n<p>Some cases</p>\n\n<ul>\n<li><strong>InsR/FoxO1 Signaling Curtails Hypothalamic POMC Neuron Number</strong> [1]: <em>it's possible that the hormonal and nutrient milieu contributes to alterations in POMC neuron development</em>.</li>\n<li><strong>Early-Life Exposure to Testosterone Programs the Hypothalamic\nMelanocortin System</strong> [3].</li>\n<li>Study about testosterone and basal metabolic rate [2].</li>\n</ul>\n\n<p>Nuclei</p>\n\n<ul>\n<li>hypothalamus lateral nucleus</li>\n<li>hypothalamus tuberal medial perifornical nucleus [4]</li>\n<li>hypothalamus arcuate nucleus (appetite and energy expenditure - POMC-CART; upregulative NPY AGRP)</li>\n</ul>\n\n<p>Receptor</p>\n\n<ul>\n<li>androgenic (NR3C4) (adipose tissue; more in visceral) (no link)</li>\n</ul>\n\n<p>where I found no receptor existing directly between those two events - appetite and testosterone secretion by comparing the NCBI gene databases between those two processes.\nIt is much more easier to show the thing first in the embryologic studies and then by using the gene found in bigger studies.\nAt the moment, more work is needed in these studies in Embryology.</p>\n\n<p>My initial clause is based on some of my notes in Embryology. \nThere are researches who are trying to show this link between studies in embryology. \nThe problem is at the moment in the development of hypothalamus and something else. \nI will update this post when I remember about the situation better and when finding the right things from my notes.</p>\n\n<h2>Sources</h2>\n\n<ol>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271107/#!po=14.0625\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271107/#!po=14.0625</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402517/\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402517/</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060636/\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060636/</a></li>\n<li>John E. Hall. Guyton and Hall Textbook of Medical Physiology. 12Th edition.</li>\n</ol>\n"
}
] |
19,514
|
<p>It is said that the stonefish (Synanceia) is able to stay out of the water for up to 24 hours. I wonder how they get oxygen from the air. Could someone explain this?</p>
|
[
{
"answer_id": 19511,
"pm_score": 4,
"text": "<p>Brain's main energy source is glucose. It uses about 20% of total glucose [1]. Brain hypoglycemia causes depressive-like behaviors in mice through adrenergic pathways [2].</p>\n<p>When it comes to humans, here is a study that claims low glucose leads to increased aggression in married couples (see <a href=\"http://o.canada.com/health/hunger-in-the-form-of-low-blood-sugar-leads-to-greater-aggression-and-anger-in-married-couples-study-finds\" rel=\"noreferrer\">this</a> too):</p>\n<blockquote>\n<p>Self-control requires energy, part of which is provided by glucose. For 21 days, glucose levels were measured in 107 married couples. To measure aggressive impulses, each evening participants stuck between 0 and 51 pins into a voodoo doll that represented their spouse, depending how angry they were with their spouse. ... As expected, the lower the level of glucose in the blood, the greater number of pins participants stuck into the voodoo doll, and the higher intensity and longer duration of noise participants set for their spouse [3].</p>\n</blockquote>\n<p>However, the conclusion is disputed:</p>\n<blockquote>\n<p>Bushman et al.'s study does not demonstrate that fluctuations in blood glucose affect individuals' self-control abilities. As an important consequence, there is no reason to assume that giving couples a sugary “boost to their self-control energy” (p. 3) will reduce intimate partner violence. Because the glucose model of self-control lacks empirical foundation, it does not qualify as a framework for scientifically based intervention strategies [4].</p>\n</blockquote>\n<p>What is sure, is that hypoglycemia activates sympathetic nervous system:</p>\n<blockquote>\n<p>... the neurogenic symptoms of hypoglycemia are largely the result of sympathetic neural, rather than adrenomedullary, activation [5].</p>\n<p>Hypoglycemia increases plasma levels of both epinephrine and norepinephrine. These catechols are released primarily from the adrenal medulla. However, it is well documented that hypoglycemic increases muscle sympathetic nerve activity, and that both alpha and beta adrenergic activity increase [6].</p>\n</blockquote>\n<p>And this leads to behavioral changes (at least in animals):</p>\n<blockquote>\n<p>Noradrenaline is involved in many different functions, which all are known to affect behaviour profoundly. ... Part of these effects may arise in indirect ways that are by no means specific to aggressive behaviour, however, they are functionally relevant to it. Other effects may affect brain mechanisms specifically involved in aggression. Hormonal catecholamines (adrenaline and noradrenaline) appear to be involved in metabolic preparations for the prospective fight; the sympathetic system ensures appropriate cardiovascular reaction, while the CNS noradrenergic system prepares the animal for the prospective fight. ... It appears that neurons bearing postsynaptic alpha2-adrenoceptors are responsible for the start and maintenance of aggression, while a situation-dependent fine-tuning is realised through neurons equipped with beta-adrenoceptors [7].</p>\n</blockquote>\n<hr />\n<p>References:</p>\n<ol>\n<li>Wikipedia contributors, "Human brain," Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Human_brain&oldid=615456836\" rel=\"noreferrer\">http://en.wikipedia.org/w/index.php?title=Human_brain&oldid=615456836</a> (accessed July 6, 2014).</li>\n<li>Park MJ, Yoo SW, Choe BS, Dantzer R, Freund GG. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/21820138\" rel=\"noreferrer\">Acute hypoglycemia causes depressive-like behaviors in mice.</a> Metab. Clin. Exp. 2012 Feb;61(2):229-36. doi: <a href=\"http://dx.doi.org/10.1016/j.metabol.2011.06.013\" rel=\"noreferrer\">10.1016/j.metabol.2011.06.013</a>. PubMed PMID: 21820138.</li>\n<li>Bushman BJ, Dewall CN, Pond RS, Hanus MD. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/24733932\" rel=\"noreferrer\">Low glucose relates to greater aggression in married couples.</a> Proc. Natl. Acad. Sci. U.S.A. 2014 Apr 29;111(17):6254-7. doi: <a href=\"http://dx.doi.org/10.1073/pnas.1400619111\" rel=\"noreferrer\">10.1073/pnas.1400619111</a>. PubMed PMID: 24733932.</li>\n<li>Lange F and Kurzban R (2014) Sugar levels relate to aggression in couples without supporting the glucose model of self-control. Front. Psychol. 5:572. doi: 10.3389/fpsyg.2014.00572</li>\n<li>DeRosa MA, Cryer PE. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/14970007\" rel=\"noreferrer\">Hypoglycemia and the sympathoadrenal system: neurogenic symptoms are largely the result of sympathetic neural, rather than adrenomedullary, activation.</a> Am. J. Physiol. Endocrinol. Metab. 2004 Jul;287(1):E32-41. doi: <a href=\"http://dx.doi.org/10.1152/ajpendo.00539.2003\" rel=\"noreferrer\">10.1152/ajpendo.00539.2003</a>. PubMed PMID: 14970007.</li>\n<li>Hoffman RP. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/18220670\" rel=\"noreferrer\">Sympathetic mechanisms of hypoglycemic counterregulation.</a> Curr Diabetes Rev. 2007 Aug;3(3):185-93. PubMed PMID: 18220670.</li>\n<li>Haller J, Makara GB, Kruk MR. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/9491941\" rel=\"noreferrer\">Catecholaminergic involvement in the control of aggression: hormones, the peripheral sympathetic, and central noradrenergic systems.</a> Neurosci Biobehav Rev. 1998;22(1):85-97. PubMed PMID: 9491941.</li>\n</ol>\n"
}
] |
[
{
"answer_id": 19615,
"pm_score": 2,
"text": "<p><em>This is a short review about the issue and not complete.\nThis and the earlier answer are not proofs of the link between the two proceses.</em></p>\n\n<p>To investigate this better, I think it would be much easier first to narrow the case to </p>\n\n<ul>\n<li>testosterone and energy homeostasis (Embryology; or better formulated research case)</li>\n<li>catabolism and anger</li>\n<li>anger and aggressive behaviour.</li>\n</ul>\n\n<p>Then, think about specific cases. \nThink genes which are associated with aggressive behaviour and violence in catabolism (criminal studies). </p>\n\n<p>Terms</p>\n\n<ul>\n<li>Satiety</li>\n<li>Appetite</li>\n<li>Hunger </li>\n</ul>\n\n<p>I was not sure in which specific area you are particularly interested. \nAt this stage, we cannot provide a proof between hunger and aggressive behaviour. \nIt depends so much on the individual (life style; genomics) what is the end result.\nHere follows little general pieces of information:</p>\n\n<p>Some cases</p>\n\n<ul>\n<li><strong>InsR/FoxO1 Signaling Curtails Hypothalamic POMC Neuron Number</strong> [1]: <em>it's possible that the hormonal and nutrient milieu contributes to alterations in POMC neuron development</em>.</li>\n<li><strong>Early-Life Exposure to Testosterone Programs the Hypothalamic\nMelanocortin System</strong> [3].</li>\n<li>Study about testosterone and basal metabolic rate [2].</li>\n</ul>\n\n<p>Nuclei</p>\n\n<ul>\n<li>hypothalamus lateral nucleus</li>\n<li>hypothalamus tuberal medial perifornical nucleus [4]</li>\n<li>hypothalamus arcuate nucleus (appetite and energy expenditure - POMC-CART; upregulative NPY AGRP)</li>\n</ul>\n\n<p>Receptor</p>\n\n<ul>\n<li>androgenic (NR3C4) (adipose tissue; more in visceral) (no link)</li>\n</ul>\n\n<p>where I found no receptor existing directly between those two events - appetite and testosterone secretion by comparing the NCBI gene databases between those two processes.\nIt is much more easier to show the thing first in the embryologic studies and then by using the gene found in bigger studies.\nAt the moment, more work is needed in these studies in Embryology.</p>\n\n<p>My initial clause is based on some of my notes in Embryology. \nThere are researches who are trying to show this link between studies in embryology. \nThe problem is at the moment in the development of hypothalamus and something else. \nI will update this post when I remember about the situation better and when finding the right things from my notes.</p>\n\n<h2>Sources</h2>\n\n<ol>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271107/#!po=14.0625\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271107/#!po=14.0625</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402517/\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402517/</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060636/\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060636/</a></li>\n<li>John E. Hall. Guyton and Hall Textbook of Medical Physiology. 12Th edition.</li>\n</ol>\n"
}
] |
19,515
|
<p>A steroid, testosterone was injected in female body which led to development of secondary sexual characters but these characters were not developed over night (Response was very slow). What could be possible explanation of this phenomenon</p>
<ol>
<li>a Steroid hormones produce a slow response because they do not have secondary messenger </li>
<li>Slow response is due to lack of cell membrane receptors and amplification enzymes</li>
<li>Movement of this hormone is very slow in blood</li>
<li>None of the above</li>
</ol>
<p>I think option 3 is correct because steroid hormones are hydrophobic in nature and cant be transported in the blood without the help of any carrier protein so this may be the reason but I am not sure about this.. </p>
|
[
{
"answer_id": 19511,
"pm_score": 4,
"text": "<p>Brain's main energy source is glucose. It uses about 20% of total glucose [1]. Brain hypoglycemia causes depressive-like behaviors in mice through adrenergic pathways [2].</p>\n<p>When it comes to humans, here is a study that claims low glucose leads to increased aggression in married couples (see <a href=\"http://o.canada.com/health/hunger-in-the-form-of-low-blood-sugar-leads-to-greater-aggression-and-anger-in-married-couples-study-finds\" rel=\"noreferrer\">this</a> too):</p>\n<blockquote>\n<p>Self-control requires energy, part of which is provided by glucose. For 21 days, glucose levels were measured in 107 married couples. To measure aggressive impulses, each evening participants stuck between 0 and 51 pins into a voodoo doll that represented their spouse, depending how angry they were with their spouse. ... As expected, the lower the level of glucose in the blood, the greater number of pins participants stuck into the voodoo doll, and the higher intensity and longer duration of noise participants set for their spouse [3].</p>\n</blockquote>\n<p>However, the conclusion is disputed:</p>\n<blockquote>\n<p>Bushman et al.'s study does not demonstrate that fluctuations in blood glucose affect individuals' self-control abilities. As an important consequence, there is no reason to assume that giving couples a sugary “boost to their self-control energy” (p. 3) will reduce intimate partner violence. Because the glucose model of self-control lacks empirical foundation, it does not qualify as a framework for scientifically based intervention strategies [4].</p>\n</blockquote>\n<p>What is sure, is that hypoglycemia activates sympathetic nervous system:</p>\n<blockquote>\n<p>... the neurogenic symptoms of hypoglycemia are largely the result of sympathetic neural, rather than adrenomedullary, activation [5].</p>\n<p>Hypoglycemia increases plasma levels of both epinephrine and norepinephrine. These catechols are released primarily from the adrenal medulla. However, it is well documented that hypoglycemic increases muscle sympathetic nerve activity, and that both alpha and beta adrenergic activity increase [6].</p>\n</blockquote>\n<p>And this leads to behavioral changes (at least in animals):</p>\n<blockquote>\n<p>Noradrenaline is involved in many different functions, which all are known to affect behaviour profoundly. ... Part of these effects may arise in indirect ways that are by no means specific to aggressive behaviour, however, they are functionally relevant to it. Other effects may affect brain mechanisms specifically involved in aggression. Hormonal catecholamines (adrenaline and noradrenaline) appear to be involved in metabolic preparations for the prospective fight; the sympathetic system ensures appropriate cardiovascular reaction, while the CNS noradrenergic system prepares the animal for the prospective fight. ... It appears that neurons bearing postsynaptic alpha2-adrenoceptors are responsible for the start and maintenance of aggression, while a situation-dependent fine-tuning is realised through neurons equipped with beta-adrenoceptors [7].</p>\n</blockquote>\n<hr />\n<p>References:</p>\n<ol>\n<li>Wikipedia contributors, "Human brain," Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Human_brain&oldid=615456836\" rel=\"noreferrer\">http://en.wikipedia.org/w/index.php?title=Human_brain&oldid=615456836</a> (accessed July 6, 2014).</li>\n<li>Park MJ, Yoo SW, Choe BS, Dantzer R, Freund GG. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/21820138\" rel=\"noreferrer\">Acute hypoglycemia causes depressive-like behaviors in mice.</a> Metab. Clin. Exp. 2012 Feb;61(2):229-36. doi: <a href=\"http://dx.doi.org/10.1016/j.metabol.2011.06.013\" rel=\"noreferrer\">10.1016/j.metabol.2011.06.013</a>. PubMed PMID: 21820138.</li>\n<li>Bushman BJ, Dewall CN, Pond RS, Hanus MD. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/24733932\" rel=\"noreferrer\">Low glucose relates to greater aggression in married couples.</a> Proc. Natl. Acad. Sci. U.S.A. 2014 Apr 29;111(17):6254-7. doi: <a href=\"http://dx.doi.org/10.1073/pnas.1400619111\" rel=\"noreferrer\">10.1073/pnas.1400619111</a>. PubMed PMID: 24733932.</li>\n<li>Lange F and Kurzban R (2014) Sugar levels relate to aggression in couples without supporting the glucose model of self-control. Front. Psychol. 5:572. doi: 10.3389/fpsyg.2014.00572</li>\n<li>DeRosa MA, Cryer PE. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/14970007\" rel=\"noreferrer\">Hypoglycemia and the sympathoadrenal system: neurogenic symptoms are largely the result of sympathetic neural, rather than adrenomedullary, activation.</a> Am. J. Physiol. Endocrinol. Metab. 2004 Jul;287(1):E32-41. doi: <a href=\"http://dx.doi.org/10.1152/ajpendo.00539.2003\" rel=\"noreferrer\">10.1152/ajpendo.00539.2003</a>. PubMed PMID: 14970007.</li>\n<li>Hoffman RP. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/18220670\" rel=\"noreferrer\">Sympathetic mechanisms of hypoglycemic counterregulation.</a> Curr Diabetes Rev. 2007 Aug;3(3):185-93. PubMed PMID: 18220670.</li>\n<li>Haller J, Makara GB, Kruk MR. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/9491941\" rel=\"noreferrer\">Catecholaminergic involvement in the control of aggression: hormones, the peripheral sympathetic, and central noradrenergic systems.</a> Neurosci Biobehav Rev. 1998;22(1):85-97. PubMed PMID: 9491941.</li>\n</ol>\n"
}
] |
[
{
"answer_id": 19615,
"pm_score": 2,
"text": "<p><em>This is a short review about the issue and not complete.\nThis and the earlier answer are not proofs of the link between the two proceses.</em></p>\n\n<p>To investigate this better, I think it would be much easier first to narrow the case to </p>\n\n<ul>\n<li>testosterone and energy homeostasis (Embryology; or better formulated research case)</li>\n<li>catabolism and anger</li>\n<li>anger and aggressive behaviour.</li>\n</ul>\n\n<p>Then, think about specific cases. \nThink genes which are associated with aggressive behaviour and violence in catabolism (criminal studies). </p>\n\n<p>Terms</p>\n\n<ul>\n<li>Satiety</li>\n<li>Appetite</li>\n<li>Hunger </li>\n</ul>\n\n<p>I was not sure in which specific area you are particularly interested. \nAt this stage, we cannot provide a proof between hunger and aggressive behaviour. \nIt depends so much on the individual (life style; genomics) what is the end result.\nHere follows little general pieces of information:</p>\n\n<p>Some cases</p>\n\n<ul>\n<li><strong>InsR/FoxO1 Signaling Curtails Hypothalamic POMC Neuron Number</strong> [1]: <em>it's possible that the hormonal and nutrient milieu contributes to alterations in POMC neuron development</em>.</li>\n<li><strong>Early-Life Exposure to Testosterone Programs the Hypothalamic\nMelanocortin System</strong> [3].</li>\n<li>Study about testosterone and basal metabolic rate [2].</li>\n</ul>\n\n<p>Nuclei</p>\n\n<ul>\n<li>hypothalamus lateral nucleus</li>\n<li>hypothalamus tuberal medial perifornical nucleus [4]</li>\n<li>hypothalamus arcuate nucleus (appetite and energy expenditure - POMC-CART; upregulative NPY AGRP)</li>\n</ul>\n\n<p>Receptor</p>\n\n<ul>\n<li>androgenic (NR3C4) (adipose tissue; more in visceral) (no link)</li>\n</ul>\n\n<p>where I found no receptor existing directly between those two events - appetite and testosterone secretion by comparing the NCBI gene databases between those two processes.\nIt is much more easier to show the thing first in the embryologic studies and then by using the gene found in bigger studies.\nAt the moment, more work is needed in these studies in Embryology.</p>\n\n<p>My initial clause is based on some of my notes in Embryology. \nThere are researches who are trying to show this link between studies in embryology. \nThe problem is at the moment in the development of hypothalamus and something else. \nI will update this post when I remember about the situation better and when finding the right things from my notes.</p>\n\n<h2>Sources</h2>\n\n<ol>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271107/#!po=14.0625\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271107/#!po=14.0625</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402517/\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402517/</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060636/\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060636/</a></li>\n<li>John E. Hall. Guyton and Hall Textbook of Medical Physiology. 12Th edition.</li>\n</ol>\n"
}
] |
19,540
|
<p>does the order of genes within a chromosome matter? or is the main thing that the genes are there.</p>
<p>so for example, our DNA is very similar to that of apes not only by the genes themselves but also by the arrangement of those genes in the chromosomes.</p>
<p>is the order of this arrangement significant? Or if it were shuffled around, then the functional impact would be more or less the same?</p>
<p>Another example, an <a href="http://www.genome.gov/page.cfm?pageID=10005831" rel="nofollow noreferrer">international study</a> in the mouse genome has revealed that virtually all mouse genes have direct counterparts in humans, i.e. humans and mice contain virtually the same set of genes. is the difference between humans and mice due primarily to the different order of the genes or to the slight differences in the genes themselves?</p>
<p>This question was raised from a claim <a href="https://biology.stackexchange.com/a/5568/6202">here</a> which seems to imply it does not matter.</p>
<blockquote>
<p>The chances are infinitesimal that human chr 2 were to resemble those
of other primates at random. This is what you say in science when you
mean 'impossible'. One simply doesn't see a segment of DNA the size of
Chr 2A and 2B being so similar for such a length when we look at rats,
dogs, worms or any more distantly related living thing.</p>
</blockquote>
|
[
{
"answer_id": 19555,
"pm_score": 4,
"text": "<blockquote>\n <p>is the difference between humans and mice due primarily to the\n different order of the genes or to the slight differences in the genes\n themselves?</p>\n</blockquote>\n\n<p>The latter.</p>\n\n<blockquote>\n <p>This question was raised from a claim here which seems to imply it\n does not matter.</p>\n</blockquote>\n\n<p>You are talking about two different things. Gene expression is often controlled by nearby DNA sequences that don't code for protein. Moving a gene away from the DNA that controls it can change its expression a lot, and have huge consequences on the organism. But in many cases, you can move a whole gene, including its controlling sequences, to another place, and nothing much will happen.</p>\n\n<p>People were bringing up synteny as evidence of evolutionary relatedness, not as the cause for all primates looking similar.</p>\n"
}
] |
[
{
"answer_id": 19541,
"pm_score": 2,
"text": "<p>Ye, the order matters. This can be seen in chromosomal translocations which can cause cancer.\nA example for that would be the translocation of IRF4 which happens in a subtype of multiple myeloma. The translocation is permanently activating the transcription factor. See here for details: </p>\n\n<ul>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/21487109\" rel=\"nofollow noreferrer\">Translocations activating IRF4 identify a subtype of germinal\ncenter-derived B-cell lymphoma affecting predominantly children and\nyoung adults.</a></li>\n</ul>\n\n<p>The main reason for this is the regulation of the genes - when the order is changed, the regulatory elements which are important for regulating the expression are missing. A lot of these regulatory elements are located many kB away from the gene and are still important for its activation or silencing.\nThis can look like the image below (image from <a href=\"http://pbil.univ-lyon1.fr/members/sagot/htdocs/team/projects/chromo_net/purpose_chromo_net.html\" rel=\"nofollow noreferrer\">here</a>): </p>\n\n<p><img src=\"https://i.stack.imgur.com/kOGzE.jpg\" alt=\"enter image description here\"></p>\n\n<p>Regarding the mouse question: On which chromosome a gene is located is not really important if you compare different species. The gene I worked on for a while is functionally equivalent between mouse and human (the human version works perfectly in mouse), but they are located on different chromosomes. It again comes down to different regulation and in some cases also a different amino acid sequence. Also mice (as other animals as well) have quite a number of genes which are unique for them and which make a difference between the two species. There are a few interesting papers on that topic:</p>\n\n<ul>\n<li><a href=\"http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1000112\" rel=\"nofollow noreferrer\">Lineage-Specific Biology Revealed by a Finished Genome Assembly of\nthe Mouse</a></li>\n<li><a href=\"http://hmg.oxfordjournals.org/content/12/7/701.full\" rel=\"nofollow noreferrer\">Comparison of the genomes of human and mouse lays the foundation of\ngenome zoology</a></li>\n</ul>\n"
}
] |
19,545
|
<p>What features make one plant able to withstand dry spells better than another with relatively similar structure? For instance, one of my <a href="http://en.wikipedia.org/wiki/Rudbeckia" rel="nofollow">Rudbeckias</a> is wilting from drought at the moment, and an <a href="http://en.wikipedia.org/wiki/Oenothera" rel="nofollow">Oenothera</a> next to it is not yet showing signs of dryness.</p>
<p>Or like <a href="http://plants.usda.gov/core/profile?symbol=IMCA" rel="nofollow">jewelweed (Impatiens capensis)</a>, which wilts even while the soil is damp, in full sun, and <a href="http://en.wikipedia.org/wiki/Ambrosia_artemisiifolia" rel="nofollow">ragweed (Ambrosia artemisiifolia)</a>, which will grow in very dry locations without being phased.</p>
<p>Is it caused by a faster transpiration rate in some plants than in others?</p>
|
[
{
"answer_id": 20092,
"pm_score": 3,
"text": "<p>The difference may be related to how the plants fix carbon. While all plants convert CO₂ and H₂O to glucose and oxygen, there are at least three pathways that are used to do it. The C3 pathway is older and less efficient than the CAM and C4 pathways. Many drought tolerant plants use the CAM or C4 pathways because less water is needed. The C4 pathway is better than C3 in drier climates, hotter climates, and when CO₂ or nitrogen are limited. The hard part about this answer is that I'm not a botanist. Wikipedia lists some plants that use C4, CAM, and C3, but there is no comprehensive list, so I can't match up all the plants you mentioned in your question. In general, a higher percentage of monocots, especially grasses, use C4, but a wider diversity of dicots use C4. But you still can't draw conclusions about families of plants, because while corn and sorghum use C4, rice and barley use C3. Ragweed, a plant you say grows well in dry conditions, is a member of Asteraceae, which includes many plants that use C4. However, rudbeckias are also members of Asteraceae, but don't do as well in dry conditions. The C4 pathway has appeared and disappeared in several different plants, making any general claim hard to make. Here are some links that might help:</p>\n\n<ul>\n<li><a href=\"http://www.en.wikipedia.org/wiki/C4_carbon_fixation\" rel=\"nofollow\">http://www.en.wikipedia.org/wiki/C4_carbon_fixation</a> </li>\n<li><a href=\"http://www.en.wikipedia.org/wiki/C3_carbon_fixation\" rel=\"nofollow\">http://www.en.wikipedia.org/wiki/C3_carbon_fixation</a> </li>\n<li><a href=\"http://www.en.wikipedia.org/wiki/Crassulacean_acid_metabolism\" rel=\"nofollow\">http://www.en.wikipedia.org/wiki/Crassulacean_acid_metabolism</a></li>\n<li><a href=\"http://www.brown.edu/Research/Edwards_Lab/reprints/sage_etal_2011jexb.pdf\" rel=\"nofollow\">http://www.brown.edu/Research/Edwards_Lab/reprints/sage_etal_2011jexb.pdf</a></li>\n</ul>\n\n<p>If you know more about plants than me, that last link might be helpful, it's about the evolution of C4 pathway in plants and includes lists, but uses the formal species names I just don't recognize.</p>\n"
}
] |
[
{
"answer_id": 19589,
"pm_score": -1,
"text": "<p>Plants in drier conditions usually have reduced surface area, thick waxy cuticle covering the epidermis, reduced number of stomata, and water storage tissues that presides in its roots and leaves.</p>\n\n<p>This means that even if the plants are similar, one of them might express more of one of the features shown above.</p>\n"
}
] |
19,548
|
<p>It seems like being nearsighted for much of your life due to elongated eyes would make it easier in general to focus on near objects rather than far since the lens would not have to change much. Since in old age we lose the ability to focus close images due to a hardening of the lens over time, wouldn't having eyes shaped more for near images be helpful in maintaining the ability to see close up, and thus nearsighted, or myopic people, would be less likely to develop farsightedness, or hyperopia, with age? It seems then that nearsightedness is more of an adaptation that occurs at a young age, so that these people can work up close for longer periods of time both in the the short term(studying) and long term(age). I'd love to hear if any research has been done on this subject, and any other input you have.</p>
|
[
{
"answer_id": 19551,
"pm_score": 3,
"text": "<p>It is generally understood that we tend to become hyperopic as we age (<a href=\"http://www.journalofvision.org/content/8/4/29.short\" rel=\"nofollow\">reference</a>). As to whether this aids in decreasing myopia is stated as marginal in papers. One paper titled \"<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/12482270\" rel=\"nofollow\">Is there a hyperopic shift in myopic eyes during the presbyopic years?</a>\" states that</p>\n\n<blockquote>\n <p>it was found that almost all hyperopic and <a href=\"http://en.wikipedia.org/wiki/Emmetropia\" rel=\"nofollow\">emmetropic</a> eyes showed an\n age-related hyperopic shift; but only a small proportion of myopic\n eyes shifted toward hyperopia, with others remaining relatively stable\n and still others increasing in myopia.</p>\n</blockquote>\n\n<p>In a second study titled \"<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/10892850\" rel=\"nofollow\">Age-Related Decreases in the Prevalence of Myopia: Longitudinal Change or Cohort Effect</a>?\", it was found that there is a decline in the prevalence of myopia in older adults. </p>\n\n<p>Some people in personal experiences have stated that their myopia has decreased (<a href=\"http://ask.metafilter.com/76846/Myopia-reduction-with-age\" rel=\"nofollow\">reference</a>) while others found themselves wearing bifocals (<a href=\"http://msgboard.snopes.com/cgi-bin/ultimatebb.cgi?ubb=get_topic;f=35;t=001797;p=1\" rel=\"nofollow\">reference</a>). In closing, I would say that this is something that your Ophthalmologist may be able to predict better but it is not a given that your myopia would decrease. It may or may not be so with many factors like your eye shape coming into play.</p>\n"
}
] |
[
{
"answer_id": 24026,
"pm_score": 1,
"text": "<p>Let me see whether I can explain this quickly. The eye size is tightly regulated genetically. Babies don't have big eyes, they have exactly the same sized eyes like adults, only their head is smaller. Myopic eyes are larger than normal and hyperopic eyes are smaller than normal, even though the difference is only 1 to a few millimeters. When you focus to the far point, the light focusses to the nearest point possible in the back of your eye. When you come closer to an object, the focus point inside the eye moves further out. Thus, the farsighted person with the small eye can only see when the object is away. Moving closer moves the focal point inside the eye to behind the retina. The opposite is true for myopic people with too large eyes. When a person gets old, the lens gets stiff and cannot adjust the focal point inside the eye to the distance of the retina. Thus, the lens remains stiff in the most relaxed state (extended), or - in other words - at the most distant focal point the person had when it was young. A normal-sighted person has his old-age focal point at the horizon and since his lens is stiff, can only see sharp from the horizon to a few meters in front of him (depending on the intensity and wavelength of the light - blue light better than red). A short-sighted person is of disadvantage when old, since his far point remains to be at short distance. He gains a little sharpness over the normal sighted person in the short distance, but loses it in the distance like he always did. You can calculate this nicely, actually. All physics.</p>\n"
}
] |
19,575
|
<p>I'm studying a TCGA dataset trying to find correlations between gene expression and clinical data which might shed light on some pathways. One column of the clinical data provides a list of chemotherapy drugs the patient received and I'm pretty sure there's a wealth of possibility in this column but I don't know anything about how chemotherapy drugs work or what kinds of things it makes sense to classify about them. </p>
<p>I'm making a spread sheet that will have the following columns: </p>
<pre><code>Drug_Name
Number_of_Patients_Received
Mechanism
Associated_Drugs
</code></pre>
<p>But I don't know what else is important to know about these drugs. What would you think is important to know to help understand how these drugs might have played an interactive role with the pathways. Also, if you have any recommendations of online resources, I'll appreciate you mentioning them with a short explanation of what I might find there.
But my primary question is else should I look up about these drugs to help me understand their role/impact.</p>
|
[
{
"answer_id": 19579,
"pm_score": 3,
"text": "<p>There's <a href=\"http://www.pharmgkb.org/\" rel=\"nofollow\">this database</a> of genetic/drug interactions, which I think is pretty much exactly what you're looking for. </p>\n\n<p>Probably your best approach is to classify your drugs into a couple different categories of action. Some drugs will have to be in several categories at once(I'm lookin at you anthracyclines) Dose-dependent mutagens(cisplatin), growth-dependent mutagens(fluorouracil), topoisomerase inhibitors, tyrosine kinase inhibitors, microtubule inhibitors, retinoid signaling, immune adjuvants, and then 'misc'. </p>\n\n<p>Alkylating agents and platinum-containing drugs like cisplatin directly damage DNA, while there are other drugs(methotrexate,fluorouracil) destroy or damage DNA by pretending to be nucleotides and breaking things that way. </p>\n\n<p>Anthracyclines bind into DNA strands damaging it, directly create free radicals, disable topoisomerase II, and displace histones.</p>\n\n<p>There are the topoisomerase inhibitors which prevent cell growth by preventing DNA from being unwound for replication.</p>\n\n<p>There is a fairly diverse(chemically) class of 'mitotic inhibitors' that screw up microtubule formation or proper microtubule dissolution, any of which prevents mitosis.</p>\n\n<p>Sunitinib blocks tyrosine kinases, which are involved in blood vessel formation(and nerve formation and some other things). Other tyrosine kinase inhibitors are more specific to vascular endothelial growth factor(VEGF) receptors, but most tyrosine kinases target more or less specifically VEGFR and related receptors. Some are antibodies, some are just small molecules that bind TKRs.</p>\n\n<p>There are a few retinoid-related drugs most of which influence the vitamin A pathways, like tretinoin, bexarotene, etc. Dual use in skin creams.</p>\n\n<p>Immunoadjuvants are designed to activate the immune system to aid in tumor cell destruction. Interferon-alpha, imidazoquinoline, et cetera.</p>\n\n<p>In the miscellaneous category: Bortezomib, a short peptide that interferes with proper protein degradation. L-asparaginase slows all protein production by destroying asparagine, an amino acid. Some blood cancers respond to corticosteroids, and some ovarian/testicular cancers are treated with sex hormone inhibitors. Nearly any blood-borne poison works as a chemotherapy agent due to the <a href=\"http://en.wikipedia.org/wiki/Enhanced_permeability_and_retention_effect\" rel=\"nofollow\">EPR effect</a>, so heavy metals or radioactive isotopes also are sometimes used. Arsenic trioxide, for instance, is just arsenic. </p>\n\n<p>It's also worth looking at the steroids that are given along with cancer treatment(dexamethasone) to mitigate side effects. As regulatory hormones, there's going to be a hefty impact on genetic regulation from regular steroid injections. If nothing else it's a confounding effect you'll need to control for.</p>\n\n<p>The preparations/solvents of chemotherapy agents can also be significant. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/11527683\" rel=\"nofollow\">Cremophor</a> was used to suspend some anticancer drugs, but <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/21575719\" rel=\"nofollow\">recent developments</a> imply that might be on its way out.</p>\n"
}
] |
[
{
"answer_id": 34644,
"pm_score": 1,
"text": "<p>Resonating provided a good general classification scheme that could be implemented for categorizing chemotherapeutic agents. Another resource that could be used is the following: <a href=\"http://www.genome.jp/kegg/drug/\" rel=\"nofollow\">http://www.genome.jp/kegg/drug/</a>. This is a pretty good classification of drugs based on ATC resource (<a href=\"http://en.wikipedia.org/wiki/Anatomical_Therapeutic_Chemical_Classification_System\" rel=\"nofollow\">http://en.wikipedia.org/wiki/Anatomical_Therapeutic_Chemical_Classification_System</a>). These two resources are good starting points.</p>\n"
}
] |
19,590
|
<p>In <a href="http://www.simonsfoundation.org/quanta/20140710-hints-of-lifes-start-found-in-a-giant-virus/#comment-142465" rel="nofollow">this piece</a> about giant viruses and the origin of life, in the context of the move from RNA world to DNA world, virologist Valerian Dolja states:</p>
<blockquote>
<p>In order to move from RNA to DNA, you need an enzyme called reverse transcriptase</p>
</blockquote>
<p>Is this true though? Don't many DNA polymerases work with both, ssDNA and ssRNA templates, i.e. they function as reverse transcriptases although they're not "true" reverse transcriptases. So, in order to move from RNA to DNA, a reverse transcriptase was not a necessity like ribonucleotide reductase was for RNA to Uracil-DNA and thymidylate synthase was for Uracil-DNA to DNA?</p>
|
[
{
"answer_id": 19579,
"pm_score": 3,
"text": "<p>There's <a href=\"http://www.pharmgkb.org/\" rel=\"nofollow\">this database</a> of genetic/drug interactions, which I think is pretty much exactly what you're looking for. </p>\n\n<p>Probably your best approach is to classify your drugs into a couple different categories of action. Some drugs will have to be in several categories at once(I'm lookin at you anthracyclines) Dose-dependent mutagens(cisplatin), growth-dependent mutagens(fluorouracil), topoisomerase inhibitors, tyrosine kinase inhibitors, microtubule inhibitors, retinoid signaling, immune adjuvants, and then 'misc'. </p>\n\n<p>Alkylating agents and platinum-containing drugs like cisplatin directly damage DNA, while there are other drugs(methotrexate,fluorouracil) destroy or damage DNA by pretending to be nucleotides and breaking things that way. </p>\n\n<p>Anthracyclines bind into DNA strands damaging it, directly create free radicals, disable topoisomerase II, and displace histones.</p>\n\n<p>There are the topoisomerase inhibitors which prevent cell growth by preventing DNA from being unwound for replication.</p>\n\n<p>There is a fairly diverse(chemically) class of 'mitotic inhibitors' that screw up microtubule formation or proper microtubule dissolution, any of which prevents mitosis.</p>\n\n<p>Sunitinib blocks tyrosine kinases, which are involved in blood vessel formation(and nerve formation and some other things). Other tyrosine kinase inhibitors are more specific to vascular endothelial growth factor(VEGF) receptors, but most tyrosine kinases target more or less specifically VEGFR and related receptors. Some are antibodies, some are just small molecules that bind TKRs.</p>\n\n<p>There are a few retinoid-related drugs most of which influence the vitamin A pathways, like tretinoin, bexarotene, etc. Dual use in skin creams.</p>\n\n<p>Immunoadjuvants are designed to activate the immune system to aid in tumor cell destruction. Interferon-alpha, imidazoquinoline, et cetera.</p>\n\n<p>In the miscellaneous category: Bortezomib, a short peptide that interferes with proper protein degradation. L-asparaginase slows all protein production by destroying asparagine, an amino acid. Some blood cancers respond to corticosteroids, and some ovarian/testicular cancers are treated with sex hormone inhibitors. Nearly any blood-borne poison works as a chemotherapy agent due to the <a href=\"http://en.wikipedia.org/wiki/Enhanced_permeability_and_retention_effect\" rel=\"nofollow\">EPR effect</a>, so heavy metals or radioactive isotopes also are sometimes used. Arsenic trioxide, for instance, is just arsenic. </p>\n\n<p>It's also worth looking at the steroids that are given along with cancer treatment(dexamethasone) to mitigate side effects. As regulatory hormones, there's going to be a hefty impact on genetic regulation from regular steroid injections. If nothing else it's a confounding effect you'll need to control for.</p>\n\n<p>The preparations/solvents of chemotherapy agents can also be significant. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/11527683\" rel=\"nofollow\">Cremophor</a> was used to suspend some anticancer drugs, but <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/21575719\" rel=\"nofollow\">recent developments</a> imply that might be on its way out.</p>\n"
}
] |
[
{
"answer_id": 34644,
"pm_score": 1,
"text": "<p>Resonating provided a good general classification scheme that could be implemented for categorizing chemotherapeutic agents. Another resource that could be used is the following: <a href=\"http://www.genome.jp/kegg/drug/\" rel=\"nofollow\">http://www.genome.jp/kegg/drug/</a>. This is a pretty good classification of drugs based on ATC resource (<a href=\"http://en.wikipedia.org/wiki/Anatomical_Therapeutic_Chemical_Classification_System\" rel=\"nofollow\">http://en.wikipedia.org/wiki/Anatomical_Therapeutic_Chemical_Classification_System</a>). These two resources are good starting points.</p>\n"
}
] |
19,593
|
<p>why plants can only synthesize D-glucose why not L-glucose along with D glucose. I know it very well that plants have only enzymes which can synthesize D-glucose but Why not they have enzymes which can also manufacture L-glucose. So that we could have mixture of L and D glucose molecules? What is the significance of synthesis of only D-glucose by the plants ?</p>
|
[
{
"answer_id": 19579,
"pm_score": 3,
"text": "<p>There's <a href=\"http://www.pharmgkb.org/\" rel=\"nofollow\">this database</a> of genetic/drug interactions, which I think is pretty much exactly what you're looking for. </p>\n\n<p>Probably your best approach is to classify your drugs into a couple different categories of action. Some drugs will have to be in several categories at once(I'm lookin at you anthracyclines) Dose-dependent mutagens(cisplatin), growth-dependent mutagens(fluorouracil), topoisomerase inhibitors, tyrosine kinase inhibitors, microtubule inhibitors, retinoid signaling, immune adjuvants, and then 'misc'. </p>\n\n<p>Alkylating agents and platinum-containing drugs like cisplatin directly damage DNA, while there are other drugs(methotrexate,fluorouracil) destroy or damage DNA by pretending to be nucleotides and breaking things that way. </p>\n\n<p>Anthracyclines bind into DNA strands damaging it, directly create free radicals, disable topoisomerase II, and displace histones.</p>\n\n<p>There are the topoisomerase inhibitors which prevent cell growth by preventing DNA from being unwound for replication.</p>\n\n<p>There is a fairly diverse(chemically) class of 'mitotic inhibitors' that screw up microtubule formation or proper microtubule dissolution, any of which prevents mitosis.</p>\n\n<p>Sunitinib blocks tyrosine kinases, which are involved in blood vessel formation(and nerve formation and some other things). Other tyrosine kinase inhibitors are more specific to vascular endothelial growth factor(VEGF) receptors, but most tyrosine kinases target more or less specifically VEGFR and related receptors. Some are antibodies, some are just small molecules that bind TKRs.</p>\n\n<p>There are a few retinoid-related drugs most of which influence the vitamin A pathways, like tretinoin, bexarotene, etc. Dual use in skin creams.</p>\n\n<p>Immunoadjuvants are designed to activate the immune system to aid in tumor cell destruction. Interferon-alpha, imidazoquinoline, et cetera.</p>\n\n<p>In the miscellaneous category: Bortezomib, a short peptide that interferes with proper protein degradation. L-asparaginase slows all protein production by destroying asparagine, an amino acid. Some blood cancers respond to corticosteroids, and some ovarian/testicular cancers are treated with sex hormone inhibitors. Nearly any blood-borne poison works as a chemotherapy agent due to the <a href=\"http://en.wikipedia.org/wiki/Enhanced_permeability_and_retention_effect\" rel=\"nofollow\">EPR effect</a>, so heavy metals or radioactive isotopes also are sometimes used. Arsenic trioxide, for instance, is just arsenic. </p>\n\n<p>It's also worth looking at the steroids that are given along with cancer treatment(dexamethasone) to mitigate side effects. As regulatory hormones, there's going to be a hefty impact on genetic regulation from regular steroid injections. If nothing else it's a confounding effect you'll need to control for.</p>\n\n<p>The preparations/solvents of chemotherapy agents can also be significant. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/11527683\" rel=\"nofollow\">Cremophor</a> was used to suspend some anticancer drugs, but <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/21575719\" rel=\"nofollow\">recent developments</a> imply that might be on its way out.</p>\n"
}
] |
[
{
"answer_id": 34644,
"pm_score": 1,
"text": "<p>Resonating provided a good general classification scheme that could be implemented for categorizing chemotherapeutic agents. Another resource that could be used is the following: <a href=\"http://www.genome.jp/kegg/drug/\" rel=\"nofollow\">http://www.genome.jp/kegg/drug/</a>. This is a pretty good classification of drugs based on ATC resource (<a href=\"http://en.wikipedia.org/wiki/Anatomical_Therapeutic_Chemical_Classification_System\" rel=\"nofollow\">http://en.wikipedia.org/wiki/Anatomical_Therapeutic_Chemical_Classification_System</a>). These two resources are good starting points.</p>\n"
}
] |
19,612
|
<p>This plant was found growing in Germany. I have never seen it before, reverse Google image search did not help either. Can you help me identify what type of plant this is?</p>
<p><img src="https://i.stack.imgur.com/2YcJL.png" alt="Full view">
<img src="https://i.stack.imgur.com/MrjTJ.jpg" alt="Flower">
<img src="https://i.stack.imgur.com/GPiDX.jpg" alt="Root"></p>
<p>Thanks, looks like it is something like this:</p>
<p><a href="http://pflanzen-enzyklopaedie.eu/stauden/amerikanische-kermesbeere-phytolacca-americana/#more-4034" rel="nofollow noreferrer">http://pflanzen-enzyklopaedie.eu/stauden/amerikanische-kermesbeere-phytolacca-americana/#more-4034</a></p>
<p>Related question:</p>
<p><a href="https://gardening.stackexchange.com/questions/2609/what-is-this-fast-growing-plant-with-blue-black-berries/2610#2610">https://gardening.stackexchange.com/questions/2609/what-is-this-fast-growing-plant-with-blue-black-berries/2610#2610</a></p>
|
[
{
"answer_id": 19618,
"pm_score": 4,
"text": "<p>This looks like some species of <em>Phytolacca</em> to me.</p>\n\n<p>It's possibly <em>Phytolacca americana</em>, which is native to the US (in fact it's an enthusiastic 'volunteer' in my garden) but <a href=\"http://books.google.com/books?id=5vd_ZE7UDV8C&lpg=PA1018&ots=tmnF-2RlZr&dq=european%20phytolacca&pg=PA43#v=onepage&q=phytolacca&f=false\">naturalized in Europe</a>.</p>\n\n<p>If you still have any in the ground, once they ripen, the berries are intensely purple and <a href=\"http://www.efloras.org/florataxon.aspx?flora_id=1&taxon_id=220010427\">can be used as dye (or even eaten?)</a></p>\n\n<hr>\n\n<p><a href=\"http://www.efloras.org/florataxon.aspx?flora_id=1&taxon_id=220010427\">Mark A. Nienaber & John W. Thieret. Phytolaccaceae. In: Flora of North America Editorial Committee, eds. 1993+. Flora of North America North of Mexico. New York and Oxford. (link goes to entry of P. americana)</a></p>\n"
}
] |
[
{
"answer_id": 55311,
"pm_score": 1,
"text": "<p>It is <a href=\"https://fr.wikipedia.org/wiki/Phytolacca_acinosa\" rel=\"nofollow noreferrer\">Phytolacca acinosa</a> because the flowers grow upwards and the fruits are ribbed. <a href=\"https://en.wikipedia.org/wiki/Phytolacca_americana\" rel=\"nofollow noreferrer\">Phytolacca americana</a> has downward pointing flowers and smooth fruits.</p>\n"
}
] |
19,648
|
<p>Is it possible for a device to measure how much air we breathe in and out over the entire day and at what rate? I think if we have access to this data we can compare it across people.</p>
|
[
{
"answer_id": 19682,
"pm_score": 3,
"text": "<p>What you are looking for is a spirometer. There are different types of spirometers serving different purposes like the Incentive spirometer and the peak flow meter. I would suggest that you go through the <a href=\"http://en.wikipedia.org/wiki/Spirometer\" rel=\"nofollow noreferrer\">wikipedia page on it</a> to get more info. </p>\n\n<p><img src=\"https://i.stack.imgur.com/jnvac.gif\" alt=\"enter image description here\"></p>\n"
}
] |
[
{
"answer_id": 19684,
"pm_score": 1,
"text": "<p>Another possibility is <a href=\"http://www.serinth.gr/en/products/ergospirometers/portable-ergospirometers/cosmed-k4b2.html\" rel=\"nofollow\">K4 device</a> and <a href=\"http://www.cosmed.com/en/products/cardio-pulmonary-exercise-testing/k4-b2-mobile-cpet\" rel=\"nofollow\">K4 device</a>. Beyond spirometry it can measure other variables such as: </p>\n\n<ul>\n<li>Pulmonary Gas Exchange (VO2, VCO2)</li>\n<li>Breath by Breath Technology</li>\n<li>Telemetry Data Transmission up to 1000m</li>\n<li>Indirect Calorimetry</li>\n<li>Integrated GPS System</li>\n<li>Integrated Oxygen Saturation (SpO2)</li>\n<li>Integrated 12-lead Stress Testing ECG</li>\n</ul>\n"
}
] |
19,653
|
<p>I recently watched the video <a href="https://www.youtube.com/watch?v=R3unPcJDbCc">This Is Not Yellow</a> explaining how red, green, and blue pixels can be used to create images of all other colors. Since yellow is created with red and green pixels, how is a person with red-green colorblindness (me, for instance) able to perceive yellow on a monitor?</p>
|
[
{
"answer_id": 96315,
"pm_score": 1,
"text": "<p>Below is a summary of the information found <a href=\"https://commandcenter.blogspot.com/2020/09/color-blindness-is-inaccurate-term.html\" rel=\"nofollow noreferrer\">here</a> and from how <a href=\"https://enchroma.com/pages/how-enchroma-glasses-work\" rel=\"nofollow noreferrer\">Enchroma glasses work</a> (although, I've tried the glasses and the effect is too subtle for me to wear them regularly).</p>\n<p>Human color vision works because there are three different color-sensitive receptors called <a href=\"https://en.wikipedia.org/wiki/Cone_cell\" rel=\"nofollow noreferrer\">cones</a> that detect short-wavelength light (bluish), medium-wavelength light (greenish), and long-wavelength light (reddish). The charts below show the sensitivity of these receptors in people with different genetics.</p>\n<p><a href=\"https://i.stack.imgur.com/JKewc.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/JKewc.jpg\" alt=\"Charts of the sensitivities of color receptors\" /></a></p>\n<p>Chart taken from <a href=\"https://rads.stackoverflow.com/amzn/click/com/0521496454\" rel=\"nofollow noreferrer\" rel=\"nofollow noreferrer\">Color Art and Science, edited by Trevor Lamb and Janine Bourriau</a></p>\n<p>The bottom chart, marked (c), shows the sensitivities of eyes of people with normal color vision. Short-wavelength (blueish) cones detect a distinct patch of light while the medium- (greenish) and long- (reddish) wavelength cones overlap, but are still separated enough to reliably distinguish between the two color ranges.</p>\n<p>The middle chart, marked (b), shows mild protananomaly or deutananomaly color blindness in which the color regions that medium (greenish) and long (reddish) cones react to are more overlapped than in people with normal vision. This can lead to trouble distinguishing these colors since the overlap causes both receptors to light up for more colors.</p>\n<p>The top chart, marked (a), shows complete protanopia or deutanopia, where the long (reddish) and medium (greenish) receptors completely overlap in their sensitivity ranges. This can also happen if one receptor is entirely missing from the retina.</p>\n<p>I was under the impression that all red-green color blindness was of the protanopia/deutanopia type, meaning that the yellow generated on a computer screen should look red because the green light wouldn't be activating any of the non-functional medium (greenish) cones. In actuality, I only have a mild protananomaly/deutananomaly, so my eyes are still sensitive to the differences between red and green light, just less so than normal people. The yellow I see may be subtly different than other people, but I can still differentiate.</p>\n<p>Enchroma glasses work for mild colorblindness by filtering out light in the overlap region of medium (greenish) and long (reddish) cones. This creates more separation in the detection region of those cones, thus making some colors more distinct at the cost of blocking some light.</p>\n"
}
] |
[
{
"answer_id": 19661,
"pm_score": 2,
"text": "<p>Normal people see color due to the bellow mentioned combination of red, green and blue:</p>\n\n<p><img src=\"https://i.stack.imgur.com/l99xj.jpg\" alt=\"enter image description here\"></p>\n\n<p>But due to genetic factors, The graph Distorts:</p>\n\n<p><img src=\"https://i.stack.imgur.com/KNOdh.jpg\" alt=\"enter image description here\"></p>\n\n<p>Now,If consider the normal <a href=\"http://www.rapidtables.com/web/color/Yellow_Color.htm\" rel=\"nofollow noreferrer\">Color code for yellow</a>:</p>\n\n<p>Yellow = R(255) + G(255) + B(0)</p>\n\n<p>Or in other words</p>\n\n<p>Max. Red + Max. Green + no Blue = Yellow</p>\n\n<p>That means even if you can see a little of Red and Green, you can still a little deeper or lighter shade of yellow.</p>\n\n<p>So Summing it up in the images:</p>\n\n<p><img src=\"https://i.stack.imgur.com/qzJT7.png\" alt=\"enter image description here\"> </p>\n\n<p><strong>Normal</strong></p>\n\n<p><img src=\"https://i.stack.imgur.com/KBPaq.jpg\" alt=\"enter image description here\"> </p>\n\n<p><strong>Red ColorBlind</strong></p>\n\n<p><img src=\"https://i.stack.imgur.com/6Sv7V.jpg\" alt=\"enter image description here\"> </p>\n\n<p><strong>Green ColorBlind</strong></p>\n\n<p><img src=\"https://i.stack.imgur.com/QzpTp.jpg\" alt=\"enter image description here\"> </p>\n\n<p><strong>Blue ColorBlind</strong></p>\n\n<p>Source: </p>\n\n<p><a href=\"http://www.color-blindness.com/coblis-color-blindness-simulator/\" rel=\"nofollow noreferrer\">Coblis — Color Blindness Simulator</a></p>\n\n<p><a href=\"http://wearecolorblind.com/article/a-quick-introduction-to-color-blindness/\" rel=\"nofollow noreferrer\">A quick introduction to colorblindness</a></p>\n"
}
] |
19,656
|
<p>I'm aware that our earliest records of many major animal and plant phyla come from the Cambrian or Precambrian periods, and I'm also vaguely aware of some of the objections raised with general concept of phyla. With this in mind, I'm curious which of widely accepted biological phyla appeared most recently, and what evidence do we have of their relatively recent appearance? </p>
<p>I'm most interested in animals, but I'd also welcome any information about other organisms.</p>
|
[
{
"answer_id": 19659,
"pm_score": 4,
"text": "<p>In my view, we simply don't have good enough data to answer this question. The fossil evidence is too sparse prior to the Cambrian and the evidence that we do have suggests that the phyla were already too separated. Meanwhile, the depth of time and the different lifecycles and circumstances of the species involved mean that any \"genetic clocks\" we might use are likely to be too poor at keeping time and, indeed, different attempts have delivered different estimates of the time of divergence.</p>\n"
}
] |
[
{
"answer_id": 19657,
"pm_score": 2,
"text": "<p>As far as I know there is no phylum which appeared after the Cambrian. Every discussion beyond that is close to speculation, as the divergence estimates of different studies vary significantly. \nYou might want to look into one of the resources mentioned below:</p>\n\n<ul>\n<li><a href=\"http://www.timetree.org/index.php\" rel=\"nofollow\">http://www.timetree.org/index.php</a></li>\n<li><a href=\"http://www.onezoom.org/\" rel=\"nofollow\">http://www.onezoom.org/</a></li>\n</ul>\n"
}
] |
19,658
|
<p>I'm a computer scientist who is starting to dabble with biology. My eventual goal is to model different kinds of cells with a computer program. As of right now, I'm just trying to take some smaller steps.</p>
<p>First, I downloaded a complete human genome from <a href="http://hgdownload.cse.ucsc.edu/downloads.html#human" rel="noreferrer">http://hgdownload.cse.ucsc.edu/downloads.html#human</a> There is a FASTA file for each chromosome.</p>
<p>Then, I wrote a java program which can convert FASTA DNA sequences into the appropriate amino acid chain.</p>
<p>Next, I made my program look for the "start" code (ATG) and "stop" codes (TAA, TAG, TGA).</p>
<p>So, now I have sequences of amino acids which might theoretically end up folding into proteins. But, before I start diving into protein folding, I wanted to try to verify that the steps I took so far were done correctly. I looked up some important human genes in an online database and found their amino acid sequences. I then searched through my program's data for those sequences and confirmed that they were there. However, the gene was in a different base-pair location than the database said that it should be in.</p>
<p>This led me to some questions, which, so far I have been unable to answer and hopefully people here will be able to help shed some light.</p>
<ol>
<li><p>I know there are a lot of different publicly available genomes. Maybe the UCSC one that I downloaded is different from the one used by the gene database. How much does each genome vary from each other genome and in what ways do they vary?</p></li>
<li><p>In attempting to answer that first question, I was going to download a bunch of genomes from the 1000genomes website and do some comparisons, but I wasn't sure which files to download. Each of the files begins with either ERR or SRR and I'm not sure what that means. This is the folder I'm currently looking in <a href="ftp://ftp-trace.ncbi.nih.gov/1000genomes/ftp/data/HG00239/sequence_read/" rel="noreferrer">ftp://ftp-trace.ncbi.nih.gov/1000genomes/ftp/data/HG00239/sequence_read/</a></p></li>
<li><p>Lets say I'm trying to model a white blood cell. How do I know which parts of the genome get turned into proteins for that type of cell?</p></li>
</ol>
<p>Sorry if anything I said doesn't make sense. As I said, my expertise lies in programming, not biology/genetics.</p>
|
[
{
"answer_id": 19662,
"pm_score": 5,
"text": "<p>No, your approach will not work, you are taking a very simplistic view of an extremely complex system. Some of the problems you are ignoring are:</p>\n<ul>\n<li><p>Genes (eukaryotic genes anyway) are <a href=\"https://en.wikipedia.org/wiki/RNA_splicing\" rel=\"nofollow noreferrer\">spliced </a>to produce mRNA, a process that removes <a href=\"https://en.wikipedia.org/wiki/Intron\" rel=\"nofollow noreferrer\">introns</a> and leaves only the <a href=\"https://en.wikipedia.org/wiki/Exons\" rel=\"nofollow noreferrer\">exons</a>. If you just translate the entire chromosome file you will get noise.</p>\n</li>\n<li><p>Splicing also changes the <a href=\"https://en.wikipedia.org/wiki/Reading_frame\" rel=\"nofollow noreferrer\">frame</a> a gene is read in, you don't mention frames at all in your question but you can't work with sequences unless you deal with them.</p>\n</li>\n<li><p>Many genes (most even, in some species) are <a href=\"https://en.wikipedia.org/wiki/Alternative_splicing\" rel=\"nofollow noreferrer\">alternatively spliced</a>. One gene can give rise to multiple protein sequences. Which one is produced at any one time can depend on a multitude of factors ranging from pure chance, through environmental conditions to the cell type where the gene is expressed.</p>\n</li>\n<li><p>Genes can be present on both strands of DNA and a gene on the + strand can overlap with a gene on the - strand. In some cases they can even overlap on the same strand (<a href=\"https://en.wikipedia.org/wiki/Nested_gene\" rel=\"nofollow noreferrer\">nested genes</a>). You need to check <em>both</em> strands for coding sequences.</p>\n</li>\n<li><p>You're assuming that all coding sequences start with ATG (most do, not all) and you seem to be assuming that an ATG always starts a coding sequence. A given gene can have dozens or hundreds of ATG codons, how can you know which one is used as a START codon?</p>\n</li>\n</ul>\n<p>The process of identifying the parts of the genome that get translated into protein is not trivial. It is the subject of countless PhD theses, mine for example. There are many programs (gene predictors) that are designed specifically to detect genes in genomic sequences. Having spent many years working with them I can assure you that they're not something you can just whip up one afternoon. They tend to involve very complex models of coding vs. non-coding sequences and are way more sophisticated than simply looking for START and STOP codons. Trying to write one without knowing a <em>lot</em> more about biology than you seem to is just a waste of time.</p>\n<p>Your specific questions are basically irrelevant because of the points mentioned above. Nevertheless, the answers are:</p>\n<ol>\n<li><p>They vary but not much. For well annotated genomes like the human one, the differences will be negligible. That is not why you have strange results though as I explained above.</p>\n</li>\n<li><p>All public FTP sites tend to have a README file that explains what the files provided are. You should read the relevant README from <a href=\"ftp://ftp-trace.ncbi.nih.gov/1000genomes/ftp/\" rel=\"nofollow noreferrer\">ftp://ftp-trace.ncbi.nih.gov/1000genomes/ftp/</a></p>\n</li>\n<li><p>Answering that question will get you a Nobel prize. There simply is no way of predicting what genes will be activated in a particular cell. We're not even <em>close</em> to that level of understanding of how a cell works but I can tell you that it will not depend on the sequence, you will never be able to predict whether a gene is active in a particular cell based on its DNA sequence alone. It will depend on various things including the gene's <a href=\"https://en.wikipedia.org/wiki/DNA_methylation\" rel=\"nofollow noreferrer\">methylation</a> state and is largely an emergent quality of the cell's complexity (think of various proteins interacting with one another, leading to the activation of a gene). The best you can do is get a list of genes that are known to be active from the literature.</p>\n</li>\n</ol>\n<p>In summary, if you want to do something as complex as modelling a cell I suggest you first take the time and study some basic biology so you can understand the system you are trying to model a bit better. The cell is not only an extremely complex system that we don't fully understand yet, it is also not wholly deterministic and contains a lot of stochasticity that you seem to be ignoring completely.</p>\n"
}
] |
[
{
"answer_id": 19664,
"pm_score": 2,
"text": "<p>Why bother predicting proteins badly from DNA sequence when you could have just as well downloaded the manually curated human proteome?</p>\n\n<p>As to your questions:</p>\n\n<ol>\n<li><p>Are you asking about human genomes or genomes in general? The vast majority of the variance in human genomes is in non-coding sequence. As to genomes in general, they vary in pretty much every imaginable way.</p></li>\n<li><p>I think those files are quality filtered Illumina reads. SRA = Sequence Read Achieve. SRR = SRA RUN accession. ERA = EMBL SRA. ERR = ERA RUN accession.</p></li>\n<li><p>You should look into transcriptomics data. Predicting such stuff in silico is currently pretty much undoable.</p></li>\n</ol>\n"
}
] |
19,668
|
<p>Take for example the human and the chimpanzee, they are "closely related" species since they are "close" to each other in a phylogenetic tree. However, this terminology seems pretty informal, what would be the formal way to specify that two or more species are "closely related"?</p>
|
[
{
"answer_id": 19673,
"pm_score": 3,
"text": "<p>Are you looking for something like \"<a href=\"http://en.wikipedia.org/wiki/Sister_group\" rel=\"nofollow\">sister lineage</a>\" (or \"sister taxon\" or \"sister group\")</p>\n\n<p>This term may be more specific than what you're looking for, and to use it correctly you'd want to be a little careful – I guess in this case you might have to say something like: </p>\n\n<blockquote>\n <p>\"the lineage that includes chimpanzees and bonobos is sister to the\n lineage of which humans are the only extant species\"</p>\n</blockquote>\n\n<p>or</p>\n\n<blockquote>\n <p>\"the lineage that includes chimpanzees and bonobos and the lineage of\n which humans are the only extant species are sister lineages\"</p>\n</blockquote>\n\n<p>both referring to <a href=\"http://tolweb.org/Hominidae/16299\" rel=\"nofollow\">this phylogeny</a>.</p>\n\n<hr>\n\n<p>It's also possible that explaining exactly what you mean by 'close', or what it entails, would be appropriate, be it Ilan's suggestion of % genetic similarity (or maybe genomic similarity?), # of nodes between your two taxa (again, this would have to be in reference to a specific phylogeny), or if you have a dated phylogeny you could refer to the time since divergence, as in \"coding DNA divergencies ...place the most recent common ancestor of humans and chimpanzees at between 5 and 6 million years ago.\"(<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/12766228\" rel=\"nofollow\">Wildman et al 2003</a>).</p>\n"
}
] |
[
{
"answer_id": 19672,
"pm_score": 2,
"text": "<p>As <a href=\"http://en.wikipedia.org/wiki/Genus\" rel=\"nofollow\">genus</a> comes above species I'd consider using this term for the species which are close genetically (\"these two species are from the same genus\"). Above genus comes family etc...</p>\n\n<p>On the other hand, the proximity or similarity of species could be probably \"measured\" by degree of <a href=\"http://en.wikipedia.org/wiki/Biodiversity\" rel=\"nofollow\">biodiversity</a>, and especially <a href=\"http://en.wikipedia.org/wiki/Genetic_diversity\" rel=\"nofollow\">genetic diversity</a> considering two close species having low biodiversity and very different species as having higher biodiversity. </p>\n\n<p>Thirdly, and I feel that this is the most strong term to use, you can \"express\" the genetic closeness of species as being \"genetically similar\":</p>\n\n<p>\"Some monkeys and humans have 98% genetic similarity\" or \"are up to 98% genetically similar\" or \"... DNA similar\"... </p>\n"
}
] |
19,708
|
<p>As steroid hormones can pass through the plasma membrane by simple diffusion because they are lipid derived hormones, it means that they are capable of passing through every cell of our body, BUT why are only specific cells responsive against steroid hormones?</p>
<p>For example, all of our body cells almost contains the genes for the development of secondary sexual characters but why do only specific cells show a response against these steroid hormones because the development of secondary sexual characters occur only in specific region of our body, that is, beard formation occur only in a specific region of the face, etc.</p>
<p>IN SUMMARY: When steroid hormones can pass through every cell of our body then why do they show only a localized response?</p>
|
[
{
"answer_id": 20402,
"pm_score": 3,
"text": "<p>Unlike other types of hormones, steroid hormones do not have to bind to plasma membrane receptors. Instead, they can interact with intracellular receptors that are themselves transcription activators. Steroid hormones too hydrophobic to dissolve readily in the blood travel on specific carrier proteins from their point of release to their target tissues. In the target tissue, the hormone passes through the plasma membrane by simple diffusion and binds to its specific receptor protein in the cytoplasm. The receptor-hormone complex then translocates into the nucleus where it acts by binding to highly specific DNA sequences called <strong><em>hormone response elements (HREs)</em>,</strong> thereby altering gene expression. \nHormone binding triggers changes in the conformation of the receptor proteins so that they be- come capable of interacting with additional transcription factors. The bound hormone-receptor complex can either enhance or suppress the expression of adjacent genes. \nThe DNA sequences (HREs) to which hormone- receptor complexes bind are similar in length and arrangement, but differ in sequence, for the various steroid hormones. Each receptor has a consensus HRE sequence to which the hormone-receptor complex binds well, with each consensus consisting of two six-nucleotide sequences, either contiguous or separated by three nucleotides, \nThe ability of a given hormone to act through the hormone-receptor complex to alter the expression of a specific gene depends on the exact sequence of the HRE, its position relative to the gene, and the number of HREs associated with the gene.</p>\n"
}
] |
[
{
"answer_id": 19709,
"pm_score": 3,
"text": "<p>The quick answer is that only certain cell types express the required <a href=\"http://en.wikipedia.org/wiki/Steroid_hormone_receptor\">steroid hormone receptors</a> that are necessary to induce signaling and gene regulation when bound to their target steroid hormones, like estrogen, testosterone, cortisol, etc. If no receptor is present, the steroid doesn't effect any change.</p>\n\n<p>The second part of the answer involves the particular signaling pathways induced by the ligation of certain receptors by certain classes of hormones. <a href=\"http://en.wikipedia.org/wiki/Testosterone\">Testosterone</a>, for example, has numerous effects across the body, from promoting the growth of hair to building muscle mass to effects on mental well-being. Testosterone and its primary metabolite 5α-dihydrotestosterone bind primarily to the cytoplasmic <a href=\"http://en.wikipedia.org/wiki/Androgen_receptor\">androgen receptor</a>, which then translocates to the nucleus, binds DNA at <a href=\"http://en.wikipedia.org/wiki/Hormone_response_element\">hormone response elements</a>, and alters the transcriptional activity of genes (either increasing or decreasing, depending on the gene and the cell type). Testosterone can also be metabolized to <a href=\"http://en.wikipedia.org/wiki/Estradiol\">estradiol</a> and bind <a href=\"http://en.wikipedia.org/wiki/Estrogen_receptor\">estrogen receptors</a>, which function similarly to the androgen receptor (although it can have DNA-independent effects as well).</p>\n\n<p>So, depending on the cell type, receptor expression levels, other DNA regulatory elements, the presence or absence of various testosterone-metabolizing enzymes, and other factors like age, gender, etc., a single steroid hormone can have a multitude of effects throughout the body.</p>\n"
}
] |
19,725
|
<p>In an animal cell, especially neuron and in particular its axon, while there is electrical resistance and capacitance mechanism in the cell, which play essential roles in the cable theory model of neuronal action potential transmission, is there a prominent self <a href="http://en.wikipedia.org/wiki/Self_inductance" rel="nofollow noreferrer">inductance</a> mechanism in the sense of electromagnetism?</p>
|
[
{
"answer_id": 20252,
"pm_score": 4,
"text": "<p>What one thinks, no matter how intuitive it may appear is not particularly relevant in science. The inductance associated with a neural axon has been well documented since Cole (1966). Its role in the propagation of neural signals is developed extensively in <a href=\"http://neuronresearch.net/hearing/pdf/7Projection.pdf#page=39\" rel=\"noreferrer\">http://neuronresearch.net/hearing/pdf/7Projection.pdf#page=39</a> . The actual development begins earlier in Section 7.4 on page 322 of that document.<br>\nFailure to consider the inductance associated with any alternating electrical signal passed along a coaxial cable leads to disaster. The first undersea cable based on the ideas of William Thompson,Lord Kelvin, and described as an RC cable by Hermann (page 322 in the above document) was a technical and financial disaster. Two years later, a more sophisticated RLC cable based on Maxwell's Equations for a coaxial structure was laid with great success. No RC cable has ever been used in practice since that time. For unknown reasons, the biological community keeps trying to ignore the inductance of the coaxial myelinated axon (leading to ridiculous modeling data). This appears to be the result of introductory courses in electricity for non-engineers trying to avoid the necessary mathematics to understand electromagnetic signal propagation through space and along various types of cables and waveguides.</p>\n"
}
] |
[
{
"answer_id": 78594,
"pm_score": 1,
"text": "<p>There surely is inductance in neurons. This inductance is introduced by two different mechanisms. \n1. The coil structure of myelin sheaths can introduce a real electrical inductance. The solid evidence for this is the opposite spiraling directions between the adjacent myelin sheaths. </p>\n\n<p>Here I quote the description on Wikipedia:<em>At the junction of two Schwann cells along an axon, the directions of the lamellar overhang of the myelin endings are of opposite sense.</em> You can also check the details in this paper: Uzmman B. G.; Nogueira-Graf G. (1957). \"Electron microscope studies of the formation of nodes of Ranvier in mouse sciatic nerves\". Journal of Biophysical and Biochemical Cytology. 3 (4): 589–597. doi:10.1083/jcb.3.4.589</p>\n\n<p>The opposite spiraling directions can introduce a positive mutual inductance between adjacent myelin sheaths then further enhance the propagation speed of the neural signal. Meanwhile, it is easy to predict that the myelinated nerve can be stimulated by a magnetic field because of this coil inductor. Because of this opposite spiraling direction, the stimulation result is determined by the spatial gradient of the magnetic field. This phenomenon was validated by years and can be easily understood now.</p>\n\n<ol start=\"2\">\n<li>The piezoelectric effect of the plasma membrane. If you check the molecular structure of the lipid bilayer of the plasma membrane, you will find that it is naturally a piezoelectric layer. The definition of the piezoelectric layer is a layer consists of two crystal layer with opposite polarities, which is exactly the same as the lipid bilayer. The equivalent circuit of this piezoelectric layer will be a RLC circuit, which contains an equivalent inductor. Since the inductor is not a real one, the value is only used to match with the mechanical resonance frequency. When the mechanical resonance frequency is very low, which is the case for a soft and thin plasma membrane, this inductance will be huge. This is why in Cole's paper for measurement of the squid axon, this inductance is 0.2H. Then as a direct prediction, there should be a mechanical wave accompany with the electric signal of the action potential. \nThis mechanical wave has been measured in this paper: Gonzalez-Perez, A., Mosgaard, L.D., Budvytyte, R., Villagran-Vargas, E., Jackson, A.D. and Heimburg, T., 2016. Solitary electromechanical pulses in lobster neurons. Biophysical chemistry, 216, pp.51-59.</li>\n</ol>\n\n<p>I think here I already give a comprehensive answer to this question. You can check all the details in this paper on bioRix:<a href=\"https://www.biorxiv.org/content/early/2018/10/22/343905\" rel=\"nofollow noreferrer\">https://www.biorxiv.org/content/early/2018/10/22/343905</a></p>\n\n<p>Here I may talk something more, but these things will make most of the people in neuroscience unhappy.\nIf this inductance introduced by the coil structure of myelin and the piezoelectric effect is true, then the whole neuroscience is wrong from the Day 1. The H-H model is built based on a RC circuit and so many people have developed their theories and models based on this H-H model. But ridiculously, everyone claims his model or theory is correct and can explain the data when tha basis is wrong. I have seen so many absurd explanations to bypass this inductance, such as the frequency-dependent capacitor, virtual cathode, negative resistor, and even negative capacitor. \nAnd indeed, more and more people begin to realize the so-called neuroscience is a complete failure. You can see in the homepage of Neuralink(<a href=\"https://neuralink.com/\" rel=\"nofollow noreferrer\">https://neuralink.com/</a>), they officially claim that they do not need any neuroscience experience, quote here:<em>No neuroscience experience is required</em>\nAlso, there are many groups now only use deep learning or machine learning to study neurons. </p>\n"
}
] |
19,744
|
<p><a href="https://cooking.stackexchange.com/a/45589/11251">An answer on another SE site</a> mentions that sugar "at a certain level acts as a preservative". I've always been taught that microorganisms eat sugar and expel acids, that is why sugary food are damaging to teeth. <strong>How is it that sugar acts as a preservative, then?</strong></p>
<p>Googling the question I've found <a href="http://sciencefocus.com/qa/how-does-sugar-act-preservative" rel="nofollow noreferrer">conflicting</a> <a href="https://answers.yahoo.com/question/index?qid=20080423133918AAt7NvX" rel="nofollow noreferrer">answers</a> though I don't credit the sources as being especially reputable. What is the real reason that sugar can act as a preservative?</p>
|
[
{
"answer_id": 19748,
"pm_score": 4,
"text": "<p>Sugar in high concentrations acts osmotic. This means that the water available in the cells is drawn towards the high concentration of a solutant (sugar), like in the image below (this is demonstrated with a plant cell, but the principle is the same for bacteria and other microorganisms):</p>\n\n<p><img src=\"https://i.stack.imgur.com/ZciJU.png\" alt=\"enter image description here\"></p>\n\n<p>Since microorganisms can not survive without water, they are not able to grow or reproduce. This effectively safes food. The same mechanism works when salt is used to conserve meat or fish.</p>\n"
}
] |
[
{
"answer_id": 43042,
"pm_score": 2,
"text": "<p>Sugar participate in food preservation only at high concentrations. When microbes are introduced to high sugar concentrated environment, water inside the microbial cell diffuses out to the high sugar concentrated solute due to the phenomenon called <strong>osmosis</strong>. As water is very much needed for cell functioning and metabolism the dehydrated cells fail to perform its function and eventually die. This is called <strong>sugar curing</strong>, a food preservation technique. Also hard sugary sweet is less susceptible to microbes than soft sugar sweet because of its high sugar content that makes it intolerant for microbial growth and also the absence of moisture (important factor for microbial growth) in the hard sweet as compared to soft sweet makes it less susceptible to microbial attack.</p>\n"
}
] |
19,749
|
<p>I have some protein-ligand complexed that I have been docking with some other software and just want to use Autodock to evaluate those complexes. So, basically I just want to use it as a scoring function to take a look at the energy components - I don't want to re-dock the ligands into the protein binding sites.
From what I have found on the internet, I came up with this procedure, but I am not sure if this is the right approach, and also I get an error in the last step saying that "atoms are outside the grid".</p>
<p>It would be nice if someone could take a look at it and tell me whether this make sense and if this is the right procedure (and maybe a suggestion for the error source)</p>
<p><strong>1) Preparing the receptor</strong></p>
<ul>
<li><p>need to add hydrogens if not present</p></li>
<li><p>adds gasteiger charges to peptide</p></li>
</ul>
<p><strong>input</strong></p>
<ul>
<li>protein.pdb</li>
</ul>
<p><strong>output</strong></p>
<ul>
<li>protein.pdbqt</li>
</ul>
<p><strong>script:</strong> </p>
<ul>
<li>prepare_receptor4.py -r protein.pdb [options]</li>
</ul>
<hr>
<p><strong>2) Preparing the ligand</strong></p>
<ul>
<li>add hydrogens if not present </li>
</ul>
<p><strong>input:</strong> </p>
<ul>
<li>ligand.pdb or ligand.mol2</li>
</ul>
<p><strong>output:</strong> </p>
<ul>
<li>ligand.pdbqt</li>
</ul>
<p><strong>script</strong></p>
<ul>
<li>prepare_ligand4.py -l ligand.mol2 [options]</li>
</ul>
<hr>
<p><strong>3) Generate grid parameter file</strong></p>
<p><strong>inputs</strong></p>
<ul>
<li>ligand.pdbqt</li>
<li>protein.pdbqt</li>
</ul>
<p><strong>output</strong></p>
<ul>
<li>protein.gpf</li>
</ul>
<p><strong>script:</strong> </p>
<p>prepare_gpf4.py -l ligand.pdbqt -r protein.pdbqt [options]</p>
<hr>
<p><strong>4) AutoGrid: generate maps and grid data file</strong></p>
<p><strong>inputs:</strong> </p>
<ul>
<li>protein.pdbqt </li>
<li>protein.gpf</li>
</ul>
<p><strong>outputs:</strong></p>
<ul>
<li>protein.glg Grid Log File</li>
<li>protein.*.map affinity maps for different atoms</li>
<li>protein.maps.fld Grid data file</li>
<li>protein.d.map desolvation map</li>
<li>protein.e.map electrostatic map</li>
</ul>
<p><strong>command:</strong></p>
<p>autogrid -p protein gpf</p>
<hr>
<p><strong>5) Generate docking parameter file</strong></p>
<p><strong>inputs</strong></p>
<ul>
<li>ligand.pdbqt</li>
<li>protein.pdbqt</li>
</ul>
<p><strong>output</strong></p>
<ul>
<li>ligand_protein.dpf</li>
</ul>
<p><strong>script:</strong> </p>
<p>prepare_dpf4.py -l ligand.pdbqt -r protein.pdbqt [options]</p>
<hr>
<p>**
**</p>
<p><strong>6) Prepare .dpf file and run autodock for re-scoring</strong></p>
<p>**
**</p>
<p>Remove seach parameters and append the "epdb" keyword, so that an
examplary .dpf would look like this:</p>
<p>autodock_parameter_version 4.2 # used by autodock to validate
parameter set </p>
<p>outlev 1 # diagnostic output level </p>
<p>intelec # calculate internal
electrostatics </p>
<p>ligand_types C HD N NA OA # atoms types in ligand </p>
<p>fld rec.maps.fld # grid_data_file </p>
<p>map rec.C.map # atom-specific affinity map </p>
<p>map rec.HD.map # atom-specific affinity map </p>
<p>map rec.N.map # atom-specific affinity map </p>
<p>map rec.NA.map # atom-specific affinity map </p>
<p>map rec.OA.map # atom-specific affinity map </p>
<p>elecmap rec.e.map # electrostatics map </p>
<p>desolvmap rec.d.map # desolvation map </p>
<p>move lig.pdbqt # small molecule </p>
<p>about 17.6 22.2 32.6 # small molecule center </p>
<p>epdb # small molecule to be
evaluated </p>
<p>**
**</p>
<p><strong>inputs</strong></p>
<ul>
<li>ligand_receptor.dpf</li>
</ul>
<p><strong>command:</strong> </p>
<p>autodock -p ligand_protein.dpf</p>
<h1>Edit</h1>
<p>I managed to use AutoDock Vina for re-scoring now, however, the output is not as detailed as the one that would be produced by AutoDock 4.2.</p>
<p>For example, what I get is:</p>
<p>Affinity: -2.06943 (kcal/mol)
Intermolecular contributions to the terms, before weighting:<br>
gauss 1 : 51.97697<br>
gauss 2 : 1133.84012<br>
repulsion : 7.41516<br>
hydrophobic : 34.56441<br>
Hydrogen : 0.00000 </p>
<p>(what is also weird is that the <code>prepare_ligand4.py</code> script to generate the .pdbqt file from the mol2 file removed the hydrogens)</p>
<p>In AutoDock4.2, the output would be, for example,</p>
<p>epdb: USER Estimated Free Energy of Binding = -6.54 kcal/mol [=(1)+(2)+(3)-(4)]<br>
epdb: USER Estimated Inhibition Constant, Ki = 15.95 uM (micromolar) [Temperature = 298.15 K]<br>
epdb: USER<br>
epdb: USER (1) Final Intermolecular Energy = -7.14 kcal/mol<br>
epdb: USER vdW + Hbond + desolv Energy = -6.33 kcal/mol
epdb: USER Electrostatic Energy = -0.81 kcal/mol<br>
epdb: USER (2) Final Total Internal Energy = -0.20 kcal/mol<br>
epdb: USER (3) Torsional Free Energy = +0.60 kcal/mol<br>
epdb: USER (4) Unbound System's Energy [=(2)] = -0.20 kcal/mol </p>
<p>Anyone knows if this might be available through VINA somehow?</p>
|
[
{
"answer_id": 20001,
"pm_score": 3,
"text": "<p>Okay, I finally figured it out. Basically there are those following 6 steps:</p>\n\n<ol>\n<li>Preparing a protein</li>\n<li>Preparing a ligand</li>\n<li>Generating a grid parameter file</li>\n<li>Generating maps and grid data files</li>\n<li>Generating a docking parameter file</li>\n<li>Running AutoDock</li>\n</ol>\n\n<p>Since the details are a little bit too lengthy for this post, I have written it up as a tutorial. A lot of people (like me) seemed to struggle to get it to work, so I thought this write-up could be a useful reference: <a href=\"http://sebastianraschka.com/Articles/2014_autodock_energycomps.html\" rel=\"nofollow\">AutoDock4.2 re-scoring tutorial</a></p>\n"
}
] |
[
{
"answer_id": 19751,
"pm_score": 2,
"text": "<p>You can use Autodock Vina. It provides an option to calculate local score only.</p>\n\n<blockquote>\n <p>displaying the individual contributions to the intermolecular score, before weighting (these are shown with \"--score_only\")</p>\n</blockquote>\n\n<p>Autodock is better tool in speed and accuracy than Autodock itself.</p>\n\n<p>For using it, you need :</p>\n\n<p>1) Protein.pdbqt</p>\n\n<p>2) Ligand.pdbqt</p>\n\n<p>3) Config.txt (the confguration file):</p>\n\n<blockquote>\n <p>receptor = hsg1/rigid.pdbqt </p>\n \n <p>ligand = ligand.pdbqt</p>\n \n <p>center_x = 2 # Center of Grid points X</p>\n \n <p>center_y = 6 # Center of Grid points Y </p>\n \n <p>center_z = -7 # Center of Grid points Z</p>\n \n <p>size_x = 25 # Number of Grid points in X direction</p>\n \n <p>size_y = 25 # Number of Grid points in Y Direction</p>\n \n <p>size_z = 25 # Number of Grid points in Z Direction</p>\n</blockquote>\n\n<p>Run your code as :</p>\n\n<pre><code>vina --score_only --config config.txt --log your_filename.log\n</code></pre>\n\n<p>for mmore information type:</p>\n\n<pre><code>vina --help_advanced\n</code></pre>\n\n<p>source: <a href=\"http://vina.scripps.edu/manual.html#faq\" rel=\"nofollow\">http://vina.scripps.edu/manual.html#faq</a></p>\n\n<h2>UPDATE:</h2>\n\n<p>Use:</p>\n\n<pre><code>prepare_ligand4.py -A 'hydrogens'\n</code></pre>\n\n<p>for Adding hydrogen</p>\n\n<p>For understanding the scoring of Vina:</p>\n\n<p><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3041641\" rel=\"nofollow\"><strong>AutoDock Vina: improving the speed and accuracy of docking with a new scoring function, efficient optimization and multithreading</strong></a></p>\n"
}
] |
19,809
|
<p>Cooperativity in gene expression is an important feature of many regulatory networks. Described using the <a href="http://en.wikipedia.org/wiki/Hill_equation_(biochemistry)" rel="nofollow">Hill function</a>, the most common example is a transcription factor (TF) that when bound to its target regulatory site, increases the rate of binding of other transcription factors (usually through TF-TF dimerization). </p>
<p>There are numerous example of TF dimerization-based cooperativity in the literature. However, I am trying to find examples of positive transcriptional cooperativity that involve mechanisms <em>other than</em> TF dimerization. In the dimer model, an unbound TF binds to its cognate promoter (containing multiple enhancers) with a certain affinity. With the first TF bound, another identical TF now has increased affinity for its target - binding to the enhancer and binding (dimerization) to the first TF. The expression profile is sigmoidal (near binary) and represents sharp on/off switching in activity. </p>
<p>Although peer-reviewed articles experimentally or theoretically characterizing alternative mechanisms are preferred, I'm also interested in user hypotheses and discussions that are more speculative. Specifically, I'm interested in positive cooperativity that occurs without feedback from the regulated genes.</p>
<p>One potential mechanism could involve a DNA-binding TF consisting of a transcriptional activator domain and a chromatin remodeling or DNA methylation domain. When the TF binds it not only activates transcription but remodels local chromatin. If the remodeling increases affinity for the next TF, they act cooperatively (and positively). Perhaps something similar to this has already been described. </p>
|
[
{
"answer_id": 19825,
"pm_score": 3,
"text": "<p>Positive co-operativity without feedback from the downstream genes:</p>\n\n<p>I guess Polycomb/Trithorax complexes will fit this criterion nicely.</p>\n\n<p>Polycomb group (PcG) represses Hox and other differentiation related genes (such as neurogenin) while Trithorax (TrxG) group promotes their expression. They are not like usual transcription factors that bind to promoters and recruit/exclude RNA-polymerase; they bind at regions called Polycomb Response Elements/Trithorax Response Elements and mediate epigenetic regulation of nearby genes by histone modifications (primarily methylation). </p>\n\n<p>PcG froms two main complexes PRC1 (Polycomb Repressive Complex-1) and PRC2. Different components of the complex have different molecular functions. For e.g SuZ has a Zinc finger domain and can bind to DNA/RNA, Ezh has histone methyltransferase activity etc.</p>\n\n<p><a href=\"http://www.annualreviews.org/doi/full/10.1146/annurev.genet.38.072902.091907\" rel=\"nofollow\">This</a> is an old review but is still quite informative. </p>\n"
}
] |
[
{
"answer_id": 19815,
"pm_score": 2,
"text": "<p>Interesting question. I think I have two examples for you which might be interesting.\nThe first is the co-regulation of the microphthalmia-associated transcription factor (MITF) in pigmentation by SOX10 and PGC1a/b. See this paper:</p>\n\n<ul>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/23201126\" rel=\"nofollow\">PGC-1 coactivators regulate MITF and the tanning response.</a></li>\n</ul>\n\n<p>The second is about the regulation of brown fat tissue by PGC1a and IRF4 which seem to interact in these cells. See this paper:</p>\n\n<ul>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/24995979\" rel=\"nofollow\">IRF4 Is a Key Thermogenic Transcriptional Partner of PGC-1α.</a></li>\n</ul>\n\n<p>In both cases a transcription factor (SOX10 or IRF4) interacts with the co-activator PGC1 proteins to regulate gene expression. If the co-activator is missing, the expression is at least downregulated. These activations are not so atypical or rare but are occurring quite often. If you have problems in getting these articles, let me know.</p>\n"
}
] |
19,811
|
<p>I have an ant queen in a jar. This is what she looks like:</p>
<p><img src="https://i.stack.imgur.com/jTC29.jpg" alt="black ant queen captured in jar"></p>
<p>Because I'm planning to start an artificial ant nest, I'd like to learn something about that specific species of ant. This particular queen is very common in the Czech Republic, central Europe. It's also very common in cities.</p>
<ol>
<li>Could you tell what kind of queen is that?</li>
<li>Is there any image reference that would help me find out? Ideally with some location search possibility.</li>
</ol>
|
[
{
"answer_id": 71876,
"pm_score": 2,
"text": "<p>This cannot be a Lasius queen, it is a Formica queen. Although one of the main characteristic is the shape of the first segment of the funicula which cannot be seen on this picture, the general aspect of this queen (elongated, with red legs, does not have a bulky aspect) indicates this queen is from the genus Formica. It is similar in shape and coloration to many queens in the subgenus Serviformica, for example Formica cunicularia, Formica cinerea.</p>\n"
}
] |
[
{
"answer_id": 19826,
"pm_score": 2,
"text": "<p>As @skymnige said it is definitely <strong>Black garden ant (<em>Lasius niger</em>)</strong></p>\n\n<p><img src=\"https://upload.wikimedia.org/wikipedia/commons/4/4c/Lasius_Niger_wingless_queen.jpg\" alt=\"\"></p>\n"
}
] |
19,827
|
<p>Can epistaxis or nosebleeds be a cause of death?</p>
<p><img src="https://i.stack.imgur.com/o3wRX.png" alt=""></p>
|
[
{
"answer_id": 19831,
"pm_score": 5,
"text": "<p>Yes, it can, but it is extremely rare.</p>\n\n<blockquote>\n <p>... nosebleeds are rarely fatal, accounting for only 4 of the 2.4 million deaths in the U.S. in 1999 [1].</p>\n</blockquote>\n\n<p>The main issue is that epistaxis can be a sign of potentially fatal diseases:</p>\n\n<blockquote>\n <p>The instances in which nosebleed is potentially fatal are those in which there is a history of recent head injury, severe arteriosclerotic cardiovascular disease or an underlying vascular tumor in the nasal chambers. Fatal nasal bleeding has not been reported in children [2].</p>\n</blockquote>\n\n<p>Here are some causes which can lead to fatal complications if left untreated [3]:</p>\n\n<blockquote>\n <ul>\n <li>Leukaemia</li>\n <li>Hypertension</li>\n <li>Coagulation disorders</li>\n <li>Hepatitis</li>\n <li>Head injury</li>\n <li>Myelodysplastic syndromes - Epistaxis</li>\n </ul>\n</blockquote>\n\n<p>Death by massive hemorrhage can occur when epistaxis is the result of a ruptured aneurysm [4, 5, 6]:</p>\n\n<blockquote>\n <p>An instance of fatal epistaxis is reported in a patient with an unsuspected aneurysm of the infraclinoid portion of the internal carotid artery. There was no known history of trauma. The aneurysm was subsequently detected on an old X-ray film. Epistaxis from an aneurysm at this site is nearly always preceded by significant head trauma and is associated with cranial nerve palsies, a syndrome with a high mortality. Epistaxis from rupture of a non-traumatic aneurysm is very rare [4].</p>\n</blockquote>\n\n<hr>\n\n<p>References:</p>\n\n<ol>\n<li>Work Table I. Deaths from each cause by 5-year age groups, race and sex: US, 1999 Page 1922. U.S. Centers for Disease Control Published 2001-05-11. Via Wikipedia contributors, \"Nosebleed,\" Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Nosebleed&oldid=617613780\">http://en.wikipedia.org/w/index.php?title=Nosebleed&oldid=617613780</a> (accessed July 21, 2014).</li>\n<li>QUINN FB. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/13738727\">Fatal epistaxis.</a> Calif Med. 1961 Feb;94:88-92. PubMed PMID: 13738727. </li>\n<li>Right Diagnosis (tm). Epistaxis Deaths. Available from <a href=\"http://www.rightdiagnosis.com/symptoms/epistaxis/deaths.htm\">http://www.rightdiagnosis.com/symptoms/epistaxis/deaths.htm</a> (accessed 21.07.2014)</li>\n<li>HORNIBROOK, J. and RHODE, J. C. (1981), <a href=\"http://onlinelibrary.wiley.com/doi/10.1111/j.1445-2197.1981.tb05942.x/abstract\">FATAL EPISTAXIS FROM AN ANEURYSM OF THE INTRACRANIAL INTERNAL CAROTID ARTERY.</a> Aust. N.Z. J. Surg., 51: 206–208. doi: 10.1111/j.1445-2197.1981.tb05942.x</li>\n<li>P. N. Pathak (1972). <a href=\"http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=1141168\">Epistaxis - due to ruptured aneurysm of the internal carotid artery.</a> The Journal of Laryngology & Otology, 86, pp 395-397. doi:10.1017/S0022215100075423. </li>\n<li>Urso-Baiarda F, Saravanappa N, Courteney-Harris R. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/14988378\">An unusual cause of massive fatal epistaxis.</a> Emerg Med J. 2004 Mar;21(2):266. PubMed PMID: 14988378. </li>\n</ol>\n"
}
] |
[
{
"answer_id": 19830,
"pm_score": 3,
"text": "<p>Any injury, that results in external bleeding can lead to death, since it is a breach in the body's defenses and an entry point for pathogens.</p>\n\n<p>Explanation:</p>\n\n<p>When you have nose bleeding the blood must be coming from somewhere. Usually from inside your body. </p>\n\n<p>That means there is a hole in your body which is big enough for blood to stream out.</p>\n\n<p>That in return also means that through the same hole things can get back inside your body.</p>\n\n<p>For example any kind of virus or bacteria. </p>\n\n<p>That does not mean every bleeding is potentially lethal. But depending on the environment the body is in the chance of infection is certainly greater with a lesion (hole in the circulatory system) than without it.</p>\n"
}
] |
19,836
|
<p>I am trying to convert a MOL2 file (includes partial charges and hydrogen atoms) into a PDBQT file for re-scoring in AutoDock Vina. However, both approaches that I tried don't keep the hydrogen atoms from the MOL2 file (the PDBQT file doesn't contain hydrogen atoms).</p>
<p>The command I used for OpenBabel is </p>
<pre><code>babel -i mol2 my.mol2 -o my.pdbqt
</code></pre>
<p>When I look at the documentation, they babel has a dedicated "-d" flag for removing hydrogens. So I assume that this shouldn't happen by default?</p>
<p>The same thing happens if I use MGLTools</p>
<pre><code>prepare_ligand4.py -l my.mol2
</code></pre>
<p>Any ideas of what might be going on here?</p>
<p>Thanks for your help!</p>
<p>will append the MOL2 file if someone wants to try it:</p>
<pre><code>@<TRIPOS>MOLECULE
mymol2
25 25 0 0 0
SMALL
USER_CHARGES
@<TRIPOS>ATOM
1 C1 -1.0341 29.2934 -14.5590 C.ar 1 <0> -0.1745
2 C2 -0.1917 29.9513 -13.6630 C.ar 1 <0> -0.1483
3 C3 -2.3919 29.1585 -14.2689 C.ar 1 <0> -0.1608
4 C4 -0.7068 30.4744 -12.4770 C.ar 1 <0> -0.0956
5 C5 -2.9070 29.6816 -13.0828 C.ar 1 <0> -0.1543
6 C6 -2.0573 30.3323 -12.2033 C.ar 1 <0> -0.0209
7 C7 -5.0136 30.3602 -8.9792 C.2 1 <0> 0.9092
8 C8 -1.1556 29.8264 -9.1470 C.2 1 <0> 0.9071
9 C9 -2.6151 30.8987 -10.9189 C.3 1 <0> -0.0262
10 C10 -3.5221 30.2951 -8.6255 C.3 1 <0> -0.1568
11 C11 -2.5717 29.8912 -9.7583 C.3 1 <0> -0.1554
12 O1 -5.7013 31.2223 -8.3667 O.co2 1 <0> -0.8817
13 O2 -0.7003 30.9084 -8.6799 O.co2 1 <0> -0.8929
14 O3 -5.3714 29.5329 -9.8669 O.co2 1 <0> -0.8807
15 O4 -0.6188 28.6818 -9.1887 O.co2 1 <0> -0.8571
16 H1 -0.6331 28.8861 -15.4824 H 1 <0> 0.0899
17 H2 0.8655 30.0564 -13.8891 H 1 <0> 0.1079
18 H3 -3.0478 28.6460 -14.9665 H 1 <0> 0.0917
19 H4 -0.0427 30.9855 -11.7849 H 1 <0> 0.2049
20 H5 -3.9661 29.5717 -12.8653 H 1 <0> 0.1145
21 H6 -2.0757 31.8190 -10.6595 H 1 <0> 0.0142
22 H7 -3.6485 31.2140 -11.1119 H 1 <0> 0.0547
23 H8 -3.4370 29.5769 -7.7988 H 1 <0> -0.0109
24 H9 -3.2268 31.2722 -8.2199 H 1 <0> 0.0482
25 H10 -2.8394 28.8903 -10.1212 H 1 <0> 0.0739
@<TRIPOS>BOND
1 1 2 ar
2 1 3 ar
3 2 4 ar
4 3 5 ar
5 4 6 ar
6 5 6 ar
7 6 9 1
8 7 10 1
9 7 12 1
10 7 14 2
11 8 11 1
12 8 13 1
13 8 15 2
14 9 11 1
15 10 11 1
16 1 16 1
17 2 17 1
18 3 18 1
19 4 19 1
20 5 20 1
21 9 21 1
22 9 22 1
23 10 23 1
24 10 24 1
25 11 25 1
@<TRIPOS>SUBSTRUCTURE
</code></pre>
<h1>EDIT:</h1>
<p>The solution to the problem with <code>prepare_ligand4.py</code> would be</p>
<pre><code>prepare_ligand4.py -l my.mol2 -U \""" -C
</code></pre>
<p>to keep the partial charges and hydrogen atoms (oddly, <code>-U ""</code> didn't work for me: <code>prepare_ligand4.py: option -U requires argument</code>)</p>
|
[
{
"answer_id": 19837,
"pm_score": 3,
"text": "<p>You saw my last <a href=\"https://biology.stackexchange.com/questions/19749/how-to-use-autodock-just-for-rescoring\">answer of your question</a>? you can do that easily, just use </p>\n\n<pre><code>prepare_ligand4.py -l my.mol2 -A \"hydrogens\"\n</code></pre>\n"
}
] |
[
{
"answer_id": 34897,
"pm_score": 0,
"text": "<p>In babel: </p>\n\n<pre><code>babel my.mol2 my.pdbqt -xh\n</code></pre>\n\n<p>-x states options for writing .pdbqt files\n-h says keep hydrogens</p>\n"
}
] |
19,891
|
<p>There are approximately 20k protein-coding genes found in the human genome. This number is presumably very small when considering all the genomes found in the diverse microbes associated with the human body. </p>
<p>Is there an estimate for the total number of protein-coding genes found in human microbiome? </p>
|
[
{
"answer_id": 19897,
"pm_score": 4,
"text": "<p>The Human Microbiome Project collected samples as shown in the image below from healthy volunteers:</p>\n\n<p><img src=\"https://i.stack.imgur.com/FMnKs.jpg\" alt=\"enter image description here\"></p>\n\n<p>They give an estimate of about 8 Million genes in the human microbiome, which is about 360x the number of genes in the human genome. See <a href=\"http://www.nih.gov/news/health/jun2012/nhgri-13.htm\" rel=\"nofollow noreferrer\">here</a> for their press release with a lot of information. Additionally these two articles are as well interesting, if you want to dive deeper into the stuff:</p>\n\n<ul>\n<li><a href=\"http://www.nature.com/nature/journal/v486/n7402/full/nature11209.html\" rel=\"nofollow noreferrer\">A framework for human microbiome research</a></li>\n<li><a href=\"http://www.nature.com/nature/journal/v486/n7402/full/nature11234.html\" rel=\"nofollow noreferrer\">Structure, function and diversity of the healthy human microbiome</a></li>\n</ul>\n"
}
] |
[
{
"answer_id": 19894,
"pm_score": 2,
"text": "<h2>Human Microbiome Project</h2>\n\n<p>According to Published data on HMP website:</p>\n\n<ul>\n<li>The human microbiome consists of all the microorganisms that reside in or on the human body. </li>\n<li>They may cause illness but some are necessary for good health.</li>\n<li>There total count is 10 times more than Human cells.</li>\n<li>~800 genomes had been sequenced.</li>\n<li>~5000 Human sample had been used.</li>\n<li>Include 14 disease project samples.</li>\n<li>Total data stored on the DACC resource is 14 terabytes.</li>\n<li>Total protein(~8 million) coding genes found to be 360x of number of human genes</li>\n</ul>\n\n<p>Source:</p>\n\n<p>[1] <a href=\"http://en.wikipedia.org/wiki/Human_Microbiome_Project\" rel=\"nofollow\">http://en.wikipedia.org/wiki/Human_Microbiome_Project</a></p>\n\n<p>[2] <a href=\"http://commonfund.nih.gov/hmp/index\" rel=\"nofollow\">http://commonfund.nih.gov/hmp/index</a></p>\n"
}
] |
19,942
|
<p>The metabolic rate measures how much energy an organism <strong>expends</strong> over a unit of time. Its breakdown for the human body in terms of its functions is well documented : so much for the heart, for the brain, etc.</p>
<p>In West et al, 2002 I have found an estimate for the metabolic rate of a single cell. But how does this breakdown in terms of elementary functions in the cell?</p>
<p>E.g., how much of the energy made available from nutrients is used in the process of replicating genome, of expressing proteins, of trafficking...?</p>
<p>Following Jeremy Kemball's link suggestions, I find in <a href="http://www.ncbi.nlm.nih.gov/pubmed/7492307%2C7708012?dopt=Abstract" rel="nofollow">this paper</a> the fraction of ATP consumption for the following processes:</p>
<pre><code>Protein synthesis 0.34
Na+/K+ ATPase 0.16
Ca2+ ATPase 0.17
RNA/DNA synthesis 0.25
Unidentified 0.09
</code></pre>
<p>(which adds up to 1.01 rather than 1 for spurious reasons). Their measurement is indirect, based on $O_2$ consumption for an assumed steady-state regeneration of ATP. I wonder how GTP-based processes are accounted for? Or are they negligible compared to ATP ones?</p>
<p>This is for a specific cell type, rat thymocyte, is there a reason to expect that this will be hugely different for say a fibroblast? Also, they stimulate their thymocyte with concanavalin A. I understood they are not getting RNA/DNA consumption signal without Con-A, but didn't get why it would be so.</p>
<p>Finally, what would be in the remaining 9% ? One candidate for ATP consumption suggested by Jeremy Kemball is actin turnover, I guess it fits only in the "unidentified" line. Tubulin turnover is a GTP process, not sure about intermediate filaments (do they turnover?). All ATP-molecular motors (myosin, kinesin, dynein at least?) have to be there too. What else?</p>
<p>I am particularly interested in the total amount of ATP energy that goes to myosin.</p>
|
[
{
"answer_id": 20031,
"pm_score": 4,
"text": "<p>I was musing on this and did some strange googling, and have some ballpark figures for a bunch of different organisms. It's far from a complete answer but it's at least a start, and all this won't fit in a comment.</p>\n\n<p>DNA replication, I assumed, was a huge metabolic drain on the cell. Turns out that is far from the case. Many helicases are passive, requiring no ATP, and the amount of ATP-equivalent triphosphates to synthesize the entire genome is pretty small compared to the amount that gets used and recycled every day.</p>\n\n<p>According to <a href=\"http://bionumbers.hms.harvard.edu/search.aspx?task=searchbytrmorg&log=y&unt=y&trm=Body%20weight%20ATP/day&org=%25\">these guys</a> humans go through their bodyweight in ATP every day, about 50% of which is actin turnover, and <a href=\"http://bionumbers.hms.harvard.edu/bionumber.aspx?&id=110441&ver=7&trm=ATP/day\">30% is synthesis</a> (60% or more in rapid bacteria). Proteins cost about <a href=\"http://kirschner.med.harvard.edu/files/bionumbers/Estimated%20specific%20costs%20of%20component%20processes%20of%20protein%20turnover.pdf\">4-5 ATP</a> per AA to break down and rebuild.</p>\n\n<p>You're not going to get a really good general breakdown, I don't think, but in crop plants or E. coli there are <a href=\"http://bionumbers.hms.harvard.edu/search.aspx?log=y&task=searchbytrmorg&trm=ATP\">number</a>s for this, sort of. A lot of them are based on indirect measurements of protein uptake/turnover and ATP cost per AA or BP. They're fascinating but insane and often contradictory.</p>\n"
}
] |
[
{
"answer_id": 20149,
"pm_score": 1,
"text": "<p>A significant amount of heat generated by the cell does not come from the hydrolysis of an NTP. ATP is generated by a H+ gradient in the mitochondria, and this gradient is created by mechanisms which rely only in part by ATP. Most of the energy stores in our bodies are not in the NTP pool. This is why CO₂ and urine are used to measure energy expenditure during physical exercise. On the scale of individual cells, it is a challenge to conceive a protocol which would account for all confounding variables. However, on the scale of a human, confounding variables in energy use are easily controlled. If you are interested in the energy expenditure of a single biological process, this would seem a better project rather than quantifying all processes simultaneously. </p>\n"
}
] |
19,967
|
<p>Besides religious prohibition, there are several non-religious arguments against eating pork. A few of which are: </p>
<ol>
<li>Pigs and swine are so poisonous that you can hardly kill them with strychnine or other poisons. </li>
<li>Swine and pigs have over a dozen parasites within them, eg tapeworms, flukes, worms, and trichinae. There is no safe temperature at which pork can be cooked to ensure that they will be killed</li>
<li>The swine carries about 30 diseases which can be easily passed to humans</li>
</ol>
<p>I would like to hear some scholarly verification regarding these points. Simple Yes-No-Yes will be enough, elaboration is welcome, though.</p>
<p>Thank You</p>
|
[
{
"answer_id": 19968,
"pm_score": 6,
"text": "<blockquote>\n<p>Pigs and swine are so poisonous that you can hardly kill them with strychnine or other poisons.</p>\n</blockquote>\n<p>This is a <em>non-sequitur</em>. An animal being poisonous does not imply that it resists to poison, nor the reverse is true.</p>\n<p>In any case, to the extent of my knowledge pigs do not produce any specific poison. Obviously, if you could provide a more specific claim, this could be tested a bit more in depth.</p>\n<p>The second part, instead, is plain false. You can definitely kill a pig with strychnine.</p>\n<p>Both the <a href=\"http://www.merckmanuals.com/vet/toxicology/strychnine_poisoning/overview_of_strychnine_poisoning.html\" rel=\"noreferrer\">Merk veterinary manual</a> and <a href=\"http://books.google.co.uk/books?id=IPOsWhQgNPkC&pg=PA977\" rel=\"noreferrer\"><em>Diseases of swine, 9th edition</em></a> report an oral lethal dose of 0.5-1 mg/kg.</p>\n<p>For comparison, <a href=\"http://www.cdc.gov/niosh/idlh/57249.html\" rel=\"noreferrer\">the CDC</a> reports a probable lethal oral dose of 1.5-2 mg/kg for humans.</p>\n<blockquote>\n<p>Swine and pigs have over a dozen parasites within them, eg tapeworms, flukes, worms, and trichinae.</p>\n</blockquote>\n<p>Sure, pigs do have parasites. <a href=\"http://books.google.co.uk/books?id=IPOsWhQgNPkC&pg=PA904\" rel=\"noreferrer\">Chapter 55</a> of <em>Diseases of swine</em> is specifically on parasitic infections.</p>\n<p>Now, do ALL pigs have them? The answer is no, some parasites are more common than other, and the amount of parasites depends on the health status of the farm.</p>\n<p>For instance:</p>\n<p><strong>Northern Europe</strong> (<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/9650867\" rel=\"noreferrer\">Roepstorff et al. 1998</a>)</p>\n<blockquote>\n<p>In Denmark (DK), Finland (FIN), Iceland (I), Norway (N), and Sweden (S), 516 swine herds were randomly selected in 1986-1988. Individual faecal analyses (mean: 27.9 per herd) from eight age categories of swine showed that Ascaris suum, Oesophagostomum spp., Isospora suis, and Eimeria spp. were common, while Trichuris suis and Strongyloides ransomi-like eggs occurred sporadically. Large fatteners and gilts were most frequently infected with A. suum with maximum prevalences of 25-35% in DK, N and S, 13% in I and 5% in FIN. With the exception of the remarkably low A. suum prevalence rates in FIN, no clear national differences were observed. Oesophagostomum spp. were most prevalent in adult pigs in the southern regions (21-43% in DK and southern S), less common in the northern regions (4-17% adult pigs infected), and not recorded in I. I. suis was common in piglets in DK, I, and S (20-32%), while < 1% and 5% were infected in N and FIN, respectively. Eimeria spp. had the highest prevalences in adult pigs (max. 9%) without clear geographical differences. I. suis and Eimeria spp. were recorded for the first time in I, and I. suis for the first time in N.</p>\n</blockquote>\n<p><strong>USA</strong> (<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/10223350\" rel=\"noreferrer\">Gamble et al. 1999</a>)</p>\n<blockquote>\n<p>To determine Trichinella infection in a selected group of farm raised pigs, 4078 pigs from 156 farms in New England and New Jersey, employing various management styles, were selected based on feed type (grain, regulated waste, non-regulated waste).<br />\n[...]<br />\nA total of 15 seropositive pigs on 10 farms were identified, representing a prevalence rate of 0.37% and a herd prevalence rate of 6.4%. A total of nine seropositive pigs and one suspect pig from six farms were tested by digestion; four pigs (representing three farms) harbored Trichinella larvae at densities of 0.003-0.021 larvae per gram (LPG) of tissue; no larvae were found in six pigs.</p>\n</blockquote>\n<p><strong>China</strong> (<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/15710534\" rel=\"noreferrer\">Weng et al. 2005</a>):</p>\n<blockquote>\n<p>The prevalence of intestinal parasites was investigated in intensive pig farms in Guangdong Province, China between July 2000 and July 2002. Faecal samples from 3636 pigs (both sexes and five age groups) from 38 representative intensive pig farms employing different parasite control strategies were examined for the presence of helminth ova and protozoan oocysts, cysts and/or trophozoites using standard techniques. Of the 3636 pigs sampled, 209 (5.7%) were infected with Trichuris suis, 189 (5.2%) with Ascaris, 91 (2.5%) with Oesophagostomum spp., 905 (24.9%) with coccidia (Eimeria spp. and/or Isospora suis) and 1716 (47.2%) with Balantidium coli. <strong>These infected pigs were mainly from farms without a strategic anti-parasite treatment regime</strong>.</p>\n</blockquote>\n<p>However, note that <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/10831052\" rel=\"noreferrer\">Boes et al. 2000</a> reports higher percentages.</p>\n<blockquote>\n<p>The prevalence of helminths in pigs was investigated in five rural communities situated on the embankment of Dongting Lake in Zhiyang County, Hunan Province, People's Republic of China, in an area known to be endemic for Schistosoma japonicum. The helminth prevalences identified on the basis of faecal egg count analysis were: Oesophagostomum spp. (86.7%), Ascaris suum (36.7%), Metastrongylus spp. (25.8%), Strongyloides spp. (25.8%), Trichuris suis (15.8%), Globocephalus spp. (6.7%), Gnathostoma spp. (4.2%), Schistosoma japonicum (5.0%) and Fasciola spp. (1.3%).</p>\n</blockquote>\n<p><strong>Kenya</strong> (<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/18509940\" rel=\"noreferrer\">Nganga et al. 2008</a>):</p>\n<blockquote>\n<p>A total of 115 gastrointestinal tracts (GIT) from 61 growers and 54 adult pigs were examined between February 2005 and January 2006. Seventy eight (67.8%) had one or more helminth parasites, of which thirty six (31.3%) were mixed infection. Ten types of helminth parasites encountered in descending order of prevalence were, Oesophagostomum dentatum (39.1%), Trichuris suis (32.2%), Ascaris suum (28.7%), Oesophagostomum quadrispinulatum (14.8%), Trichostrongylus colubriformis (10.4%), Trichostrongylus axei (4.3%), Strongyloides ransomi (4.3%), Hyostrongylus rubidus (1.7%), Ascarops strongylina (1.7%) and Physocephalus sexalutus (0.9%).</p>\n</blockquote>\n<hr />\n<blockquote>\n<p>There is no safe temperature at which pork can be cooked to ensure that they will be killed</p>\n</blockquote>\n<p>False. Proper cooking, as well as freezing (but see below) are effective in killing worms.</p>\n<p><a href=\"http://www.cdc.gov/parasites/trichinellosis/gen_info/faqs.html\" rel=\"noreferrer\">The CDC</a> suggest:</p>\n<blockquote>\n<p>The best way to prevent trichinellosis is to cook meat to safe temperatures. A food thermometer should be used to measure the internal temperature of cooked meat. Do not sample meat until it is cooked. USDA recommends the following for meat preparation.</p>\n<p><strong>For Whole Cuts of Meat (excluding poultry and wild game)</strong><br />\nCook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest part of the meat, then allow the meat to rest for three minutes before carving or consuming.<br />\n<strong>For Ground Meat (excluding poultry and wild game)</strong><br />\nCook to at least 160° F (71° C); ground meats do not require a rest time.</p>\n</blockquote>\n<p>Also</p>\n<blockquote>\n<p>Curing (salting), drying, smoking, or microwaving meat alone does not consistently kill infective worms; homemade jerky and sausage were the cause of many cases of trichinellosis reported to CDC in recent years.<br />\nFreeze pork less than 6 inches thick for 20 days at 5°F (-15°C) to kill any worms.<br />\nFreezing wild game meats, unlike freezing pork products, may not effectively kill all worms because some worm species that infect wild game animals are freeze-resistant.<br />\nClean meat grinders thoroughly after each use.</p>\n</blockquote>\n<hr />\n<blockquote>\n<p>The swine carries about 30 diseases which can be easily passed to humans</p>\n</blockquote>\n<p>Again, sure pigs can carry diseases that can be passed to humans, but proper storing and cooking of meat is effective in getting rid of the great majority of bacteria.</p>\n<p>Finally in 2012 <a href=\"http://www.hpa.org.uk/NewsCentre/NationalPressReleases/2012PressReleases/120613HPAissuesfoodsafetyreminder/\" rel=\"noreferrer\">Public health England</a> reported food poisoning caused by red meat as accounting for 17% of all food poisoning incidents, with pork accounting for 3%. By comparison, poultry accounted for 29% of food poisoning events (although people eat more poultry than red meat).</p>\n<p>Similarly, the <a href=\"http://www.cdc.gov/foodborneburden/attribution-1998-2008.html\" rel=\"noreferrer\">CDC report on the Attribution of Foodborn Illness</a> (1998-2008) puts red meat accounting for 12%, pork as accounting for 5.4% and poultry 9.8%.</p>\n"
}
] |
[
{
"answer_id": 19969,
"pm_score": 3,
"text": "<p>First: There is no biological reason to not eat pork. These bans (Jewish and Islamic) are based on religious rules, so this is more a cultural, not so much a biological answer.</p>\n\n<p>The reasoning that pork meat would deteriorate pretty fast in warm climates is true, but it is also true for all other sorts of meat (like cattle, goat or sheep). Besides cultural reasons (think of India, where cows are holy) there is another reason according to the antrologist Marvin Harris. </p>\n\n<p>In his book \"The Sacred Crow and the Abominable Pigs\" (you can find a chapter on pigs <a href=\"http://etnologija.etnoinfolab.org/dokumenti/82/2/2009/harris_1521.pdf\" rel=\"nofollow\">here</a> and another interesting article on that topic <a href=\"http://aurora.icaap.org/index.php/aurora/article/view/53/66\" rel=\"nofollow\">here</a>) he says that feeding habits are important, too. While goats, cows and sheep can be fed a grass only diet, this is not possible for pigs. They need a grain-based diet (where they compete with the humans for the food) or at least rich woods to survive. As these were depleted by the humans in the middle east, pigs couldn't be held sustainable.</p>\n"
}
] |
19,972
|
<p>As a child I watched tiny fiddler crabs living in conical shells, and many years later I find that people study fossil turritellids. So now I wonder: how old are shells, typically, that you see on beaches? Do they wear out after a year of sand abrasion? 100 years, a million? Is it known? </p>
|
[
{
"answer_id": 39960,
"pm_score": 4,
"text": "<p>Mollusk shells found on typical east coast (US) beaches can range from days old (the animal that made the shell died recently) to thousands of years old. Some shells in our state, North Carolina, have been dated as 40,000 years old. A high number of \"seashells\" found on east coast beaches are from mollusks that lived in the marsh on the back side of the island. The presence of these shells on ocean beaches provides evidence of island migration - the island has moved landward over the marsh until what was once the marsh is now the ocean shore. Once buried in the sand, the shell is well preserved until erosion uncovers it. Occasionally, fossilized shells are washed up on beaches after having been dislodged from offshore limestone deposits - these shells can be millions of years old.</p>\n\n<p>-Richard -\nCarolina Ocean Studies</p>\n"
}
] |
[
{
"answer_id": 19981,
"pm_score": 2,
"text": "<p>Ages of shell as a piece can be checked or counted. </p>\n\n<p><img src=\"https://njsurfriderdrafts.files.wordpress.com/2012/03/seashells1.jpg\" alt=\"\"></p>\n\n<p>Procedure:</p>\n\n<p>1) Examine the shell's ridges with a magnifying glass.</p>\n\n<p>2) Tabulate the number of ridges. You can approximate by number of cell per unit length.</p>\n\n<p>3) Divide the total number of ridges by 365. Each day the little mollusk\n earns a new ridge, thus total will give you its age.</p>\n\n<p>But, that is age of one shell. If you are asking the age of all of them in a beach, my guess would be as old as the beach. </p>\n\n<p>Read more : <a href=\"http://www.ehow.com/how_6331956_tell-age-seashell.html\" rel=\"nofollow noreferrer\">http://www.ehow.com/how_6331956_tell-age-seashell.html</a></p>\n"
}
] |
19,998
|
<p>Which part of the brain is the first place (from top to bottom) where all 31 pairs of spinal nerves (on each side) meet? Or if they all start at one place - where is that?</p>
<p>Nominally, the beginning of the spinal cord is the medulla oblongata, but perhaps the spinal nerves or some sort of "root" of every nerve start at the Thalamus?</p>
|
[
{
"answer_id": 21289,
"pm_score": 4,
"text": "<p>They don’t meet. </p>\n\n<p><strong>Some framework:</strong> </p>\n\n<ul>\n<li>Spinal nerves contain motor, sensory, and autonomic fibers. Each of these have different pathways. </li>\n<li>Spinal nerves don’t go to the brain. Rather, they synapse in the spinal cord with other neurons which in turn go to the brain (sometimes requiring one more synapse).</li>\n<li>In the case of motor neurons, we talk about <em>upper</em> and <em>lower</em> motor neurons. In the sensory system, we talk about <em>first order</em> and <em>second order</em> neurons. Explanation below. </li>\n</ul>\n\n<p><strong>Regarding sensory (afferent) neurons:</strong> </p>\n\n<ul>\n<li>Touch and limb position sense are mediated by the dorsal column-medial lemniscus system. The <em>first order</em> (primary sensory) neurons from the spinal nerves, synapse on a <em>second order</em> neuron in the dorsal column in the medulla. There it decussates (i.e. courses to the contralateral side) and ascends via the medial lemniscus to the thalamus. There it synapses with a third neuron that courses via the internal capsule to the primary somatic sensory cortex.</li>\n<li>Pain, itch, and temperature sense are mediated by the anterolateral system. These <em>first order</em> (primary sensory) neurons synapse at the spinal level they enter. The <em>second order neuron</em> decussates at that level and courses rostrally via the anterolateral column, ending up in the thalamus. There it synapses with a third neuron that courses via the internal capsule to the primary somatic sensory cortex.</li>\n</ul>\n\n<p>Conclusion: It takes three neurons (inclusive) to get from the spinal nerve to the primary sensory cortex in the postcentral gyrus of the parietal lobe. </p>\n\n<p><strong>Regarding motor (efferent) neurons:</strong> </p>\n\n<ul>\n<li>Limb muscles are innervated by circuits beginning in the primary motor cortex. These <em>upper motor neurons</em> descend to the medulla, decussate here, and continue caudally via the lateral corticospinal tract. At the level of the spinal nerve, they synapse with neurons in the lateral ventral horn. These are the <em>lower motor neurons</em> that become the spinal nerve.</li>\n<li>Axial/girdle muscles are innervated by circuits that also begin in the primary motor cortex. These <em>upper motor neurons</em> synapse in the midbrain, descend, and decussate at the appropriate spinal level. They synapse there with the <em>lower motor neurons</em> that exit the spinal cord and end up in the muscles.</li>\n</ul>\n\n<p>Conclusion: It takes two neurons (inclusive) to get from the primary motor cortex in the pre-central gyrus of the frontal lobe to a spinal nerve. </p>\n\n<p>In the cortex, these circuits also don’t all come together. They are actually quite diffusely organized across the sensory and motor cortices. Here is a representation of the sensory cortex.* It is a schematic of the post-central gyrus with pictures to indicate where the signals from various body parts end up. The motor cortex is similar. (<a href=\"https://www.google.com/?gfe_rd=ssl&ei=gmwWVPSbMMSc8Aazp4G4DQ#q=homunculus&spell=1)\" rel=\"nofollow noreferrer\">Google <em>homunculus</em> if interested.</a>)</p>\n\n<p><img src=\"https://i.stack.imgur.com/YMs7P.jpg\" alt=\"sensory\"></p>\n\n<p>In addition the pathways described for cognitive perception and control, there are others that help with sub-conscious control of movement (e.g. those involving the cerebellum and basal ganglia), sub-cortical perception of pain signals (e.g. amygdala), and even spinal reflex arcs that never reach the brain. Not all circuits that begin or end in the spinal nerves are destined for or originate from the cortex</p>\n\n<p>This is already considerably over-simplified, and the <a href=\"http://en.wikipedia.org/wiki/Autonomic_nervous_system\" rel=\"nofollow noreferrer\">autonomic system</a> is more complex yet and is not confined to spinal nerves, so I won’t detail it. These signals originate in and feed back to an entirely different area of the brain (mostly hypothalamus). Similar to the motor and sensory systems, at least one synapse is required to connect the brain to the peripheral nerve. </p>\n\n<p>Conclusion: they don’t meet. </p>\n\n<hr>\n\n<p><sup>\nReference:\n</sup>\n<sup>\n<a href=\"http://rads.stackoverflow.com/amzn/click/007138183X\" rel=\"nofollow noreferrer\">Martin, John. <em>Neuroanatomy: Text and Atlas.</em> McGraw-Hill Medical; 3 edition (March 27, 2003)</a>\n</sup><br>\n<sup>\n*The source of this image is: <a href=\"http://www.mindtrippingshow.com/mind-trip-of-the-week-17-how-do-we-feel-the-world\" rel=\"nofollow noreferrer\">http://www.mindtrippingshow.com/mind-trip-of-the-week-17-how-do-we-feel-the-world</a>\n</sup></p>\n"
}
] |
[
{
"answer_id": 20296,
"pm_score": 0,
"text": "<p>I am not sure whether I grasped the gist of your question appropriately, but let me provide some clarifications. </p>\n\n<p>$\\text{Nerve}$ is simply a collection of axons. Therefore, all the spinal nerves are just bundles of assorted nerve axons. </p>\n\n<p>Now, the origin of nerve is slightly ambiguous as far as its meaning is considered. It can mean the <strong>physical origin</strong>, the place where the particular branch of nerve starts off from a main trunk or some other nervous organ. It can also mean the location of the cell bodies the axons of which comprise the nerve, the <strong>functional origin</strong>. </p>\n\n<p>Now coming back to the question, the <em>physical</em> origin of the spinal nerves is not common. Each pair of spinal nerves originates from a specific segment of the spinal cord via two roots, the dorsal and the ventral. Therefore, each nerve originates separately and different spinal nerves cannot be traced back to a common physical origin. (The <a href=\"http://en.wikipedia.org/wiki/Cauda_equina\" rel=\"nofollow\">cauda equina</a>, is actually a collection of several spinal nerves which move dorsally and periodically gives of the nerves out of the vertebral column. Although the nerves comprising the Cauda Equina, second lumbar nerve onwards, appear to have a common origin, they actually originate from their own specific segment and then move caudally as a bundle to overcome the developmental constraint of spinal cord being shorter than the vertebral column, necessitating the caudal movement of nerves within the column to emerge at appropriate points) </p>\n\n<p>The <em>functional</em> origin is a bit more complicated. This is because each spinal nerve has a variety of nerve fibres. There are some sensory fibres with cell bodies in the dorsal root ganglion, there are motor fibres with their cell bodies in spinal cord, there are sympathetic fibres with cell bodies in the series of collateral or the <a href=\"http://en.wikipedia.org/wiki/Sympathetic_ganglion\" rel=\"nofollow\">sympathetic ganglia</a>, connected to the spinal nerve via gray and white <a href=\"http://en.wikipedia.org/wiki/Ramus_communicans\" rel=\"nofollow\">ramus communicans</a>. There can also be cell bodies located directly in medulla which passes nerve fibres in cranial nerves as well as through its branches into the sympathetic ganglia and ultimately into the spinal nerves. Sacral nerves also contain parasympathetic nerve fibres functionally originating in the CNS. Thus, considering the functional origin, though each spinal nerve has a lot of origins, there is a slight convergence of origins for different nerves. The sympathetic ganglia and the spinal cord are two places where the origins of different spinal nerves may coincide or be structurally and functionally integrated. But it must be kept in mind that this is a very limited convergence. There is an appreciable uniqueness to the functional origin of each spinal nerve and hence we cannot say that they \"meet\".<br>\n<a href=\"http://upload.wikimedia.org/wikipedia/commons/8/87/Spinal_nerve_CAT.svg\" rel=\"nofollow\">IMAGE</a></p>\n"
}
] |
20,002
|
<p>Let's say I drink some Kefir Milk, what happens to the lactic acid in the Kefir Milk that has entered my digestive system?</p>
|
[
{
"answer_id": 20012,
"pm_score": 4,
"text": "<p>First, there are two different isomers of the lactic acid, the L(+)- and the D(-)-form. Both differ in the position of the OH-group in the molecule:</p>\n\n<p><img src=\"https://i.stack.imgur.com/FdfH2.png\" alt=\"enter image description here\"></p>\n\n<p>Both turn polarized light in different ways, the D(-) to the left and the L(+) to the right. The physiological form of lactic acid for the human body is the L(+) form, which is taken up in the gut and then metabolized by the <a href=\"http://en.wikipedia.org/wiki/Lactate_dehydrogenase\" rel=\"nofollow noreferrer\">L-Lactatdehydrogenase</a> to form pyruvate and NADH.</p>\n\n<p>For the D(-)-Lactate is has been thought the the D-Lactatedehydrogenase is only present in some lower animals and bacteria and that this lactate isoform is mostly excreted. This seems not to be true and there is some D-Lactatedehydrogenase in humans (and other mammals) as well. </p>\n\n<p>See these publication for more information:</p>\n\n<ul>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/15987839\" rel=\"nofollow noreferrer\">D-lactate in human and ruminant metabolism.</a></li>\n</ul>\n"
}
] |
[
{
"answer_id": 20003,
"pm_score": 3,
"text": "<p>Lactic acid has been found to act as a fuel for the muscles. Refer to: <a href=\"http://www.nytimes.com/2006/05/16/health/nutrition/16run.html?_r=0\">http://www.nytimes.com/2006/05/16/health/nutrition/16run.html?_r=0</a></p>\n\n<blockquote>\n <p>Most athletes consider lactic acid their enemy, and think that training helps eliminate the metabolic waste product from their muscles so the muscles will function longer and harder. But UC Berkeley physiologist George Brooks has found that training actually teaches muscle cells how to use lactic acid as a fuel to get more bang for the buck. With training, mitochondria grow, take in more lactate via a shuttle and burn it to generate more energy.</p>\n \n <p>\"I gave rats radioactive lactic acid, and I found that they burned it faster than anything else I could give them,\" Dr. Brooks said.</p>\n</blockquote>\n\n<p>You may also refer to <a href=\"http://www.eatmoveimprove.com/2009/11/the-truth-about-lactic-acid/\">http://www.eatmoveimprove.com/2009/11/the-truth-about-lactic-acid/</a> for details on lactic acid metabolism.</p>\n"
}
] |
20,006
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<p>I sometimes use <a href="http://www.ruralking.com/agristar-2-4-d-amine-1-gallon.html?utm_medium=cse&utm_source=google&CAWELAID=1624250989&CAGPSPN=pla&catargetid=520009190000031013&cadevice=c&gclid=CjwKEAjwxtKeBRDMzoeQmYn5uHcSJACGCF3Dhs22FITlehPhZgOacOeZU5_PbIz8W8iI4BOsuTyoPBoCeW7w_wcB" rel="noreferrer">2,4-Dichlorophenoxyacetic acid</a> to control broadleaved weeds in lawns. It is selective, and quickly kills the dicot weeds, while other plants are unharmed.</p>
<p><img src="https://i.stack.imgur.com/tGMsm.png" alt="enter image description here"></p>
<p>2,4-D is a synthetic auxin, a class of plant hormones. It is gets taken in through the stomata on the leaves, and is transported to the meristems of the plant. This causes uncontrolled, unsustainable growth, and the plant wilts, and dies.</p>
<p>Why doesn't this affect most monocotyledons?</p>
|
[
{
"answer_id": 20138,
"pm_score": 4,
"text": "<p>According to <a href=\"http://www.purdue.edu/newsroom/research/2011/111122MurphyTransporter.html\" rel=\"noreferrer\">this link</a> from Purdue, the seed of the answer is this:</p>\n\n<blockquote>\n <p>The herbicide is used to kill broadleaf weeds, which are dicots, while monocot grasses, such as sorghum and corn, are more resistant. That's because grasses inactivate 2,4-D inside the plant, while broadleaf dicots do not.</p>\n</blockquote>\n\n<p>But on the other hand, <a href=\"http://sourcedb.cas.cn/sourcedb_xtbg_cas/yw/ywlw/201312/P020131220579582246464.pdf\" rel=\"noreferrer\">Song 2014</a> has this to say about 2,4-D:</p>\n\n<blockquote>\n <p>However, the underlying molecular mechanism of how auxinic herbicides selectively kill\n dicots and spare monocots is not\n understood yet (Grossmann 2000; Kelley\n and Riechers 2007; McSteen 2010). The mechanisms of auxin biosynthesis, transport,\n and signal transduction\n are conserved in monocots and dicots make this question more complex (McSteen 2010). Early research has\n proposed that the selectivity of auxinic herbicide is because of\n either limited translocation or rapid degradation\n of exogenous auxin, altered vascular anatomy, or altered perception of auxin in monocots (Monaco et al. 2002;\n Kelley and Riechers 2007). Auxin transport is influenced by plant vascular\n systems (Mattsson et al. 1999;\n Scarpella et al. 2006). The difference in vascular tissue structure between dicots\n and monocots may contribute\n to the selectivity of auxinic herbicides. In monocot\n stems, the vascular tissues (the phloem and xylem) are\n scattered in bundles, and lack a vascular\n cambium; in dicot stems, the vascular tissues are form\n ed in rings and\n possess a cambium. </p>\n</blockquote>\n\n<p>So in other words, we don't know yet. It seems to be very strongly tied to auxin transport, but we do not have the full mechanism of action; since auxin is such an important plant hormone, and the pathway is therefore highly conserved (that is, the genes tend to be nearly identical on the parts of the sequence that affect the phenotype), the general conclusion is that the pathway itself is not affected, but an accessory pathway clears up auxin in levels excess of any normal amount in monocots.</p>\n\n<p>Edit: Whoops, got the author's first/last names mixed up.</p>\n"
}
] |
[
{
"answer_id": 88996,
"pm_score": -1,
"text": "<p>The specificity of 2,4 D may be due to either limited translocation or rapid degradation ,altered vascular anatomy or altered perception of auxin in monocot</p>\n"
}
] |
20,019
|
<p><a href="https://i.stack.imgur.com/lZrzJ.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/lZrzJ.jpg" alt="enter image description here"></a></p>
<p>In the picture above (Source: <a href="http://ecx.images-amazon.com/images/I/71zKixilmEL._SL1500_.jpg" rel="nofollow noreferrer">Amazon.com</a>, United Scientific MCT001 Hand Microtome) we can see a microtome. How is it operated?</p>
|
[
{
"answer_id": 20022,
"pm_score": 3,
"text": "<p>The imnstrument is shown here upside down. If it is turned around, it looks like this:</p>\n\n<p><img src=\"https://i.stack.imgur.com/cwWXG.jpg\" alt=\"enter image description here\"></p>\n\n<p>The glass disc are placed around the middle tube. The operation principle can be seen in this image:</p>\n\n<p><img src=\"https://i.stack.imgur.com/o88u7.gif\" alt=\"enter image description here\"></p>\n\n<p>The specimen is placed in the tube in the middle and pushed out by turning the knob at the bottom. The minimal increment for this kind of microtome is 10 micrometers. The razor knife is used to cut the slices of the specimen.\nAn operation manual can be found <a href=\"http://www.unitedsci.com/sites/www.unitedsci.com/files/activity-guides/MCT001.pdf\" rel=\"nofollow noreferrer\">here</a>.</p>\n"
}
] |
[
{
"answer_id": 58826,
"pm_score": 1,
"text": "<blockquote>\n <p>Also, are these still used in everyday biological research? Teached\n for students?</p>\n</blockquote>\n\n<p>It's a hand microtome allright. As Chris explained, these are used to section thin slices of plant tissue, to be examined using a transmitted light microscope. They're still availlable from several sources, for example from Euromex in The Netherlands. I still have one of those, but it's years ago I used it:</p>\n\n<p><a href=\"https://i.stack.imgur.com/j2YSt.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/j2YSt.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Those are hardly used anymore in research, but they are still being used by amateur biologists/botanists/microscopists. </p>\n\n<p>The only uses I can imagine in research would be to use it to section a sample to see whether or not it is interesting enough to be processed and sectioned using more contemporary techniques, such as paraffin embedding followed by rotary-/sledge-/base sledge microtomy. Or perhaps in the study of life processes.</p>\n\n<p>Depending on the skills of the operator (including his skills to sharpen/strop his knives!) and the nature of the sample, slices as thin as 20 µm can be sectioned, using a hand microtome. </p>\n\n<p>That's often thin enough to make for a more or less acceptable botanical slide, temporary or permanent, but as kind of a norm, \"regular\" paraffin botanical/histological/histopathological/... sections for light microscopy are sectioned these days at any thickness between 2 - 10 µm. </p>\n\n<p>That's not possible with this type of microtome. </p>\n\n<p>The impossibility to section samples at a thickness thin enough to make for really clear microscopic images has burdened scientists for ages. </p>\n\n<p>It wasn't untill 1883 that an American mechanic, Adam Pfeiffer, came up with a usable machine to make that happen. Pfeiffer worked further on the idea provided by two others, Cowles and Richards, who made a first prototype in 1879. </p>\n\n<p>In 1886, Charles Minot, an American as well, came up with the first really usable rotary microtome. </p>\n\n<p>That \"Minot-microtome\" is up to the present day, the workhorse in the botanical, histological and histopathological lab. </p>\n\n<p>It's an interesting story, but the rotary microtome is based on a fundamentally different concept, compared to a hand microtome. </p>\n\n<p>The real offspring of the hand microtome is the (base) sledge microtome, as it mimics more or less the movements of an operator using a hand microtome. But without all those impossible to controll variables.</p>\n\n<p>This is a base sledge microtome, I finished restoring only a few weeks ago. It's the legendary <em>Jung Heidelberg Tetrander II</em>. The Tetrander was put on the market in 1910 and some of those are still in use. They're used to section large and hard samples (hard wood, bone, teeth, ...), which can't be sectioned using a rotary microtome. </p>\n\n<p>At the time it appeared on the market, a popular joke amongst German histotechnicians was, that it was named \"Tetrander\" because it took four man to handle it... In reality it was named \"Tetrander\" because it was designed by four German scientists, amongst them the legendary Paul Mayer (yes, that Mayer's hemalum staining solution guy).</p>\n\n<p>This one (it is operational) is capable of sectioning samples as large as about 5cm * 7cm (ca. 2in * 3in), section thickness adjustable between 1 and 50 µm. </p>\n\n<p>Larger, motorized models are capable of sectioning things as hard as a concrete bloc, having the size of a modest tree. And that's no exageration...</p>\n\n<p><a href=\"https://i.stack.imgur.com/UvHTM.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/UvHTM.jpg\" alt=\"enter image description here\"></a></p>\n"
}
] |
20,034
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<p><strong>Dry Humping</strong>, is:</p>
<blockquote>
<p>dry humping is the process of two people repeatedly moving up and down and back and forth on top of each other fully clothed( or missing various pieces, but the penis must not come in contact with the vagina with out some sort of fabric separating them ex: boxers,panties, or even sheets!!)</p>
</blockquote>
<p>We all know that the basic rule for impregnation is that the sperm must come in contact with the egg, and even be able to fertilize it. While sperm can get through clothes, semen (but this is yet been proven or disproved) gets stuck, thus the sperm dies.</p>
<p>What is your opinion about this? If two people are on top of each other, fully clothed, and the male comes to ejaculation, is there any chance that pregnancy can happen, in the <strong>realistic</strong> and biological look at it (and not some probability or statistical way)? What advice should be given to teens on the matter?</p>
<p>I am a computer scientist with no biology knowledge, and am very interested in getting the opinion of biologists.</p>
<p>But since I know that the stackexchange community likes to see work done before asking questions, I did my own research (I am used to googling code and algorithms):
Very few research has been done on the subject. There is one shining research that concluded, as I recall, that:</p>
<blockquote>
<p>If the underwear is <strong>completely saturated</strong> with semen, and is in <strong>direct</strong> contact with the woman's vagina, pregnancy is <strong>possible</strong> statistically, but <strong>highly unlikely</strong>.</p>
</blockquote>
|
[
{
"answer_id": 20036,
"pm_score": 5,
"text": "<p>If there has been an ejaculation by the male, and semen is present, there is a chance of getting pregnant. Period. Teens really need to know that.</p>\n<p>I think you may have your terms confused - semen is the overall fluid released during an ejaculation, sperm are the cells with tails that are produced in the testes and fertilize the egg. At any rate, according to the WHO, a normal sperm count is over 15 million per milliliter, with some counts much higher (>50e6/ml ), and an average between 20 and 40 million. The volume of the ejeculate tends to be anywhere from 1-6 ml. If you take a healthy young male at the peak of his reproductive capabilities, this equates to a very large number of sperm being released during a sexual encounter. All it takes is for one to reach an egg and fertilize it. Sperm are very very small, much smaller than the pore size of average fabric, so clothing will do very little to stop them. The female is likely sexually aroused during this activity as well, and produces additional fluids and lubricants that promote the survival and motility of sperm, among other things.</p>\n<p>So, it depends on many factors. If both parties are fully clothed (at least 4 layers of clothing between their respective reproductive organs) and there is a minumum of soaking through, the chances of pregnancy are correspondingly quite low. On the other hand, if only one partner is wearing just their underwear, it's essentially like there is no clothing present at all, and the relative chances go up significantly.</p>\n<p>Safe sex practices can't be emphasized enough to young people, as education and awareness is so much better than ignorance and myths. Even aside from pregnancy, if condoms are not utilized properly to contain all the semen there is the chance of sexually-transmitted diseases, ranging from herpes and gonorrhea to AIDS. None of these require penetration to be passed along, and one might argue that the additional presence of potentially irritating fabrics could open up raw areas or cuts and enhance their transmittal.</p>\n<hr />\n<h2>Take home message</h2>\n<p>Now, all this being said, the chances of impregnation through clothing without direct penetration of the penis into the vagina is quite low compared to "typical" unprotected fully-penetrating intercourse, especially depending on where the female is in her fertility cycle. According to <a href=\"http://www.demographic-research.org/Volumes/Vol3/5/default.htm\" rel=\"noreferrer\">this study</a>, a woman's most fertile day is two days before ovulation (as had been postulated before), and the chances of pregnancy on that day are about 25% (assuming penetrating intercourse). Overall, the chance of pregnancy throughout the month is about 5%.</p>\n<p>I don't have any hard numbers on the pregnancy chances when one or both partners have at least some clothing on, as obviously it will vary greatly depending on who is wearing what, the volume of ejaculate, contact time after ejaculation, etc. Just for fun, let's assume it's 100 times lower. That means the chances of impregnation two days pre-ovulation would be 0.25%, or 1 in 400. While rather low, this is still a non-zero chance.</p>\n<p>Condoms are about 98% effective if used properly during penetrative vaginal intercourse. Various other birth control methods such as contraceptive pills, intrauterine devices, implants and injections are quoted as being 99% effective on their own, although they do not protect against sexually transmitted diseases. I'm certainly not one for preaching abstinence, but done properly it should be 100% effective. Ultimately, it is up to both partners to decide what their risk tolerances are, together. It is much better to seriously talk about it beforehand than to be panicked and unsure afterwards.</p>\n<hr />\n<p>Hopefully this addresses your concerns, please leave comments if you have additional questions.</p>\n"
}
] |
[
{
"answer_id": 43572,
"pm_score": -1,
"text": "<p>It is effectively impossible to get pregnant by <a href=\"http://beforeplay.org/2014/01/can-sperm-go-through-clothes-and-get-a-woman-pregnant/\" rel=\"nofollow\">dry-humping</a> because the conditions that would have to be met for sperm to pass through multiple layers of clothes, survive on skin, find the vaginal opening, survive in the vaginal environment and finally impregnate an egg are simply unrealistic. </p>\n\n<p>The barrier of clothing that we can assume present during 'dry humping' is significant. Semen begins to die as soon as it begins to <a href=\"http://www.healthcentral.com/sexual-health/c/question/953442/146810/\" rel=\"nofollow\">dry out</a> and any clothes you're wearing are likely to draw water away from the sperm cells through adhesion of water to the fabric. One layer is absolutely not <em>\"like there is no clothing present at all\"</em>. </p>\n\n<p>Assuming some sperm cells made it through all that and onto skin, their motion isn't directed towards the vaginal opening, so a sizable fraction will be literally lost at that step. Skin is also a toxic environment on its own, so these improbable sperm have a very limited time to find their way. </p>\n\n<p>That last battle buddy team of sperm has very little chance of surviving the vaginal environment. A lot of sperm need to enter the vaginal environment together to ensure that just a few survive. </p>\n\n<p>As far as dry humping is concerned, there's no realistic reason to worry about pregnancy.</p>\n"
}
] |
20,086
|
<p>Can you please give me some advice for a book in (evolutionary) <a href="http://en.wikipedia.org/wiki/Conservation_genetics" rel="nofollow">conservation genetics</a> that offers an in-depth review of the mathematical formulations used in this field.</p>
<p>I read the book <a href="http://www.amazon.fr/Evolutionary-Conservation-Biology-R%C3%A9gis-Ferri%C3%A8re/dp/0521116082/ref=sr_1_3?ie=UTF8&qid=1406725200&sr=8-3&keywords=evolutionary%20conservation%20biology" rel="nofollow">Evolutionary Conservation Biology (Ferrière and Dieckmann, 2009)</a> and I really liked it. I'm seeking for another book of the same kind that goes further on the part A (Theory of Extinction) and especially on the concern of the importance of population structure and the genetic load. I am also interested in <a href="http://en.wiktionary.org/wiki/landscape_genetics" rel="nofollow">landscape genetics</a>.</p>
|
[
{
"answer_id": 20101,
"pm_score": 3,
"text": "<p>This book \"<a href=\"http://www.cambridge.org/se/academic/subjects/life-sciences/ecology-and-conservation/primer-conservation-genetics\" rel=\"nofollow\">A primer of conservation genetics</a>\" would suit quite well I think. In particular chapter five deals with \"Genetics and Extinction\" and is preceded by a lot of population genetics based theory. A beginner might also combine it with \"A primer of ecological genetics\" (Hartl & Conner) but you seem to have enough Pop gen knowledge to not need it!</p>\n\n<p>The landscape genetics is perhaps a bit lacking from this book though. Maybe a better and more comprehensive solution, but slightly more advanced, is <a href=\"http://rads.stackoverflow.com/amzn/click/0470671459\" rel=\"nofollow\">this book</a> which does feature some aspects of landscape genetics in chapter 15 along with good population genetics type coverage of extinction.</p>\n"
}
] |
[
{
"answer_id": 20115,
"pm_score": 2,
"text": "<p>If you're interested in learning about the mathematics of population genetics, <a href=\"http://onlinelibrary.wiley.com/book/10.1002/0470047356\" rel=\"nofollow\">Population Genetics and Microevolutionary Theory</a> by Alan Templeton is an absolutely amazing resource.</p>\n\n<p>If you check out the index, here are entries under population structure:\nassortative mating, admixture, linkage disequilibrium, coarse-grained spatial heterogeneity, gene flow, gene flow and population history, gene flow vs admixture, microevolution modeling, multiple inheritance modes, natural selection, adaptation, and fitness.</p>\n\n<p>Heterozygosity and other mathematical descriptors are particularly relevant to conservation (the author has been involved in various conservation projects). Furthermore, there are various entries on viability.</p>\n\n<p>Plus there's plenty of information in it about the effects of landscape on gene flow and other population structural features.</p>\n"
}
] |
20,129
|
<p><strong>Very simple:</strong> Why (and how) is regenerated skin different from original ?</p>
<p>As we know we lose skin cells that becomes the dust in out homes and it always grows back to full thickness right ? So when I have a cut, I imagined it to heal provisionally with whatever possible and then after some time to replace itself with the normal skin that is coded in my chromosomes. So why doesn't it do that ? Scars remain and the color is always different from the neighbor parts.</p>
<h2>Update:</h2>
<ul>
<li>Why we get scars?</li>
<li>What about skin transplants ? </li>
<li>Why doesn't skin actually grow/replace itself? </li>
</ul>
<h2>Update 2:</h2>
<ul>
<li>(I've been thinking) Skin has lots of different layers, right ? So when an area is damaged does it regenerate all layers or just one for being simple and efficient (in "hope" the subject will take precautions not to damage this part of body again, so that regenerating everything back to 100% would be overkill) ?</li>
<li>I'm not a scientist, I have only the basics from school, so I'll probably not understand most of the technical terms</li>
<li>also I'm more interested about an explanation that goes towards the "survival of the fittest" rule, and not so much about the biochemical reactions in our bodies (because it was just some random mutation that turned out to be the better choice for us → why?)</li>
</ul>
|
[
{
"answer_id": 20210,
"pm_score": 4,
"text": "<p>Human skin is made up of three layers [1]:</p>\n\n<ol>\n<li>Epidermis; it contains no blood vessels; it has 5 cellular layers (starting from surface):\n\n<ul>\n<li><strong>stratum corneum</strong></li>\n<li>stratum lucidum</li>\n<li>stratum granulosum</li>\n<li>stratum spinosum</li>\n<li>stratum germinativum</li>\n</ul></li>\n<li>Dermis; it is separated from the above by the <strong>basal membrane</strong>; made up of connective tissue (with blood vessels and nerve endings)</li>\n<li>Hypodermis - it is not even considered part of the skin</li>\n</ol>\n\n<p><a href=\"http://commons.wikimedia.org/wiki/File:Gray940.png#mediaviewer/File:Gray940.png\" rel=\"nofollow noreferrer\"><img src=\"https://upload.wikimedia.org/wikipedia/commons/1/18/Gray940.png\" alt=\"Gray940.png\"></a><br>\"<a href=\"http://commons.wikimedia.org/wiki/File:Gray940.png#mediaviewer/File:Gray940.png\" rel=\"nofollow noreferrer\">Gray940</a>\". Licensed under Public domain via <a href=\"//commons.wikimedia.org/wiki/\" rel=\"nofollow noreferrer\">Wikimedia Commons</a>.</p>\n\n<blockquote>\n <p>Why (and how) is regenerated skin different from original ?</p>\n</blockquote>\n\n<p>Why? Skin is a very important organ. It protects from pathogens, it maintains body temperature, it keeps body water [1], etc. How? That depends on what causes the regeneration. I've emphasized two terms in the above list.</p>\n\n<ul>\n<li><em>Stratum corneum</em> represents the \"skin cells that becomes the dust in our homes and it always grows back to full thickness\". It is lost during a physiological process called desquamation [2]. The cells that are lost are non living corneocytes. Their only purpose is to from a protection barrier [3].</li>\n<li><em>Basement membrane</em> holds the germinativum layer of the epidermis. Injuries that do not affect it are repaired by complete regeneration of all destroyed layers. However, if the injury destroys membrane continuity, the germinative cells on the edges will fail to \"reconnect\" with each other, thus the layers derived from them will follow the same rule. A process of fibrosis is triggered. The result of extensive fibrosis is a scar, containing collagen secreted by the granulation tissue with dermal origins. Yet, the germinative layer tends to join back together [6], but probably the excess collagen production, without the limiting basement membrane, bulges into the epidermis and limits germinative layer extension. That's why keeping the edges of the tissue close to each other reduces excessive fibrosis and allows germinative layer regeneration, thus resulting in none to small, barely visible scars.</li>\n</ul>\n\n<p>How deep should an injury be in order not to affect basement membrane? No more than 0.06 to 0.08 mm [5].</p>\n\n<blockquote>\n <p>What about skin transplants ?</p>\n</blockquote>\n\n<p>Skin grafts contain at least a part of dermis [4], which will allow granulation tissue formation thus permitting revascularisation and making the graft stick. Otherwise it would fall off and/or be lost by necrosis.</p>\n\n<hr>\n\n<p>References:</p>\n\n<ol>\n<li>Wikipedia contributors, \"Skin,\" Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Skin&oldid=619454074\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/w/index.php?title=Skin&oldid=619454074</a> (accessed August 4, 2014).</li>\n<li>Wikipedia contributors, \"Desquamation,\" Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Desquamation&oldid=614028888\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/w/index.php?title=Desquamation&oldid=614028888</a> (accessed August 4, 2014).</li>\n<li>Wikipedia contributors, \"Stratum corneum,\" Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Stratum_corneum&oldid=615247326\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/w/index.php?title=Stratum_corneum&oldid=615247326</a> (accessed August 4, 2014).</li>\n<li>Wikipedia contributors, \"Skin grafting,\" Wikipedia, The Free Encyclopedia, <a href=\"http://en.wikipedia.org/w/index.php?title=Skin_grafting&oldid=603324006\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/w/index.php?title=Skin_grafting&oldid=603324006</a> (accessed August 4, 2014).</li>\n<li>Sandby-Møller J, Poulsen T, Wulf HC. <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/14690333\" rel=\"nofollow noreferrer\">Epidermal thickness at different body sites: relationship to age, gender, pigmentation, blood content, skin type and smoking habits.</a> Acta Derm. Venereol. 2003;83(6):410-3. doi: <a href=\"http://dx.doi.org/10.1080/00015550310015419\" rel=\"nofollow noreferrer\">10.1080/00015550310015419</a>. PubMed PMID: 14690333. </li>\n<li>Dawn A. Tamarkin, Ph.D. <em>Repair of skin.</em> 2011 STCC Foundation Press. Available from <a href=\"http://faculty.stcc.edu/AandP/AP/AP1pages/Units1to4/skin/repairof.htm\" rel=\"nofollow noreferrer\">http://faculty.stcc.edu/AandP/AP/AP1pages/Units1to4/skin/repairof.htm</a> (accessed 04.08.2014)</li>\n</ol>\n"
}
] |
[
{
"answer_id": 20147,
"pm_score": 2,
"text": "<p>You're confusing an emergent system with a determined system. Your cells have programming which emerges as the form you see. You are using determinism to decide what your form should be. Determinism gives one reaction for every action. Biology is emergent, not deterministic. The biological mechanisms which are responsible for healing exist in a different information space, with different evolutionary pressures from those which generated your form. The close approximation of scar tissue to undamaged flesh is an emergent property of these two instructions sharing the same physical location. There is no communication between the information which patterned your form and the information which heals your body. </p>\n"
}
] |
20,176
|
<p>There are many plants and animals named for the naturalist Charles Darwin, such as Darwin's Frog <em>(Rhinoderma darwinii)</em>, but which were named by him? I'm finding it difficult to find such a list.</p>
|
[
{
"answer_id": 20200,
"pm_score": 4,
"text": "<p>I've discovered that searching for <a href=\"http://eol.org/search?q=darwin&type%5B%5D=taxon_concept\" rel=\"nofollow\">Darwin on the Encyclopedia of Life</a> (EOL) appears to prioritise in its search results those species named by Darwin rather than for him. The first page of results includes many barnacle species (as noted by 3cat). The first five species are:</p>\n\n<ul>\n<li><em>Amphibalanus amphitrite</em> (Striped Barnacle)</li>\n<li><em>Megabalanus coccopoma</em> (Titan Acorn Barnacle)</li>\n<li><em>Balanus glandula</em> (Acorn Barnacle)</li>\n<li><em>Elminius modestus</em> (New Zealand Barnacle)</li>\n<li><em>Balanus nubilus</em> (Giant Barnacle)</li>\n<li>...</li>\n</ul>\n\n<p>There are 370 results, but some of them are not species level (e.g. Chthamalidae), and some other entries are mixed in (e.g. <a href=\"https://en.wikipedia.org/wiki/S.C.Darwin\" rel=\"nofollow\">S.C. Darwin</a> and S.P.Darwin), and later results include, for example, <em>Nemoria darwiniata</em>, so it's hard to quantify the results.</p>\n\n<p>I might try writing an SQL query for the downloaded <a href=\"http://www.catalogueoflife.org/\" rel=\"nofollow\">Catalogue of Life</a>, as its online interface doesn't seem to allow the relevant query.</p>\n\n<p><strong>EDIT:</strong></p>\n\n<ul>\n<li>The complete list: <strong><a href=\"http://eol.org/collections/12085\" rel=\"nofollow\">Species described by Charles Darwin (EOL)</a></strong>, listing 81 species. (Pointed out in comments. Thanks 3Cat)</li>\n</ul>\n"
}
] |
[
{
"answer_id": 20186,
"pm_score": 3,
"text": "<p>I don't know if these are his earliest descriptions but Darwin did describe several species of Planaria, such as <em>Planaria vaginuloides</em>, <em>P. oceania</em>, plus a new genus, <em>Diplanaria</em> in 1844.</p>\n\n<p><a href=\"http://darwin-online.org.uk/content/frameset?itemID=F1669&viewtype=text&pageseq=1\">Darwin, C. R. 1844. Brief descriptions of several terrestrial planariæ, and of some remarkable marine species, with an account of their habits. Annals and Magazine of Natural History 14 (October): 241-251, 1 plate.</a></p>\n\n<p>Perhaps his best known taxonomic work is on barnacles (Cirripedia). He described several species in his monograph first monograph on the group.</p>\n\n<p><a href=\"http://darwin-online.org.uk/content/frameset?itemID=F339.1&viewtype=text&pageseq=1\">Darwin, C. R. 1851 [=1852]. A monograph of the sub-class Cirripedia, with figures of all the species. The Lepadidæ; or, pedunculated cirripedes.. London: The Ray Society. Volume 1</a></p>\n\n<p>The first monograph was followed by three other monographs on living and fossil Cirripedia. </p>\n\n<p>I believe that most of his writings after publication of <em>On the Origin of Species</em> focused on expanding his evolutionary ideas rather than on descriptions of new species.</p>\n\n<p>You can read nearly all of Darwin's writings online at <a href=\"http://darwin-online.org.uk\">http://darwin-online.org.uk</a>. With careful searching you can find all (or nearly all) species descriptions.</p>\n"
}
] |
20,215
|
<p>I've been looking at some sequenced exomes and found an interesting point mutation that causes a Proline-to-Leucine amino acid change in the protein. This seems like it could have a big impact on the protein's functionality but before I go any further I want to explore whether or not the variant is a sequencing artifact. </p>
<p>I looked at the coverage for this particular region of the genome and found that in some samples, the point mutation is seen in every single read covering the base in question while in others the point mutation is seen in approximately half of the reads. In all my samples, the base in question is covered by at least 15 separate reads but usually its more than 20. </p>
<p>My primary question is: <strong>how should I interpret the cases where the point mutation is seen in some but not all of the reads covering its location?</strong></p>
<p>I'm also interested in any suggestions/advice on the more general topic of determining whether or not the mutation I've found is a sequencing artifact.</p>
|
[
{
"answer_id": 20216,
"pm_score": 4,
"text": "<p>I don't know, whether the organism you are working with is diploid, but suspect it's an animal (or even a mammal), so the most parsimonious explanation would be that you have <a href=\"https://en.wikipedia.org/wiki/Zygosity#Homozygous\">homozygotes</a> and <a href=\"https://en.wikipedia.org/wiki/Zygosity#Heterozygous\">heterozygotes</a> at this SNP-position.</p>\n"
}
] |
[
{
"answer_id": 20236,
"pm_score": 0,
"text": "<p>Also I don't know what kind of genetic input your given but if there is variation in origin ie some saliva some cheek skin then there could be a tissue based difference in the genome. </p>\n"
}
] |
20,217
|
<p>I saw this pic while crawling online and it was a bit different for me to predict which worm is this. </p>
<p><img src="https://i.stack.imgur.com/grEvP.jpg" alt="enter image description here"></p>
<p><strong>Source:</strong> <a href="http://www.seafishingtackle4u.com/softbaits/ragworms-latex-lures/" rel="nofollow noreferrer">http://www.seafishingtackle4u.com/softbaits/ragworms-latex-lures/</a></p>
<p>It appears somewhat different form other annelids as parapodia or setae are somewhat transparent and very attractive too.</p>
<p>What worm is this?</p>
|
[
{
"answer_id": 20219,
"pm_score": 2,
"text": "<p>As Cornelius correctly pointed out, it's not a living worm :)</p>\n\n<p>As to the question, what kind of worm they tried to imitate, I'd say, they had a <a href=\"https://www.google.com/search?channel=fs&q=nereidae&tbm=isch\" rel=\"nofollow\">nereid</a> (errant, i.e. wandering) in mind and were likely inspired by the segmentation of <em><a href=\"https://www.google.com/search?channel=fs&q=arenicola&tbm=isch\" rel=\"nofollow\">Arenicola</a></em> (sedentary), which together created this appearance, unrealistic for an errant polychaete: with the body segments outnumbering parapodia.</p>\n\n<p><strong>EDIT:</strong></p>\n\n<p>They also paid no attention to the head (a very important body part in polychaete systematics!), which seems to be absent. This feature could also be \"inherited\" from <em>Arenicola</em>, the head end of which is not prominent and bears no appendages.</p>\n"
}
] |
[
{
"answer_id": 20218,
"pm_score": 2,
"text": "<p>If you would have read the text from the source of that image (which by the way you didn't mention, I did a Google Image search and edited your question to include it), you would have known that what is seen in the picture is not a living thing, it is a latex <a href=\"http://en.wikipedia.org/wiki/Fishing_lure\" rel=\"nofollow\">fishing lure</a>:</p>\n\n<blockquote>\n <p>Product Description: Sandworm/Ragworm 8″ size, sure fire fish catching lures. Costing less than live worms, but lasting much longer, never be without worms again. </p>\n</blockquote>\n\n<p>Source: <a href=\"http://www.seafishingtackle4u.com/softbaits/ragworms-latex-lures/\" rel=\"nofollow\">http://www.seafishingtackle4u.com/softbaits/ragworms-latex-lures/</a></p>\n"
}
] |
20,225
|
<p>Haven't looked into this to very long, but an initial search didn't return anything. </p>
<p>HIV uses certain co-receptors to enter our cells. Could we flood the blood stream with specially designed proteins that mimic cell receptors, either locking the virus out of vulnerable cells, or even causing the virus to release its genetic material (pre-mature ejc. for viruses... :|), so it can't accidentally get away and infect a cell anyway? It seems like an obvious idea, so the fact that it may not already be happening must mean there are a host of challenges to it? Basically we design a protein that acts like a strait jacket, with tags that allow our body to recognize it as a 'friendly' body. T-cells use the same receptor though, so are there ways to identify a T-cell compared to a HIV virion?</p>
<p>Obviously this wouldn't prevent some viruses managing to infect actual cells, but over time, if we can attack enough, say 2/3 of the virions, for each generation, we could seriously harm the population, and maybe keep it in check?</p>
|
[
{
"answer_id": 20231,
"pm_score": 4,
"text": "<p>Yes, that should be possible. And it is one of the ways antibodies work. It is already used as a treatment against <a href=\"http://en.wikipedia.org/wiki/Rabies#Treatment\">rabies</a>. There you get a dose of immunoglobulins directed against the rabies virus together with the vaccine. The immunoglobulins neutralize the virus.</p>\n\n<p>The same is possible when you vaccinate against the surface proteins which a virus uses to dock to a cell. With the resulting antibodies this docking is at least hindered if not completely prevented. And there are interesting results from the Ebola research which used a small molecule inhibitor to identify the protein which is important for cell binding of the virus. It is called NPC1, when the receptor on the virus surface is blocked, no docking can take place. This will be one of the approaches to make a therapeutic. See <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230319/\">here</a> for more details.</p>\n\n<p>And it is of course possible to design more of the molecules - the problem is to find substances which do not interfere with body functions or which stimulate other pathways.</p>\n"
}
] |
[
{
"answer_id": 64317,
"pm_score": 1,
"text": "<p>This approach actually works on almost anything, given enough proteins and nanoscale \"griefing\".</p>\n\n<p>There was an experiment a few years back where scientists wrapped normal cell membranes around polyurethane beads. The surface looks like a normal cell, allowing it to soak up toxins and trap viruses.</p>\n\n<p>Then there's the offensive approach where proteins are used to block structures on a virus, preventing it from recognizing and entering host cells. Alternately you could include immune-reactive structures on those proteins, painting them for clean-up.</p>\n\n<p>This approach also works on bacteria. Block membrane channels used to get rid of waste, or outright cover the bacteria in sticky garbage \"griefing\" gunk preventing them from eating. Build exceptionally heavy proteins that bind to bacterial flagella and stop them from moving.</p>\n\n<p>Scale it up to worm parasites. Build proteins that stick to their mouths and refuse to leave. While you're at it, build another set that sticks to the opposite end of the worms' digestive tracts, preventing them from eating or removing waste. It's a major headache and a pain in the behind - at the same time.</p>\n"
}
] |
20,264
|
<p>According to my textbook, Davson-Danielli's model of a phospholipid bilayer sandwiched between two layers of globular protein was incorrect. The nonpolar protein portions would separate the polar portions of the phospholipids from water, causing the bilayer to dissolve. Meaning, the Davson-Danielli model is not only incorrect, but it is also impossible.</p>
<p>I understand why the model is incorrect, but not why it is impossible. In my view, the nonpolar proteins would remain together in a micelle shape due to hydrophobic exclusion. Because of this, the phospholipid bilayer sandwiched on the inside would remain isolated from the water.</p>
<p>Why would a bilayer dissolve if the proteins were in contact with water and the phospholipids were isolated from the water? </p>
<p>I think that my confusion stems from many misunderstandings about the chemistry and structure of the cell membrane. In depth illustration of the error that my book mentioned would be most helpful.</p>
|
[
{
"answer_id": 20265,
"pm_score": 4,
"text": "<p>The original figure that Danielli and Davson proposed looks like this (from the <a href=\"http://onlinelibrary.wiley.com/doi/10.1002/jcp.1030050409/abstract\" rel=\"nofollow noreferrer\">original publication</a>):</p>\n\n<p><img src=\"https://i.stack.imgur.com/ZVnDo.png\" alt=\"enter image description here\"></p>\n\n<p>It shows the phospholipid bilayer of the membrane (which is correct) embedded between two layers of globular proteins. The hydrophobic tails of the lipids are orientated towards each other, while the hydrophilic heads are oriented to the outside.</p>\n\n<p>Although the membrane composition is correct (this was already published 1925 by <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/19868999\" rel=\"nofollow noreferrer\">Gorter and Grendel</a>), there are some problems with the proposed model:</p>\n\n<ul>\n<li>Membranes are not identical. The differ in thickness and the ratio of\nproteins:lipids.</li>\n<li>Membranes have distinct inside and outside layers (defined by the\nmembrane proteins which are present on the surface of the membrane)</li>\n<li>Other than predicted by the model, the membrane proteins do not have\na very good solubility in water - in fact they are amphiphatic,\nmeaning they have hydrophilic and hydrophobic regions. The\nhydrophobic side is anchored inside the membrane.</li>\n<li>When the membrane proteins would cover the lipid bilayer, their\nhydrophobic regions would be in contact with water, which\ndestabilizes this construct. Even if they would be oriented towards\nthe membrane, they would face towards the hydrophilic heads of the\nphospholipids causing the same effect. Additionally the proteins\nwould also seperate the hydrophilic phospholipid heads from the\nwater. So there is no real stable solution in embedding the membrane\nwith proteins.</li>\n</ul>\n"
}
] |
[
{
"answer_id": 24051,
"pm_score": 0,
"text": "<p><strong>Problems with the davson danielli model :</strong></p>\n\n<ol>\n<li><em>freeze-etched micrographs</em>:</li>\n</ol>\n\n<p>This is a technique of rapidly freezing the cell and then fracturing them. The fracture occurs along lines of weakness and in these micrographs there were two prominent dark lines which indicate the phospholipid bilayer and but there were transmembrane proteins even in between the phospholipid bilayer unlike what the davson danielli model suggested (that the phospholipid bilayers contained two layers of proteins on top and on bottom.)</p>\n\n<p><img src=\"https://i.stack.imgur.com/OH8I1.jpg\" alt=\"enter image description here\"> <img src=\"https://i.stack.imgur.com/xw8cr.jpg\" alt=\"enter image description here\"> </p>\n\n<p>2)<em>structure of membrane proteins :</em></p>\n\n<p>improvements in biochemical tech allowed people to extract proteins from the membranes. They were different sizes and globular in structure.They were unlike the type that would form continuous layers on the periphery of the membrane. Proteins were hydrophilic in nature and hence should have been attracted to the tails and not the heads.</p>\n\n<p>3)<em>Fluorescent anti-body tagging</em> :</p>\n\n<p>red and green markers were attached to the antibodies that bind to membrane proteins. these two cells were fused together and 40 minutes later it was seen that the red and green markers were mixed throughout the membrane of the fused cells. therefore the proteins were free to move within the membrane rather than being fixed in a peripheral layer.</p>\n"
}
] |
20,266
|
<p>I understand that in PCR we're able to amplify only selected portions of the DNA... however despite reading it from multiple sources, I cannot figure out how this selection actually takes place.</p>
<p>I know that by using proper primers, one each for coding and template strands, we can direct the DNA polymerases to specific sites to start with. I also understand that these primers make the replication proceed in opposite directions, towards each other. Like follows:</p>
<p><img src="https://i.stack.imgur.com/9N6Ug.png" alt="My understanding of so far"></p>
<p>However, I wonder what makes the replication terminate when the polymerase reaches the primer at the other end? Because as far as I understand, replication should continue indefinitely until the physical end of the sample strand is reached... such that we may decide the starting points but never the ending points.</p>
|
[
{
"answer_id": 20267,
"pm_score": 4,
"text": "<p>Note: In your PCR program you always set extension time.</p>\n\n<p>Case:</p>\n\n<ul>\n<li>Product length = 500bp</li>\n<li>PCR extension time = 50sec</li>\n<li>Assuming that polymerase adds 1000 nt/min</li>\n</ul>\n\n<p>Cycle 1:</p>\n\n<ul>\n<li>Strand that binds FP: extends ~800nt to the right (as per the polymerization rate): 300 bp ahead of RP complementary site. This product is lets say <code>P1</code></li>\n<li>Strand that binds RP: extends ~800nt to the left: 300bp ahead of FP complementary site. This is <code>P2</code></li>\n</ul>\n\n<p><img src=\"https://i.stack.imgur.com/vhjVq.png\" alt=\"enter image description here\"></p>\n\n<p>Cycle 2: </p>\n\n<p>The products of cycle-1 become templates for next round. \nFP binds to <code>P2</code> -300nt from its 3' end. Similarly RP binds to <code>P1</code> -300nt from its 3' end.\nThe resultant products will be 500nt which give rise to a 500bp perfect dsDNA.</p>\n\n<p><img src=\"https://i.stack.imgur.com/WYfGy.png\" alt=\"enter image description here\"></p>\n\n<p>Some <code>P1</code> and <code>P2</code> will keep forming at a linear rate; since your template is low in amount compared to the amplified cycle1 and cycle-2 products, your expected PCR product will be much higher (which gets produced at an exponential rate).</p>\n"
}
] |
[
{
"answer_id": 20268,
"pm_score": 2,
"text": "<p>I'm not completely clear when you say \"what makes the replication terminate when the polymerase reaches the primer at the other end\" since when you perform a PCR you go through three phases. The denaturation, whereby the two DNA strands become single stranded, then the annealing, which is when primers attach to their appropriate matching site (but the original DNA template is still single stranded) and extension, which is when DNA polymerase use the primers to extend make the matching strand the primer is attached to (<a href=\"http://en.wikipedia.org/wiki/Polymerase_chain_reaction\" rel=\"nofollow\">http://en.wikipedia.org/wiki/Polymerase_chain_reaction</a>). DNA polymerase continues to make the strand until it essentially either drops off or until the cycle is over and it is time for the cycle to repeat itself. The way you make sure to terminate a specific DNA replication at an appropriate length is to use the extension time as a control since as pointed in the above answer by @WYSIWYG the extension is largely assumed to be 1000 nt/min so if your product of interest is 500 bp, then you do 30-40 sec of extension in your PCR extension cycle program and if the product of interest is 1000 bp you do 60 sec of extension and so on.</p>\n\n<p>In the training I received, it is usually not recommended to PCR DNA template which is very large such as an entire plasmid such as pUAST. The main issue even with high fidelity/proff-reading DNA polymerases is that you can get errors in replication if the strand is very long. what often happens is that you amplify a section of DNA if you want to check for the presence of something or if you need to use the amplified fragment then you design restriction sites at either end of your fragment by incorporating it in the primers itself then you go ahead with you digestion and fragment purification and then you sequence your fragment to make sure you do not have any errors although PCR has much much more applications.</p>\n"
}
] |
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