text:
Doing a medical study on yourself?
What research guidelines is a person legally mandated to follow if they want to do medical experimentation on themselves?
There is a large amount of variation in the types of medical experiments so I wanted to ask people focusing on the change in practice as a function of the type of medical experimentation you do in the biological sciences (e.g., drugs, blood samples, tissue regeneration, testing medical equipment), including invasive and non-invasive studies. This question seemed almost equally suited to academia and biology SE, but given the focus on different types of biological experiments I felt this might be the more suitable site.
I am most interested on research practices in the United States, and anything touching FDA regulations would be great.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3298919/ seems to be a very relevant paper.

I can't cite any sources, but self experimentation is far less likely to be regulated than trials on other people. We had a seminar speaker who was giving high doses of some molecule his lab was working on to himself and looking for side effects. Unfortunately I can't remember his name or his molecule. He did say that the university committee on human subjects didn't care if it was just himself.

And you are not going to be a able to statistically prove any thing with just one individual. There will be inherent bias in the experimental design, and ultimately worthless imo.

Barry Marshall had drunk a solution of H.pylori to "prove" that it causes ulcer !

@RoverEye A self study could still be very useful in the case of a type of study that would be providing a massive stream of data even if conducted on one individual.

This is perhaps too broad because there are a huge number of experiments that one could do to themselves, each with its own legal minefield (e.g. taking drugs), and as already mentioned it would be a massively flawed study and wouldn't contribute a great deal to the scientific community

@biogirl sure, I remember. But that was more of luck and the experiment itself (he postulated) wont end up killing him. I personally feel that it is more of a statement rather than an experiment (yes, I know its published in a peer reviewed journal, but still). You cant do that, with the way science has grown since then.

There's also the guy that did the knuckle cracking on one hand to him self for years...

@rover eye I agree. Doing experiment on one individual does not prove anything. But it amuses me to see to what length scientists can go to prove themselves :)

One of the cornerstones of research ethics worldwide is the Nuremberg code, which was formulated shortly after the Second World War and set off by the cruelties performed by the Nazi Doctors. The Declaration of Helsinki, which is currently widely used as the guiding principle of research ethics, was directly inspired by the Nuremberg code.
Interestingly, article 5 in the Nuremberg code reads, and I quote:

No experiment should be conducted where there is an a priori reason to believe that death or disabling injury will occur; except, perhaps, in those experiments where the experimental physicians also serve as subjects.

Basically what this tells you is that when you are a physician, you are not only ethically allowed to experiment on yourself, even when you can reasonably expect death may follow, you are even allowed to put others at that risk(!) Admittedly, it does not specifically talk about non-physicians. Nonetheless, with regard to your question, this Nuremberg article implies that self-experimentation is allowed, regardless the risks.
Annas (2010), rightfully argues that, even where risks are minimal, prior ethics committee review of research should always be sought, if only to confirm the reasonableness of the risk assessment and regardless whether investigators are subjects.
The problem then becomes whether self-experimentation (an experiment done by the investigator on himself or herself only) must be reviewed and approved by an ethics committee before it is conducted. Here Annas (2010) concludes that:

[...] When an investigator proposes to experiment only on him or herself, that activity is not properly categorized as research at all, but as self indulgence (or, some may say, self abuse). Trivial interventions masquerading as research studies are primarily a source of amusement.

Although I do not necessarily share the concluding accusations against self-experimentation, I do share her view that self-experimentation should not be regarded as proper scientific research, and therefore should not be subject to ethical review.
Reference
Annas, BMJ (2010); 341: c7103


text:
Are retroviruses cytotoxic?
There are typically hundreds of retroviruses found in healthy human beings.
Are retroviruses then cytotoxic? (In other words, are they able to kill or damage other cells).

Can you please expand your question? Actually I am not sure what you are asking.

Hundreds of retroviruses are normally found in healthy human beings. So the question is, if retroviruses are cytotoxic or it depends on the classification? Should the question  'Does all retroviruses are cytotoxic?' would be more clear? Or 'which'?

Re-phrased the question to opposite, so I think it's more clear.

The word cytotoxic in your question probably came from 'cytotoxic t cell'. Programmed cell death induced by a cytotoxic t cell is responsible for cytotoxicity, not the retrovirus itself.

Wiki says that cytotoxicity is the quality of being toxic to cells, so it's not only refered to T cells as far as I understand, but to all other natural killer cells. Please correct me if I'm wrong.

As you point out human beings (and other organisms) have hundreds of retroviruses and many can be seen in the human genome, some of which appear to be the remains of deactivated viruses, others which may be active.   Most retroviruses are not pathogenic - they don't cause disease.
This is because many retroviruses replicate slowly, budding and secreting from the cell surface in small numbers without killing their host cell.
There are several disease-causing retroviruses.  Human T-cell Leukemia Virus (HTLV) can cause T-cells to replicate in an uncontrolled fashion, resulting in leukemia.  This is not a necessary result for HTLV to replicate, but it is a result of viral infection as viral replication tweaks the cell machinery to replicate.
While it's not clear exactly how, Human Immunodeficiency Virus (HIV) kills its hosts cells.  Unfortunately HIV's hosts are CD4 immune cells.  The fact that sporadic replication of HIV can cause all host immune cells to die entirely makes HIV a pathogen.
Disease is usually thought of as a lack of adaptation of a pathogen and host: viruses do better if they do not kill their host.  Both these cases are possibly not the future for either virus: either could adapt to reproduce without causing a disease. Or they might have already , having spun off some strains into the pool of quiet retroviruses medical science does not concern itself with.

This answer gives a good background for how retro viruses may differentially damage biological function. The word cytotoxic in the question wasn't appropriate for the relationship between a cell and a virus.

@caseyr547 The upvote for the answer only says something about the quality of the answer. So even if the question doesn't make much sense it can still be possible that the answer is good. What is the case here.

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text:
Why are all human beings not black in color?
Archaeologists and historians strongly claim human beings originated from the African continent, where the default color is black for humans.
Why are all human beings not black in color?

First let's look at the difference between light skin and dark skin: darker skinned people have higher concentrations of melanin than those with lighter skin. Africa is located around the equator, a place where the sunlight is very intense. Melanin protects the skin against harsh, damaging rays, which is very beneficial in Africa. But a high concentration of melanin also decreases the skin's ability to produce vitamin D3 (1). Vitamin D3 is a vital nutrient to many physiological processes. Deficiencies in vitamin D3 has been known to cause things like rickets and osteomalacia (2).
So in Africa, having a high concentration of melanin in your skin conferred a great fitness benefit: you could go outside without getting cancer. But when humans relocated to places farther from the equator with reduced sunlight, having a high concentration of melanin in the skin actually became harmful because it would make darker skinned people more likely to have vitamin D3 deficiencies. Given this change in the fitness conferred by the trait of dark skin, individuals with lower concentrations of melanin in their skin were more likely to survive and reproduce in these new conditions. After many generations, the allele(s) that cause lighter skin became more common than those that cause darker skin.
Hope that was helpful!

T.L. Clemens, S.L. Henderson, J.S. Adams, M.F. Holick, INCREASED SKIN PIGMENT REDUCES THE CAPACITY OF SKIN TO SYNTHESISE VITAMIN D3, The Lancet, Volume 319, Issue 8263, 9 January 1982, Pages 74-76, ISSN 0140-6736, http://dx.doi.org/10.1016/S0140-6736(82)90214-8
http://www.everydayhealth.com/drugs/vitamin-d3

You can see the same effect at work in India (and I think in Australia).  The people who are native inhabitants of the southern part of India are quite dark, northerners not so much.

@jamesqf lets discuss about Africa only.

@rjames  For Suppose, I moved to Himalayas/Ice regions, but doesn't it make my skin white naturally, Still I have to choose artificial methods like plastic surgery etc to change my color.

@user11287 Evolution occurs over many generations. It takes a long time for changes like that to occur.

@user11287: Limiting the discussion to Africa only would ignore much relevant data.  For instance, while the southern Indians are dark-skinned, they aren't otherwise (judging from those I've met, anyway) like Africans in appearance.  I'll also note that when I live in northern winters, most of my skin is pretty pale, but it turns brown in the summer.

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text:
Why is the number of PCR cycles limited?
I've been told that the maximum number of cycles in PCR is between 20 and 30.
Is this true, and what are the reasons for this limitation?

I would draw the line beyond 35, but thats a bit cosmetic.
The reasons are manyfold:

due to the exponential fashion of the amplification (ideally)
reagents are used up at some point
reagents degrade, this is especially true for the dNTPs
the activity of the enzyme, despite being heat-stable is declining
over time
beyond 35 cycles the exponential curve is flattening out (reasons see
above)
if you run the PCR for too long, you will get more and more
side-products (mostly primer dimers, but mis-aligned primers can also
make problems), this is more a problem for real-time PCR than for ones run on a gel

If you need a higher sensitivity with more cycles, you can use the technique called "nested PCR". There you do a first round with a primer pair specific for the region of interest and then do a second round with primers which are located slightly to the inside of the amplified DNA. This is done to avoid the amplification of unwanted contaminations. Since you do some 50-70 rounds of PCR amplification in total, this method is extremely sensitive (also to contaminations). See the image from the Wikipedia article for details:

Thanks for the answer! Would it then be possible to terminate the PCR, isolate out all the DNA and then start a new batch in PCR with all the isolated DNA, as to renew the polymerase and have "new" primers?

Yes, thats possible and is done. But to avoid the amplification of a contamination, you use a set of primers which is located slightly to the inside of the product and which does not overlap with the primers of the first round. This technique is called nested PCR (the article also contains an image of the technique.

I have added it to the answer.

How many cycles of PCR before dNTPs run out?
Assume a 25 μl reaction.
Assume 200 μM dNTPs.
200 μM dNTPs = 200 pmol  μl -1
so in  25 μl  reaction, there are 5000 pmol of dNTPs
= 5000 x 10-12 x 6 x  1023 molecules
= 3 x 1015 molecules dNTP
Assume that we start with 1 molecule of a 1000 bp template, 50% GC
1 kb = 2000 nucleotides
So , how many of these molecules can we construct using 3 x 1015 molecules dNTP?
= 3 x 1015/2000
= 1.5 x 1012 DNA molecules
How many cycles of PCR to produce this many from a single template molecule?
2n = 1.5x 1012
nlog2 = log(1.5) + log(1012)
nlog2 =  12.18
n = 12.18/ log2 = 41 cycles
Of course this in an absolute upper limit. The estimate assumes that you start with one template molecule of 1 kb, and that dNTPs aren't being hydrolysed, or otherwise degraded.

You have to take into account, that we use four different dNTPs for PCR, so this calculation would only be valid if the bases are equally distributed.

Which is why I stated the assumption of 50% GC (and so 50% AT).

You are right, I missed that point. Sorry for that.

In my own research I've found that the amount of PCR product increased as I increased the cycles to 50 times. This was for a single pair of primers used to amplify genomic DNA extracted with a particular kit as doesn't apply to other reactions I've done. What some people seem to forget is that the PCR products don't necessarily double at each cycle at any point in the PCR because some primers don't function as well as others and reaction conditions may be suboptimal (e.g. presence of contaminants or concentration of Mg ions).
In short, provided you aren't getting reduced-quality products (e.g. smearing or non-specific priming products), then I think it's fine to increase the number of cycles well beyond 30 - it's something you have to test empirically with your particular primers, template, polymerase, buffer etc.


text:
Why did humans lose their fur?
The little amount of body hair humans have don't seem to be of much use for keeping warm.
Our Simian cousins on the other hand sport thick furs.
At which point during the species evolution and why did humans lose their fur?

possible duplicate.. at least very related http://biology.stackexchange.com/questions/2293/why-do-we-grow-so-much-hair-on-our-heads-compared-to-our-bodies (There's also numerous questions relating to the functionality of patches of hair/baldness which you might be interested in... http://biology.stackexchange.com/questions/5217/what-is-the-armpit-hair-for and http://biology.stackexchange.com/questions/13996/why-dont-we-have-hair-on-palms and http://biology.stackexchange.com/questions/5676/why-does-human-facial-and-head-hair-continue-to-grow but these don't answer your question)

@GriffinEvo yes clearly related and a partial duplicate, but I voted to keep open. The other Q doesn't cover when hominids lost their fur, but has a partial answer on why.

@fileunderwater I must admit I'm not too sure I should vote to close, as you say there is some part of  this question which is not a duplicate.

I don't see the point, either.

I've retracted my close vote

This is an interesting question, and there are a number hypotheses available to explain this phenomenon. The short answer (as far as I can say after my literature search) is that we don't know the answer for sure. The long version follows below.
The main problem with all these hypotheses is that though they may have a valid point, a definitive hypothesis hasn't been demonstrated yet. All these hypotheses are listed in the first reference, with a ton of additional references in the paper. I will summarize the different hypotheses only briefly here; for details please read the paper. The second reference is also interesting.
The point when this process started was after the last common ancestor of chimpanzee and humans when our two lines diverged. Chimpanzees are our closest relatives and still have hair coats, so this process must have started afterwards. Analyses of MC1R mutations (which affect pigmentation) suggest that human have been hairless for at least 1.2 million years. See reference 3 for details on this.
Aquatic ape hypothesis (also known as aquatic ape theory): This hypothesis states that modern humans spent some time semi-aquatic. In this lifestyle fur does not insulate very well and this led to an evolutionary disadvantage.
Cooling hypothesis: This hypothesis states that the modern humans lost their hair when they left the forests and started to live on the savannah. There they got too warm with their fur and finally lost it. This hypothesis sounds logical at first thought, but has a few problems. Naked humans have two problems: during the day they collect quite some heat via their skin, which requires them to have a cooling system (we sweat to cool us), and during cold nights we need a lot of internal energy to keep our temperature stable. Insulation however works both ways (not only keeps the warmth in, but also can keep heat out), and indeed some savannah monkeys have denser fur than their relatives in the forest. The cooling system will also lead to water loss and potential dehydration.
Hunting hypothesis: This hypothesis states that humans started becoming carnivores and therefore had the need to run for extended periods of time to hunt for meat. This leads to thermal overload; without a fur they can release this heat much faster to avoid overheating.
Bipedality hypothesis: This hypothesis assumes that modern humans, walking on two feet, have a lower direct influx of solar radiation. This lowers the chance for overheating.
Allometry hypothesis: Allometry states that species which get bigger during evolution, do not have all their organs getting bigger at the same rate. The hypothesis states that humans got bigger, the number of hairs stayed the same, and finally got lost.
Clothing hypothesis: One of the more illogical hypotheses, this assumes that hair loss wasn't critical for humans as they managed to make themselves clothes.
Vestiary hypothesis: A mix of the cooling and the clothing hypothesis: Here it is assumed that hair loss is beneficial due to more cooling and that the negative effects of too much loss of heat were counteracted by the invention of artificial insulation.
Neoteny hypothesis: Neoteny denotes the retention of of juvenile physical characteristics in adults. Humans are characterized as retarded in development (compared to the apes) and mature more slowly. Additionally, it is assumed that some characteristics (here loss of hair) of juvenile or fetal apes are maintained.
Carrion-eating hypothesis: Another strange hypothesis, this assumes that man as a messy eater (like vultures and condors, which have naked necks) have an advantage of being hairless.
Sex-related hypothesis: This hypothesis assumes that hairless skin is more sensitive to stimuli like touch, temperature and pain. This would allow more sensitive social contacts, especially between man and woman, but also between woman and child. Pubic hair is not explained by this hypothesis.
Adaptation-against-ectoparasites hypothesis: Here it is assumed that naked humans are less prone to harbour ticks, fleas and other parasites which hide and live within fur. Apes have great social rituals of removing these within their group.
References:

Evolution of nakedness in Homo sapiens
The Hairless Mutation Hypothesis Explains Not Only the Origin of
Humanization from the Human/Ape Common Ancestor but also Immature
Baby Delivery
Genetic variation at the MC1R locus and the time since loss of human
body hair.

Really good Answer Chris, covered a lot of hypotheses there. +1

The aquatic ape hypothesis coudldn't prevail itself in professional circles.

@empedokles Correct. I listed the ones I came across, no matter if they are accepted or not.

I have an alternative explanation for why we still have hair in the few places where we do: Sun protection. Think of what a sunburn on your crotch is going to do to your probability to reproduce if you're a naked protohuman living in the African Savannah a million years ago. Also, think of the sun is beating down on the top of your head if you do not have hair there. Armpit hair seems to have a dual purpose though, while the skin there is thin it's not sun exposed. That hair however would help keep sweat there, helping it cool you more as it evaporates, and there's a lot of heat there.

Africa is weird it is the only place I know of were many large mammals are all but hairless, elephants, rhinos, warthogs, Hippo, Humans. There has to be some common factor encouraging it.

The really weird thing is we have more hair than chimps (follicles per inch). Our body hair is just shorter and thinner so it is less visible. This is one reason the cooling hypothesis is gaining ground.

The short answer is that no-one knows. That no-one knows, along with a lot of popular interest, has led to wide ranging speculation. Some of that is well grounded, but much of it is not. Some has been published within relevant journals subject to peer review, whilst others have been published independently for the lay public. Despite the extent of popular interest it is not a subject of study that attracts large numbers of academics or a lot of research funding, so there may not be enough experts to keep the more egregious speculators in check.
I think "Why?" is a question that brings to light more of what we don't know that what we do. We don't know if this peculiar evolutionary development was a consequence of specific mutations that resulted abruptly in occurrences of a furless variant amongst precursor hominids or if it was an accumulation of incremental changes via sexual and/or natural selection. I'd like to think studying DNA will answer that.
Furlessness probably can't be understood without reference to other changes, including to skin pigmentation, thickness, sweat and oil glands, follicular nerve supply and sensory sensitivity. Bipedalism too. And I don't think we can leave out the abilities of smart, tool using problem solvers to adapt behaviourally to overcome physical limitations, or that those kinds of solutions can go beyond mere compensation for disadvantages to become extraordinary advantages in their own right.
The most widely accepted explanation - that it is an adaptation for improved hot weather endurance - is predicated on an improved ability to perspire. I don't think it is known if being more sweaty preceded, followed or occurred together with truncated body hair growth, or if it one element of more wide ranging changes, such as with hypotheses invoking neotony/pedomorphism. When such an important advantage as hot weather endurance is dependent upon changes other than to hairiness, it's necessary to consider how and why they came about as well.

The little amount of body hair humans have don't seem to be of much
  use for keeping warm.

This raises a fundamental question of what the functions of body hair are. Whilst keeping warm is the function of fur in mammals that most immediately comes to mind to most people it is not the only function. I don't think the "why furless?" question can be answered through consideration only of the loss or diminishing of any specific functions; the myth of body hair being effectively functionless is what first prompted my interest in questions like this.
A widely overlooked observation is that modern humans gained improved sensory sensitivity through relative increase in follicular nerve supply, to the extent that W.Montagna ("Evolution of Human Skin", 1985) likens all human hairs, regardless of size or location, to the vibrissae - dedicated feeler hairs - of related apes.
Can we properly assess the relative advantages and disadvantages that arose from loss of fur if we do not properly consider the full range of functions of the hairs involved? Curiously, the hypothesis by D. Morris ("The Naked Ape", 1967) that losing fur improved our skin's sensory abilities, with consequences for social and sexual bonding, appears based on absence of hairs - presuming hairs to be inhibitors of touch sensitivity. To be fair, Montagna's observations that the increased follicular nerve supply has made them "the principle anatomical unit of skin sensibility" came after Morris. To be less generous the role of hairs as sensory receptors is self evident - unless his didn't work - and had made it's way into journals as far back as Darwin's day. (Can't find that reference to "every hair, with it's envelope, is a sensory organ" - a scan of a page rather than something searchable. Lost the link with a change of computer.)
I don't know that I've answered the question - more like pointed out that there is no definitive answer to this question; I would like to further discuss this, especially through engagement with people better informed than I am. Would this be a suitable subject for a Chat room? (Not sure I have the privileges here to start one).

Surely the simplest explanation is that hair is a "necessary evil"; a not terribly good compromise, but the best that evolution could come up with. Hair is very expensive biologically; it requires large amounts of energy both to produce and to maintain, and it harbors parasites. True, it keeps the animal warm when the environment is cold, but it also severely limits strenuous activity when it's hot. Lions and most similar predators can only manage short bursts of high speed running, but fur-less humans can run all day, chasing down large herbivores until they collapse from heat exhaustion.
However we're only able to do without body hair because, uniquely among animals, our high intelligence allows us to develop workable substitutes: fire, clothes, houses and so on.
In short, the answer to the question: "Why, out of all the primates did humans lose their hair?" might simply be: "Because they could..."
The "Aquatic Ape" hypothesis might better be re-worked as a consequence of developing hairlessness, not a cause. Being able to dry off rapidly after going into water (and if necessary put on dry clothes afterwards) made bodies of water much more attractive as a potential food source.
Essentially, losing our body hair arguably opened up new food sources to humans, ones that were particularly abundant in the fatty acids required for proper development of the infant brain. Better nutrition would have fostered natural selection for even greater brain development, eventually leading to modern humans.

Welcome to Biology. Do you have any links or references so people can do some background reading on your answer? As of now it seems an unsupported theory. For example, fur-less humans cannot run all day and a fur-bearing horse will in fact do a much better job at that. Also, one doesn't have to enter the water to catch a fish. -1

Man vs Horse marathon - says that in hot weather, man can, and does, win over the horse, so... +1 to reseverse that -1. yes, we need links.

men and beat a horse in a marathon in any weather, humans are just better endurance animals. And short hair also aids cooling (by blocking sunlight) which is why so many desert mammals have it.

Since there is only theories I will give my opinion. I think Fire played a huge part in losing our body hair 1.2 million years ago. Since the first fire was created 3.4 million years ago evolution had time to play it's part. Simply put, fire near a fury animal is way more dangers than a fire near hairless animal. And because fire gave it user many benefits to survive they couldn't let go of it just because it's was dangers and they adapted. Also, since fire gives heat it allowed us to stay worm without fur in the cold nights.

Actually hair is quite fire-resistant, and protects bare skin from embers. There's a reason many smiths grow a nice bushy beard.

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text:
Can dietary monosodium glutamate intake induce restlestness?
The question is all in the title.
More context:
I like phở soup. I have noticed that I get restless after eating the phở soup at some restaurants. The effects are similar to the ones resulting from caffeine intake. (Ingesting a cup of Turkish coffee or a couple of espressos results in my hands shaking badly.)
The phở soups which I think trigger the reaction appear to be the most savory ones. Given that:

Monosodium glutamate (MSG) is a common ingredient in phở
MSG has flavor enhancing properties
Glutamate is a neurotransmitter

I thought there was possibly a connection. (Or perhaps not. Or perhaps it's the intake of MSG together with the consumption of an herb containing caffeine or another psychoactive drug. Phở contains herbs in large quantities.)
I found this paper which states the effects of caffeine result from an increase of glutamic acid (GA) in the posterior hypothalamus which in turns triggers wakefulness.
Thus I guess what I am asking is: does dietary intake of MSG increase blood serum levels of GA and does an increase of GA blood serum level result in an increase of GA in the brain (or in some parts of the brain)?

+1, the question of dietary glutamate consumption has been occupying my mind for a long time :) Below the result of quite some thought on the matter.

This question made me hungry.

The answer is absolutely. It definitely has the potential for restlessness, and even far worse effects. BIg Food does not want people to know this and the dangers associated with high levels of free glutamates because it is found in nearly every food in the form of "natural flavors" and many other forms including actual monosodium glutamate. The neurotoxic and neuroexcitatory effects of free glutamates is not only well-known, it is exploited by Big Food which puts it into all our food because it tricks our brains into making bland food taste better.

There is no strong evidence for MSG having any kind of neurotoxic/neuromodulatory effect.
However, A 2010 article says that, in a double blind trial, it was found that the people who consumed MSG containing soda, reported headache in significantly more numbers compared to the placebo subjects [1]. The concentration of MSG used in this study was 75-150 mg/kg. Assuming that one serving of soda would be 300ml i.e 300g, the amount of MSG consumed would be maximally 45mg, which is much less than glutamate concentration in some natural food stuffs such as tomatoes (~2000mg/kg [2,3]; a tomato that weighs 6oz/~170g contains ~340mg of glutamate). Therefore, I would doubt the findings of this article. The results could have possibly been observed because of some hidden dependent variable (such as the soda formulation).
In general, the USFDA considers MSG as GRAS (generally regarded as safe) [4].
Finally, a 2014 article concludes that dietary MSG would not lead to increase in either blood or brain levels of glutamate [5].
From the Abstract:

The sodium salt of glutamate (monosodium glutamate; MSG) imparts a
  savory/meaty taste to foods, and has been used as a flavoring agent
  for millennia. Past research on MSG/glutamate has evaluated its
  physiologic, metabolic and behavioral actions, and its safety.
  Ingested MSG has been found to be safe, and to produce no remarkable
  effects, except on taste. However, some recent epidemiologic and
  animal studies have associated MSG use with obesity and aberrations in
  fat metabolism. Reported effects are usually attributed to direct
  actions of ingested MSG in brain. As these observations conflict with
  past MSG research findings, a symposium was convened at the 13th
  International Congress on Amino Acids, Peptides and Proteins to
  discuss them. The principal conclusions were: (1) the proposed link
  between MSG intake and weight gain is likely explained by co-varying
  environmental factors (e.g., diet, physical activity) linked to the
  "nutrition transition" in developing Asian countries. (2) Controlled
  intervention studies adding MSG to the diet of animals and humans show
  no effect on body weight. (3) Hypotheses positing dietary MSG effects
  on body weight involve results from rodent MSG injection studies that
  link MSG to actions in brain not applicable to MSG ingestion studies.
  The fundamental reason is that glutamate is metabolically
  compartmentalized in the body, and generally does not passively cross
  biologic membranes. Hence, almost no ingested glutamate/MSG passes
  from gut into blood, and essentially none transits placenta from
  maternal to fetal circulation, or crosses the blood-brain barrier.
  Dietary MSG, therefore, does not gain access to brain. Overall, it
  appears that normal dietary MSG use is unlikely to influence energy
  intake, body weight or fat metabolism.

Totally false. MSG is proven to have a strong neurotoxic and neuroexitatory effect. One of many: Regarding the mode of cell death, glutamate-induced neuronal cell death has been judged originally as necrotic from the morphological appearance. https://www.ncbi.nlm.nih.gov/books/NBK6108/ This is a well-known scientific fact.

@biology there is a difference between consuming glutamate as food and adding glutamate directly to neurons. Read my answer carefully before saying that it's totally false.

Short answer
Glutamate cannot enter the brain due to the blood-brain-barrier.
Background
You are totally right that glutamate represents the principal excitatory neurotransmitter in the brain (Meldrum, 2000). However, glutamate is a regular amino acid and will be metabolized quickly. More importantly, the blood-brain barrier is extremely effective in keeping polar (hydrophylic) molecules out, and therefore especially ions are not coming through as they are extremely hydrophilic. The blood-brain-barrier is formed by the endothelium lining the blood capillaries in the brain. In the brain, the endothelial cells are coupled through tight-junctions, that effectively keep almost everything out of the brain. The only molecules that can get through are either actively absorbed through specialized channels (glucose transporters for example) or are lipophilic. Glutamate under physiological pH carries two negative charges and a positive charge (Fig. 1), and will hence never make it through the blood-brain-barrier. There are glutamate transporters in the endothelial cells, but these in fact transport glutamate out of the brain, rather than in (Hawkins, 2009).

Fig. 1. Glutamate at physiological pH. Source: WikiWand.
References
- Hawkins, Am J Clin Nutr (2009); 90(3): 867S–4S
- Meldrum, J Nutr (2000) 130(4S Suppl): 1007S-15S

Thanks for adding the molecular explanation. Despite this, there is some scepticism about MSG causing "headaches".

@WYSIWYG - that is likely not through direct entrance, but by some indirect mechanism. Increased glutamate in the brain is potentially excitotoxic and it theoretically cannot enter the brain through the blood stream via dietary intake.

Just a thought: if there are one-way channels for excess glutamate to leave the brain - is it theoretically possible that higher levels of glutamate in the blood outside the barrier could reduce the rate at which glutamate leaves the brain, due to less of a diffusion gradient? So the dietary glutamate never enters the brain, but its presence in blood reduces the rate at which glutamate already in the brain is transported out?

btw. I didn't know about wikiwand. Just installed it in my browser- it's amazing :)

How do you think glutamate gets in the brain? Obviously it enters the brain one way or another. The body doesn't just manufacture glutamate from the air you breathe. It comes in through dietary intake some way or another, indirectly or directly.

@biology - Glu's probably just synthesized de novo, but that wasn't the question


text:
Difference in variance of Cys in protein sequences
Suppose I have got two sets of proteins (amino acid sequences). In one set, I find that the variance in the percentage concentration of the Cys is way more (65.34) than the variance of Cys in the other group (0.456). Does it mean anything? Does this have any sort of biological implication?
The concentration has been calculated by dividing the total number of Cys found by the size of the protein sequence.

It may or may not mean anything. Without additional information no inference can be drawn.

What additional information is needed in this case?

A lot: mean cysteine density, other structural and biochemical properties of the protein etc. Basically just the variance in cysteine content won't tell you anything.

This question would be more answerable with an introduction to the biological context, a description of how each dataset was generated (included the sample sizes), and the relative percentages of other amino acids.

No, because it's extremely likely your sets are not a representative sample of the true distribution in proteins.
Your bias might be caused by an effect on the functionality of the protein, but it might as well be a bias in which organisms are sequenced or something caused by the alignment or the way you are searching for your sets.

If there be is a hint towards functionality of protein, what is that functionality? Any sort of hint is what I want to know

I'd say this is 99% biased searching / sequence collecting.

What would be the bias? What is the biological factor that creates this bias?

"a bias in which organisms are sequenced or something caused by the alignment or the way you are searching for your sets"


text:
Difference between Appendix and the Cecum?
What's the difference between an appendix and a cecum, and what are their functions?

In herbivores the Cecum is an area that stores plant matter and helps digest it via symbiotic bacteria. Carnivores have smaller Cecums because meat is easier to digest than plant matter. In humans the Cecum is also an anatomical landmark that delineates the change from small intestine (a digesting organ) to the large intestine (mostly a capacity/storage organ).
The Appendix is a small, previously thought "superfluous" fleshy worm-shaped organ at the junction between the small and large intestines. Recent research posits that the appendix is sort of a harbor for a person's gut flora that can re-populate the intestines should the existing bacteria die or get removed (diarrhea being the most common cause). It can also become infected, inflamed, and require surgery to remove (Appendicitis).

But, how do people survive then if their appendix is removed, if it has such a crucial function?

Its function (which is still being debated) isn't that crucial. Rarely ever is all of your gut flora wiped out, and there are other ways to repopulate. Because of its seemingly benign, if not particularly useful, existence it is only removed if it becomes a problem. However, if it is removed, practically everybody recovers fully and there are practically no side-effects.

Also see: http://biology.stackexchange.com/questions/1502/is-the-appendix-a-vestigial-structure-in-all-vertebrates

Appendix and cecum both are parts of the large intestine.
Appendix is the inferior extension of the cecum of the large
  intestine. It is a blind pouch-like structure that resembles a worm,
  hence the name ‘vermiform’.
and
Cecum is a small intraperitoneal pouch-like structure located on the
  right side of the lower abdomen.

Source - Knowyourbody.net

Multiple answers are usually appreciated because they can address different aspects of a question. However, simply repeating the point already stated by an existing answer is not really appreciated.

Hi Welcome to BIO.SE. Thanks for adding an answer. However, in addition to WYSIWYG's comment, we also discourage simply quoting large chunks of text. Instead, try to synthesize info from one or many reputable sources into your own words and formatted for this site. Thanks.


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Can allelopathy succesfully be used against algal blooms?
Algal blooms caused by man (harmful algal blooms) are a major ecological problem. An excessive amount of algae causes hypoxia and logically, most marine wildlife can't be sustained in hypoxic conditions.
Can't we use allelopathic plants to reduce the amount of algae significantly?

One problem I can see with this idea is that whereas in soil any allelopathic compound will be restricted to the immediate vicinity of the source plant, in an aqueous environment the allelopathic compound would diffuse away quickly, so that the source plant would have to produce a lot more to reach an effective concentration.

This has been tried and it sorta works.
Algae in general seems to be inhibited by rotting barley straw in the water.
There is also an observation (not universally accepted) that many plants in the water do not have as much algae.  This post is from April 2011, so it seems pretty current.

Here is a good review titled: Use of allelopathy of aquatic macrophytes for algal-bloom control.
Hu and Hung talked about Macrophyte species which have allelopathy effects on Algal-bloom.
This paper discussed the development and potential application of allelopathy of aquatic plants on algae, including the reported aquatic macrophytes having allelopathy on algae, their allelochemicals and potential modes of action on algae, possible ways for application and the prospect of using aquatic macrophytes to control algal bloom.
Plants which you want to use for allelopathy effects on algal bloom, must of course be marine.
But sometimes allelopathic agents of terresterial plants can be extracted and use for this purpose more commercial than marine planting.


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Statement about Tropical Rainforests
I made a statement about tropical rainforests, and I want to know if it's somewhat true or not:
The soil in tropical rainforests is not exceptionally fertile, because it contains few minerals. The reason that a tropical rainforest has a huge amount of vegetation is because of the quick mineralisation. If a dead leaf falls onto the ground, it immediately gets turned into minerals, which the plants immediately use for sustaining theirselves

I don't quite follow your logic of why a dead leaf should be immediately turned into minerals.

that's what happens in a rain forest, it happens much more quickly than in a temperate forest for example

I think you need to clarify that point in your statement, then.  I would not buy that it happens immediately, nor would I buy that it is degraded into "minerals", likely there is some state where it is detritus and is then processed further by microorganisms.

I didn't mean immediately in the literal sense.. in the previous sentence I also said 'quick mineralisation' which shows that..

Well, to be honest, what you have is a statement laden with ambiguities, so to claim any truth in it, you'd have to be absolutely precise with the language.  If you made this statement to scientists, most if not all would assume you would have ballpark figures for "immediate", etc. with references to back them up.  I'm not sure what anyone can offer you in an answer beyond that.

@jonsca I don't know why I am coming back to this after a month and a half, but 'laden with ambiguities' is a hyperbole. I don't appreciate hyperboles on sites like these.

It was not meant as a personal attack, there are quite a few ambiguities in you statement "huge", "quick", "immediately".  If you attempted to publish that in a scientific setting, I'm sure you would get the same response.  I don't think there was any hyperbole in my statement at all, laden="weighted down".  I think they distracted from the message you were trying to put forth, that's all.

There are many websites which describe this phenomenon. They all seem to confirm the basic premise of the question: in tropical rain forests most of the minerals are held in the biomass and rapid decomposition contributes to the recycling of these nutrients for new growth. One example is here.

Tropical rainforests are noted for the rapid nutrient cycling that occurs on the ground.  In the tropics, leaves fall and decompose rapidly.  The roots of the trees are on the surface of the soil, and form a thick mat which absorbs the nutrients before they reach the soil (or before the rain can carry them away).  The presence of roots on the surface is a common phenomenon in all mature forests; trees that come along later in succession win out in competition for nutrients by placing their roots over top of the competitors, and this pattern is seen in the temperate rainforest as well.  What does not occur in the temperate rainforest, however, is a rapid cycling of nutrients.  Because of the cold conditions and the acidity released by decomposing coniferous needles on the forest floor, decomposition is much slower.  More of the nutrients are found in the soil here than would be the case in a tropical forest, although like the tropical forest most of the nutrients are held in the plants and animals themselves.

I looked for actual evidence of these differences in rates of decomposition and I found this:

Salinas, N. et al. (2011) The sensitivity of tropical leaf litter decomposition to temperature: results from a large-scale leaf translocation experiment along an elevation gradient in Peruvian forests. New Phytologist 189: 967-977

These authors reported a comparison of rates of decomposition at various elevations in Peruvian forest. The parameter k is the decay rate of dry mass, year-1. The following data are taken from Table 3.
site          elevation (m)   mean k (yr-1; 15 species)
Tambopata     210             1.753
Tono          1000            1.424
San Pedro     1500            0.968
Trocha Union  2720            0.546
Wayquecha     3025            0.424

and this:

Jacob, M. et al. (2010) Leaf litter decomposition in temperate deciduous forest stands with a decreasing fraction of beech (Fagus sylvatica) Oecologia 164:1083–1094

These authors studied leaf decomposition in a deciduous forest in Germany, with emphasis on the effect of proportion of beech trees upon overall rates of decomposition. Using data from Table 1 and Figure 2 (values converted from mg-1 g-1 day-1 to yr-1)
% beech yr-1
  96    0.2555
  67    0.657
  21    1.022

My Conclusion
Rates of decomposition can be much higher in tropical rainforest (k=1.753 yr-1 for the Tambopata site in Peru, k=0.256 yr-1 for a beech-rich forest in Germany). However, at higher elevations tropical rain forests are characterised by much lower rates of decomposition (Wayquecha k=0.424 yr-1), comparable to those in deciduous forests.
These are all measurements of loss of dry mass from leaf litter. This will be dominated by loss of carbon, and I would expect that minerals will leach from the decaying litter more rapidly than these values. Nevertheless it seems plausible that relative rates of mineral recycling will reflect these k values.

Fantastic answer


text:
Why is the Hydra Biologically Immortal?
I have heard that the Hydra organism is biologically immortal (later I found that there are more immortal organisms). Now I know that its immortality is related to its telomerase. The thing is that we all have telomerase, but we age and Hydra don't. What are the proteins (especially telomerase) related to aging in humans and Hydra and how do they work differently?

Could you define "hydra" or find a picture of it? The only "hydra" I'm well aware of is the fictional one from Greek myths.

Dear MCM, go to this link

Hydra are just one of the many organisms which are immortal.  That is to say all their cells divide forever - there is no senescence (planned cell death) in any of their cells. Interestingly Hydrae that reproduce sexually age and die, but asexual reproduction appear to be immortal.  Animals that are immortal more often reproduce asexually... this may only be because immortality became unpopular in evolution early on and may have not developed senescence in the way other animals have, or lost it when it was not so integral to life.

Although immortal Hydra also appears to share the (TTAGGG)n telomere repeat, there is as yet no data on how or whether they avoid chromosome end depletion. These data suggest the possibility that senescence or death of asexual individuals and colonies may in part result from a failure to maintain chromosome ends that are restored by going through a sexually reproductive cycle .

So its not clear if the telomeres are protected in hydrae and other immortal animals.  I would guess they probably don't have active telomerase if they are truly immortal, though its possible the telomeres are shortened and are repaired.
There are other factors which are supposed to be important for immortality.  Yeast and single eukaryotes are not individually immortal; an individual mother cell can only divide a limited number of times. While hydrae are not a popular focus of research, there has been a concerted effort in trying to understand yeast mortality and there are more than one mechanism being pointed to.
Since there is no germline in single celled organisms, (they only have one copy of their genome to reproduce from) telomeric shortening would not be a useful mechanism for aging; Calorie restriction has been shown to prolong fission and budding yeast by activating pathways which slow aging by protecting against stress, and slowing down reproduction.  All of these findings have strong parallels in work in aging in animals which is a hot topic now.
Finding these pathways is encouraging strong thought that aging and senescence are an evolutionary adaptation rather than a biological necessity.

Our current knowledge suggests that an apoptotic program has evolved in microorganisms as a survival strategy beneficial to the group. This program is dependent on cellular pathways like the Sch9, Tor1, and Ras/PKA pathways and its activation reduces cell protection and maintenance and raises the level of superoxide production, which in turn contributes to cell damage and death. Superoxide also elevates DNA damage and mutation frequency in the aging cultures ... Aging and apoptosis are intrinsically related in yeast and the mechanisms that cause them have just begun to be elucidated. ...  will provide important information to understand the fundamental biology of aging in other species and investigate the controversial hypothesis that an “aging program” might be conserved in higher eukaryotes.

There is an open question as to whether an immortal yeast could be engineered to be immortal.  A team at Max Planck Institute did a lot of foot work and found a strain which they claim does not seem to experience individual mortality either.
So this does indicates that immortality might not be a necessity for any cell or maybe even for animals.  Occasionally, even animal and human cells can be coaxed to revert to an immortalized state, though usually it is the result of cancerous rearrangements of the genome.
This is a rich field and there are lots of telomerase focused ideas too.  Maybe someone can post something along those lines.

@It isn't correct to say that yeast cells are immortal. See here for example. I spent two years working alongside a postdoc who spent all of her time watching yeast cells age and die!

more complex organisms also have very little senescence - e.g. lobsters (http://www.ncbi.nlm.nih.gov/pubmed/9849895?dopt=AbstractPlus & http://www.fightaging.org/archives/2007/06/ageless-animals-the-lobster-edition.php) - which is linked to constant (near constant) levels of telomerase expression throughout life. From the abstract to the above paper: "We conclude that telomerase activation is a conserved mechanism for maintaining long-term cell proliferation capacity and preventing senescence, not only in cellular models or embryonic life stages but also in adult multicellular organisms.  "

it sounded like this isn't a sure thing yet so I decided not to emphasize it.  there are other wierd cases too.  nobody knows why sharks do not appear to get cancer either, even if they have a more typical planned cell death mechanism.  Lots left to understand.  its certainly possible that some mechainism for immortalizing animals will be discovered.  there is lots of work in that direction.

@shigeta now I have to search those sharks!

here's a start : http://news.nationalgeographic.com/news/2003/08/0820_030820_sharkcancer.html

@AlanBoyd you're right I'd forgotten that.  Did find some exceptions and it turned into a nice section of the post.

Actually, most adult cells do not express telomerase or express it only at a very low levels. Telmoerase is highly expressed only in cells that need to divide (e.g. stem cells), thus "immortalizing" them.
In fact, human cell lines which scientists work with can be "immortalized" by activation of telomerase (along with other things).
So you may ask yourself: why not have telomerase activated all the time in all cells? Well, allowing a cell to reproduce easily can be a pretty bad thing... that is exactly what cancer does. Indeed, one of the things a cancer has to do is to activate the telomerases in order to be able to grow. This is also why cancer cell lines are "immortal". This also suggests a potential cancer therapy - targeting telomerase - which is currently being pursued experimentally.

Thank you, Can you add some reliable articles to your answer please?

@mysky I added a link to the Wikipedia article on telomerase, which has much of this information included. I don't know if you call that "reliable" though and what technical level you would like.

Telomerase activity is just one (probably minor) facet of aging.  It takes a lot more than just basic end repair of DNA to keep a complex organism alive, especially mammals.  Just a few issues off the top of my head:

repairing oxidative stress to DNA and proteins
repairing UV damage to DNA
keeping cells clean of debris like protein aggregate buildup (think amyloid deposits like in Alzheimer's)
replacing dead cells without compromising the tissue they're in

For a solidly scientific, short, but very readable book on the subject, I personally liked "Understanding Ageing" by Robin Holliday.  For being published in 1995, it's still relevant. He had a later book that wasn't quite as good (Aging: The Paradox of Life: Why We Age, published in 2010). In large part it's because it was fairly redundant to the first one; we've known about these problems for a long time and have made fairly little progress on them.
http://www.amazon.com/gp/product/0521478022/ref=oh_details_o03_s00_i00?ie=UTF8&psc=1
Part of how hydra can get away with apparent immortality is their constant proliferation of stem cells and their ability to regenerate entire body parts. This circumvents a lot of the issues above (theoretically, but I'm not an expert on hydras). Many copies of the DNA are separately housed, so if a copy gets damaged irreversibly, it can just get trashed. Most (if not all) human organs have similar reserves of active stem cells. There isn't a single universal source (outside of the sperm and eggs), but this is less important so long as the entire stem cell supply isn't compromised by some gross organ damage.
The second part is much, much harder for humans though. While some tissues (say muscle) can easily replace dead cells, it's much harder in others, like the brain. You don't just have to replace a dead cell, but all of its connections to every other cell. And really, the brain is what this all comes down to, and an identity crisis in humans.  I don't care if you replace my liver and my left arm times, but how do you replace the brain?  I would speculate that we spend a lot more time keeping individual cells alive, because we can't replace them.
If you chop a starfish in half, you get two starfish, and would have trouble saying which was the original. Is it the same starfish if you've replaced the arms 3 times and the body twice?
If you chopped a human in half down the center, and we could magically regenerate everything, you would get two very different people from each other and the original. The problem being that there's no way to reconstruct the connections; you'd just get a blank brain to fill up.


text:
Is this an Emperor Penguin or a King Penguin?
I have a book from Dorling Kindersley called Animal Encyclopedia (the German version that I have is called Das große Tierlexikon) with images from animals.
One is titled Emperor Penguin (Kaiserpinguin) which is in my opinion clearly recognizable as a King Penguin (Königspinguin).
This is the image:

I wrote to Dorling Kindersley and they told my that their investigation revealed that it really is an Emperor Penguin.
I am not a biologist nor a penguin expert, but from all the descriptions and images I could find (even in the same book on other pages!) I think the publishing company is wrong and just too lazy or arrogant to admit this error and too miserly to release a revised version of the book.
Who is wrong? Me or Dorling Kindersley? Emperor or King?
Update 2020
They seem to inherently admit it themselves, that the book was wrong (and that they lied to me), as they used the same picture on one of their websites and with king penguin in the caption of the picture:

I know this is verrrryyy old. But yes it's a king. You can tell from the long straight beak. Emperors have a shorter curved beak

@erik Haha love the update. Much appreciated after 7 years of personal torment I'm sure! :p.  Seriously, though, thanks for updating!

Might I also suggest just accepting Alan's answer here or adding one of your own.

Found this image here. I've also seen references to the "closed orange ear patch" of the King Penguin, which fits with the image. So my vote is for the DK image being a King Penguin.

Are you an expert at this? Ornithologist or something? That would be of more value for me. I have the same opinion as you have because of the closed orange ear patch. But maybe there are other indicators which are not that obvious for us amateurs.

No I'm not an expert, just an amateur like you.


text:
How did the roar evolve from snort?
When Lions roar, or Dogs show aggression, they do that snort-roar thing. They're producing sound while inhaling. How did that come to be when all (?) other forms of sound involve exhaling?
Humans do produce sound while snoring, but that's merely a by-product of it.
And while people could very well speak by inhaling, they don't do that in their regular communication. Lions and Dogs do. Why/when did they decide that (inhaling sound production) was a better/more effective means of making sound?

Snoring involves generating sound while inhaling, and people can speak while inhaling as well.

@MattDMo Addressed your comment into my question


text:
What's the difference between diuretic veggies and alcohol that make the latter bad?
So I'm reading this article to Treat Fluid Retention and it suggests

Eat foods with diuretic properties.

But also

Avoid drinks that will dehydrate the body such as tea, coffee and alcohol.

As I understand, tea, coffee and alcohol are plenty diuretic. So what makes those veggies's diuretic nature better than alcohol's?
I know alcohol is more harmful than veggies, but I mainly wanted to know how do diuretic veggies help you when infact the diuretic alcohol actually makes you dehyderated? How's veggies' diuretic nature more helpful than the alcohol's (disregarding other side-effects of it)?

This question is primarily concerned with the mechanism behind a supposed effect of certain vegetables, and does not ask for any treatment suggestions. Voting to reopen.

Firstly I would suggest if you have concerns about suffering from symptoms fluid overload you should consult your doctor. Self diagnosis and self treatment is not a good option.
In terms of alcohol being used as a diuretic, you have to bear in mind that there are many deleterious effects of excess alcohol. By consuming alcohol as a diuretic you would most likely cause more health problems than you solve.

I was just researching remedies for Puffy face, nothing too serious. I know alcohol is more harmful than veggies, but I mainly wanted to know how do diuretic veggies help you when infact the diuretic alcohol actually makes you dehyderated? How's veggies' diuretic nature more helpful than the alcohol's (disregarding other side-effects of it)?


text:
What is the equivalent of shutter-speed in Human eye?
I just learned that in video cameras, every frame of the video has its own shutter speed.

And I know how frame-rate in human eye works out, well, not completely, hence the question.
http://en.wikipedia.org/wiki/Frame_rate

The human eye and its brain interface, the human visual system, can process 10 to 12 separate images per second, perceiving them individually.

How much (or what is the equivalent of) shutter-speed in those individual images?

Related Q?: Is it a limitation of the eyes or the brain that we cant see a moving bullet

See also http://en.wikipedia.org/wiki/Flicker_fusion_threshold

Many people can tell the difference between 60 FPS and 144 FPS monitors. Cameras and LCD's are changing from 30 to 60 to 120 FPS. Conversely, even professional gamers can't really tell the difference between 120 and 240 FPS monitors. That's not exactly equivalent to the eye shutter speed though, it can be because of eye tracking of lower FPS movement.

The light receptor of the eye is a protein called Rhodopsin.  To me the equivalent of shutter speed for the eye is the (de)sensitization of rhodopsin by phosphorylation.  The brighter the light, the more sites on rhodopsin are phosphorylated, diminishing the intensity of the signal coming from the photo receptor via the transducin G protein that conveys the visual signal onward.
This process takes a few seconds, but then it's possible to see when stepping into sunlight or in a darkened room.
This is more like a volume knob than a shutter speed since the same signal comes out at the same rate of each light sensor, but it has a similar effect — it modulates the intensity of the image.
Actually I feel dumb but there is a simple answer to this question.  You can get lost in the above physiology. The simpler answer is about 20 fps.  Whenever strobing stops and persistence of vision takes over to create a continuous image is an interesting way to answer this question.  That's how television and movies (and videos) work. 30 fps looks pretty smooth.  It's not a perfect answer because 60 or 100 fps are functionally useful for situations like video games where fast reaction time is important.

If we are comparing with a camera, I would say this is more like the ISO rather than the shutter speed.

good point.  the right answer might be the speed with which the optical nerve assembles the information from the eye.  that is harder to explain or define though.  nerves each act independently and do not synchronize the way a machine does.

There is nothing comparable to a shutter of the camera in the eye. The eyelid is like a lens hood. When the eyelid is open the image is continuously projected on to the retina unlike in a movie camera. However if the question is on frames per second (number of static images) required to produce a sense of seamless motion this article might be of some help. In video camera instead of a shutter speed it is the number of times the image on the sensor is sampled(recorded) per second electronically. The eye is more similar to a video camera. The retina has rods and cones which has variable 'refresher' rates which makes it more complicated to calculate exact figures.

Not all of your rods/cones fire at any given moment.  Exception is when a bright flash of light is viewed.  Recovery time from the resulting flash blindness is pretty slow -- seconds.  But there's some photobleaching there, so maybe that's not fair.


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Are there organisms that have incorporated plastic into their lives?
Are there organisms that have incorporated (manmade) plastic into their lives in any way? Either in their diet, or as a part of their body?

What do you mean by "plastic"? Manmade, oilbased plastics?

@Chris Yes, Manmade plastic.

It's not appropriate as an answer given the 'manmade' specification, but I have to mention the bee genus Colletes ('polyster bees') here, since they actually make their own plastic: http://www.scientificamerican.com/article/from-pollen-to-polyester/ (and http://opus.bath.ac.uk/31888/). Thanks to @george-law for drawing my attention to these in his answer here: http://biology.stackexchange.com/questions/47898/bee-identification

Biodegradable waste is a type of waste which can be broken down, in a
  reasonable amount of time, into its base compounds by micro-organisms
  and other living things, regardless of what those compounds may be.

from wikipedia

So yes, there are microbes which are capable of biodegradating manmade plastic. It depends on plastic types.
If you meant creating new pathways to biodegradate non-biodegradable plastics, then I don't think so. My opinion that by some of those plastics there are theoretical barriers (e.g. energy barriers or toxic byproducts), and by some of them evolution might create a pathway in time (I don't think in our lifetime, but nothing is impossible).
There are microbes which build plastics to store energy. They are just polymers like starch or cellulose (sugar polymers), with different building stones... Afaik the first biodegradable plastics came from here, but so they were very expensive. Nowadays we don't need microbes in the polymerization process, e.g. we can create polylactic-acid without the presence of microbes.
edit:
I have found an interesting article in the topic.

Now, for the first time, researchers have found detailed evidence that
  bacteria in an animal’s gut can safely biodegrade plastic and
  potentially help reduce the environmental impact of plastic in
  landfill and elsewhere. The animal in question? The humble mealworm –
  which turns out to be not so humble after all.
Researchers led by Stanford University in US and Beihang University in
  China found that the mealworm – the larval form of the darkling beetle
  – can safely subsist on a diet of Styrofoam and other kinds of
  polystyrene, with bacteria in the worm’s gut biodegrading the plastic
  as part of its digestive process. The findings are significant because
  it was previously thought that these substances were non-biodegradable
  – meaning they ended up in landfill (or worse, our oceans, where
  they’d accumulate for decades).

ScienceAlert - Scientists find worms can safely eat the plastic in our garbage

One example: The Satin Bowerbird (Ptilonorhynchus violaceus).
The males of this species build structures out of sticks (suprisingly called bowers) that they decorate with blue items to attract potential mates. Recent research has shown that the males have began incorporating plastics into these structures for courtship.
A google image search can confirm pictures of this. In this study: "Sexual selection drives rapid divergence in Bowerbird display traits"
researchers provided the birds with square plastic tiles, that were ultimately incorporated into bowers.

I don't know if this qualifies as "incorporated ... into their lives", but Hermit crabs use all sorts of man-made materials as housing/protection. If you do a google image search on "hermit crab plastic you will see many examples, including plastic waste.
There are also other animals that use random materials that are lying around to construct housing/cases, and I can imagine that e.g. Trichoptera larvae will occationally include pieces of plastic in their cases. At least they will use gold and pearls (when not given an option). However, these are not really examples of species that have adapted specifically to plastic to use it as a resource.


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Are autoantibodies against intracellular proteins "functional"?
Autoantibodies against intracellular proteins have been detected in some autoimmune diseases (For example, TRIM21 in Sjögren's syndrome and NALP5 in Autoimmune Polyendocrine Syndrome Type 1).
My question is are these autoantibodies functional (e.g. play certain roles in the diseases) or are they just the byproducts of pathological processes?
Regarding the first case scenario, it is highly unlikely that these autoantibodies can penetrate the cell membrane to interact with the intracellular autoantigens.
The second case scenario sounds more probable to me. For example, some processes may cause cell death and lysis, thus release intracellular proteins. Local inflammation can co-occur and may trigger the formation of autoantibodies.

This review sketches out some of the scenarios from the point of view of cancer therapy.  Some of them are unlikely, though I wouldn't say impossible, to happen naturally, but others are likely to be relevant.

@MikeSerfas Thank you. The third possibility "Antibodies can also be generated that bind cell surface major histocompatibility complex class I (MHC-I)-presented peptides that are derived from intracellular proteins." is brilliant. I should have thought of it.

Thus your question "are these autoantibodies functional" is to be answered to the positive: yes, cells presenting these antigens are led to apoptosis by T cytotocic cells? Just to make sure.


text:
Why the "cfr." in 'Cirrhipathes cfr. anguina' and not "cf."?
Recently I stumbled upon the species name Cirrhipathes anguina. In the literature it is often mentioned as Cirrhipathes cfr. anguina. What does cfr. mean? Does it carry the same meaning as cf.?
Edit: If the same, why is cfr. used in this case and not just .cf?

Thank you for the answers. Given that you answered at the same time and equally well I added another question :)

I've seen both cf. and cfr. used in literature. According to Wiktionary, cf. is an abbreviation of the Latin confer whereas cfr. is an abbreviation of the Italian confrontare, both of which mean compare. It's probably just a stylistic choice by the authors, perhaps depending on their country of origin. I doubt you'll get a better answer than the ones given.

It's the same as cf. Both abbreviate confer-- meaning the specimen has most of the defining features of the species indicated, and the ID would likely be confirmed with comparison to reference material.
Ref: Sigovini, M. et al. 2016. Open nomenclature in the biodiversity era. Methods Ecol Evol. 7: 1217-1225. http://onlinelibrary.wiley.com/doi/10.1111/2041-210X.12594/abstract

Whoaa that was a simultaneous post :-) +1

The Wikipedia page explains cf. as:

In biological naming conventions, cf. is commonly placed between the genus name name and the species name to describe a specimen that is difficult to identify because of practical difficulties, such as the specimen being poorly preserved. For example, "Barbus cf. holotaenia" implies that the specimen is believed to be Barbus holotaenia but the actual identification cannot be certain.

And from Habitas it becomes apparent that cf. is indeed synonymous to cfr., both being abbreviations for confer:

cf., cfr., confer. : Latin, compare (with)
character, taxonomic : any attribute of a member of a taxon by which
  it differs or may differ from a member of a different taxonomy.

Yup, it was indeed! Great minds and all that. :)


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Why doesn't Diabetes cause death by starvation?
The main cause for diabetes is lack of insulin in the body. Insulin is the hormone that allows body cells to absorb glucose from the blood. With out insulin, the body cells can't get glucose from the blood. So, why doesn't diabetes cause death by starvation?

I mean, the short answer is "it does". But on a cellular level, and unevenly. So the effects are a little different. Most of this stuff happens with regular starvation also: http://www.diabetes.org/living-with-diabetes/complications/ketoacidosis-dka.html

Diabetes before the advent of insulin therapy

Not all cells depend on insulin to take in glucose from blood (e.g. vascular endothelial cells). But the majority do (muscle tissue and fat tissue).
The lack of insulin causes the cell to use auxiliary metabolic pathways to generate its energy [1]:

in muscle, the protein breakdown is stimulated
liver gluconeogenesis is stimulated by low insulin levels and high amino acid levels in blood and using substrate from muscle and fat tissue
glucocorticoids stimulate lipolysis
liver starts ketone body synthesis, which along with medium chain fatty acids prove to be quite a good alternative energy source for the brain

Energy from nutritional principles is as follows:

Lipids = 9 kcal/g
Proteins = 4 kcal/g
Carbohydrates = 4 kcal/g - the most important because they are used as is. Lipids and proteins require energy from other sources to start chemical reactions which yield energy.

References:

Mark Brandt, Ph.D. Endocrine Notes Supplement from Rose Hulman Institute of Technology, pages 78-80
Wikipedia (links)

Glucose enters your cells via a family of transporters.  A primary transporter in muscle and fat cells is known as GLUT-4.  Insulin stimulates GLUT-4 to move from the interior of a cell to the cell surface, where the glucose can then bind to the GLUT-4 transporter and enter the cell.  However, there are plenty of glucose transporters on the cell surface, even when there is no insulin.  In fact, there are enough transporters on the cell surface to allow the cell to get enough glucose to sustain its energy needs.  Thus, glucose transport into cells is never truly dependent upon insulin.  Insulin enhances the uptake of glucose into cells, but it is not required for it.  In fact, when you knock out the insulin receptor in mice so that insulin cannot stimulate glucose uptake into muscle or fat cells (yet you keep the insulin receptor intact on other cells like brain and liver), the animals do not become diabetic and they have normal blood sugars.-https://www.ncbi.nlm.nih.gov/pubmed/15254588
Metabolic tracer studies have allowed us to learn how insulin operates in humans in vivo. When you take a type I diabetic off insulin, blood glucose climbs sharply. However, it's not because glucose can't get into cells. In fact, glucose uptake into cells actually increases. This is because the concentration of glucose in the blood is so much higher than the cellular concentration that glucose must move into the cells (remember, there's already enough glucose transporters on the cell surface even if there's no insulin). So why does blood glucose climb so high? Remember that the amount of glucose in your blood is both a function of how much glucose is entering the blood (the rate of appearance), as well as how much glucose is leaving the blood (the rate of disappearance). In a fasted diabetic without insulin, all of the glucose is coming from the liver. Remember that your liver helps maintain blood sugar levels when you are fasted by releasing glucose; this glucose comes from both gluconeogenesis (the formation of glucose from non-carbohydrate sources, like protein) and glycogenolysis (the breakdown of glycogen stored in your liver). Insulin acts as a brake (a chalone as Dr. Schafer described it) on these processes. Thus, when you do not have insulin, you have runaway gluconeogenesis and glycogenolysis. The high blood sugar in an uncontrolled diabetic is thus caused by overproduction of glucose from the liver, not because glucose can't get into cells.-http://m.bja.oxfordjournals.org/content/85/1/69.short


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Do insomniacs yawn?
According to wikipedia, the jury is still out on the function a yawn serves. The article referenced above however writes to say

Yawning most often occurs in adults immediately before and after sleep, during tedious activities and as a result of its infectious quality. It is commonly associated with tiredness, stress, overwork, lack of stimulation and boredom, though studies show it may be linked to the cooling of the brain

The first sentence there draws my attention. Given a yawn is almost definitely associated with sleep - being expected to occur immediately before, and after.
Does it follow that an insomniac does not yawn?
As a corollary, are there any known medical conditions which preclude the act of yawning? For instance, a comatose person probably does not yawn.

Anecdotally, YES insomniacs yawn. Especially when tired from not sleeping

Of course. As you quoted from Wikipedia:

It is commonly associated with tiredness, stress, overwork, lack of stimulation and boredom.

Insomniacs, because they can't get a good sleep, are more tired and stressed than the others.


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In what animal species is the sex ratio skewed in favour of the fertile female?
Ants have something like a single fertile female to several males. The same applies to bees, and larger animals - elephants too. Is the sex ratio universally skewed in favour of the female? What animal species exhibit this ?

You mean for animals, right? You get all sorts of crazy sex ratios (and crazy sexes!) going on in plants.

So just to be clear, you're looking for animals who have sex ratios of male:female <1:>1 in the population, right? Sex ratios within broods, as opposed to within populations can behave strangely.

@Oreotrephes: Yep. Thanks. Just updated the title

It is advantageous to have a skew towards more males. Males can be expendable as they are only required briefly for impregnation and can then focus on providing resources for the mother and young and protection. This breaks down when this is no longer the case, for example in humans we are closer to a 50/50 divide.
This article notes that in aphids, there are twice as many females as males, the same is true for daphnia. I don't think the reason behind this is known. In reptiles, the female to male ratio can depend on temperature of incubation thus this can lead to strong fluctuations.
An interesting principle is Fisher's principle:

Fisher’s principle explains why for most species, the sex ratio is
  approximately 1:1. Bill Hamilton expounded Fisher’s argument in his
  1967 paper on “Extraordinary sex ratios” as follows, given the
  assumption of equal parental expenditure on offspring of both sexes.
  Suppose male births are less common than female. A newborn male then
  has better mating prospects than a newborn female, and therefore can
  expect to have more offspring. Therefore parents genetically disposed
  to produce males tend to have more than average numbers of
  grandchildren born to them. Therefore the genes for male-producing
  tendencies spread, and male births become more common. As the 1:1 sex
  ratio is approached, the advantage associated with producing males
  dies away. The same reasoning holds if females are substituted for
  males throughout. Therefore 1:1 is the equilibrium ratio.
  Source

At least in some species, aphids have nested parthenogenic vivipary, that is, a female may be pregnant with a female child who is pregnant. Of course, this can result in rapid population growth, and if selected for would explain a higher female ratio.

In rock hyraxes, similar to elephants, the sex ratio of male to females are between 2:3 and 1:3. Since subadult males are pushed from the population by the territorial male just before they become sexually active. When looking at adult hyraxes, however, the females can outnumber the males by quite some margin.
Recent studies had shown an adult sex ratio of ♂1:♀17 & that the male to female ratio, in populations situated in residential areas, does not show such a big difference.
https://www.ncbi.nlm.nih.gov/pubmed/24899114


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Is there any evolutionary/physiological advantage to multi-lateral symmetry?
Just wondering ; I get the impression a large number of multicellular organisms are multi-lateral in their physical structure. Why would evolution/mutation have retained multi-lateral symmetry in an organism? What advantage/s does symmetry provide an organism?
EDIT:
By multi-lateral symmetry I mean at-least bi-lateral symmetry (as in the case of many beings such as elephants, crabs and fishes), but perhaps more than bi-lateral too (starfish come to mind)
END EDIT:

Could you explain what you mean by multi-lateral symmetry or give examples?

Similar to: http://biology.stackexchange.com/questions/5588/why-is-most-life-symmetrical-externally-but-not-internally

@Kevin: Thank you. The question you found is very similar; it didn't appear in my search for 'symmetry' 'physiology' when i looked - hence this question posted.

Signs of symmetry are determined by the environment. Completely isotropic ecological niche corresponds to the maximum degree of symmetry of organisms (spherical symmetry). Asymmetrization on the axis "up-down" took place under the influence of gravity field and lead to radial symmetry. Bilateral symmetry of the multicellular animals arose with movement.

Bilateral symmetry of the multicellular animals arose with movement is there any place where I could read more on that matter?

Evolution works by tinkering, not engineering.  Gaining an evolutionary advantage in a simple way is rewarded, as is simplicity generally.  Symmetry allows for relatively greater simplicity at the genetic information level (modular body parts driven by repeated application of same genetic instructions).  Without symmetry, more genetic information would be needed to construct a similarly complex organism (symmetric like), with the concomitant exposure to increased genetic degradation.


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How is hibernation/aestivation different from anesthesia?
How do hibernation/aestivation happen?
I read on wikipedia that a squirrel injected with the body fluids of a hibernating fellow is more prone to hibernation. If hibernation/aestivation are driven by biochemicals and not merely the weather, can the process be induced in higher beings such as humans to replace surgical (etc) anesthesia? How is the one different from the other?
p.s. Or perhaps to induce hibernation for the trip across the Solar System (+:

What makes you think that changes related to the seasons are not "biochemically induced"?

Because there appears to be a temperature component involved leading to either deep or shallow 'slumber'.

surely, but all of these things are mediated by hormones (or in general blood-borne molecules) at the end of the day...

I'm assuming you're referring to general anesthesia, which still encompasses many types of mechanisms. Here's an interesting article about whether humans can hibernate. It's not a true scientific paper, but it brings up some interesting points.

@nico: don't have an argument to present against that ... perhaps this is a ppoor example, but if a person has a sneezing fit whenever it's going to rain - that wouldn't necessarily mean the fit was caused by hormones

@Everyone: I said hormone, but I could have said chemical. What I mean is that if you have an external influence (wheather, temperature, humidity, whatever) on your body, it will convert it to some chemical signal at some point.

But that applies to voluntary actions too - even moving a muscle is ultimately a biochemical process ( I could be wrong though ...)

Neurons are ultimately electrochemical, but nearly all biological decision-making over minutes, hours, or longer is hormones/chemical signals in the blood or brain. Tiredness, puberty, hunger, allergies, sweating, thirst, how bees know when their queen is dead, etc are all chemical or hormonal.

I'm going to answer the question of whether aestivation/hibernation can be activated in humans or other apes, because it's more interesting.
Mammals, as a clade, have three major subgroups. Bats, shrew-likes, rodents, and then everything else including primates. One family of the shrew-likes hibernates, some rodents(but not all) and some bats can hibernate or enter a period of extended torpor. The only kind of primate that can hibernate is the dwarf lemur, which does so in a strange way(fully asleep for 6-8 months, little regulation of body temperature). Other hibernating animals regulate their temperature but keep it low, and wake to roll over or whatever every couple of days. Plus lemurs are on the edge of the mammal cladogram, so they're just pretty weird.
Phylogenetically, it's not likely(imho, but I'm not a mammalian phylogenetics expert) a primate ancestor of humans has ever had the ability to hibernate. It seems more likely that primates lost the ability if it was a capability of mammalian ancestors and dwarf lemurs re-evolved it. It's possible atavistic remnants of such a system might still exist, but extensive hormonal and possibly surgical treatments would be required to induce it. Not to mention you can wake animals from hibernation by poking them, so it probably would be a substandard anaesthesia method.


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How are geneticists able to isolate gene functions?
As an example, this Scientific American article describes a known area in the dog genome that metabolizes carbohydrates.
How is it that researchers are able to determine specific functions such as this?

Lots of ways. Gene knockout, gain of function, biochemical assays, etc...

@LanceLafontaine if you have a more detailed answer, please submit it as an answer rather than a comment.

@LanceLafontaine suggested a few ways above, but I would recommend reading this section
in Alberts' Molecular Biology of the Cell, which gives a more descriptive overview of some approaches, but even that is not exhaustive.
An extremely simplistic and also not exhaustive summary:

observe mutants, see what processes are disrupted, and map these back to particular mutations
mutate a gene and see what processes are disrupted
biochemical studies to see, for example, which proteins (which are gene products) interact in vivo and things like where they're localized, which may hint at function.
analyze structure of proteins, see how similar they are to other proteins with known function, and infer that the protein of interest probably has a similar function

EDIT: The link to Alberts is to the 2002 edition (which is free online; the latest edition of the textbook costs around $200), so things have come a long way since then, but the underlying approaches are still in use.


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What could cause hairs to gray at the tips but not the roots?
I have noticed that some of my sporadic gray hairs are gray at the tip side but oddly, not near the roots.  Some are even only gray in the middle.  I find all of this very counter intuitive, and I assure you nobody is secretly dying my hair.
How does the graying process work, and how is it that this can be happening?

I have the same, I take it a good sign though - Benjamin Button kind of vibe. Not all, but quite a few grey hair are dark at the root. If I had to guess what could be causing it - I would say: stress, keto diet, lack of sleep (causing grey hair), and once those things are removed coloured hair start growing again. Though it's pure speculation on a sample of one.

When Googled, this question only comes up with this and one Quora post with the rest about how hairs grey starting at the roots. I'll submit what was in the Quora post to help someone find information: One person claimed swimming a lot in chlorinated water could bleach the tips of hair. Another person said exposure to sunlight might do this. A final person said it could be from damaged hair (split ends, etc.), meaning the fix is a trim to get rid of the damaged hairs. That last one matched my scenario best. I'll see if my hair becomes grey at the tips again after a trim.

After years of this, I am still wondering what the heck is going on. My informal observations are that for virtually all hairs that aren't entirely grey, the grey part is the part closer to the root, with typically a fairly distinct cutoff where it becomes grey. For what it's worth, these are chest hairs.

Interesting question, I am not sure if I have a definite answer, but at least some ideas:
The pigment in the hair is made by specialized cells, the melanocytes. The make the pigment (eumelanin=dark and pheomelanin=red/yellowish) which is then deposited into the growing hair. They are located at the bottom of hair bulb and usually die at the end of each hair cycle. To have the hair of the next hair cycle colored as well, this melanocyte population in the hair bulb needs to be replenished. This is done by melanocate stem cells, which live in the hair bulge and which start to reproduce and differentiate in melanocyte which then migrate down to the hair bulb. There is an excellent article following this process:

Mechanisms of hair graying: incomplete melanocyte stem cell
maintenance in the niche.

The hair later gets grey (low pigment) and white (no pigment) when these melanocytes are not, or not fulley replenished in later hair cycles. Why this happens, there are a few hypothesis.
First, its possible, that with age the melanocyte stem cell population (which not only need to replenish the melanocytes, but also need to maintain its own population) is getting smaller and disappears over time. This process would explain gradually graying over time. See this reference:

Melanocyte stem cell maintenance and hair graying.

Another possibility is the presence of reactive oxigen species (ROS) which occur naturally in melanocytes. Over time, the enzyme which intercepts this ROS (catalase) is getting less active or present in the cells and thus oxidative damage is getting bigger, damaging the melanocytes and their ability to make pigment. It would actually bleach itself...

Senile hair graying: H2O2-mediated oxidative stress affects human
hair color by blunting methionine sulfoxide repair

Melanin has also an important role in intercepting ROS, so in this process less and less pigment is made (as the damage accumulates) and this also leads to hair, which is less pigmented for exogeneous oxidative stress:

Towards a "free radical theory of graying": melanocyte apoptosis in
the aging human hair follicle is an indicator of oxidative stress
induced tissue damage.

It could be possible (and this is a wild guess) that the phenomenon of the tips graying first is situated by this. Hair less protected against exogeneous oxidative stress (smoke, UV etc.) so the melanin is "used up" during this until the hair greys at the tip, since its the oldest and most exposed part of the hair. This article by Tobin gives also a nice overview:

The cell biology of human hair follicle pigmentation

Your hair grows out from the roots, and typically as you age, the pigments (melanin) that would normally keep your hair a certain colour are not produced anymore because the pigment producing cells (melanocytes) start to die.
They're likely different colours in the middle because that will be the result of a gradual dying off of the melanocytes at the base of that strand. As a result the root (newest part of the hair) will typically be gray when they have mostly all died off, the middle will have a bit of melanin because it was produced when there were still some functional melanocytes, and the tip (the oldest part of the hair) will still be full of melanin from when it was produced when the melanocytes were alive.
As for why this happens it's not fully understood why the melanocytes die as we age, but the gene Bcl-2 has been found to be essential for the maintenance of melanocytes. Mutations in this gene could be responsible for premature graying [1]. There is some literature on the role of Bcl2 family genes as regulators of cell death [2][3] but how these things are connected seems largely still unknown.
[1] http://www.nbcnews.com/id/6750793/ns/health-cancer/t/research-yields-clues-why-hair-turns-gray/#.UVCu21dONvJ
[2] http://www.annualreviews.org/doi/abs/10.1146/annurev.immunol.16.1.395?journalCode=immunol
[3] http://genomics.senescence.info/genes/entry.php?hgnc=BCL2
There have been some reports of people indicating that a change in lifestyle and/or diet have led to a decrease in gray hairs, or even that the hair begins to regain its colour leaving a gray section at the tip or in the middle. I've only found one relevant article which makes reference to some research into the restoration of hair growth and colour in mice[4]. An American group are studying the role of the Wnt signaling protein in controlling the activity of melanocytes. I'm just speculating here, but it could be that fluctuations in Wnt protein production (possibly influenced by diet and lifestyle and overall health) may switch melanocyte melanin production on and off. I haven't been able to find any literature to back up this hypothesis though.
[4] http://inventors.about.com/od/gstartinventions/a/Cure-For-Grey-Hair.htm

Sorry, I realized I mis-typed what actually happens.  The counter intuitive aspect is seeing gray tips or middles, not roots, like one would expect.. editing.

I edited my question; if you could please update your answer to reflect my corrected question, that would be great.

The last link is at least questionable. TRP-2 (or usually called DCT) is of course also present in follicular melanocytes in the hair, otherwise there would be not eumelanin (dark) pigmentation. The observation that Wnt may play a role is pretty broad, since Wnt signalling is essential for the melanocyte to function. I can go through my library tomorrow and write some more about it if wanted (the topic is pretty old).

This is a consistent phenomenon with me and I don't live a stressful life and eat pretty consistently, so I'm skeptical that it's environmental.  About 20 to 30% of my graying hairs are like this (black at the roots, gray on the oldest half.)  @Chris I'd love to hear more.

@JeffAxelrod Done. Took a bit longer than anticipated.

I think this is not the best answer here to the question. Chris covers the topic better, I think, since he mentions H2O2 mediated oxidative stress, and ROS, too. All answers could cover Genetics more clearly. Nevertheless, I like the mentioning of Bcl2 here.


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When a Lysosome's bonding sites all get bonded to, what is the most resource and energy efficient way to handle the used Lysosome?
Let's say a Lysosome that bonds to a hazardous material to neutralize it has all bonding sites used up. would it be more safe / efficient to excrete the entire Lysosome / hazardous material molecule or to bring it to a certain organelle / organ to unbind the material and send it for excretion and then have the Lysosome available for use again? In which way do Lysosomes in nature commonly handle this problem?

Enzymes are catalysts, i.e. by definition they don't get used up. More info on "cellular garbage disposal" can be found here: http://en.wikipedia.org/wiki/Lysosome

Are you sure that you are referring to enzymes? Sounds more like you are talking about things like hemoglobin (not an enzyme), which binds to the waste product CO2 and carries it to the lungs for excretion.

okay yeah, see, I learned something I didn't even  realize I was going to. updating question to fit Lysosomes. Does it make more sense now what I was asking?