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Does gray/white hair turn gray/white from a normal hair? or does a gray/white hair actually grow gray/white originally?
I am really curious if hair actually tuns white/gray from default color, or does it have a defect as it is made and grows out of your head a different color?

It can actually be for both reasons and it more or less depends on the age what happens. The pigment of the hair is produced by pigment cells (the melanocytes) in the hair bulge and is then integrated into the growing hair (image from here).

The pigment melanin produced by these cells can be destroyed by reactive oxigen species which then leads to grey hair which can still be pigmented at the tip.
The other possibility is connected to the hair cycle. After growing for a while the growth stops, the hair falls out and the hair follicle goes into a resting state. In this phase the pigment cells die. When the hair follicle starts a new hair cycle, the pigment cell population in the hair bulb is renewed from the melanocyte stem cells in the hair bulge. Over time the number of the melanocyte stem cells gets lower until there are none left eventually. At this point new hairs will grow without pigment and be grey/white.
There are two interesting publications about this topic:

Oxidative Stress in Ageing of Hair
Melanocyte Stem Cell Maintenance and Hair Graying

wow, this makes a lot of sense as to why old people lose hair.


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Why are there seven entries for Pimpinella dioica in the Catalogue of Life?
And six for Haliclona digitata, and five for Ichneumon varius. A couple of the duplicate entries are synonyms for other species, which is understandable, but most are the "accepted name". Shouldn't there just be one Pimpinella dioica? By my count there are 3068 species with two or more "accepted name" entries in the 2014 database. Where do these duplicate entries originate? Do they serve a purpose or are they errors?
Probably a question for catalogueoflife.org forums, but they don't seem to have any discussion area, so seeing if anyone here can answer.

While any large database may have errors that can lead to multiple entries (sensu har-wradim's answer), I think most of the multiple entries detail the taxonomic history associated with that species. Your link to the sponge Haliclona digitata provides a clear example. First, dismiss the H. digitata (Schmidt, 1862) entry. As clearly stated, it is a synonym for a different species of sponge, Tedania anhelans.
The remaining entries are all links to various homonyms of H. digitata. Skimming through the World Porifera Database entries (via the "Online resource" links), provides the necessary information. Lendenfeld's use of Chalinorhaphis is the original description. It is the senior homonym, meaning the specific epithet (digitata) has precedence over junior names. The junior names include Adocia digitata (Baer) and Gellius digitatus (Koltun). It was probably Tanita & Hoshino that transfered digitata to the genus Haliclona but I cannot verify this without seeing the article.
The taxonomic history can also be tracked for Ichneumon varius, but the linked databases don't hvae as much detail as the Porifera database for H. digitata. Still, it suggests that the description by Pontoppidan in 1763 is the senior homonym, and the subsequent uses by Cuvier, Gmelin and Muller are junior homonyms.
This is also what I think har-wradim is alluding to for Pimpinella dioica. Unfortunately, the Umbellifer database seems to have little detail in this regard.
The Catalogue of Life provides a convenient mechanims to begin a thorough search for the taxonomic history of a species.

This is because Catalogue of life is a database created and maintained via consulting other, taxonomically narrower databases. This leads to propagation of the original inaccuracies and introduction of new ones during the process of data transfer.
In the case of Pimpinella dioica, for example, the information was imported from the World Umbellifer Database. If you search there for "Pimpinella dioica" you get a list of names, only one of which is explicitly labeled as synonym (by Linné, the same one as in CoL). CoL interpreted this situation as if others were accepted as valid, BUT this was not the case: all other records are marked as "provisional" and most of them actually contain information about probable synonymy in "Comments".
Moreover, in the description of World Umbellifer Database the one can learn, that the database guarantees accuracy principally for generic names only.

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Distance matrix with different length sequences
In a project we're doing (in python), we want to create a distance matrix for a phylogenetic tree with multiple, different length sequences. However, what we've seen so far (AlignIO in biopython, etc.) requires the sequences' length to be equal. Is there any pythonic way to get the matrix with sequences of different length? Or any other indirect way that would get us to the same result?

How do you define the distance? (Sorry, cannot post comments -- moderators, please help)

Without seeing your code it's kind of hard to help. This question is much more suited for [so], please ask it over there and tag it [python] and [biopython].

Use a metric that is a function of the sequence but not the sequence itself; something like GC content. Or use end-to-end alignment such as Needleman-Wunsch algorithm

I am not a python user but it seems to me AlignIO is (similar to the bioperl counterpart) for reading/writing an already existing alignment (hence the requirement of equal sequence lengths). You could align the sequences with an external tool (like e.g. MAFFT) and then read the alignment in python with the AlignIO interface.

There are two possibilities:

Do not use the sequences per se but a scalar metric of sequence similarity for distance values
Introduce gaps in the alignment. You can also do an end to end gapped alignment such as the Needleman-Wunsch and use the alignment scores for the distance matrix.

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Why do spiders have a leaf at the bottom of a piece of web?
I've lately seen a lot of instances where a leaf is dangling from a piece of web coming down off a tree. What purpose/s does this serve for the spider? Is it some sort of mechanism for the spider to determine the wind / disturbances in that region?
I've seen a suggestion that it's to help act as a plumb during web construction to keep part of it tight, but do we actually know for sure?
Here's a national geographic image showing what I mean:

http://ngm.nationalgeographic.com/ngm/photo-contest/2012/entries/177963/view/

I would think that these leave simply got caught by the net.

It's attached to a single piece of thread, dangling about 5ft from the ground.

Could the spider have used the leaf as support for the web while it was still attached the tree, then the leaf fell off the tree and still hung on the web?

@user137 interesting idea, and would explain why I only see it in autumn. It wouldn't have to necessarily be part of the web for this to be viable.

I've also come to reason that spiders use web to move from leaf to leaf, so it may just be a leaf that's had web shot onto it by the spider and was attached to a more permanent part of the tree.

As far as I know, it has a practical effect. Spiders hunt for small insect and don't like when bigger animals damage their webs. So that they make the web visible for mammals, but in the way which doesn't prevent the prey from being caught.
I don't have reference for this, my colleague (entomologist) told me so.

I like this thought.  It's like the owl decals we put on windows to keep the birds from banging their heads on the glass.  I, for one, won't walk into a web I know is there.

It would be good to have a reference for this claim or to clarify that this is just a guess.

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Would oxygen levels be stable without photosynthesis?
I learned how the CO$_2$ cycle works in several biology classes, high school, elementary school, geology, and physics. Then today there was an article published in the NY Times claiming:

...it is a myth that photosynthesis controls the amount of oxygen in the atmosphere. Even if all photosynthesis on the planet were shut down, the atmosphere's oxygen content would change by less than 1 percent.

I'm really confused. If the earth naturally has 20% oxygen in the absence of photosynthisis, why did it spike durring Great Oxygenation Event? I reread that several times. There's no citation; no further context that can explain this. If this were coming from the climate change denier camp, I'd just shrug it off, but the credentials would say otherwise. It's in the NY Times and Nadine Unger is an atmospheric chemist at Yale.
My guess is that this is simply a misleading paragraph with a grain of truth. The question is, where is that grain? How long would the atmospheric oxygen content remain at within 1% of the current level if we turned off photosynthesis?

The answer to your question is in the first graph of the Wikipedia article you linked to: Great Oxygenation Event. In that graph, where time is measures in billions of years, you see that O2, as it was produced, was absorbed in oceans, seabed rock, land surfaces, and finally, about .85 billion years ago, O2 sinks filled and the gas accumulated in the atmosphere.[1] The spike you speak of was probably due to

the evolution of the large vascular land plants that brought about increased O2 production and increased O2 levels due to the enhanced global burial of microbially resistant, lignin-rich organic matter during the Permo–Carboniferous (Berner 2004).

More simply put, there hadn't been equilibrium established yet between the amount of oxygen being produced, the stabilization of the ocean layers and the 'burial of excess carbon' in the deepest ocean layers. Most of the O2 on earth was produced many millions of years ago; it is a myth that the O2 we breathe today is the same O2 made by, say, ocean phytoplankton yesterday.
Nadene Unger states in the NYT article that

[I]t is a myth that photosynthesis controls the amount of oxygen in the atmosphere. Even if all photosynthesis on the planet were shut down, the atmosphere’s oxygen content would change by less than 1 percent.

This is because there are tremendous oxygen sinks that store oxygen gas, such as the surface layers of the ocean. As O2 is used, the ocean would give up free O2. Because of these sinks, some estimate that

if photosynthesis were to cease, atmospheric oxygen would be depleted in 5000 years due to respiration, weathering, and combustion.[2]

while others state that

If photosynthesis were for some reason to stop, oxidation of the entire organic carbon reservoir would consume less than 1% of O2 presently in the atmosphere and there would be no further O2 loss (since there would be no organic carbon left to be oxidized). Conversely, if respiration and decay were to stop, conversion of all atmospheric CO2 to O2 by photosynthesis would increase O2 levels by only 0.2%.[3]

It is very hard to get a comprehensive answer of what would happen exactly. Do we assume all vegetation/phytoplankton suddenly disappears, or does it die (thus increasing to the carbon drain on O2)? Do we assume quick quick death of animals based on lack of vegetation/plankton, etc. as food, or would it be slower? As I said, a comprehensive answer is difficult to find. In any case, the atmospheric O2 would not fluctuate wildly in any immediate fashion.
[1] The oxygenation of the atmosphere and oceans Heinrich D Holland, Phil. Trans. R. Soc., 29 June 2006
[2] The Global Oxygen Cycle
[3] Introduction to Atmospheric Chemistry

So basically Unger's claim is based around the ideas in third reference (The last link is worth a read): carbon is the limiting reagent in the C + O2 -> CO2 reaction? My gut reaction is that in the absence of photosynthesis we don't live in a bistable system: we'd eventually return to the state from billions of years ago. But I can believe that initially there would be very little change.

Also, maybe worth clarifying what "the entire organic carbon reservoir" is referring to. I'm assuming it means all life on earth, plus all fossil fuels we could conceivably dig up.

@Shep, yes, I believe you're right. In other times, other things also needed O2, like iron, etc. but now, it's mostly carbon.


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Vitamins that could help "make us smarter"?
I was at Sprouts health store and saw a lot of vitamins/herbs that claimed to be "Study Aids" etc, so if there is any basis to it, where exactly does it hold truth? And are these supplements safe?

Can you show what effort you have made in answering the question yourself?  If you need help with something to google, try "herbal cognitive enhancers"

Are there vitamins that make us smarter?
Vitamins are micronutrients required in small quantities for normal human metabolism. Extra high (supra-physiological) doses do not generally result in improved performance. Of course, if one is deficient in certain vitamins (e.g. Vit B-1 deficiency causing Wernicke-Korsakoff encephalopathy), taking a vitamin can restore normal function. However, with adequate access to a normal diet, you are unlikely to be deficient. Commonly cited exceptions include:

strict vegans (Vit B12)
alcoholics (thiamine (B1), folate)
cultures highly dependent on maize as a staple (niacin (B3))

In people with a normal diet, taking additional vitamin supplements is usually not helpful.* (An exception may be Vitamin D depending on whom you talk to, but this is unrelated to cognitive performance.)
There have been scattered studies showing some benefit of various plant extracts and other “natural” substances. Studies such as this one about Bacopa monniera do demonstrate benefit. However, many such studies are of limited value due to sponsorship by the makers of supplements and publication in journals with questionable quality of peer review. This meta-analysis reviewing the effects of phosphatidylserine, phosphatidylcholine, citicoline, piracetam, vinpocetine, acetyl-L-carnitine, and antioxidants reached a more guarded conclusion:

for most of the "brain-specific" nutrients we review, some mildly suggestive effects have been found in preliminary controlled studies

Note that most of the substances discussed thus far are not vitamins but rather amino acids, more complex plant extracts, or — in the case of caffeine — a synthetic crystalline xanthine alkaloid. These sorts of things are commonly included in supplements found at health stores. As for vitamins specifically, this large randomized controlled trial found no effect of multivitamin and mineral supplementation on cognitive function.
What component of Cognitive Supplements are active?
The answer is usually caffeine. Caffeine is cheap, widely available, and markedly improves short-term cognitive and physical performance. By modulating adenosine activity in the central nervous system, it improves alertness, prevents impairment in neuro-plasticity associated with sleep deprivation, potentiates synaptic transmission in animal models, and may slow neurodegeneration in certain disease states.
This review article looked at ”enhancement supplements” containing taurine, guaraná, ginseng, glucuronolactone, B-vitamins, and other compounds  as well as caffeine and concluded:

there is an overwhelming lack of evidence to substantiate claims that components of [energy supplement drinks], other than caffeine, contribute to the enhancement of physical or cognitive performance.

To your question,

Are these supplements safe?

You should look at the ingredients. If it is caffeine, the answer is: usually. However, it is not recommended for those with insomnia, anxiety, palpitations, or who are underweight. As for other components of these, you need to read the label and do your research. As mentioned in the footnote, vitamins themselves are not without the possibility of harm at supra-physiological doses. For other components the danger is likely uncertain and under-researched.

*For those interested in the vitriol around this subject, check out this series of editorials that followed the paper linked above. Quoting the first of these:

 In conclusion, β-carotene, vitamin E, and possibly high doses of vitamin A supplements are harmful. Other antioxidants, folic acid and B vitamins, and multivitamin and mineral supplements are ineffective for preventing mortality or morbidity due to major chronic diseases. Although available evidence does not rule out small benefits or harms or large benefits or harms in a small subgroup of the population, we believe that the case is closed— supplementing the diet of well-nourished adults with (most) mineral or vitamin supplements has no clear benefit and might even be harmful. These vitamins should not be used for chronic disease prevention. Enough is enough.


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Why don't we develop immunity against common cold?
We all suffer from common cold, and that, frequently. Why have we not developed immunity against it till now? By immunity I mean immunity as a species.

The short answer is we do, it's just that there are so many different causes to common cold.  A slightly longer and more complete answer will note that while we know immunodominate epitopes for the 100s of rhinovirus serotypes, we are still researching why viruses like RSV are not immunogenic (my bet is on NS1, possibly NS2 proteins).  If no one has put up a good answer by 2100ish EST, I should be back on then to post one.

What kind of immunity are you talking about? Immunity as a species? Immunizations? Can you clarify?

Long lasting immunity is obtained by means of the adaptive immune system, and mainly involves the development of antibodies that identify specific parts (epitopes) of the pathogen's proteins. Common cold is typically caused by a type of virus called rhinovirus. Viruses have very high mutation rates, which alter the sequence of the virus proteins, modifying their antigenic properties. This consequently alters the ability of antibodies to recognize a particular antigen.
In other words, we do develop long lasting immunity against the virus that causes us a cold today, but the virus that causes us a cold a few months later is somewhat different, and the adaptive immune system has to start from scratch.

Why do viruses have high mutation rates? Because thay divide so fast?

@kinshukkashyap it is because the higher error rate in the genome replicating enzymes. For example, retroviruses use reverse transcriptase that has high error rates (due to lack of proofreading).

@kinshukkashyap, but, it is also connected to faster replication times. If you divide very fast and can produce a large amounts of copies (offspring) then you can accept higher replication errors that may render some of the copies useless, but may lead to some advantage to some other copies (e.g. drug resistance).

@ddiez I'm not sure if mutation rates are the most important factor here, as forward genetic experiments with HRV don't show the virus changing serotypes often.

@AtlLED, could you provide reference for that experiment? Indeed, there are several mechanisms for immune evasion. Serotype changing is one of them. In viruses there is also antigenic drift (caused by mutations) and shift (caused by exchange of sequences between viral strains), Ref Janeway's Immunobiology 5th edition. It has been postulated that HRV uses antigenic drif/shift but cannot find references demonstrating that!

@ddiez sure I'll take a look.  I know from personal experience, but I see what I can find in a lit review.  You certainly can get monoclonal antibody escape variants, but we saw more genetic stability than expected with HRV16 and HRV44 so we never pursued it for a paper.  I know off the top of my head of examples that indicate reinfection is of separate serotypes. I'm not postulating that there isn't genetic drift in HRV.

@AtlLED At any rate, my response to the original question is obviously a very simplified one! I appreciate your comments and insight into this interesting topic. Thank you for the example. I am interested in asthma and other complex respiratory diseases so I will read it with interest.

First, I want to note that ddiez has a good answer, but I thought this was good question to have a more expanded answer on immunology and pathogenesis.
The First thing we need to establish what is a "cold".
The most common cold is rhinovirus (HRV), but the second place holder is a little harder to define.  For example, respiratory syncytial virus (RSV) has been shown to be nearly ubiquitous by age two.  I actually disagree with the Wiki article on the common cold which puts coronaviruses (plural, which is not clear in the article) in second place.  For example, if you take look at sessional reports from hospitals, you can find that RSV and influenza are the more common.  Now this does select for those who were sick enough to seek hospital treatment, but if you look at a recent more in-depth study conducted through health clinics, you will again find coronavirus in much lower showing:

[Editorial note, if someone wants to take the time to MathJax that table in, please go ahead.  It seemed too large to insert the table as text. Here’s the original.]
Thus, a cold is an infection from any of the above viruses, with a common cold likely being HRV or RSV.  But how the body reacts to each of those is different.
Secondly, how do we mount an immune response to a cold?
There are two different kinds of immune responses in humans: innate or adaptive (to not get to technical, you can come up with responses outside of these).  Both responses are excitingly complex, and needed to fight a cold.  The innate immune system is designed to handle the initial reactions to the pathogens, but often the adaptive immune system is what "clears" (viral clearance being the removal of the infection) the infection totally.  In a novel infection, the adaptive immune system takes a few days to ramp up, which is why a cold can last for a few days to two weeks. This is when you get B-cells producing enough antibody to clear the infection.  Then the next time you are infected by something of the same serotype you will have a reservoir of cells already primed to make an immune response, and it will happen quicker.  At least that is what the human body is trying to do.  Viruses are trying to "evade" the immune system and proliferate (acknowledging of course that is a personification of viruses, and that they are not "trying" to do anything).
The key word in the adaptive response is "novel."  If the pathogen is different enough, that is the epitopes are different enough, then the immune system won't recognize it.  This is the principal strategy used by HRV.  Depending on who you ask there are between 96-120 serotypes of HRV, so using a number of about 100 seems reasonable (120 is a much more recent number and the increase has largely correlated with better diagnostic tools).  There don't seem to be additional stereotypes developing/mutating quickly (though conceivably they could), so as opposed to being infected by a mutated version of the cold you had last year, you're getting a different strain/serotype that was already in circulation.  Thus if you got a different HRV infection once a year, you have about 100 years of rihno viruses colds (when you actually get that old you have senescence problems in the immune system).
RSV is a different story.  You don't mount a lasting immune response to the virus in the first place:
 (Table 10.6.  Fields Virology; 6th Edition.  LWW 2013)
In fact, I know a researcher who would infect his lab members with the exact same strain of RSV every 6 months for years (before people would stop such a thing...).  Why RSV doesn't elicit lasting immunity--and in fact notably shorter immunity--is the subject of current research.
As you can see in Table 10.6, mucsal responses are generally not as long lasting as systemic infections.  This can make sense from a macro view—the mucus successfully prevented the pathogen from spreading to the rest of the tissues in the body, so it's not as critical to respond to.  On a more specific level we know that more IgA is produced and the cytokines can be different.  But RSV seems specifically reduced. One leading idea is that two of the proteins produced by the virus, NS1 and NS2, cause an immune response to not be properly mounted.  In other words, the virus is making materials that deliberately interfere with adaptive immune response.  An interesting paper that just came out addresses this idea for a possible vaccine candidate.

This should be the accepted answer.


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What are the application areas of Pattern formation studies specific to biology?
I was reading about reaction-diffusion processes, morphogenesis concept by Alan Turing and works of Murray in describing pattern formation on animals etc. But one question which came to my mind was even if we describe these processes in mathematical and physical contexts, are there any application areas awaiting for the results?

What do you mean "awaiting for the results?" Do you mean, are there unsolved problems in pattern formation that would have implications for biology, if the answer was known?

Yes. Specifically can such advancements help in any area like repairing an organ or so?

Ok, I'm not quite sure if we are at the repairing an organ phase, but here are a few interesting examples:
1. Philip Maini at Oxford has used pattern formation to give insight into jaguar patterning: Paper. He also has a book chapter Pattern formation and wound healing that could of of interest, although I'm not sure if this is a direct application as much as a heuristic understanding of how wound healing happens.

From the biomedical side, Michael Levin at Tufts is doing amazing work in regenerative medicine, and a lot of what he does is inspired by pattern formation as well, although I am not sure if it explicitly uses the theory - his papers.
This paper is one of my favorite from Ron Weiss - engineered pattern formation. Will most likely have important biomedical applications some day, although not currently.

It is quite interesting to know this. Tissue engineering, biomaterial fabrication and
biosensing.


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How does isopropyl alcohol disinfect less in higher concentration?
Isopropyl alcohol (2-propanol) can be used as disinfectant.
For increasing concentration of it in water, the effect as disinfectant increases, and then decreases again.
Typical concentrations for use as disinfectant seem to be 60-75% isopropyl alcohol in water.
Wikipedia: Isopropyl alcohol - Medical mentions membrane pores of bacteria that will not open without water.
That does not feel like the full explanation to me; I expect there are bacteria with membrane pores of diverse kind.
Does 100% isopropyl alcohol not disinfect at all - or just more slowly? What abour the effect on other pathogens?

The main reason why alcohols (isopropanol and ethanol mostly) can be used as disinfectants is that they denature (bacterial) proteins. This is also the reason why they work on such a broad spectrum of microorganisms (bacteria, fungi, viruses), but not on spores, as these are better protected.
The higher the concentration of the alcohol is, the faster this denaturation is happening. And this can cause problems: When you denature the proteins of the bacterial cell wall, they will form some kind of protective layer around some of the cells which allows their survival. Diluting the alcohols makes the disinfection happening slower and thus gives the alcohols more time to get into the cell.
For more information about concentrations and also for a ton of references, have a look into the CDC's disinfection guidelines in the subchapter on alcohols.
More details can be found in this review:

Antiseptics and Disinfectants: Activity, Action, and Resistance

So this is a good question.
70% is optimal for most cell types, especially those with a cell wall like prokaryotes.
Wikipedia is a little off here. The reason you add water is to make the solution hypotonic.
The alcohol disrupts the hydrophobic forces holding the phospholipids of the membrane while dehydrating any peptidogylcan of the wall enough to cause it to become less fluid/more brittle.
Now that you have essentially made the protection of the cell like brittle glass, the hypotonicity causes the cell to swell and now easily burst.
Bacteria aren't going to last long in 100% either. They fix instead, which although irreversible takes a little longer to occur.
It's also a little more economical and less wasteful to use 70% if it's just as, if not a little more, effective

Can you please add some references?

The sentence "They fix instead..." - it that related to nitrogen fixation? I don't understand that part.

Or do they just get immobile with no way to recover?

@VolkerSiegel Fixation in this context is referring to histological fixation, which can actually be one of several chemical processes. This Wikipedia page is a good starting place.


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Why does botulinum toxin seem to be more dangerous to humans than to other mammals?
Various mammals seem to get away with eating parts of carcasses that we would prefer to not even touch, and that we assume will make us sick.
Because of that, I assume botulinum toxin is more dangerous to humans than many animals.
Is that right so far - can they handle more of some toxins compared to us?
Or are they better in avoiding harmful substances based on more suited olfactory sense?
Or are we just more afraid?
Assuming the differences exist - what is the cause for it?
Are there plausible explanations in terms of evolutionary pressure?

How do you come to the conclusion that is is more dangerous for us? Botulinus is a strict anaerobic bacteria, so you will not likely find it on relatively fresh carcasses.

Humans have a tendency to can things and put food in jars, which is more or less a recipe for botulism. Vultures have a huge list of fascinating adaptations for eating rotting carcasses but that's an answer for a different question.

@Chris Yeah, I was not that sure with it - that's why I called it assumption. So part of it is the "Or are we just more afraid?"... And right, the vultures deserve a separate question!

@JeremyKemball makes sense, the fact that most other animals never tried to keep a carcasse until next summer seems to be important, worth making it answer.

It's an interesting question other than your assumption about botulinum toxin, which is incorrect and seemingly irrelevant. Perhaps you should remove it. http://www.sciencedirect.com/science/article/pii/S0300908400002169?via=ihub#TABI

From a food safety point of view, you don't get botulism from "carcasses" (meat). Common botulism vectors are plants, especially the parts growing around dirt (making homemade garlic oil is a really bad idea), and honey (a danger to infants, adults can stomach the spores and they can't form a colony of living bacteria in honey). So, if there are animals which come frequently into contact with botulism, they aren't vultures. Actually, I might have to write an answer about that...

Because of that, I assume botulinum toxin is more dangerous to humans than many animals.

Couldn't find too many examples but, there are some things to consider (according to [1]):

there are seven distinct types of toxin with variable action among animals
different dose / effect intensity ratio between toxin types
toxins A, B, E and F cause disease in humans
toxin C and D are more common to birds, cattle, horses

And here are some numbers:

cattle median lethal dose: 0.388 ng /kg [2] of C type toxin
mouse median lethal dose ( 12.88 times more than cattle): 5 ng/kg [2] of C type toxin
human median lethal dose: 1 ng/kg [1] of A type toxin

When it comes to carcasses toxicity, there are some papers to consider:

Smith GR, Turner A. Factors affecting the toxicity of rotting carcasses containing Clostridium botulinum type C. Epidemiol. Infect. 1987 Jun;98(3):345-51. PubMed PMID: 3297745. - Persistent toxicity at 20 and 37 degrees Celsius even for a long time. No toxicity at 16 degrees Celsius
Smith GR, Turner A, Till D. Factors affecting the toxicity of rotting carcasses containing Clostridium botulinum type E. Epidemiol. Infect. 1988 Jun;100(3):399-405. PubMed PMID: 3288491. - Maximal toxicity at 30 degrees Celsius that is lost in time.

are they better in avoiding harmful substances based on more suited olfactory sense?

Not if we are talking about nonproteolytic B, E and F type bacteria. Indeed, Clostridium botulinum, proteolytic type A, B and F types produce odor [3].

Or are we just more afraid?

I don't see how fear could (significantly) influence pharmacodynamics and pharmacokinetics of the toxin.

References:

CIDRAP - Center for Infectious Disease Research and Policy. Botulism. Available from http://www.cidrap.umn.edu/infectious-disease-topics/botulism
Moeller RB, Puschner B, Walker RL, Rocke T, Galey FD, Cullor JS, Ardans AA. Determination of the median toxic dose of type C botulinum toxin in lactating dairy cows. J. Vet. Diagn. Invest. 2003 Nov;15(6):523-6. PubMed PMID: 14667014.
P. Kendall. Botulism. Colorado State University Extension. Available from http://www.ext.colostate.edu/pubs/foodnut/09305.html

I think he means 'fear' in the sense that humans worry about botulism, and vultures apparently do not. Some explanations: vultures are less affected by botulinum toxin, vultures aren't exposed, and vultures just don't worry about things. Seems to be a blend of 2 and 3, but it's interesting to point out that in certain temperature/time windows carcasses might be poisonous to humans but not to vultures, due to differences in relative toxicity/toxin type. A faulty assumption is sometimes right.

You seem to not understand how botulism works. It is impossible for vultures (or anybody else) to get botulism from a carcass.
First, you have spores. They are ubiquitous in nature, and you have probably eaten lots of them. They are especially common on vegetables growing around/in dirt, like garlic. The spores are

indestructible when using common cooking methods
dormant under normal food storage conditions
not dangerous to humans above 1 year of age. They remain dormant in the human body and get excreted without causing anything.

Then, you have botulinum bacteria colonies. To get a colony going, you need to take some spores and cut off the oxygen supply. For example, storing raw garlic in oil provides both a possible contamination route and a perfect growth environment.
The bacteria themselves are
  - easy to kill off with heat
  - not prone to establishing a colony in your body.
The problem with the bacteria: Once there has been a colony, it starts producing the toxin. This toxin is very poisonous even in minute amounts, and stays around to harm you even after you have killed the bacteria which produced it (e.g. with acid). It is not especially heat stable, certainly not as stable as the spores.
So, the way you get botulism is:

Start out with food contaminated by the spores (meat is rarely such food, vegetables are more common. Of course, cross contamination in your kitchen is possible.)
Cut off all oxygen supply for some time. A colony forms.
Sterilizing the food by placing it in boiling water for some time doesn't matter, the spores will survive it easily. (This is why industrial food is canned at much higher temperatures, and safe home canning recipes are quite acidic).
eat the food after it has been stored with the colony inside.

So, vultures don't have any special resistance to botulism toxin, they just don't come in contact with it.
On a side note, there are quite a few other pathogens which are common in meat, and vultures are probably more resistant to them than humans. But it is normal for bacteria to be able to only make one species, or a small range of species sick. Just ask the poor medical researchers trying to heal human disease in mouse models - there are huge differences.


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What is this woodlouse doing?
I picked an apple from the ground, it was wet with dew and a woodlouse was stuck to it, with its back against the apple. When it got loose, it started flexing its "tail" like this for a while. Why?

That's a really nice little video.

It was moistening its respiratory and osmoregulatory organs:
Woodlice as all other terrestrial arthropods face the major challenge of preserving water balance. In their case the two systems that immediately suffer from desiccation are osmoregulation itself and respiration. In woodlice these two functions are carried out mostly by the pleopods: modified leaf-like appendages on the ventral side of the hind body part ("tail") (see here and here some annotated photos and drawings of ventral side of woodlice).
To maintain these structures in moist state woodlice have a number of adaptations, one of them being the ability to "pick up water from external sources via uropodal dipping, with the water moving upwards by capillarity" (see here). Uropods are the tiny rod-like appendages on the tip of the "tail", and dipping of the uropods is exactly what you were observing.


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Can two Hfr strains of E. coli conjugate?
Genetics textbooks (and some internet searching) yield abundant examples of Hfr strains conjugating with F- cells, but these sources are surprisingly silent regarding the results of an Hfr encountering another Hfr strain. Will conjugation occur in both directions, or will it not occur at all? Similarly, can F+ cells conjugate with other F+ cells?


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Mutation-drift equilibrium and among loci variance in heterozygosity
At mutation-drift balance, the increased heterozygosity brought by new mutations is exactly equal to the loss of heterozygosity due to genetic drift. At equilibrium, the expected heterozygosity for a given locus is:
$$\hat h = \frac{4Nu}{1+4Nu}$$
The expected heterozygosity is only the first moment of the whole distribution of locus specific heterozygosity. What is the (among loci) variance in heterozygosity?

In The Distribution of Gene Frequencies in Populations, Sewall Wrights derivates a continuous approximation to the probability distribution for the frequency of an allele in a panmictic population under the pressure of drift and mutation on a bi-allelic locus. In his paper, he reports several version of the same equation. Below is one of them, where $\phi(q)$ is the probability density of the one specified allele to be at frequency $q$.
$$\phi(q) = C q^{4N\nu -1}(1-q)^{4N\mu -1}$$
, where $C=\frac{\Gamma(4N\mu+4N\nu)}{\Gamma (4N\mu) \cdot \Gamma (4N\nu)}$ is a constant, $\mu$ and $\nu$ and the forward and backward mutation rate The heterozygosity is then a simple one-to-one function of the allele frequency.


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How does Pothos grow in only water?
The popular potted plant, Pothos aureus (or Epipremnum aureum) is happy to grow in a jar, with only water, for years. How is this possible when other plants need at least Nitrogen, Phosphorus and Potassium?

Pothos needs those nutrients as well, but they are more tolerant of poor nutrition than most plants, therefore rendering them better houseplants (most people don't fertilize their plants properly). But with no nutrients, the plant will begin to fade. A good hydroculture system includes a nutrient solution, to keep the plant fed, and an aerator, to add oxygen to the root zone.

"Tolerant" is an understatement... the plant is putting on mass for years, without those nutrients at all.  How is this possible?

This is a good question but unfortunately you are making the false assumption that the water has no nutrients in it. Pothos probably is simply very efficient at extracting these nutrients from water.

It is not possible, that a plant grows without any nutrients. Magnesium for example is needed in every chlorophyll, so there is no photosynthesis without magnesium. Another point is that plants can not get nitrogen from the air, so they have to get it from the soil and nitrogen is present in every amino acid, which build the plants proteins. Proteins are essential for every living organism. This are only two points and there are many many others why every plant needs nutrients like nitrogen phophorus, magnesium...
If it seems that Epipremnum aureum does only need water, maybe the plant gets its nutrients from a place you don't expect. Maybe the water is contaminated. Are there leafs falling into the water for example? Another possibility could be that Epipremnum aureum stored a lot of nutrients before it got only water but this won't last for ever.
I read your comment, thats why i think the nutrients have to come from the water. Additionally I found this publication about Calcium Deficiency Symptoms of Epipremnum aureum
I think you know that tap water or rain water isn't pure H2O. We just measured the tap water in Cologne, by ICP-MS. This is no official measurement, and we measured only once but I think its nice to see whats else in tap water.     Unfortunately we couldn't measure nitrogen, because normally the machine is used for plant extracts and there would be to much nitrogen.

Maybe your Epipremnum aureum gets enough nutrients from the water, I don't know if this is possible and how often you change the water.
Your pot could also be a source for nutrients if its not sealed up.
In conclusion the answer is that in general it is not possible, that your plant grows without nutrients. So there is a source which can be only detected by yourself, because you know the exact conditions under which your plant grows. I hope I could give you some hints.

Tap water does contain a significant amount of metal ions in solution, and this applies to all water sources (rainwater, groundwater) with the exception of ultrapure (eg distilled or reverse osmosis water).
For example, the official analysis of the NYC water supply in 2015 shows that there are significant quantities of nitrogen, phosphorus and potassium in the tap water samples taken.

In short, pothos does in fact require minerals to grow, and these minerals are provided by the water.

I owned a commercial soil/plant/water testing laboratory for 28 years, and have written 3 books on Tropical Foliage Plants, including Epipremnum (pothos). There are likely a lot more minerals in your water in that vase than you think there are, enough obviously to keep the plant alive and to some extent growing for years. I find nothing wrong in this  answer. You will find small amounts of nitrates, sulfates, calcium, magnesium, boron and several other plant nutrients in most tap and well waters. My reference is 35 years of analyzing water samples; also refer to the book Groundwater and Wells.


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Is there an association between environmental and mutational robustness?
The robustness of a genotype is the ability of this genotype to resist (always produce the same phenotype) to various parameters such as mutations and environment. The ability of a genotype to resist to mutations is called mutational robustness while the ability of a genotype to resist to varying environmental variables is called environmental robustness.
Is there a correlation between environmental and mutational robustness?
In other words the above question is: is there a among-species/populations/genotype correlation between mutational robustness and environmental robustness? i.e., Knowing that species $A$ has high mutational robustness, is species $A$ more or less likely than a randomly picked species $B$ to have a high environmental robustness? Or are the concepts of environmental and mutational robustness completely different and involve completely different genes and genetic architecture? Both theoretical and empirical studies that offer insights to this question are welcome.

Hansen (2006) says (middle of page 140):

A link between genetic and environmental robustness is plausible, because genetic en environmental disturbances may often affect the same functional pathways in the organism, and ny increase in the robustness of a pathway leads to both genetic and environmental canalization. Evidence for a correlation between environmental and genetic robustness has been fund in studies of RNA folding (Ancel & Fontana 2000), in the effects of heat-shock proteins (Stearns et al. 1995).

He also cites Rifkin et al. (2005) who also showed evidence for this correlation. Finally Hansen cites Dworkin (2005) who did not find this link.
Hansen does not cite any theoretical paper and does not offer clear arguments of why this link exist but it is the best I could find


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What do you see when your eyes are closed?
If you are in pitch black and you close your eyes, you sometimes can see strange shapes of various colors. A lot of the time these shapes and colors change as you observe them. This phenomenon still occurs if you are not in complete darkness.
I am wondering what this is that you are `seeing'? Is this phenomenon classified as seeing, as how can we be looking at something if our eyes are closed?
If you are not seeing these shapes and colors, then what you observe is pure darkness. What is this pure darkness that you are seeing? Since you are seeing it, is something stimulating the vision parts of your brain? Is it the back of your eyelid?

I'm not asking about floaters, although I have always wondered what those were.

I retracted my vote.

Floaters are different. That's due to collagen fibers in the vitreous "gunk" of the eye interrupting light transmission to the retina (shadowing, basically). Because this requires light hitting the retina, it's not in the category I described below. If you want more info, ask another question (although that one is eminently google-able).

I some times see what i call the theater. Its random images but it plays like a movie, but changes scenes every 15 seconds or so. Like right now, i'm seeing a bear in a meadow.

OK, I'm having a huge moment of confusion here... "sometimes" see strange shapes of various colors when you close your eyes ? Don't we always see such patterns (we just don't usually pay attention to them) when we close our eyes or have I just discovered I'm weird ?

This is called a phosphene — the experience of perceiving light in the visual cortex without light actually entering the eye. This commonly happens due to stimulation of the retinal ganglion cells by something else. The most frequent source in normal individuals is pressure to the retina (e.g. rubbing a closed eye.) It is also possible for phosphenes to occur due to neuronal stimulation at the cortical level. Most people have had the experience of “seeing stars” when you stand up too quickly. This happens because orthostatic hypotension results in transiently decreased cerebral perfusion; it is the metabolic shift in oxygenation and/or glucose delivery to cortical neurons that causes the perception of light. Something similar occurs with brief rises in intracranial pressure that occurs with sneezing or coughing.* Magnetic stimuli can also induce this phenomenon.
Phosphenes can also be pathologic (i.e. disease-associated). Migraine headache sufferers may experience a visual “aura” prior to a headache, which is a type of phosphene, likely mediated at the cortical level. There is some evidence to suggest that preventing the phosphene may also reduce headache frequency. Other conditions associated with phosphenes include abnormalities of the optic nerve** and retina — just as stimulation of a peripheral somatic sensory nerve might cause a pain signal to arrive in the brain in the absence of true tactile stimulation, disorders of the optic nerve can generate disorganized signals that the brain perceives as light.

*Increased intracranial pressure leads to decreased perfusion due to the differential between peripheral and cerebral pressures.

**If you read nothing else linked to this question, take a look at that paper (free in PMC). It describes optic neuropathy associated with auditory-evoked phosphenes. The patients perceived sound as light!

Thank you for the great answer. So in layman terms, is it correct to say that the same part of the brain that is activated when your eyes are open gets activated, in some way, when your eyes are closed. This part of the brain being activated is what causes you to 'see' those strange objects?

@JonHerman You got it! The visual cortex in the occipital lobe.

Interesting article on auditory-evoked phosphenes.  I've personally experienced unexpected loud sounds as flashes of light for years (though without any other associated visual issues like the subjects in the paper.)  I do have an epileptic focus in my temporal lobe, however, which perhaps is interacting with the LGN somehow, causing a similar symptom via a different mechanism.  In any case, fascinating read.

I just got another question. If there is nothing stimulating the visual cortex, but you put your attention on what you're seeing, you see pure darkness. What is this pure darkness, it has to be something because I can see it. Is it the back of the eyelid or something like that?

This phenomenon is also known as Prisoner's Cinema

@CoreyOgburn - good point. The pathologic form in optic neuropathy is at least in part due to de-afferentation (lack of normal incoming signals). I suppose the prolonged absence of any environmental light can have something like the same effect.

Retinal implants generate electrically evoked spots of light also called phosphenes. Some of them rely on light entering the eye, such as the alpha-IMS. Hence your definition of phosphene may not be entirely appropriate. Nitpicky. Great answer +1


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Why is green fur not a thing?
In most biomes on earth, and certainly in the most densely-populated, the best camouflage color or pattern for an animal would be a variant of green, so as to blend in with the leaves and grasses of the surrounding environment.  Whether predator or prey, the art of not being seen is hugely important in the natural world, and yet to the best of my knowledge there isn't a single mammal on the planet with fur that is even partially green.
Is there a reason for that?  It seems like animals have evolved some pretty crazy color patterns to break up their silhouette or blend into the background, but why haven't any mammals taken the obvious route of "look like leaves"?
Is it really THAT not-easy being green?

I don't know if this is related, but I've done enough computer graphics programming to know that brown is hard color to reproduce on a computer. It's a mixture of red and green. If animals don't have good color vision, they might not be able to tell the difference between red and green, and it all looks brown anyway, kind of like colorblind men. However, I don't know how many animals have this issue, I think lack of blue vision is more common than lack or red or green.

i wonder if its because small mammals started out as terrestrial - bound to the ground where green is not as much a color.  certainly birds can be green when they need to be.

But we clearly need it for the Green-beard effect

The technical answer is: Because the coloration of skin and hair is done by the two forms of melanin: Eumelanin, which is dark brown to black and Pheomelanin which is yellow to red. This enables colors from white (not pigmentation) to black (dense eumelanin pigmentation) and also colors in between by different ratios of the two pigments.
The evolutionary answer is that it obviously made no evolutionary advantage to have other colors. If you look closer at this, you will see that most habitats are not green or only for a part of the year. If you think about african plains, these are mostly brown, something like artic landscapes are only green for a very short timeframe in the summer, for the rest of the year these are white to brown. And even tropical rainforests are mostly dark to brown on the ground. They would clearly stick out of the environment with green colored hair.
For all these different habitats the animals living there have adapted their hair color. It is not uncommon for artic animals to change their hair color with the course of the year, dark to brown in the summer and white in the winter (artic foxes and snow hare) for example. Animals which live in deserts will have a paler color than those which live in dark colored mountain areas.
See this article for more information: "The Adaptive Significance of Coloration in Mammals"
Also interesting in this context is this article which looks at the reason for zebra stripes: "The function of zebra stripes"

Whoever downvoted me, can you please explain why? If there is criticism on my answer, it will be helpful to know about it, so I can improve the answer.

+1, I am not a biologist, but I would also expect a kind of an evolutionary baggage argument. Reptiles tend to be in similar habitats and grow to the same sizes in comparison to plants as many mammals, yet they developed chromatophores and mammals just melanocytes. It would also be interesting to understand bio/chemically why melanogenesis produces such a limited variety of colors.

I am not much into chromatophores, I know this only for zebrafish. There three different pigments are available, dark melanophores, blue xantophores and silvery iridophores. It doesn't happen there, but it is imaginable to combine blue and yellow (pheomelanin) to get green. Still it didn't happen evolutionary.

Just to add a different dimension to the answer from @Chris. Not all animal colouration is produced by melanin. A whole range of bright colours in insects, birds and reptiles comes under the heading of structural colouration, which basically involves having a repeating structure at the microscopic level to interact with light. This is the basis for macaw colours, peacock feathers, and some butterfly wing colours.
It also occurs in mammals - see for example the mandrill. In this case the coloured patches are bare skin containing ordered collagen fibres to create the effect, (science here). I have no idea if collagen could be structured to produce a green colour.
Finally, an anecdote: a number of years ago a polar bear in the San Diego zoo was seen to develop green patches. Upon investigation this was found to be due to damaged hair shafts in areas where the animal rubbed against surfaces in its enclosure. In the polar bear the hair shafts are hollow, for insulation, and the damaged hairs were being colonised by algae. So you could imagine a green mammal could evolve by using this effect.

That algae colonize the sloth happens quite regulary. But I would see this under the pigmentory aspect. See here for details.

I would be surprised if collagen structures could make red and blue but not green, as green is between the two in wavelength. I had no idea mammals did structural colouration.

Polar bears have hollow hair shafts? Forget alpaca and mink, I want to knit polar bear yarn!

Tropical tree-dwelling sloths often have green fur, the pigments due to possibly symbiotic algae; see this.

A dimension not explored by the other (excellent) answers has to do with color perception under trees. Leaves are green while on the tree, which tends to make mostly green light available to the understory.
Viewed under green light, a green-furred animal would appear bright green, roughly the same as a white creature viewed under green light. A red or brown creature would appear grey-brown or black, and reflect much less light.
Orangutans apparently do this for camouflage, according to this book I haven't read:

Russon, Anne E.  2000.  Orangutans:  wizards of the rain forest.  Firefly Books, Buffalo, New York, USA.

which I was told about by these guys. It's not the first place I've heard this factoid, but it does make first-pass sense.
There is a difference between looking the same as a background of green leaves under sunlight and looking the same as a background of tree trunks or leaf litter under a greenish light.

Very good point.


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TV's so loud when I turn over
Scenario: I'm about to fall asleep with the T.V. on. Having completely forgotten that it was, no longer even hearing it, just before falling asleep I turn over with a 'fresh' ear and it's blaring. If I roll back over it will be noticeable, but quiet again. Waking hours my ears are fine, no worries. Is this some weird sleep induced brain shut-down going on?

I've noticed a similar thing. I think your ear adapts to the sound level it is being hit with, so when you turn over, the ear that was used to hearing absolutely nothing comes up, adapted to find the weakest signals. You can do something similar with your eyes. Cover one for a few minutes, then open it and close the other. The room will seem quite bright. Or, look through a cardboard paper towel tube with one eye for a while. The view through the tube will get much brighter, as that eye is being hit with considerably less light.


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Which factors may affect a choice of an oviposition place in nocturnal moths?
Winter Moth (Operophtera brumata) is a small brachypterous (females have stunned wings - unable to fly) moth which places eggs on thick branches.
I would like to know which abiotic and biotic factors may play a role in selection of place for oviposition. Taking into account that level of humidity is probably the same on whole tree (and probably whole forest) and the branches are so thick that they are not distinguishionable from surrounding environment (and there is no accumulated heat to identify their orientation (south, north etc.)
What other factors may play a role?

The winter moth's preferred host plants are mainly deciduous trees, oak being the main food plant and also many fruit trees, birch and hazel. Females generally deposit eggs in bark crevices, under bark scales, bark snags and under lichen along tree trunks of host species. Eggs are initially small and green but gradually change colour to orange and then red before hatching (reference 1 and reference 2).
Though the oak is preferred,

There does not seem to be much discrimination in selection of host
  plant or oviposition site by the female (Wint 1983), as the choice of
  larval food plant depends on the female's pupation site and the
  direction she takes on emerging, as she just climbs up the nearest
  tree. So it might be fair to say that the larvae contribute more to
  host plant choice than the adults, as the larvae can balloon if the
  host plant is unsuitable. However there is the possibility that year
  after year each generation of females will climb up the same tree as
  their mother, and oaks (one of the most common host plants) can be
  hundreds of years old, so there could have been hundreds of
  generations of winter moth on the same tree (reference).

So that in effect means, that the thickness of branches or being indistinguishable should not be a factor. Regarding abiotic and biotic condition, the main abiotic conditions are precipitation, temperature and photoperiod.
An increase in temperature leads to more activity and a faster metabolism (reference) Since leaf buds open faster, there is a chance for eggs to be laid faster according because the larva needs to burrow into the buds before the leaf opens (bud-burst) Hatching is temperature dependant but I do not think that it effects the number of eggs much. Biotic factors like the presence of parasitic predators reduce population but does not seem to reduce the number of eggs.. (reference)


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How many humans have been in my lineage? Is it almost the same for every human currently living?
If I were to count my father, my grandfather, my great-grandfather, and so on up till, say chimps, or the most common ancestor, or whatever that suits the more accurate answer, how many humans would there have been in my direct lineage?
And would it be almost the same for every human being currently living?

Closely related question: Initial population when i count backwards?

Note that when pedigrees collapse, there are not necessarily the same number of generations on each leg. So even for an individual there isn't a single number which is "the number of generations back to the last human/chimp common ancestor" since the number depends which route you take, although you could for example take the minimum. Consider for example Prince William (Windsor) whose parents were 7th cousins once removed (http://users.uniserve.com/~canyon/ancestor.htm) as well as other relationships. This isn't specifically aristocratic inbreeding, they're just better at keeping records :-)

@SteveJessop: I think when you only consider male ancestors, there's only one route, which bypasses that issue

@MooingDuck Whether you consider female ancestors or not is irrelevant if you are looking for a common ancestor, because the amount of time between each generation differs at each link in the chain.  Hence the "once removed" part can occur where these differences added up to a whole generation.

@Michael: Ah right.  I was pointing out that each person only has a single chain, thus pedigree collapse and "depends on which route you take" are incorrect.  However, you raise a good point that not all people's chains are the same length.

A quick back-of-the-envelope answer to the number of generations that have passed since the estimated human-chimp split would be to divide the the split, approximately 7 million years ago (Langergraber et al. 2012), by the human generation time. The human generation time can be tricky to estimate, but 20 years is often used. However, the average number is likely to be higher. Research has shown that the great apes (chimps, gorilla, orangutan) have generation times comparatble to humans, in the range of 18-29 years (Langergraber et al. 2012).
Using 7 million years and 20 years yields an estimated 350000 ancestral generations for each living human. A more conservative estimate, using an average generation time of 28, would result in 250000 generations. However, some have argued that the human-chimp split is closer to 13 million years old, which would mean that approximately 650000 generations have passed (using a generation time of 20 years).
The exact number of ancestral generations for each human will naturally differ a bit, and some populations might have higher or lower numbers on average due to chance events or historical reasons (colonizations patterns etc). However, due to the law of large numbers my guess would be that discrepancies are likely to have averaged out. In any case, the current estimates of the human-chimp split and average historical generation times are so uncertain, so that they will swamp any other effects when trying to calculate the number of ancestoral generations.
However, this is only answering the number of ancestral generations. The number of ancestors in your full pedigree is something completely different. Since every ancestor has 2 parents, the number of ancestors will grow exponentially. Theoretically, the full pedigree of ancestors can be calculated using:
$$N_\text{ancestors} = \sum_{i=1}^t 2^i \hspace{1em} \text{or} \hspace{1em} 2^{t+1}-2$$
where t is the number of generations. However, this will yield an unreasonably large number of ancestors (~$2.3*10^{105}$ over just 350 generations), since it assumes that all of your ancestors are unrelated. Basically, you run into something called pedigree collapse, which means that your pedigree will have many overlaps (due to inbreeding, overlapping generations etc), so all of your ancestors cannot be seen as unrelated. In practice, this means that the number of ancestors in successive generations will stop doubling for each generation you go back, and will eventually start shrinking, which will drastically reduce the number of unique ancestors. For more on this, see answers to the question Initial population when i count backwards?. That question is basically asking about the same issue, but less specifically. There might be studies that have tried to calculate the average number of ancestors to living humans, but I haven't seen any. Therefore, I cannot say anything more specific about the average number of unique ancestors for a living human individual.

This estimation is the number of generations, not ancestors. Ancestors should double after every generation, since a human has a father and a mother. Thus, the number of ancestors in 350000 generations should be 350000^2 = 122500 million humans. (Sorry, deleted previous comment for it being not really precise. My mistake there)

I have a question about this answer. I know the OP specified males, but... (if it were only male lineage) wouldn't it look more like a tree with the single trunk pointing to him, since he has two grandfathers, and they each have two grandfathers, so 2 + 4 + 8 + 16 + 32 + 64... for x generations of grandfathers?

@ederbf As I've added, I read the Q as asking for the number of "direct" ancestors. I agree that the full pedigree is something completely different, and have added a section on this, with a link to a related Q asking specifically about the full family tree.

@ederbf Doubeling in every generation is 2^350000, not 350000^2.  Exponetial, not polynomial.  So the actual number would have been about 10^115000 - Except for the pedigree collapse that fileunderwater describes.

@Taemyr, That is true. I rushed too much writing, editing and such...

Did a major rewrite of my answer, since I'm unclear about exactly what the poster is asking (full family tree, "direct" ancestors etc). This is not a full answer, but could work as a starting point.

I would argue that the total number of ancestors would vary significantly between people, due to your last point about how pedigree tend to overlap over time.  decreases in pedigree due to shared ancestors.  To give an extreme example imagine someone who's parent's were brother and sister.  They have only 2 grandparents instead of the standard 4, their total number of ancestors is in theory half that of someone produced from a non incesterous relationship.  That also implies people from areas with smaller breeding pools, like island nations, japan etc, would have fewer ancestors.

Everyone on earth shares a single most common recent ancestor around 3500 years ago (source), and given the vast depth of time between this ancestor and the human/chimp split it seems reasonable to assume that the number of ancestors derived via this route vastly outweighs all other ancestors so it makes sense to conclude that the difference in number of ancestors between people is a small proportion of the total number.
As for estimating how large that number is, I'm really not sure how you'd do it.

Are you claiming that two people from the native populations of Australia and South America share a common ancestor 3500 years ago?

@JackAidley: http://en.wikipedia.org/wiki/Most_recent_common_ancestor "the human MRCA may have lived 2,000 to 4,000 years ago. This estimate is based on a non-genetic, mathematical model that assumes random mating and does not take into account important aspects of human population substructure such as assortative mating and historical geographical constraints on interbreeding."

@MooingDuck: Perhaps you'd like to read the link I gave.

@Joe: It's not my claim. It's the number given in the primary literature source I linked to. Other estimates exist but even then they only push it back to around 8000 years ago, still a small period of time in comparison to the time since the human/chimp split.

The link you gave says almost exactly the same thing, that their model "ignores essential aspects of population substructure, such as ... the relative isolation of geographically separated groups."

@Joe: It's a model. Any model will be, by it's nature, limited. The limitations are discussed in the paper, as is there potential impacts on the resulting number.

@Joe: You misread the abstract.  "the random mating model ignores essential aspects like...geographically separated groups.  Here we show that recent common ancestors also emerge from two models incorporating substantial population substructure." http://www.nature.com/nature/journal/v431/n7008/fig_tab/nature02842_ft.html shows that they do indeed take into account geographic seperation and migration.

Another factor not mentioned is that the number of generations will be a range even when accurately calculated for one individual. If, for example, my dad's dad's dad's etc generation was 25 years on average and my mum's mum's mum's etc generation was 20 years then you don't have to go back very far to have for them to be different. In the example 100 years ago in my dad's side is 4 generations and on my mum's side it's 5 generations.

We could try to cut the answer out:

the Population Reference Bureau estimates that about 107 billion
people have ever lived
today's population is about 7.6 billion
only 0-14 of them which are in your direct linage (parents up to grand-grand parents) are alive
world population of year 1500, when exponential growth started, is estimated to about 425 million
(https://www.wolframalpha.com/input/?i=world+population+1500). This
is about 25 generations ago. Almost all of them are not your
ancestors (by integration you should get a number of about 20 billion
people which are NOT your ancestors, while about 500.000 are)
world population 8000 b.c. is estimated to about 5 million, and 10000 b.c. to about 1 million.
majority of people before 10000 b.c. might be your ancestors. This could well be more than 10 billion people (much insecurity and definition problems here)

.. which means, we "only" need an estimation of 10000 b.c. to 1500 a.c. After playing around with Excel, I believe, it should be in the ballpark of 1 billion.
hence my best estimate would be 11 billion (10 billion before 10000 b.c. and 1 billion after).

mixed people should have more ancestors. My bet is that Children of mixed Mexicans and Chinese have most ancestors.

at some point back in history, more than 2 children on average (per parent couple) go into your ancestor tree. This is why additions shrink further back in time.

billions of people died throughout mankind history without having siblings living today.


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Is the quality of sleep dependent on sleep duration?
I've been facing this lately, where I will wake up in the middle of the night after sleeping for perhaps 2-3 hours and be wide awake, but when I go back to sleep, I wake up more tired than before.
Can anyone shed some light on this?

Sleep duration certainly affects the quality of sleep, but it is nowhere near a simple correlation. It is just one of many factors, and these factors don't work in isolation. Statistically speaking, it's a multivariate model - and one which includes a differential equation, because the way sleep duration affects your sleep today depends on the sleep quality (and also the sleep duration) from yesterday. For example, if you go several day with too little sleep, but keeping firm going-to-bed and waking-up times, the ratio of your sleep phases changes significantly, giving you much more deep sleep. This is what compression therapy is based on.
And beyond that, the way you feel upon waking is also dependent on sleep quality in very complicated ways, and other factors (for example the synchronisation of the time at which you woke with your circadian cycle) play a much larger role than the sleep quality you got. Also, there are some unexpected effects, where getting too little sleep making you feel good - it's a kind of lightheaded, giddy state, somewhat comparable to having had a small glass of champagne.
So yes, there is a dependence, but you cannot expect that having had lots of sleep will make you feel good in the morning.

My experience that it depends on it. You sleep in cycles, each cycle has about a 90 min duration. I think the quality depends on how many cycles you ended. It seems like you need to sleep more by an interruption.

Sleep was recorded on 10 nights in each of seven older subjects (mean
  age 55) and nine younger normal subjects (mean age 22). The duration
  of the NREM-REM (non-rapid eye movement—rapid eye movement) sleep
  cycles was determined, starting from the onset of NREM sleep.
In the older group an intra-individual comparison was made between the
  mean duration of cycles interrupted by one period of spontaneous
  wakefulness, within their NREM part, and the duration of intact
  cycles. The interrupted cycles were found to be on average 20 min
  longer than the intact ones, despite the mean duration of intervening
  wakefulness being only 10 min.
In the younger group an intra-individual comparison was made between
  the mean duration of intact cycles ranked as containing a large amount
  of stages 3+4 and the mean duration of intact cycles ranked low for
  stages 3+4. Similar comparisons were made in respect of the amount of
  stage REM, and also the summed amount of stages 3+4 and REM. The
  cycles containing higher amounts of stages 3+4, REM, and of 3+4+REM
  were found to be on average 9, 18 and 18 min longer.
The effect of cycle content on cycle duration was most manifest for
  the first cycle, and least for the third cycle of the night.
The results demonstrate that whereas there may be an average cycle
  duration of about 90 min individual cycles are very variable. The
  contents of a cycle influence its duration, and the onset of the REM
  period is not a strictly time-locked phenomenon.

1974 - Sleep cycle content and sleep cycle duration

If you wake up in the middle of a cycle or if you are interrupted often, then you will be tired. I think what happens by sleeping is much more complex, so this is just a short answer.

From experience I cannot say quality is dependent on duration. For example, you can take a 30 minute power nap and feel much more refreshed than sleeping 8 hours. It may have something to do with dehydration and hunger during the long periods of sleep that disrupt our REM sleeping, our deep-sleep.


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Where do the electrons and protons formed from biological reactions go?
In a reaction like disulphide bond formation protons and electrons are released. These particles are presumably damaging in high levels. What systems are in place to prevent a build up of electrons and protons?

I've reproduced the diagram that you linked to. It shows the oxidation of a pair of thiols to create a disulphide. What is missing from this scheme is the accompanying oxidising agent. So for example this could be carried out without catalysis in a reaction with molecular oxygen, in which case hydrogen peroxide would be formed. So the electrons and protons have ended up on the oxygen.
In a biological system this oxidation would usually be carried out by an enzyme, in which case the oxidising agent would probably be FAD (flavin adenine dinucleotide) or NAD+(nicotinamide adenine dinucleotide). These are by far the most commonly used redox cofactors. In a typical eukaryotic cell these would end up either (a) being reduced either by the mitochondrial electron transport chain (in which case the ultimate electron acceptor would again be oxygen); or (b) when they were used as a reducing agent in a metabolic reaction.

Additionally often Glutathione (either oxidized or reduced depending on the reaction) is part of it.

@Chris thanks, I forgot about glutathione. Of course the diagram could actual be the oxidation of glutathione!


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What Causes Shin Splints?
My shin splints are clearly tied to running. Though the pain level doesn't seem to correlate  to my running intensity. So what is it about running that causes shin splints?
My real hope is that if I understand the cause clearly enough I can adjust to fix them.

By shin splints you probably mean the pain on the inner front side of the lower 2/3 parts of the shins? This is called medial tibial stress syndrome (MTSS).
Causes, mechanism, prevention and treatment of shin splints are still poorly understood.
From what I managed to find, custom-made cushion insoles are the only proven prevention that can help in some cases.
What has not been proven to help (I'm not saying it does not help, only it has not been firmly proven):

various types of shoes (supinator/pronator)
taping
stretching/strengthening exercises
various running techniques (pose-tech, chi-running, barefoot...)

Possible causes:

running downhill or on an uneven terrain with heel striking and forefoot slapping
sudden increase in running intensity, mileage or frequency
a way of running with moving the hips (left , right) forward
(my experience): running in a forced, conflicting way, like you feel you should not run and you still go...

Possible mechanism: vibration stress in the shinbone (tibia) and the pulling force of the muscles and tendons attached to it and possible local inflammation of then periosteum.
Do not try to run through the pain. The pain will go away but on the long-term, shin splints may worsen.
Source: Shin Splints (MTSS) (Ehealthstar)


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What governs the size of animal bodies?
Million of years ago there lived dinosaurs up to 36 m high. About 10,000 years ago lived Machairodontinae -compared to cats today they were huge. About 400,000 years ago lived Mammuthus trogontherii: it reached over 4 m at the shoulder. And these are just some examples.
Todays biggest living creatures look small compared to previous. So my question is, why are all creatures getting smaller? Why doesn't evolution generate any big creatures with size comparable to the dinosaurs?

The blue whale http://en.wikipedia.org/wiki/Blue_whale is the largest animal that has ever existed on Earth, and it is available to ride right now.

IF you want to ride a dinosaur, ride an ostrich. :)

For the record - both my comment and that from Mike Taylor make no sense now that the question has been edited. It originally mentioned wanting to ride a dinosaur.

This question about dinosaur size might be helpful. African elephants would fit right in with many of the largest (non-sauropod) dinosaurs.

This post is so relevant to this question that it might almost be a duplicate.

It's strange that nobody has mentioned human impact. Consider the following.

I agree with other commenters that we are not necessarily living in a time of small body masses.
Here is a paper on a body mass distribution. It's quite mathematical, but the first author (Aaron Clauset) is good.
For individual body masses, you can look at Kleiber's law - this says that body mass and metabolism are related by a power law.

There are lots of parameters that influence body size. Here is a non-exhaustive list:

visibility to predators
ability to hunt bigger preys or to manipulate smaller preys
running faster
be more impressive
fighting ability
energy consumption for maintaining a body
Quantity/quality of food to be found
homothermy (heat loss)
sustaining its own weight
Rooms for the organs
Attractiveness to the other sex
being more able to move freely (in viscous environment (water))
mechansisms for bringing nutrients and air to the tissues
density of the body (water)
excretion of wastes
moving in small habitats
Hiding in small areas
bearing big and complex structures
Parental care
flying better
artificial selection
etc..

Saying that today's species are smaller than previous species is maybe over generalize. For example, the largest species that is thought to have ever lived is currently extant, it is the blue whale (it can weight more than 200 tons). The tyrannosaurus is roughly the same weight that the african elephant (7 tons). However it is true that insects were typically bigger before than they are today. It is also true the the sauropoda are particularly impressive as some of them were 3 or 4 times taller than a giraffe and weight around 100 tons. [Bruhathkayosaurus](The http://en.wikipedia.org/wiki/Bruhathkayosaurus), the largest land animal that ever lived may have had a weight comparable to the blue whale!
A common argument to account for the big size of dinosaurs and especially of insects during  the triassic is the oxygen concentration in the atmosphere (ref). It is particularly relevant for insects as they have no hemoglobin, meaning that the oxygen has to be dissolved into their body liquid (mostly water) to be brought to the cells. From Henry's law, the concentration of a gas such as oxygen in a liquid is a function of the concentration of this gas in the atmosphere. Therefore, the highest is the oxygen concentration, the easiest it is to bring oxygen to all the cells of a big body and therefore the lowest is the cost of having a big body.


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Answer the questions in one word with help of clues and images given
Name the things associated with Antonie Van Leeuwenhoek - (6 pictures are given for help and four of them are associated with these clues)
a)Leeuwenhoek was the first to describe these and hence called the "Father of Microbiology"
b)He found many of these (rotifers) in the rainwater collected in ditches and canals
c)Leeuwenhoek was the first to describe plant vessels in this cross section of an ash tree
d)Leeuwenhoek used this to observe microorganisms.

Homework questions are off-topic unless you show some effort to solve them yourself.

How far did you come? What did you find out?

I found the following - A) Microorganism B) Rotifera C)Fraxinus D) Microscope

These answers look fine for me.

right click the image, "search google for this image"

Wanted to post this as an answer but can't since your question is on hold. So I'll post the links to the answers. 1) http://www.infection-research.de/perspectives/view/detail/23/shape_matters_why_bacteria_care_how_they_look/ 2) image of a rotifer http://upload.wikimedia.org/wikipedia/commons/2/2d/Bdelloid_Rotifer.jpg 3) ash tree cross-section http://en.wikisource.org/wiki/Popular_Science_Monthly/Volume_45/July_1894/Sunshine_Through_the_Woods 4) http://www.history-of-the-microscope.org/anton-van-leeuwenhoek-microscope-history.php  ... You go through these pages and you will get all your answers

Since you have apparently tried to answer the question here is my interpretation. I list the six pictures (numbered from top to bottom) and link four of them to an answer.
1 - yeast cells?
2 -  ash tree section (c)
3 - rotifer (b)
4 - muscle fibre??
5 - bacteria? (a)
6 - Leeuwenhoek's microscope (d)
According to the WP page on van Leeuwenhoek he did describe the banded pattern in muscle, but there is no mention of yeast (although he would have had no trouble seeing these cells if he could see bacteria).
It's a very odd question.


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What's the duration between the binding of adrenaline to β-AR and the first translated protein?
Binding of adrenaline (epinephrine) to the β-Adrenergic receptor leads to formation of cAMP (via G protein activation), activation of protein kinase A and subsequently to the expression of specific genes related to glucose metabolism.
How long does it take (in units of time) until translation of the first protein related to the adrenalin binding event is completed?
EDIT: I can accept a reasonable guess at the time scale (+/- factor of ten). Also, it can be also any another kind of ligand/receptor system.

This is a very interesting question. I have looked now for a while to find some references, but I haven't found any so far. I don't think that there is a definite number, as the connected processes depend on several factors. One very important is the length of the gene, for E.coli the speed of transciption was between 40-80 nucleotides per second, translation is even slower with around 20 aa/sec.

Sure it depends on a lot of things, that's not surprising. However, I haven't even got an estimate on what time scale we're looking at here. Even this would already be of worth knowing.
The numbers you gave are for a single mRNA synthetase/ ribosome unit?

The numbers come from this source.

The references in the essay are definitely useful. Still, the signaling part is missing. But so, from just estimating the signaling part to take as long as the transcription/translations parts, from ligand binding to first translated protein, how about we say we're looking at minutes?

Things can certainly vary for different ligands and different levels of cascading but these are the reactions that you may consider.

Receptor activation
Nuclear translocation (lets assume it is just a part of the receptor. You can assume secondary messengers; it will add an extra step)
DNA-binding and Transcription activation
Transcription
Nuclear export of mRNA
Translation

Finally I guess what you really want is to know when steady state is reached. This will also depend on other factors such as:

Receptor deactivation rate
mRNA and protein degradation rates
Nuclear export of activated TF
Network architecture (some networks can speed up response times). This factor can be ignored and we can consider an open loop.

Phosphorylation reactions are generally much faster than transcription/translation/translocation rates and can also assumed to be equilibrium with dephosphorylation reactions.
Nuclear import rates are also dependent on cell volumes and for polarized cells like neurons it will be much higher. The average import rate is around 0.2 - 1.2 s-1 NPC-1 µM-1(cargo) [where NPC is number of Nuclear pore complexes which is again on an average 120 ] [1].
It can be, for ease, assumed to be ~0.02 min-1 [2].
In most modeling papers the transcription rate is assumed (based on experimental reports) to be 1 per min (Average polymerase speed of ~1000nt/min and gene length of 1000nt. This can vary with gene length)
Translation rates are somewhat trickier. The translation rate per ribosome translation elongation rate is ~5 codons/sec (15aa/sec)[3] or perhaps may even be lower — 3 - 9aa/s[4] ( [3] is a more recent finding). However, the overall translation rate will be dependent on number of ribosomes (Ribosomes can be assumed to be infinite unless it is some condition like stress or starvation. By no of ribosomes I meant polysomes per mRNA, which can also vary). Also, the protein synthesis rate will depend on length of mRNA. This is one parameter that can have a broad range of values (0.6-100 min-1 × mRNA).
You can set up mathematical model (based on reaction rate equations) and calculate the response times (Depending on parameters it can be 8-20 hours). Steady states can generally reach by 8 hours (based on my own experiment. But I used tetracycline to induce luciferase). Another experiment (unpublished) using IFNγ induction caused a peak in the reporter at ~12h. I am not linking all references (you can easily look up for these). Usually, for cell culture applications, there is some sort of unsaid rule to assume 12h as a general response time to persistent stimuli. Response times are also dependent on initial conditions.
Note: Response time means the time required to achieve steady state. This does not mean the delay between signal onset and protein synthesis. Other metric that is used generally is max-peaking time.


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How do Streptococcus thermophilus and Lactobacillus bulgaricus precipitate the curd of swiss cheese?
I learned in my food microbiology class that Streptococcus thermophilus and Lactobacillus bulgaricus precipitate the curd of swiss cheese. However, I was wondering what type of mechanisms do these bacteria use in order to accomplish this process.

lactic acid bacteria ferment the disaccharide lactose present in high amounts in milk to the three-carbon compound lactic acid, which acidifies the milk. this causes the proteins also present in milk to denaturate and coagulate, forming curdles. other causes/methods of curdling can be application of heat, salts or by adding the enzyme chymosin (rennin).

my bad, I am quite new here. is this satisfactory?

Well, maybe adding a better link would strengthen it a little.

all concepts in my answer are pretty googlable. I understood from Chris' comment that just dropping Wikipedia links on everything is not the best way to answer, so yeah.


text:
How many times can a human get chicken pox?
How many times can a human get chicken pox?
For example: I got chicken pox, and recovered. If I was infected with HIV, and I am exposed to chicken pox again, can it infect me second time?, According to what I've heard, chicken pox comes only one time, because of the immune system of humans. But if I am infected with HIV and so definitely have immune system damage, will chicken pox come a second time, or will the immune system still protect the body from chicken pox?

after INFECTED with HIV,i am guessing shingles will come instead of chicken pox. but i have a doubt in this.

Suggestion: I think this question would be more useful for future reference if rephrased along the lines of: Can immunocompromised individuals be infected multiple times by diseases that you normally only get once in your life?

Usually you get chicken pox only once in your life, the recurring form are usually shingles.  But: It can happen (also in people which are not immunocompromized). I know two persons which got chicken pox twice and which are otherwise normal in regards of their immune system.
Persons with an HIV infection are more at risk here. They can develop both forms and depending on how much their immune system is already affected by the HIV infection can develop severe forms of the infection. It might be necessary to treat them with antiviral drugs. So it is clearly recommended to ask a MD about this. See here for more details.


text:
Does this "fleeing spiders leaving fields of webs" phenomenon have a name?
I have recently seen images of big areas covered in spider webs:

After flood in Australia

http://news.nationalgeographic.com/news/2012/03/pictures/120307-spiderwebs-australia-floods-wagga-wagga-world-science/#/spider-webs-australia-floods-bush_49725_600x450.jpg
http://www.dailymail.co.uk/news/article-2111390/Australia-floods-Spiders-cover-fields-cobwebs-flee-rising-water.html
http://www.hoax-slayer.com/spider-fields-australian-floods.shtml
http://www.theatlantic.com/infocus/2012/03/spiders-flee-australian-flood/100265/
http://io9.com/5891091/massive-spiderwebs-engulf-australian-town-as-arachnids-escape-floods

I would like to read about this on wikipedia. So I am looking for a name of this phenomenon. Do you know how it is called?

I doubt it will be called anything specific. It's just spiders fleeing a flood like any other animal.


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Troubleshooting SDS-PAGE of trypsin-treated BSA
I am currently working on SDS-PAGE technique having 20% acrylamide concentration for hydrolyzed BSA protein. Here I attached a gel photo for trypsin hydrolyzed BSA. I don't know , is it a good result and how do I interpreted this result?

A 20% SDS gel? How big are the fragments you are expecting? The concentration seems rather high for me.

why do you need to know (is this for a report, assignment, or research?) it may affect the type of answer, and some more detail of method might be needed & what you are testing

I am doing research on drug delivery. This my initial task to check hydrolysed protein on PAGE. protein hydrolyzed by trypsin chmotrypsin and pepsin in our stomach.

her I am using 20% because on 15% I got band at bottom of GEL, nearer to edge.

It looks like your trypsin works, at least. Is there something else you were expecting? I don't do very much SDS-PAGE(so take with a grain of salt), but I would lower the thickness of your gel and let the large blurry bands run off. The BSA and hydrolyzed protein fragments are those thin lines at the top.

What percentage is your stacking gel?

The stacking gel should be 4%, and the separating gel is usually no greater than 16% (and that's to separate really large proteins). What molecular range bands are you expecting to see, and why is the separating gel percentage so high?

In 15% i got no any band.

At 15% did the large digested band also disappear? Again it will be great if you repeat the experiment and use a ladder, just to see how proteins of 66 kDa MW and lower gets resolved.

@kt123 Can you show an image of the 15% gel? I still doubt this makes sense based on my experiences. Your digested samples hardly enter the gel and the undigested protein doesn't enter it at all. Can you add your gel recipe? Based on my experience with similar sized proteins I would say an 7-8% gel should do the trick. Don't run it too long (until the first dye band which runs at the front is down at the bottom) to loose samples.

I'm going to treat this as a partial homework question but provide some guidance as to how you can potentially address your question and have solid theory to back it up. Chymotrypsin preferentially cleaves peptide amide bonds where the carboxyl side of the amide bond (the P1 position) is a large hydrophobic amino acid (tyrosine, tryptophan, and phenylalanine). So one solution which is often used by experimental biologists (such as myself) performing mass spectrometry (MS) is to put their protein sequence (in this case BSA) in an algorithm such as PeptideCutter (from ExPASy), which performs a theoretical digest of the protein sequence having chosen the desired enzyme or combination of enzymes) and see what peptide fragments are expected to be produced and work out their length/molecular weight and compare that to your experimental data.
Having had an initial look, I noticed that your protein marker/ladder is missing, which is quite important in figuring out the peptide sizes produced! Also what is 1-8 lanes? are they different concentration of enzymes? if so then it looks ok to me since the higher the enzyme concentration from left to right, the higher the amount of digest products you have. If the peptide sizes obtained are not the ones expected then perhaps increase or decrease the digestion time since you could have a problem due to either incomplete digest or unspecific digestion, depending. I guess since BSA MW is ~ 66kDa your gel concentration is appropriate since you have a problem with the 15% gel as the products are too small and too abundant to resolve.

I disagree on the gel percentage. I did run a lot of gels wit proteins in the 50-70 kDa range and I used 7 or 8% gels for that. The density here is ways too high, the undigested protein doesn't even enter the resolving gel, it stays at the border between stacking and resolving gel. At this position I would expect proteins around 100-120 kDa. What didn't work in the 15% gel? Can you use a marker?

I agree that 20% gel is quite high but OP in the comment section says using 15% gel fails to resolve the digested bands (which are many from the pic) as all collect at the bottom although I will be surprised if the large digested band also disappears. Hence the resolving gel (i assume) was used at 20%, which gave better results. It is important however to use a protein ladder just to see how proteins migrate as it is hard to tell at the moment what we are looking at. I personally use gradient gels 4-12% pre-made but thats ideal for proteins between 60-220kDa as I get an excellent resolution.

We don't know why the 15% gel failed as we never heard anything else about it. I see only one band per lane, the rest are the dyes used in the buffers. Additionally I wonder how he handled and stained a 20% gel, as these should be really brittle. I do 15% gels for oligo analysis from time to time and these are already hard to handle.

I expect most of BSA digestion products are to be small and various in size (smear like), which is what he is seeing, except that one band since the enzyme does not digest too specifically. Hence I do not think the smears he is seeing is non-washed stains since in between the lanes the SDS-PAGE gel is clear so he has got most of the unbound coomassie stain off although I do not know of his wash procedure. Oligos give a similar result to the above but I did not know you can run them in a SDS-PAGE as I just come across them in my agarose gel work.

It would however be nice for the OP to do an overnight wash (with a slightly modified wash buffer composition) to see if he/she gets a better resolution. Almost 100% of the times overnight washes work best and show bands, which were unresolved for me! but @Chris I agree about the general thrust of your argument specially the gel brittleness issue!


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Where can I upload non-human Genotype data?
I have genotype data from few chicken population and I want to (need to) upload them somewhere online with free access. I have searched the web but I haven't found any place for non-human genotype data!
Does anyone have an idea where I can upload it, which is publicly available and user friendly?
bests

Does this Website help?

Thanks @Chris I checked the link. As long as I understood all those links are for "new variants discovered" or "data for GWAS study". I just have genotypes.

Isn't here any repository for this animals?

I did not find any site like that. You can upload the file in your university/lab website.

I don't think there is an answer for this question, as such a repository for chicken data does not exist.

@Chris: isn't that a suitable answer then?

@ChrisStronks This is basically is link answer, which obviously doesn't help. Or do I see this wrong?

I don't think that it is necessary to upload to a specialist or targeted repository if none are obvious. For some data types there is an obvious repository such as dbSNP. It does not sound like such exists.
Probably things have changed since the question was posted, but nonetheless I think that this is a useful question to have answered.
There are a variety of data repositories to which you can upload unstructured data that do not require you to host it yourself:

Open Science Foundation: free, non-profit dedicated to ensuring data access and scientific reproducibility.
FigShare: has free accounts, for-profit company.
Dryad: free, non-profit.
Zenodo: non-profit.


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Evolutionary motivation behind number of neurons in DCMMP
I'm studying neuro-anatomy right now and I was surprised to learn that there are only three neurons along the Dorsal Column Medial Lemniscal Pathway (DMLP) which relays mechanical sensations from the limbs to the brain. Is this the same across all mammals? Is there an evolutionary motivation behind having exactly three neurons, instead of 4 or 2?

The species you want to look at for this are giraffes and, to some extent, elephants.  This article is talking about information flow in the other direction (corticospinal tract) but it might have some insights into the sensory pathways.  I did not read it yet, though.