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Why are there no wheeled animals?
In physics, "almost everything is already discovered, and all that remains is to fill a few unimportant holes." (See Jolly.) Therefore, on Physics SE, people are veering off into different directions: biology, for example.
Thus, it happens that a question about bicycles generates some discussion about evolution in biology and animals with wheels.
Three explanations are offered for the apparent lack of wheely animals (also on Wikipedia, where, by the way, most Physics SE questions are answered perfectly).

Evolutionary constraints: "[A] complex structure or system will not evolve if its incomplete form provides no benefit to an organism."
Developmental and anatomical constraints.
Wheels have significant disadvantages (e.g., when not on roads).

Now, I suggest that all three can be "solved".

With time.
With a symbiotic relationship between a wheel-like animal and a "driver"-like animal, although this gets awfully close to a "driver"-animal to jump onto an actual (man-made) wheel. (So, perhaps, you can suggest a better loophole around this constraint.)
Roads are presumably not the only ecological niche where animals with wheels could thrive. I'm thinking of frozen lakes, although there skates would be better than wheels.

What, therefore, is the explanation for there not being any wheeled animals?
Please consider, in your answer, the counterfactual: What assumption of yours would be falsified once a wheely animal is discovered?

There is no one single explanation for such questions, we can only speculate (with well-reasoned arguments, I hope) about this.

You may enjoy reading the Uplift Saga books by David Brin (quite an accomplished astrophysicist himself). They contain some of my favorite aliens in sci-fi, including the wheeled G'Kek!

There's a nice video from VSauce about that topic, explained for the average Biology Joe like me: http://www.youtube.com/watch?v=sAGEOKAG0zw Michael answers various questions of this type on his channel, very interesting and entertaining.

His Dark Materials gives a good answer to this (spoiler: it has wheeled animals)

@KonradRudolph it does? Damn, I should read it again, I don't remember them.

@terdon Hehe, and I likewise forgot about the G’Kek. But re-reading the Uplift Saga is time well spent anyway. ;-)

For the same reason why humans cant fly. It was never selected for.

Here is a very good video on this subject from vSauce: https://www.youtube.com/watch?v=sAGEOKAG0zw

Damn... didn't see it. Sorry.

@RaduMurzea No worries. Let's delete our comments please.

Not exactly what you asked, but possible a step in the direction; The Dutch graphic artist M.C. Escher devised a "wentelteefje" or "curl-up" animal. see here (i don't know how to embed a youtube video here)

There is an entire wikipedia article dedicated to this question.

If there is any "rolling-organ", that need not revert-back, would be disconnected from whole body; like the cart-wheel is physically disconnected from its axial rod.

I'm voting to close this question as off-topic because it is unanswerable and ridiculous.

You answered yourself, because there are no roads in the nature therefore it is not selected naturally.

@WYSIWYG -Nice link, interesting read.

Wheels are possible on the molecular level — bacterial flagella are rotating cores inside a molecular motor, but wheels larger than the flagellum have not really been found.

Defining a wheel as a freely rotating joint that can rotate indefinitely in one direction, a single animal with a wheel is an improbable* development that would require a single animal have two separate parts (axle/wheel and body).
[*read as: pretty much impossible]
It's hard to imagine how such a thing could evolve.  A wheel and axle would need to be made of living tissue, otherwise it would be vulnerable to wear and tear.  Wheels also have problems going over uneven terrain, which is really all terrain animals live in.  It's difficult to imagine what sort of selection conditions would be strong enough to push animals away from legs.
If you include driver-vehicle symbionts where the 'car' and 'wheel' are actually two animals, then they have evolved. Parasites can have all sorts of symbiotic control over their victims including as means of transport. The Jewel Wasp is one which is the most suggestive of what you may be thinking. The wasp stings its victim (a cockroach) in the thorax to immobilize the animal and then again just behind its head.  After this, the wasp can ride the beetle, steering it by holding its antennae back to its nest where the roach is immobilized to feed the wasp larvae there.
(see section "Pet cockaroaches" in this reference.)
As to the three schools of thought you added to the question, I would probably rather say there were two strong arguments against.  The first is whether there is an evolutionary path to wheels (argument 1 in your question), which I doubt.  Given even a large amount of evolutionary time you will not see a naked human being able to fly on their own power.  Too many structural characteristics of the body plan have been made to all be reversed so that wings or other means of aerial conveyance will show up. The same can be said for wheels when the body plans have fins/legs/and wings already.
Argument 3, which I also tend to agree with, is perhaps more convincing.  By the time a pair of animals makes a symbiotic relationship to do this, or a single macroscopic animal evolves wheels, they will literally develop legs and walk away. When life came onto the land this happened, and since then it's happened several times.  It's sort of like saying that the random movement of water molecules might line up to run a stream uphill. There's just such a strong path downwards, that the statistical chances of you seeing it happen are nil.
This is a hypothetical case, but arguing this in a convincing way I think you would need to lay out:  a) an environment whose conditions created enough of a selective advantage for wheels to evolve over legs or other similar adaptations we already see. Perhaps based on the energy efficiency of wheels;   b) some sort of physiological model for the wheels that convey a reasonable lifestyle for the wheel.
There are lots of questions that would need to be satisfied in our thought experiment.  Here are some: "the symbiotic wheel would be spinning constantly; if it died the driver creature would be completely defenseless"; "if the ground were bumpy, all these wheeled animals would get eaten"; "the wheel symbiont — how would it eat while its spinning all the time? Only fed by the driver? Even symbionts such as barnacles or lampreys on the flanks of sharks still have their own ability to feed."
For many similar questions the same sort of discussion ensues where there are many disadvantages which outweigh advantages for animals. e.g. "why are all the flying animals and fish and plants even more similar to airplanes than helicopters?"
Sorry if I seem negative, but way back in grad school I actually did go over some of these angles.

UPDATE: First Gear found in a Living Creature.
A European plant-hopper insect with one of the largest accelerations known in biology has been found to have gears!  (There's a movie on the article page.
)
The little bug has gears in its exoskeleton that synchronize its two jumping legs.  Once again selection surprises.

The gears themselves are an oddity. With gear teeth shaped like cresting waves, they look nothing like what you'd find in your car or in a fancy watch.  There could be two reasons for this. Through a mathematical oddity, there is a limitless number of ways to design intermeshing gears. So, either nature evolved one solution at random, or, as Gregory Sutton, coauthor of the paper and insect researcher at the University of Bristol, suspects, the shape of the issus's gear is particularly apt for the job it does. It's built for "high precision and speed in one direction," he says.

The gears do not rotate 360 degrees, but appear on the surface of two joints to synchronize them as they wind up like a circular spring.  The gear itself is not living tissue, so the bug solves the problem of regenerating the gear by growing a new set when it molts (i.e. gears that continually regenerate and heal are still unknown).  It also does not keep its gears throughout its lifecycle.  So the arguments here still stand; the exception still supports the rule.
Additional Note: In his book "the God Delusion" (Chapter 4 somewhere) Richard Dawkins muses that the flagellar motor is the only example of a freely rotating axle that he knows of, and that a wheeled animal might be a true example of 'irreducibly complexity' in biology... but the fact that there is no such example is probably to the point.

Thanks! (Is there a word missing or something else wrong in the 2nd paragraph? I can't understand the sentence properly.) Should I take your answer as follows: Wheeled animals must have two separable parts; that is unlikely, because it hasn't happened.

I did an edit for clarity.  It is just a theory as they say, but i don't think its really possible for a single animal to be made of two separable and rejoinable parts such as would be required to have an axle of a wheel.   Nothing even remotely like this has ever occurred in biology as far as I can see. That's not at all to say that we have seen everything that biology can do.  I'll try to formulate a specific principle it violates, but really two living independent parts are two creatures... symbionts don't really live this way.

So, "this" refers to the flagellum? 2) Also, I shifted my speculations to exoskeletons turning into wheels. :)

@Gugg you're right its a sentence fragment caused by my sporadic dementia.  I have outlined a response to the exoskeleton idea; legs have a lot going for them.  Its always possible... but it just might never show up.

OK, great! Now, onto my request in the question. Suppose a wheeled animal would be discovered tomorrow (and you wouldn't be given further information than that). What assumption would you drop first/doubt most?

I guess that would be my assumption that the animal somehow managed to nourish a living wheel/axle system and not be separate from the rest of the animal.  the exoskeleton is not a bad idea.  Another possibility is that somehow that legs / wings are better forms of locomotion than wheels for all environments that animals currently live in.

Thanks. That seems to put you (primarily) in the anatomical camp 2. (And secondarily in camp 3.)

You are getting more clear with your argument for, but there is still a ways to go -I added some response to my answer here.  Its a good exercise to think this through.  Good one.

I think I would argue that there are serious issues in all three categories here.  Maybe the anatomical arguments are less important than the evolutionary constraints.  I guess that would be #1 for me since the anatomical argument is based on the idea that the anatomy of wheels are just too many adaptations away from what we have now.  The inefficiencies of wheels make that evolutionary distance even greater.

Many thanks for your thoughts on this! Quite helpful to a layman.

you're not so much a layman anymore ! :) good question.

Heh, I just saw the geared animal article and came back to this question to make a comment about it.  But shigeta beat me to it! :)

here's a +1 anyway :)

Having two symbiotic creatures, one wheel and one body would be interesting. A bit like a wheelbarrow but with back legs that kick to propel the creature forward, resting on the front wheel creature. It is hard to imagine it being a practical or survivable.

I guess there is also nothing preventing two or more creatures being gestated simultaneously in one parent forming separate wheel(s) and body offspring, except for it being overly complicated not seeming to be very survivable.

Very good answer. One additional thought: The "wheel symbiont" and the "body symbiont" must also have a mechanism to transfer torque between them (an "engine") to actually propel the whole thing forward, otherwise they could only roll downhills. This makes it anatomically even more complicated and more difficult to see an evolutionary pathway.

@Beo Your wheelbarrow (front wheel, back legs) is an interesting idea. But if the wheel gets stuck, it would have to be able to also stand up on its legs to pull the wheel out again. Unless it lives on a hard smooth surface, it would probably have to get up and walk a lot, so what's the advantage of having the wheel?

There are co-gestated symbionts of course - but they are usually symbiotic microorgansms.  Id not be surprised to find a parasite that co-gestated... Parasites are not symbionts of course.  For some reason animals have a hard time living together completely symbiotically.

@shigeta - such a great answer! Wish you were still answering questions here. :)

thanks! it was a great way to work on my writing :) at one time i had 20% of the content here (!) I am still on occasionally but so many good people on the site now :) I am still looking for questions that i can really do a special service for.

Dawkins also reviews reasons large animals would be unlikely to have wheels in The Ancestor's Tale. Fortunately, they don't apply to gears in Issus coleoptratus.

In your question, you mention frozen lakes and rightly say that skates would be far easier than wheels, but you could have used salt flats as an example.
I think the reason there are no actual wheels is a mixture of ontogenetic and phylogentic barriers, maintenance (nutrition), lubrication and control (nerve connections). There would have to be severe and sustained evolutionary incentives to go from something simple, cheap and extant (legs) to something way more difficult and complex.
However, there are several species of plants and animals that use rolling as a form of locomotion. Tumbleweeds are a good example of plants, and for animals, there are spiders, caterpillars and salamanders.
It only takes a small evolutionary development to take something like this from a passive motion (rolling down hill to escape predators) to active (perhaps creating waves of flexion to roll like... ahem, caterpillar tracks).

Thanks. 1) Why "severe"? Since, if there is no functional intermediate, I presume it has to happen in one jump, only making it (much) less probable (?). I don't see how such chances would improve by the severity of the "incentives". 2) I was thinking along the lines of a some sort of an exoskeleton, that, in time, separates, but does remain pierced through the animal. (Is that unthinkable?) It could have the form of two wheels and an axle. :)

Something as complicated as wheels (if even possible with multicellular animals) could never happen as a result of a single, lucky mutation. The term 'exaptation' is where evolution takes an existing functional unit, and starts using it for a different purpose. It takes many generations so the evolutionary pressure would have to be sustained. It would have to be severe to be more beneficial than just sticking with legs.

Shigeta's molecular answer is spot on. However, at the large scale level I think the key problem with a biological wheel needs to be spelled out clearly: how does an organism with separate parts maintain these parts? Let's suppose that an organism evolves a fully rotational joint, how do they then provide nutrients to the tissue on the other side? If they don't provide nutrients how does self-repair in this tissue continue without nutrients?
Mind you, I'm not sure that the biological problems with a wheel are the real answer. I'm not sure how a wheel evolves. What's the functional intermediate? How does a semi-connected wheel out-perform a limb? Remember than evolution is canalised by what has gone before.

Thanks. I take it that your tentative suggestion is that the anatomical barrier is (at least among) the critical one(s), right?

Um, I not sure which argument is strongest. I think I favour the evolutionary angle, myself. Both are though, I think, sufficient answers but the evolutionary one probably better reflects the historical reality of matter. Wheels didn't evolve because there was no beneficial intermediate for them to pass through.

OK. So, hypothetically, if a wheeled animal was discovered tomorrow, this would make you doubt the theory of evolution? :) Or would you conclude that there must have been some beneficial intermediate? Or what? Show your cards! :)

Equally I'd conclude there must be some anatomic way it works too.

What do you mean with "equally"? Do you think all your assumptions are equally likely true?

I mean that finding an animal with wheels would demonstrate both that it is anatomically possible and that it is evolutionarily possible. I consider both to be good arguments as to why we'll never find such a thing but I suspect the reality is that the space of possible organisms that might be anatomically possible has never actually been explored because there's no evolutionarily advantageous pathways that leads there.

There's a basic philosophical problem with asking why there aren't such-and-such.  We could as easily ask why there are no six-limbed vertebrates, or creatures that use hydrogen to fly like balloons.  It's not (necessarily) that they're mechanically or biologically impossible, it's just that evolution started down another pathway first, and (by changing the nature of the "adjacent possible") that closed off the paths that led to such creatures.

@JackAidley Which-canalisation? this  one? for which-one phenomenon? doesn't seem other uses would apply.

Probablity of evolution of wheel legs, helicopters birds and propellor fish and also depends on:

The strength of the advantage gained (wheels are inefficient in 99% of biological habitats, forests, praries, wheras salt flats have adverse conditions)

The ease of development of intermediate forms: Small wheels and half weels have little to no efficiency.


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Size of classical liver lobule across species
A classical liver lobule is made up of a central vein and the portal triads.  A typical human liver weighs around 3 lbs. , while a typical bovine liver weighs around 12 lbs.  I was wondering if anyone had a reference that might discuss the size of a bovine liver lobule vs. the size of a human liver lobule.  Specifically, is the bovine liver lobule also larger than a human liver lobule?

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Role of Fbx15 in ES cells and its use in assaying for iPS cells (Yamanaka paper and others)?
I am trying to understand the assay for iPS cells in the Takahashi & Yamanaka 2006 paper.
They inserted a beta-geo cassette, which contains the neomycin resistance gene, into the Fbx15 gene.  The idea is that the beta-geo cassette will be expressed when Fbx15 will be expressed, thus conferring G418 resistance to only those cells expressing Fbx15.
They say that "Although specifically expressed in mouse ES cells and early embryos, Fbx15 is dispensable for the maintenance of pluripotency and mouse development."  Does this mean that Fbx15 will be expressed in induced pluripotent stem cells, and won't be expressed upon differentiation? (What is special about Fbx15 that will distinguish iPS cells from somatic cells, including those that might derive from iPS cells, as when pluripotency is not maintained?)

Another paper from Yamanaka's group explains Fbx15.
It says:

Inactivation of Oct3/4 in ES cells led to rapid extinction of Fbx15 expression.
Fbx15-null ES cells were normal in morphology, proliferation, and differentiation. These data demonstrate that Fbx15 is a novel target of Oct3/4 but is dispensable for ES cell self-renewal, development, and fertility.

So Fbx15 wont be expressed in Oct4⁻ cells.
I haven't seen any paper describing the function of this gene but in the case of cassette insertions the locus would prove useful in expressing the inserts specifically in Oct3/4⁺ cells

So, Fbx15 is a nonessential marker of iPS cells? As in, it's expressed only in iPS cells, but disrupting the gene with a cassette isn't expected to have any effect on the iPS cell?

Seemingly. [as per the paper]

Ok thanks. I don't think it's going to get much clearer than this.

there are only 9 reports on this gene in pubmed. Only one tries to attribute some function. It is in cancer cells, though: FBXO15 regulates P-glycoprotein/ABCB1 expression through the ubiquitin-proteasome pathway in cancer cells

@dd3 I don't know if Fbx15 is so much a marker of iPS cells as it is just a target of the Oct4 transcription factor, meaning its expression will be active in Oct4+ cells, providing a convenient way of driving exogenous (and then endogenous) expression of the Yamanaka factors long-term.

@MattDMo.. Yamanaka factors :P

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HIV and T helper cells
As far as I know and could understand from reading about HIV, T helper cell is one of the main reasons to develop AIDS in patients infected with HIV virus, that because the absence of helper T cell suppresses the immune system because no T cell cytokines released to allow other white blood cells to attack or release antigens.
Q1. Did I understand it correctly?
Q2. Now if my understanding is correct, why don't scientists find a way to produce T cell cytokines in the lab? and then inject it to patients with HIV? wouldn't that in theory revive the immune system and perhaps heal them or at least make them live longer?
P.S. My knowledge is close to nothing in this topic, so excuse me if the question itself is wrong :)

Q1: Partially. T cells are important for the immune response through pathways other than cytokine release. Being activated by contact with another immune cell presenting their corresponding antigen, T cells proliferate and themselves activate their compatible B cell counterpart. These then produce antibodies specific to that antigen, the basis of the adaptive immune response (see figure below, from Wikipedia). The important part here is that this mechanism requires cell-to-cell contact, not simply cytokines. Without it, any pathogen for which memory B cells do not exist yet will not produce an adaptive immune response - and will persist if the infection is not cleared by the innate immune response.

Q2: I expect because merely injecting T cell cytokines would not be sufficient in order to replace the essential function of T cells. Aside from that, WYSIWYG's point about the general response is probably also true: the side effects would be horrendous.

yes
[Purely my guess] :

I think it will be difficult when simultaneously several infections pop up. There is no antigen presentation (as there is no receiver); it will be difficult to manually deliver different kinds of responses by cytokine injection.
Moreover most cytokines are paracrine i.e they act locally; injecting them would cause a systemic response which may be harmful.
Plus, it might be expensive to perform a cytokine therapy. [interferons are used in certain viral infections and what I vaguely remember is that the therapy is expensive]

yes you understand how helper T cells work in the body.
no. Cytokines are not enough and injecting T cells will just make HIV persist. The only solution to not getting AIDS and having your HIV cured is an HIV vaccine and the people making the vaccines do produce some HIV vaccine.


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Up to date B cell review
Where would I find an up to date (last 6-7 years max) review on B cells? I've tried searching through pubmed with filters, cochrane library, medline and various other resources including searching old questions. A textbook would be fine too, but I'm not sure which one would give me detailed information. I'm a BSc student studying immunology. I'm not trying to create a war of "best" answers, any answer that fits these criteria I will accept.

what specifically about B cells are you interested in? The possible subject matter is so broad that I doubt you'll find reviews covering all of B cell biology and function. A recent immunology text might be better.

@MattDMo Essentially a standard textbook on immunology level detail but more up to date like novel knowledge on how BCR are activated (for example I read that the cross linking model is widely disputed) etc. Not something that just focuses on the concrete but delves a little further and includes up to date research

Do you have any references for the BCR cross linking model dispute? I'm not working directly in the field now, so I'm not as up to date as perhaps I should be...

Cellular and Molecular Immunology by Abul Abbas et al. is pretty good, and you can't beat Charlie Janeway's Immunobiology either. Both will give a good introduction to B-cells, antibodies, BCR signaling, and how they fit in to the immune system's structure and function. I own earlier editions of both, and their different perspectives are good for getting a more holistic understanding of the field. Good luck in your studies, it's a fascinating subject!

looking into these! Thanks. And totally agree I love it like anything

@AndroidPenguin If you're looking for reviews on specific subjects in journals, some of the journals I turn to include Annual Reviews in Immunology, Trends in Biochemical Sciences, Cell, Nature Reviews, Nature Reviews Immunology, and Trends in Immunology, among others. It's quite possible to find great reviews in lower-impact journals like the Journal of Immunology, and you'll often find more esoteric reviews there as well, but for now I'd stick with the real biggies like the ones I mentioned.

I agree entirely with Matt, Abbas and Janeway's books are the standard for even graduate-level introductory Immunology. Both are easy to read and well organized. Definitely start here.
However, depending on what you have access to and the depth of reading you want to do, there was an Annual Review of Immunology issue some years ago (maybe 2003?) that discussed a number of B Cell topics (signaling, fate decisions, etc). I also see that there is a newer article:
"B Cell Signaling and Fate Decision"
Annual Review of Immunology 28: 21-55 (Volume publication date April 2009)
Tomohiro Kurosaki, Hisaaki Shinohara, and Yoshihiro Baba
that might be pretty general if you have access through a university.
Good luck.
By the way, I think the disagreement about BCR crosslinking is for survival/development (i.e., are 'tonic' signals sufficient to allow cells through development?) As for activation, B cells are triggered either by antigen-specific BCR crosslinking or more general TLR activation (e.g., LPS).

could you post Pubmed/DOI links so others can find the article you're referencing? They're more likely to be "permanent" (long-lasting) than are direct journal URLs, which can and do change.

Good point. Done.


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Why do sloths come down from the trees to defecate?
I'm under the impression that most sloths exhibit this behavior, but why? They are slow moving and so have no way of escaping from predators when on the ground. Not to mention the energy they expire to break from their normally sedentary lifestyle.
They may only have to defecate and urinate once a week, but it strikes me as an unnecessary risk.  Why not let gravity do all the hard work?

From Wikipedia:

Sloths go to the ground to urinate and defecate about once a week, digging a hole and covering it afterwards. They go to the same spot each time and are vulnerable to predation while doing so. The reason for this risky behaviour is unknown, although some believe that it is to avoid making noise while defecating from up high that would attract predators. Consistent with this, they reportedly relieve themselves from their branches during storms in the rainy season. Another possible explanation is that the middens provide the sloths with one of their few methods of finding one another for breeding purposes, since their sense of smell is far more acute than their eyesight or hearing. It has also been pointed out that individual sloths tend to spend the bulk of their time feeding on a single "modal" tree; by burying their excreta near the trunk of that tree, they may help nourish it. [Source]


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Why do ion concentrations change with different secretion rates in pancreatic juice?
Why is it that when secretory rate increases in the pancreas the concentration of chloride ions decreases, and the concentration of bicarbonate increases in the production of isotonic NaCl secretion?
The modification that goes on in the duct of the acinus is dependent on flow. If the flow is faster, then less ions can be reabsorbed from the primary secretion. In the pancreas, chloride ions are removed, so surely their concentration should go up as the flow increases?
Bicarbonate on the other hand is added to the primary secretion in the duct. So shouldn't its concentration in the secretion stay the same or even increase as flow increases?

This is an approximation of the graph given in our lecture notes; from Boron & Boulpaep, Medical Physiology, 1st Ed, p919 - Sorry for the bad quality reconstruction

" In the pancreas, chloride ions are removed, so surely their concentration should go down as the flow increases?"   According to the logic of your question I think this should be "should go up".

An interesting question!
I am attaching the picture from Boron & Boulpaep, Medical Physiology, 2nd Ed, p921 here to clarify the details left out in the hand drawn picture.

The flow of the digestive pancreatic enzymes increase mainly during food consumption. This is brought about by a number of redundant systems. The fasting secretion of pancreatic enzymes depends on the MMC (migrating motor complex).

Bicarbonate ions are exchanged with chlorine ions in the apical membrane of the acinar cells through a Chloride Bicarbonate Exchanger. This process is driven by:

Secretin - most important humoral factor - Increases secretion
ACh through muscarinic receptors - Increases secretion
GRP (Gastrin Releasing Peptide) - Increases secretion
Substance P - Decreases secretion

Mechanism of action of secretin seems to be through activation of cAMP. However even small amounts of secretin which do not raise the cAMP levels measurably can stimulate bicarbonate secretion. This suggests secretin response may be by

Unmeasurably small amount of increase in cAMP
Raise in cAMP levels in localised compartments
Activation of alternative second messenger pathways

In case of GRP the second messenger is not known.
The answer to your question is that when secretin is secreted, the Bicarbonate-Chloride transporter is accelerated to achieve the result displayed. This mainly happens when food enters the small intestine so as to neutralize the acid permitting the digestive enzymes to function at the optimal pH.
The Chloride-Bicarobonate Transporter is an exchange transporter which explains why there is a sharp fall in the chloride levels.

Taken from the same text book quoted above


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Can animals, like monkeys, be homosexual?
I heard that some monkeys can be homosexual? a friend of mine was saying that he saw a male monkey having sex with another male monkey in the zoo, I honestly didn't believe him, I think he just got confused or he made it up.
Could this be true? can monkeys become homosexuals? does homosexuality (other than human) exist in the animal kingdom?

its likely they saw right.  many animals have been shown to exhibit homosexual behavior.  http://en.wikipedia.org/wiki/Homosexual_behavior_in_animals

I have seen dogs doing so.I do believe that sexuality [ homo or bi or hetero ] is one's right.

I would just like to point out that there is a difference, most obvious in humans, between homosexual behavior and a homosexual orientation.  The former is often very dependent on cultural norms and context: for example, holding hands or kissing on the cheek may or may not be considered homosexual behavior or indicative of sexual orientation depending on what country you're in.

Cases of homosexuality have been described in numerous species, including primates, and the wikipedia link posted by @shigeta lists and describes some of them.
It could be difficult to untangle the difference between an animal not being able to identify sexes very well, or, deliberately mating to anyone and those actively making a choice to engage in intercourse with a same sex individual.
I there are some species where sexes are very difficult to tell apart so they may just go around having sex with anything that looks like the right species because the mating is relatively low cost so doesn't matter if the partner was male or female. This is one such example in sea snails:

"In a laboratory mate-choice experiment, male N. radiata preferred to
  mate with females, indicating precopulatory sex identification. They
  copulated with males, however, at the frequency of 37%, perhaps
  because of sex misidentification."

Other likely candidates are those with little sexual dimorphism and those with sneaker males that mimic females.
I have also heard theoretical discussions (oh the joys of lunchtime in an evolutionary biology department!) which suggest it may be a way of individuals (particularly males) practising or keeping up fitness relating to sex or stimulating better sperm production etc.
Once you decide what constitutes "a homosexual animal" then it is perhaps easier to examine. I would say a homosexual animal is one that mates exclusively (or highly preferentially) with same sex individuals when given the choice.
Models of genetic and epigenetic inheritance have been used to suggest just how homosexuality could evolve and you can read more about it in this Biology.Stackexchange post.
So it seems that monkeys, and other animals, have been documented to exhibit homosexuality, reasons for them to do so could exist, and it could be a heritable trait which persists despite seemingly strong negative selection.

Just as a comment, I'd be surprised if animals got confused and couldn't tell the gender of the individuals they are trying to mate with.  If a vet can tell the difference, which is the case in most animals, the animals themselves shouldn't have any problem.

"Everything in the world is about sex except sex.  Sex is about power." ~Oscar Wilde

@shigeta here is one such example - the males mated with the wrong sex 37% of the time http://link.springer.com/article/10.1007%2Fs10164-005-0159-1 "In a laboratory mate-choice experiment, male N. radiata preferred to mate with females, indicating precopulatory sex identification. They copulated with males, however, at the frequency of 37%, perhaps because of sex misidentification."
.. other likely candidates are those with little sexual dimorphism and those with sneaker males that mimic females.

@rg255 I wasn't disputing you could find such examples.  I suppose there may be animals that can't tell the difference between genders or individuals, but on the average I would doubt it.  Even microoganisms can be specific; this would be an evolutionary 'feature' not a 'bug'.  So its possible if there were something it does for the organism because there is a cost - disease spreads easily and there is some opportunity cost to mating.  Competition would be on sperm competition rather than mate choice.   They ought to be induced to mate with inanimate objects with specific visual cues.

bisexuality for instance is very much a feature for bonobos - it creates their social structure...

@shigeta I wasn't suggesting that mistaken identity was responsible for all cases of homosexuality in animals - there are other explanations and cases where species are very easy for the individual to distinguish sexes, I was just giving it as one possible explanation for this observation. Also: +1 for the Bonobos example, they are a really cool system - I knew there was some species where that occurred but couldn't remember which.

@rg255 right on - science is all about the details. I feel that if jumping spiders can identify prospective mates by touching the dragline silk (a fact from another answer here) then there is typically a lot of drive for the evolution of gender and mate evaluation.  such confusion would be rare and probably for a reason... imho

Here's a Ted talk about a case of homosexual necrophilia in mallard duck. The speaker lists a few other examples of weird animal mating (frog with a fish). Apparently animals may have non-traditional preferences as well as humans.
The talk does not deal with whether this is a pathology or not, just lists a few weird examples.
Additionally, there's this section on sexual dimorphism of hypothalamus, which does mention pathology of hypothalamus. The statement below lacks a proper citation at the time of this writing, so it may be incorrect:

If a female rat is injected once with testosterone in the first few
  days of postnatal life (during the "critical period" of sex-steroid
  influence), the hypothalamus is irreversibly masculinized; the adult
  rat will be incapable of generating an LH surge in response to
  estrogen (a characteristic of females), but will be capable of
  exhibiting male sexual behaviors (mounting a sexually receptive female

there is an entertaining paper that accompanies that

http://www.chemistry.bristol.ac.uk/sillymolecules/papers/duck.pdf


text:
Why dogs move their noses when smelling?
I read on Wikipedia that:

The wet nose, or rhinarium, is essential for determining the direction of the air current containing the smell. Cold receptors in the skin are sensitive to the cooling of the skin by evaporation of the moisture by air currents.

That explains why their noses are wet. Why they're slightly moving them when smelling, like on this video (see the close-up in the second part)? Could this very little movement create enough air currents around the nose to determine what smells are coming from what directions? Or is there another reason?

Might just be mechanical, note that your nose also moves if you inhale strongly enough.

The dog's ability to smell the world around him and to interpret these odors depends on a complicated chemical sensory system. First of all, it possesses mobile nostrils, that help to determine the direction of the smell. Then comes sniffing, the ability to disrupt the air with a regular pattern of breathing that, through laboratory testing, is structured in a series of 3 to 7 snorts. Most of the sensory organs of the dog's nose, the septal organ, are probably responsible for the outbreak of sniffing behavior.
The air is scented, it passes over a bony structure called "projection sub-ethmoid", that man does not possess, and nasal membranes that cover it. The area above the protrusion is not sweep, when the dog exhales air and it allows olfactory molecules to settle and accumulate.
When a dog breathes normally, air is introduced into the nasal passages, it continues its way to the lungs. The action of smell allows air to remain "at rest" in the nasal passages. The intricate complex surrounds the maxillo-turbinate bones of the skeleton provides that the nasal membranes are capable of creating models of air flows odors that lead content in the air to hit the regions of the olfactory receptors.
The odor molecules disintegrate and are concentrated in the nasal mucus that adheres to the receptor cells. Once the mucus, load odor, adheres to the microscopic hairs of receptor cells, the chemical signal odor turns into an electric signal and is sent to the cerebral cortex and the limbic system, ie, the part of the brain that regulate behaviors feeding, drinking and sex. Small molecules stimulate the olfactory nerve of smell. Big odor molecules stimulate the trigeminal nerve, one of the largest nerves of the skull, and the volatiles of sex hormones probably stimulate the vomeronasal organ, the other part of the anatomy of the dog that does not exist in primates.

http://www.ucsuggiatevedano.it/l-olfatto

EDIT @ kmm
Their nostrils can move, like the eyes to focus and channel the light energy. Or the highly mobile ears of many predatory animals, including cats and owls, which can rotate, also independently one from the other, not only to improve the perception, but also to identify the direction of the sound.
The principle is the same as the frontal binocular vision, which allows us to calculate the distance.

EDIT II @ terdon
When the dog sniffs, "taste" a smell with a series of inhalations shorter and faster than normal, as we do when we feel a bad smell, breathes quickly several times to understand what smell is that.
Of course we are well-educated people and we do not do this in public. But the gesture is the same. =-]

EDIT III @Petr
"Smell is the ability to detect and discern the odorous emanations from the air. The snuff is the ability to intercept and discern the odorous emanations from the ground. They act with a pattern of regular breathing and is structured in a series of one / three smells accompanied by a series of three / seven snuffs.
The behavior is controlled by the organs of sense of smell nasal septum."
(Section 3.3.3.4.1 and the following)

http://www.fongaros.it/ana2.pdf
http://www.cacciapassione.com/cani-e-cacciatori/1956-olfatto-del-cane-tutta-questione-di-naso.html

The dog is able to absorb the chemicals present in the air, thanks to the characteristics enjoyed by its olfactory cells. To further stimulate their sense of smell to the dog no choice but to expand with some emphasis their nostrils sneaking in a strong "suction" of odors. The air will be retained more or less long and the dog will recognize odors also very weak.

http://www.ucsuggiatevedano.it/l-olfatto
http://en.wikipedia.org/wiki/Olfaction

The nose of the dog is also called truffle, at its end there are the nostrils or the cavity, through which sucks air, and the vibrissae, equipped with sensory hairs. The dog's nose is particularly sensitive, is equipped on the inside of an organ said "of Jacobson", which allows to perceive any kind of substance, able to distinguish between a million of specific molecules, over that of perceiving pheromones, i.e. substances that indicate important information about the physical and mental state of others like it.

http://www.comeaddestrareuncane.com/blog/tag/cani-molecolari/

In the dog, the surface of the olfactory mucosa varies between 70 and 150 cm2 - in this tissue the number of olfactory receptors varies from 250 to 280 million - In 1962, Becker et al. showed that dogs are able to recognize substances in dilutions from 1/100 to 1/10.000.000.
- http://milano.corriere.it/milano/notizie/cronaca/12_febbraio_19/cani-olfatto-parere-esperto-1903358352720.shtml
Have you noticed how a dog sniffs the urine of a female "tasting it"? It is the same action that makes the viper when it follows the track of the mouse: it evertes the tongue and carries on it the odorous particles in the buccal cavity, and this organ has a function in the middle between the olfactory and gustatory ones. "Pointing dogs" is as pointing "the wild" taste the smell.
"Eat the scent", in the jargon, because savored, not only in terms of smell, the smell of the wild. The Jacobson's organ is then a second organ capable of perceiving odors, the first we've said is represented ciliated epithelium of the mucous membrane of the nose.
But there is a third organ called the "Rodolfo-Masera" which also serves to sense the emanations chemical (not yet known which), that way you could explain a specialization of these organs to perceive certain groups of biochemicals than others.
- http://www.laciotola.net/Cani/la-funzione-olfattiva-del-cane.html

Could you explain what you mean by "nostril furniture" and how this helps them determine the direction of the smell (which seems to be the crux of the question)?

What do you mean by "3:00 to 7:00 snorted"?

A thorough answer, thanks. Could you please elaborate how the movement of nostrils helps to improve the perception of smells? In particular, my question is focused on the barely noticeable, shivering-like movement of dogs' nostrils. This can be observed when a dog tries to analyze a faint smell in the air coming from some distance - it stays completely still and only smells and moves its nostrils (as in the second part of the video).

"The odor molecules disintegrate". Huh? Not sure what that was supposed to mean. The molecules are dispersed in the air, are breathed in, and bind to receptors.

Animals smell in stereo. Just the way you need 2 ears to know the direction of sound, you need 2 nostrils to know the direction of odor source. Sniffing around helps in doing exactly that as you sample from different locations; there is inter-nostril concentration difference and inter-nostril timing difference of when the molecules hit the olfactory membrane.
Here are links to well known studies in this area:
Rats smell in stereo
Humans smell in stereo
Dogs smell in stereo


text:
Why it is so difficult to treat leukemia?
I want to ask what is the reason that T315I type CML leukemia is currently untreatable. I have read quite a few papers in this subject. Why the current genetic oriented engineering drugs failed to stop the leukemia stem cell's expansion but can only slow the secondary leukemia stem cell's expansion? I found it to be utterly hopeless for a patient to be in such a position, as chemical therapy does not work well and radiation therapy can only target specific area. There are experimental drugs in the developmental stage but from what I know they are mostly unreliable.

The T315l mutation of BCR/ABL gene produce the complete resistance of CML leukemia to all currently available BCR/ABL inhibitors.
There is a idea that is not yet tested for such patients - allogenic hematopoietic transplatation.
More information:
http://www.ncbi.nlm.nih.gov/pubmed/20657522
http://www.ingentaconnect.com/content/maney/hem/pre-prints/1607845412Y.0000000050

While this helps, it does not answer my question. But thanks.


text:
Understanding these SNP annotations
I am looking at the PharmaPGKB database for SNPs and trying to understand what the following annotation means:
rs1801131 at 1:11854475 in CLCN6, MTHFR (VIP)

Ok, the SNP identified by rs1801131 occurs in the first chromosome, at position 11854475.
Then, the two genes' identifiers come. The position 11854475 is inside the gene MTHFR. Why do they also annotate the SNP to the gene CLCN6 (which is a "neighbour" of MTHFR) ?

It is because the two genes overlap:

CLCN6 is on the plus strand and MTHFR is on the minus strand. The SNP is annotated to both because it falls in a region of the genome claimed by both genes.


text:
What chemicals and structures control the *direction* of plant growth in leaves, stems and roots?
If you want a specific plant, let's say the snap peas I am growing that I bought at Agway. I noticed that they grow towards the light source through the nearby window. Also I think roots work the same way for water/minerals. also don't various kinds of ants find food conceptually identically?
How much of this is true? Please correct:

I think analogous to ant colonies, plants will attempt to grow every which way initially, and will only continue growing in directions that give the most/enough light/water/minerals. If a direction is or becomes unfruitful, that section withers. After the initial state the plant will start branching in directions off of locations on still growing sections of plants and that cycle continues until none of the plant can be supported and the whole thing withers (perennials) or slows its metabolism down to the point where it could survive those conditions until they picked up again (such as winter seasonal survival of tree species). Also, it is not as if they decide which direction to go in. that type of decision would forgo going in another direction. And not sure, but I don't think plants have decision capabilities anyways. they grow in directions they grow best.

Your title is unclear.  Is the last question the question you would like answered? If so, I would recommend changing the title.

I don't unfortunately have time to write a full answer right now, but you will want to look at tropism on Wikipedia, particularly geotropism and heliotropism

PART 1 : Phototropism
The movement of plant shoot towards light is called phototropism. This process is mainly stimulated by the blue light. The photoreceptor involved is called Phot1 (Phototropin 1) or JK244.
Auxins such as IAA (indole acetic acid) are plant hormones, expressed highly in meristem, which cause shoot growth. On illumination this phototropin, through currently unknown messengers, causes inhibition of polar Auxin transport in the illuminated side. This causes the non-illuminated side to grow more and thus bending the plant towards light.

The image represents an older model which proposed lateral movement of auxin. The mechanism mentioned in last paragraph is the currently accepted model. The below figure illustrates 'polar auxin transport'

For details refer to this nice review on phototropism.
PART 2 : Geotropism and Hydrotropism
Geotropism or gravitropism is movement of roots towards earth (gravity) and hydrotropism is movement of roots towards water. Both phenomena interact with each other and share some common pathways. But hydrotropsim can inhibit geotropism and it is evident in conditions when root goes towards an adjacent water source.
Ethylene and Auxin signaling is involved in root growth both in geotropism and hydrotropism. In geotropism the auxin is stimulated by statoliths (clustered and membrane bound grains of starch) in the amyloplasts- the organelles which store starch. The model suggests that amyloplst sediments under the influence of gravity and thereby affect auxin polar transport (the second figure co-incidentally illustrates polar auxin transport in geotropism).
The exact moisture sensor is unknown but Abscissic acid (ABA), which is well known for its involvement in drought tolerance, is known to affect hydrotropism.
MIZ1/2 are some proteins uniquely involved in hyrdotropism.
Both pathways are dependent on Calcium as a secondary messenger.
To conclude, these pathways are not as clear as those of phototropism.
Reference:

http://www.academicjournals.org/ajar/pdf/Pdf2006/Nov/Dexian%20and%20South.pdf
http://www.sciencedirect.com/science/article/pii/S1360138504002717
http://www.plantphysiol.org/content/133/4/1677.full

Thank you :) .. and Thanks to the asker for making me revisit plant biology:)

Your statement is partially correct, but not entirely.

As an animal embryo, the seed, still closed, is already formed, with the distinction between root, stem and leaves. Tiny but already there are.
All the rest of the seed (in this case two cotyledons) is a kind of food dough, and serves as a food reserve for the seedling, until the time of rooting and the achievement of energy independence.

As animals, the plant seeks, first of all, water. The first need of water is determined by the need to break the skin that closes the seed. If there is no presence of water,  the seed dried and does not sprout.
If it "feel" the water, the seed drinks, swells and the skin breaks down. At this stage we can also say that the seed is aware of where it can find water. I do not think that they have been studies done on the awareness of the high and low (orientation). On the edge of rivers and lakes the seed can also find favorable ground above itself.
The direction of the water determines an effort, which can also lead to the rotation of the seed in the right position to emit the radicle towards the water (and the earth). In this time the embryo "eats" the nutritional reserves contained in the seed.
Then precisely they decide which direction to go in. When the place and position are correct, the seed has open and the part to eat is almost eaten, then more light. The radicle grows to first, both in size and as the length. It hooks to the soil and establishes a firm basis. Starts to drink directly (and not by absorption of the tissues of the seed) and starts to push out the seedling, typically in the opposite direction.
The seedling "feel" the light energy and go to that.

If the plants have ability of decision or not, has not yet been established. But to me personally it seems that a functional DNA must be able to allow each subjet to handle each situation (consistent with its structure) in the best way to itself.
This seems to have been ascertained for the animals. A certain capacity of thought, namely to make decisions, is absolutely functional in a huge energy saving on the need for encoding and on the structure of DNA

I know little about the life of the colonies of ants. But I know all about bees. A swarm that is detached from the hive to found a new colony, it also stops two or three times. Sends forward scouts, followed by architects and, if the place is right, the architects have a network, and bees wax begin to build.
Your mention of the ants is not sufficient to me to find similarities.

so DNA encoding is allowed to "program in" "make a guess" "functions"? growing in every direction and only continuing to grow in directions the plant found suitable probably is very inefficient compared to making a guess based on a stimulus.

Yes, to me yes - that is more efficient and request less energy/structure than encoding each single decision. But, actually, you have you've piqued my curiosity about the lives of ants, that I know only superficially. But I figure that the marvelous discoveries, behavioral and chemical, which I did on bees, I can make too delving into my knowledge on the ants.


text:
Hardy-Weinberg Equilibrium: To compute probability of finding two siblings (random mating)
I've been working a little with M. G. Bulmer's Principles of Statistics (Dover, 1979) and cannot see how to properly compute half of one question. This should be a basic probability computation, but I am not getting the same answer as the book's suggestion.
Here is the question (Chapter 2, Problem 2.4): If the three genotypes (i.e., AA, Aa, aa) are all distinguishable, find the probabilities that a) a pair of siblings and b) a pair of unrelated individuals will appear the same when p=q=.5.
The book offers .59 for a) and .38 for b). I can get b correctly, but I don't understand how to properly compute part a).
This does not seem like a complicated exercise!

I got .59. In response to WYSIWYG:
(Note: I'm using A and a for the two alleles. My copy of Bulmer uses B for the second, which makes a little more sense if the alleles are codominant.)
a.) The AA x aa cross should be twice as common as the AA x AA and aa x aa crosses, just as HT is more common than HH or TT when we toss a pair of identical coins. In particular, this cross should occur with frequency 2*(.25*.25)= .125. Same goes for AA x Aa, AA x aa, and Aa x aa.
b.) In an Aa x Aa cross, there is a 3/8 probability that two offspring will have the same genotype. I reasoned as follows:

There is a 0.5 probability that the first offspring will be heterozygous (Aa). In that case, there is a 0.5 probability that the second offspring will also be heterozygous.
There is a 0.25 probability that the first offspring will be homozygous AA: In that case there is a 0.25 probability that the second offspring will also be AA. Likewise for aa.
Summing these: (1/2)^2 + (1/4)^2 +(1/4)^2 = 1/4 + 2/16 = 3/8.

I believe that resolves the issue. Apologies if I've missed something.

this seems to be right. Thanks for correcting.

Are you sure it is 0.59 because I am getting 0.5625 for part (a) and this is how I computed.
To check genetic similarity of siblings we first have to pick up mating pairs. Six mating pairs possible with following offspring probabilities (choice of first mate x choice of second mate x same offspring genotype freq).

AA x AA : will always give same type of offspring: prob = 0.25x0.25x1
aa x aa : will always give same type of offspring: prob = 0.25x0.25x1
AA x aa : will always give same type of offspring: prob = 0.25x0.25x1
Aa x Aa : will give Aa in half the number of times: prob = 0.5x0.5x0.5
Aa x AA : will give two types of similar offsprings, half the number of times - AA and Aa: prob = 0.5x0.25x0.5x2
Aa x aa : will give two types of similar offsprings, half the number of times - aa and Aa: prob = 0.5x0.25x0.5x2

Total probability = 3x(0.5x0.5x0.5) + 3x(0.25x0.25) = 0.375+0.1875 = 0.5625
Assumptions:

Population is infinite
Population in equilibrium

For what it's worth, I repeated this calculation in my own peculiar way and also got 0.5625

@AlanBoyd: can you tell me how you approached it ?

By peculiar I meant I did it in a spreadsheet - probably it is exactly the same logic as your calculation. See https://www.dropbox.com/s/k46xhff3x0p1oc7/HW2png.png

Thanks to you both for your comments. .5625 is what I got as when I did this, too. It may simply be an error on the solutions page, but I couldn't rule out that I was making an error.


text:
How do animals/plants change for each season?
The question pretty much sums it up. How do animals/plants change for each: Spring, Summer, Autumn, and Winter?
A detailed explanation on distinct behaviour and appearance changes would be nice.

i'll answer the mechanism for plants as of now.

I flagged this question as "too broad" because, well, isn't it ? Could you maybe give some reason why you're asking this or share some research you've already done on the question to help people orient their answers more precisely ?

There are various parameters that describe change of seasons such as day length, temperature, humidity. But it can be assumed that most of these parameters ultimately depend on one parameter- day length.
The response of plants towards the length of day/night cycle is called photoperiodism (which dictates spring flowering).
This article explains the effect of a gene called CONSTANS(CO) on spring flowering. CO is post transcriptionally regulated by cryptochromes and phyochromes.

The circadian rhythm in CO mRNA abundance was proposed to represent a photoperiod response rhythm, in which exposure to light coincides with CO expression only under LDs (Long Day) and thereby triggers flowering.
......
We propose that early in the day phyB promotes the degradation of CO whereas in the evening cryptochromes and phyA antagonize this degradation and stabilize CO protein,

However, my knowledge of plant molecular biology is not that great and I would advise that you refer the mentioned article and the cross references cited in that.

Thanks for the reply, can't wait for the follow up on animals.


text:
What are the long-term negative effects of going without water/food for a period of time
There are no good answers anywhere. so asking: this is not about days of survival without water. This is about long-term negative effects induced from not drinking water for at least the mentioned days.
Please link the most reliable link (has to be heavily-reviewed, meticulously-designed studies) that answers this question so I can look into it futher. Multiple studies are needed for it to be reliable.
A related question is the same question for going without food, but with water (I'll ask this in a seperate question if the answer isn't already in the answer you provide).
This is for modern human beings as it applies to the majority of people. Also you can comment with the most reliable resources on the topic so we can read into it.
Important: NO comments without reliable scientific sources are relevant or reliable (has to be heavily-reviewed, meticulously-designed studies) so we can look into it further by ourselves. Please don't comment/answer without one.

This is the second time this EXACT question has been asked. Complete with bolded sections and all. Like the last time it was asked, you will not get any answers. You are asking for studies that do not exist, and as far as I'm aware there simply aren't any known long-term affects from temporary starvation or dehydration.

Please read the FAQ section on etiquette when posting: "Treat others with the same respect you’d want them to treat you".  I don't believe that this requirement has been met with your tone in this question.  Regarding @MCM's comment, don't vandalise content you have previously posted to the community.  I realise that the cross posting issue has been resolved Skeptics side, however a more constructive course of action would have been to flag your original question for reopening.

Besides its confrontational style, the way this question was asked suggests the author hasn't really looked into this or at least isn't clear on what questions they should be asking.  It is true that, in modern scientific culture, you cannot get approval to lock a bunch of college kids in a room for a week without food or water so you can check in with them years later and look for long term health effects.
But there are a LOT of indirect ways to study this, either by studying populations that have suffered starvation (through famine or war) or brought it upon themselves (anorexia). Or you can look at animal studies, which might not give precise consequences for humans, but can be far better controlled (you can lock them up for a week and keep them around for a year). And they will have strong implications for humans, even if the results are numerically different.
Back at human population studies, you also don't need full starvation studies (X days without any food) to find that there are long term consequences, simple caloric restriction (CR) is well established as having long term negative consequences. I don't think it's a big stretch to assume that full starvation would (at the least) exacerbate these effects. On the other hand, there's a lot of recent age-related research showing controlled CR can extend lifespan from yeast up through mice. Though it's also well established that it can (for instance) reduce fertility at the same levels.
I'll just give a couple links on population studies on starvation. Starvation is much easier to research because (as I recall) people can live for about a month without food or sleep, but a week without water and you're just dead. Population studies seem like the best way to get at the question you're asking (consequences of chronic starvation).  But as I said, these aren't controlled studies, you have to go out and find a relevant population and get what data you can. You're not going to just run across a dozen people who all went for exactly one week without food in 1943 and then went back to their normal lives. These are single study papers, but they each cite at least a dozen related papers (including reviews) and should be more than sufficient to nucleate further literature searches.
Severe caloric restriction in young women during World War II and subsequent breast cancer risk
http://onlinelibrary.wiley.com/doi/10.1111/j.1742-1241.2012.02966.x/full
Comparison of metabolic profiles of acutely ill and short-term weight recovered patients with anorexia nervosa reveals alterations of 33 out of 163 metabolites
http://www.sciencedirect.com/science/article/pii/S0022395612002488
If these don't address what you're after, then please be more clear about what you actually need (and WHY this isn't it).  And, you know, this is a public forum that runs simply by the good graces of interested and knowledgable scientists. So please try and be a little nicer in how you phrase your questions.


text:
Could a person become physically transgender through artificial means?
Let's say there's a girl who carries a few masculine traits not normal in most girls, such as a high level of testosterone; we know there are countless reasons why something like this could happen, but could that girl have actually been concieved as a boy but modified before birth to become almost fully female, with only slight traces of male traits left? Is that possible through any sort of technology, or does biology even work that way?
For instance, if a male baby was injected with high amounts of female hormones before his birth, or really, anything else that could alter his gender, in any case could he start morphing into a girl, even if not fully? (Say, to the extent where he became more of a girl but still possesed a few common but not very specific/clear/exclusively male traits such as excessive body hair, etc.?)

A "high level of testosterone" must be made within the context of a particular sex. Men tend to have much higher levels of testosterone than women, but the testosterone production and levels within women vary widely - just as many hormones. Genetics, environment, diet, drugs, and workout regimes can all affect testosterone levels. A qualified physician will be able to tell where a person is after a test.
As for the rest... Every case of gender reassignment I've heard of and read about has occurred after birth. Read through this Johns Hopkins Magazine article from Sept. 2000 to get a fairly good understanding of when gender reassignment occurs and how it's handled. Here's a quick rundown (summaries, NOT quotes from the article):

Inadequate exposure to Testosterone in utero can result in ambiguous genitalia or other conditions such as 'micropenis' for an XY fetus. Up until the 1990's, regardless of chromosomal gender, children with the conditions would be reassigned as 'female' and had reconstructive surgery very early on.
Androgen Insensitivity is when an XY fetus is genetically incapable of utilizing male hormones and can involve several levels of insensitivity from "Complete" to "Partial". Complete insensitivity usually leads to fully feminine genitalia, while "Mild" or "Partial" can lead to partially or fully masculinized genitalia. Genitoplasty is an option for the latter cases.
CAH - congenital adrenal hyperplasia. This genetic disease causes the adrenal glands to produce excess androgens--the steroids that cause masculinization--a process that begins in the womb and can result in ambiguous genitals. However, CAH girls are generally more aggressive and display behavioral tendencies that more closely coincide with boys of the same age. Important to note: CAH children are genetically female (XX) and identify as female.

An extensive review of gender reassignments in 1997 had this to say about the consequences of surgically altering an infant's sex:

Considering this case follow-up, and as far as an extensive literature review can attest, there is no known case where a 46 chromosome, XY male, unequivocally so at birth, has ever easily and fully accepted an imposed life as an androphilic female regardless of the physical and medical intervention.

HOWEVER - as with all things scientific - there is dissent from the Johns Hopkins article above:

Preliminary analysis of the data, says Migeon, indicates that almost all of the patients are content with the gender in which they were raised. All but two showed a gender identity and gender role in accordance with their gender of rearing.

There is significant divergence that has not been reconciled in any trustworthy article I could find. The modern practice is to raise the child as their genetic sex unless significantly afflicted.
In adult transgender individuals, things like Hormone Replacement Therapy are part of a regime - along with surgery, acclimatization courses, and psychological evaluations - that can successfully result in a person presenting themselves and physically resembling another sex.
With adequate surgery, hormone therapy, and proper treatment all-around, it is practically impossible to tell whether a person is transgender without getting invasive or performing genetic tests.
As with all things that veer into a hazy area between medical knowledge (medical advice is not allowed on this website) and human biology: DO NOT use the above information to diagnose yourself or anybody you know. ONLY a qualified medical professional can perform the necessary tests required and give a qualified interpretation of the results.


text:
What organs are absolutely needed by the human body?
The title is my question: what organs are absolutely needed (fatal if injured/removed) by the human body and perhaps animals in general?
I'm not asking which organs are mechanically replaceable, but more what organs cannot be removed (and not replaced) in order to maintain human life.
--update--
To clarify the question, I'm wondering what organs when removed (and applied no medical intervention) would cause fatal effects in a short amount of time, or cause semi-fatal effects (ex. shortened lifespan). A list perhaps of importance, if possible, would be nice.
note: I have no medical knowledge so I'll leave 'short' open to interpretation.

well.. i think it is only the brain which has no mechanical replacement as of now.

@WYSIWYG I've updated my question to clarify. I've been reading in wikipedia that ex. removal of the liver, pancreas is potentially fatal - and was wondering what other organs have the same effect.

I think you can rather ask which organs are dispensable. easier to answer

@WYSIWYG If this is something in dispute or unclear for some organs, I'd prefer to hear what those disputes are surrounding them than change the direction of my question just for easier answering.

Just to clarify, are we looking for organs that once removed would be fatal without medical intervention?  For example the body can be maintained for a long time without kidneys if dialysis is applied.

@RoryM +1 Thanks for the comment. My original intent was in asking what organs when removed would cause fatal effects within a short amount of time(or drastically shorten lifespan), but reading your comment, it would be great if someone could also add in their reply how it would change depending on medical intervention.

As the comments are gradually illustrating, I think this question is too vague to really be answered effectively.  There are some clear examples of organs that can be removed w/o immediately causing death with varying degrees of medical intervention but you could likely keep any small amount of human tissue alive for weeks in the lab so the answer would be all of them except for that piece* (lots of medical intervention required).

@KennyPeanuts +1 Thanks, I see the side question on the effects of medical intervention makes the question itself a bit too vague. I've removed it from the question, hope it makes this clearer to answer.

You can't remove most organs. The heart, lungs and brain are the ones that without you'll die in seconds. The rest you'll live a few hours or more. All depends how long you wish to live. The best way to see which organs are most required is to look at the order organs are shut down when there isn't enough oxygen or blood. That tells you which area most and least important.

+1 Do you perhaps know of a link or source of some sort that covers the shut down list you've mentioned?

Usually when a person has lost blood they'll lose blood to their skin, followed by muscles (excluding heart/diaphragm), gut (from oesophagus to anus). Meanwhile the blood reserve in the spleen is being mobilised, releasing lots of things to help clot the blood etc. Last to go are lymph nodes (involved in the immune system), liver (similarly involved) then heart and brain closely together.

There is a list of "vital organs" on which there is a consensus that if such organs are removed, the body dies within hours/minutes. Yet people can live long with only one lung or one kidney.
Another list could include other organs that are semi-vital: we could live for a relatively long period without them, but their absence has to be compensated with a continuous treatment (pancreas, thyroid, etc.).
In contrast, people can live in "good health" with non-vital organs removed such as legs, eyes, teeth...

+1 Thanks for the reply and vital organs link, is there perhaps also a source you know that covers the semi-vital organs you've mentioned?

I'm not a medical professional, so this isn't exhaustive or guaranteed 100% accurate:
You can live a (*mostly) normal life without your:

appendix
tonsils
spleen
gallbladder
pancreas
portions of your liver (pieces can be removed and it will regenerate)
portions of your small or large intestines
both lungs (one is needed)
both kidneys (one is needed)
uterus
testes
ovaries

*there are some side effects such as lowered immune function or difficulty digesting fatty foods, but for the most part, you might not even notice.
You can live with some **detriment to your quality of life without:

colon
bladder
up to half your brain
stomach
thyroid

** surgical interventions can replace the colon and bladder with pouches of intestine, drugs can regulate the loss of the thyroid. Losing half your brain messes up a lot, but it's survivable.

Can you add at least one reference for this list?

I could be wrong but the question asks which organs are required for life and not with ones are not too important for it.


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Why are trichromat cone cells unable to sense ultraviolet and infrared radiation?
I understand that cone cells vary in the color they sense, is this because of wavelength, frequency, something else, or a combination of the previous? I also understand that tetrachromats can see an extended spectrum of color because they have four as opposed to three (for trichromats) color channels, hence, I believe, an extended variation of cone cells.

The range of color perception in humans is primarily limited by the sensitivity of cone cells (specifically, the opsin proteins in cone cells) to various frequencies of light.  This sensitivity drops off at 700 nm on one side and 380 nm on the other, which is where infrared and ultraviolet begin, respectively.
Even with hypothetical infrared or ultraviolet cones, we wouldn't necessarily be able to perceive color much further beyond our current range anyway.  The various parts of the eye (cornea, lens, and the liquid inside) block both ultraviolet (starting around 400 nm) and infrared (starting maybe at 1400 nm) beyond certain wavelenghts.
http://en.wikipedia.org/wiki/Color_vision
Tetrachromaticity, at least in humans, does NOT confer an extended spectrum of color perception.  Tetrachromaticity results from a mutation on one of the light sensing proteins, changing its peak sensitivity by a few nanometers. So a tetrachromat can't see beyond the normal color spectrum, but they can probably distinguish shades of green and blue more precisely than trichromats. This has been an area of active scientific research recently; I think most scientists didn't think they existed.  Now studies suggest they're 2-50% of the population.  Humans with 5+ cone types are also hypothesized, and with the ubiquity of genome sequencing I imagine we'll be learning a lot more about that soon.
Other species have more diverse color perception, with ultraviolet being especially common in insects and birds. The mantis shrimp has an astounding 16 different kinds of photo receptors, plus a few specialized eyes for detecting polarized light. For a loving account of mantis shrimp, I recommend this comic. http://theoatmeal.com/comics/mantis_shrimp

Wikipedia says "the rods and cones located at the back of the human eye cannot detect the short ultraviolet wavelengths" but you say otherwise, could you possibly give evidence for your claim? Edit: Also mutation could also change the trough, right?

I also understand that ultraviolet radiation is absorbed by varios tissues of the eye (which is what causes photokeratitis, is this the same for infrared?

Sorry, I meant that as a hypotical, i.e. if we DID have extra chromophores, they still might not work.  I did see one reference that infrared doesn't actually start getting absorbed until 1400 nm by the eye though, so we might be able to extend a fair distance in that direction, but not infinitely.

I indeed read somewhere (and have never been able to find the source) that it would only take a single base pair mutation for us to see much further into ultraviolet. But that it wouldn't matter because our lens starts absorbing it very close to our existing limit. There is apparently no true infrared vision, possibly because the photons are too low energy. Animals that "see" infrared do it through other types of organs.  So I wouldn't bet on a mutation on that end.

You mean that if we had extra chromophores, humans still might not be able to see them or that the chromophores just wouldn't work?

I still need to know, do cones act on frequency, wavelength or both?

Scientists have genetically engineered mice (normally dichromats) to give them their missing red chromophore (I think).  The mice used them just fine. So the point is just that, at some point, the physiology of the lens and cornea would be the limiting factor. As for frequency vs. wavelength, I suggest you go look up wavelength on wikipedia.

For a more complete answer, human opsin proteins are limited to these ranges. There are bacterial opsins and recombinant opsins that can detect well into the UV and infrared ranges.


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Why do dogs try to cover their poop?
It may seem obvious to us humans to hide our excreta, but this is not quite normal behavior for animals.
Interestingly, dogs have the habit to pee all over the place. It's know that they do so to mark their territory. So when they want to mark their territory, why do they cover up their poop?
I found an old web article where someone asks the same question, without getting a credible answer. He quotes a Yahoo Answers answer making the following claim:

This behavior is natural in dogs. They cover up their "waste" so that
  an enemy does not find them, from the scent of the poop or pee. It is
  an instinct handed down from wolves, who hid their scent by covering
  up their feces in leaves, sticks, soil, or other nearby natural
  materials. They also rolled in animal carcasses to hide the scent of
  them. Your dog is just using her natural instinct to protect herself
  from predators.
Another things that dogs do, called marking, is when the dog pees in a
  certain area. They do not cover it up, as it is marking a territory as
  their own. Male dogs usually do this on trees, wooden posts,
  furniture, and other things. Female dogs do this in heat. Dogs do not
  poop to mark something, only pee. When you dog pees or poops and then
  covers it up, this does not mean she is marking her territory. Just
  wanted to add it so you don't get confused. :)

I find it hard to believe these two opposite claims. One time dogs want to mark their territory and the other time it's scared from predators. I know many dogs that do not cover their pee, but do cover their poop, sometimes even within the same walk (and so the same territory).
If this is true, why do dogs do both in the same walk?
On Wiki Answers I found this answer:

The animals are not actually covering up the pee or pooh but spreading
  their scent. This often happens with animals that are dominant (for
  instance show dogs).

It's so that dogs never actually cover their poop anymore, they only perform some random scratches, throwing a little sand on the turd, sometimes even nothing. That fact makes this answer quite more likely than the previous one.
Another take that's similar to the previous one is this one from Dogster:

So, why do dogs scratch with their hind legs after defecating? You
  might think the dog is trying to cover up his poop like a cat does,
  but it’s actually a way to mark territory, with the scratch marks in
  the ground pointing to the scent the dog has left.

I also found an eHow article on this subject. It seems to agree with the previous two explanations, but is more detailed.

It is normal for dogs of both sexes to vigorously kick the ground with
  their hind legs after defecating. This is called scraping or peeling
  out. Some dogs will also do it after urinating. Dogs are descended
  from wolves, which also perform this behavior. It is not a bad habit,
  but a vital part of a dog leaving a visual message and scent message
  to any other dogs that happen to pass by.

They also say that the specific reason why they spread scent with their paws is because paws just contain a lot of scent.

Dog paws contain scent glands. There are also glands in between the
  toes. The action of scraping the paws against the ground helps release
  the scent inside of the glands. Dogs scrape the ground in order to
  increase their scent on the area near the feces pile, according to
  veterinarian Dr. Justine Lee. Before domestication, dogs wandered in
  large territories. One vital way to communicate with other wandering
  dogs is through scent marking. This instinct has not been bred out of
  the domestic dog.

So, which theory is the most valid? I tent to go for the scent one. Any additions?

...maybe because dogs that didn't do that were more likely to get sick (or get members of their pack sick) and die, giving an evolutive edge to the ones that randomly started to do that. Or maybe it is so the smell doesn't cover another more important smells. Or maybe we humans selected the ones who did, because...well, obviously we prefer the ones who bury their feces without even training them to do it. Or maybe, the ones who buried them just happened to survive in greater numbers, but it may not be a relevant trait in said survival (correlation doesn't imply causation)

I cannot find any definite articles on why there would be a reason for this behaviour other than the same ones that you have mentioned in your article. It could be because it wants to mark its territory or the dog wants to hide its scent.
One point that I would also like to add is force of habit. As Charles Darwin (the father of evolutionary biology) had said in his book titled "The expression of emotion in man and animals"

‘Certain complex actions are of direct or indirect service under
  certain states of the mind, in order to relieve or gratify certain
  sensations, desires, etc.; and whenever the same state of mind is
  induced, however feebly, there is a tendency through the force of
  habit and association for the same movements to be performed, though
  they may not then be of the least use’ (reference 1 and reference 2).

It is more of a guess that we make when we see them hide their faeces but in the end, there may not be a reason at all but a habit that do not serve much purpose passed on through evolution. It is left upto our own liberty as to guess what the exact reason is.


text:
Is there a comprehensive list of human circadian-like processes, hormones or gene expressions?
I'm reading this article onblood sugar and circadian rhythms and the following question popped into my head: a lot of articles mention various diurnal or circadian rhythmicity of biological processes. Is there a "master" list of hormones, gene expressions and other processes that the modern science recognizes as "circadian"?
In other words, is there something that can give reader a clear picture of what's happening at a certain (biological)time for a human and is expected to happen tomorrow at similar time?
It would be great to take a look at such list and see what are the major processes that recur on a time-sensitive basis in humans.

There isn't a central/master website that I'm aware of, as it's still an area of active research.  I did a bit of work in the field about 10 years ago, and at that point we were still working out the circadian rhythms in the yeast mating cycle.
Since then, the field been enumerating more and more involved processes: mRNA expression, mRNA degradation, micro RNA, mRNA transport and translational regulation, then protein translation and protein regulation... Given that any single gene can be regulated at one or more of these points, and that there are at least a few different circadian cycles and they can even conflict... well, it's a bit of a mess.  Oh, and don't forget that different organs and cell types have different responses, so then you have to cross check 50 cell types.
I'd start with this review paper, which can give you an idea of what kinds of papers to search for.  If you decide you want to know about individual genes, a lot of scientists in the field have made their datasets available online in various gene expression databases.  There are several databases running currently, and maybe one of them will be specialized in circadian expression.
Circadian topology of metabolism
Joseph Bass
Nature 491, 348–356 (15 November 2012) doi:10.1038/nature11704
Published online 14 November 2012
http://www.nature.com/nature/journal/v491/n7424/full/nature11704.html


text:
How do mutations come to be shared by all cells?
It's my understanding that various hazards can damage the DNA in our cells, causing mutations.
But whenever I picture this, I see the damage being done to one of our tissues (for example, our lungs due to smoking, or our skin due to UV rays).
When I think about this, I see that... many cells in a smoker's lungs, or many cells on the back of a beach-goer's neck, may have mutations in their DNA. But only the cells in that tissue have these mutations... the other cells in our body would not have the same mutations.
In particular, sperm and egg cells would not have the same mutations, so the mutations due to smoking and UV rays shouldn't pass on to children.
Are there instances where mutations that occur over the course of our life are spread to every cell, including sperm and egg cells, so that every cell reflects the mutation, and the mutation is passed onto our offspring?

This usually happens when the mutations occur at an early stage of development, such that a precursor cell with the mutation gives rise to all other cells in the body.  Are you asking about cell-to-cell "transmission" of mutations?

Sperm/egg can be affected by the general body physiology, such as in case of starvation etc, by epigenetic mechanisms. These epigenetic changes that can be passed to next generation. See Transgenerational Epigenetic Inheritance

Goods question! Only mutations that occurred when we were in the early stages of development will affect all cells. That's why pregnant mothers shouldn't smoke. The reason for this is that one cell goes on to divide and become all our cells so any mutations in that cell are passed on to cells formed when it divides. That same principle explains your smoker example. In the lung we have two types of cells which are called Type 1 and Type 2. Type 1 cells are constantly dying as they get old and they get replaced by type 2 cells whose job it is to divide continuously to replace Type 1 cells. So we have lots of type 1 and few type 2. When type 2 divide they make one type 1 cell and one type 2 cell, so type 2 cells never run out. If smoke causes a mutation in type 1 cells generally they're okay because they'll die before enough mutations occur. Of course something that causes lots of mutations could make it cancerous before it dies but that's rare. Now if it occurs in Type 2 cells every subsequent type 1 or type 2 cell that cell makes is mutated.
The last thing you mentioned are mutations that occur to eggs and sperm. When making sperm you have the same as above. One cell makes sperm and a sperm maker cell. The sperm is like type 1 cells and the sperm maker cell is like type 2. So mutations affect them as they do above, where a mutation in a sperm maker cell is way worse. As for eggs women are born with all the eggs they'll ever have and there's no egg maker cells. So mutations just occur, and the older women are the more mutations. That's why the older a mother is the much higher risk of genetic diseases like downs. But an older man only has a slight increase in risk.
Mutations that affect eggs and sperm tend to be really harmful, as they affect every cell, so these cells or "babies" die before the mother even realises she's pregnant or as a miscarriage. I've not given the scientific names for things but if you request them, I'll give you the real names, but hope you enjoy the principles.

Hi AndroidPenguin, thank you for the explanation. I really appreciate your examples with Type I and Type II cells in the lung, as well as the analogous sperm and sperm maker cells. I didn't know that some cells were designated to be the producers of others, kind of like the factory pattern in software design.

I wonder whether these 'factory' cells always replicate through meiosis? I know that sperm maker cells do, since they produce haploid cells, but not sure about type II cells in the lung. A more general question would be, if cell A replicates to produce cells A and B, does it always do so through meiosis? As far as I understand, it's not possible to achieve this with mitosis.

Type 2 cells replicate through mitosis: one of the daughter cells differentiates into a type 1, the other stays undifferentiated as a type 2. Type 1 cells can't divide because they're so far down the maturity process, also I imagine its a protective mechanism. As for sperm maker cells, as I call them here, they divide mitotically into one sperm maker and one cell that's a pre-sperm cell (still diploid). This divides again as per meiosis to give rise to 4 haploid sperm cells. You need it to divide again for crossover (when the genes swap around so you get a random selection from your dad)

Yes, all cell division in the body is through mitosis. Meiosis is a very special form that occurs only in the ovaries and testes to produce egg and sperm cells - absolutely nowhere else!
Do note that mitosis can be asymmetrical, i.e. producing two different kinds of daughter cells rather than simply multiplying the parent (as in the example with type II cells).


text:
Does darker skin color make it easier to live under sun?
I have always thought darker colors absorb more heat from the sun, so if you are wearing a white T-shirt you will be cooler under sun than wearing a darker T-shirt, or a black piece of steel will be hotter under the sun than a shiny silvery one.
If this is true, then why is the same not applicable to skin color? It seems to me like the more sun in an area the darker the people's skin has become, isn't that the case?

Try http://skeptics.stackexchange.com/

Heat is infra red radiation.  The more dangerous form of radiation from the Sun, however, is not infrared but ultraviolet.  I'm no biologist, but I believe dark skin contains more melanin, which protects against this dangerous UV radiation (UVB anyway).  Hence there may be an evolutionary advantage to have dark skin in sunny regions?

just based on visible light and not UV in hot areas you should seen lighter skin not darker, you actually do see this animal thermoregulation, however camouflage tends to overpower this small thermal effect. Interestingly polar bears combine darks skin and hair that functions much like a fiber optic to absorb more heat from the sun. Skin color in humans has more to do with ultraviolet as has been mentioned.

It isn't about heat but ultraviolet light. Melanin is the pigment that makes our skin colour whatever it is and in darker skin there's more melanin. Melanin dissipates UV, which otherwise would cause skin cancer as it introduces mutations into DNA. Melanin production is stimulated by UV so that's why tanning beds work, our body senses the danger and responds by making our skin darker. Yes this makes us hotter but that's a small price to pay, melanin needs to be dark to do its job well.

Here's a map of skin colors of indigenous peoples: http://4.bp.blogspot.com/-GhV7vZ-zk_g/TtWrU1rrRUI/AAAAAAAAC88/fhlacsLcpxA/s1600/skin-colour-map-indigenous-people.png Darker pigmentations are at latitudes where UV is highest. Feel free to add the image to your answer if you like.

I agree with what has been said here about melanin and UV light, but I think there is a missing piece to fully understand the color variation in humans. Otherwise everyone would have just black skin and problem solved.
One of the counterparts appears to be the conversion of Vitamin D to an active form, that requires the action of sunlight. This trade-off explains the beautiful gradient of color in human populations *.
*Native populations, not migrated populations.
I'm attaching and old but interesting article about this from scientific american 2002.
http://www.direct-ms.org/pdf/VitDGenScience/Jablonski%202002%20Skin%20color.pdf

It is precisely about the balance between vitamin D and UV. Good answer.

Yes, it is true that the hotter the sun, the darker people's skin becomes (in general) because of the evolutionary advantage conferred by having melanin to protect against UV light. The reason a dark object like an asphalt road gets hot quickly is that colors like black absorb most wavelengths of light, and therefore absorb more energy in the form of thermal energy.
In the same way, the melanin in your skin absorbs the UV from the sunlight because it is so dark, and protects your skin from it.

I think that you'll need a biologist to answer your question fully. However, I can try to explain what I can in terms of physics. Generally, the darker a material is, the greater the range of wavelengths of light it absorbs. With what is perceived as a perfectly black material by a human reflecting no wavelengths of the visible light spectrum of electromagnetic radiation at all. Therefore it would be logical that in cold climates humans would have darker skin colors in order to absorb a greater range of wavelengths of light. Although at first glance this seems the correct way for humans, and in fact all organisms to evolve, it's obviously not the case. There must be other underlying reasons that have caused organisms to evolve the way they do. An interesting example of how nature seems to defy this is leaves. One would think that the chloroplasts that make up leaves should be black in order to absorb sunlight as efficiently as possible. As we know, this isn't the case.

In chloroplasts it's simple - chemical reaction needs a photon of certain energy so it could happen. Green photons are useless in this case.

Chloroplasts can't use green light for photosynthesis so they reflect it away hence we see plants as green. There are some photosynthetic organisms that don't use red light.

This does not answer the question in any way.

to answer your question from years ago maybe to better inform any new readers that read this. yes and no. we have melanin in more areas than just our skin, it's in our nervous system, in our eyes, and etc and we should also ask what "information" we obsorb in those areas. having melanin does make it easier to absorb all wavelengths on the electromagnetic spectrum, but not everyone with dark and lighter skin can live easily under the sun. also consider what i call "inorganic" or "chemical" EMF/wavelengths highly melanated beings are receiving from computers and other man made devices which there are links to cancer and other issues in the body from those unnatural EMF.  Research has shown that most bodies whether light or darker can't survive past 104F because the thermoregulatory system shuts down. now if it 120f outside does this mean that your body is the same temp,,, i don't feel so after being exposed to such weather. i have light skin, but can develop melanin rapidly with minimal damage or sunburn occurrences. but my auntie who is darker than me, who has lupus, cannot be in the sun. this is on an individual basis, but having more melanin or active melanin in general to protect you may be more in your favor, especially this 2017 and upcoming years. the color white is said to block the UV rays, but not absorb most of it. this poses the question to cancer caused by over exposure to the sun and the hue you are as man, if you are of darker hue and do not have any sun exposure, you will or may have more health problems, little to no active melanin or light skin, you may or may not have more health problems in the sun or certain longitudes and latitudes. this is good to consider whether you are aligned in a place where you are getting the correct amount of sun exposure, or consider if you are getting the incorrect amount of sun exposure. again, this answer can only be answered on an individual basis.

can you cite some references to your answer?


text:
qTERT-pcr like qRT-pcr
Is it possible to use a biologically active Telemorease Elongation Reverse Transcriptase (TERT) in the place of the Reverse Transcriptase (RT) for quantitative Reverse Transcriptase pcr (qRT-pcr)? Yes I do know that it would seemingly have no advantages. What kind of reverse transcriptase is used in qRT-pcr is there a standard like taq dna pol is used for qpcr?

What kind of reverse transcriptase is used in qRT-pcr is there a standard like taq dna pol is used for qPCR

M-MuLV (Monoley murine leukemia virus) reverse transcriptase
Some RT enzymes are engineered to remove the RNAseH domain so that template RNA persists for more rounds of RT.

Is it possible to use a biologically active Telemorease Elongation Reverse Transcriptase (TERT) in the place of the Reverse Transcriptase

Perhaps it can catalyse an RT reaction in-vitro. But commercial enzymes need to be efficient and I think using TERT won't be that advantageous.

hTERT is incapable of replacing common reverse transcriptases like MuLV or SuperScript.
hTERT is specialized to bind with its own RNA (hTR aka TERC), and not any given RNA. hTERT uses hTR as a template to extend a DNA strand with the same repeats (TTAGGG). (Cairney & Keith 2008). For qPCR it's needed to transcribe RNA into the same sequence of DNA, not something repetitive.

Could you provide links describing the biochemistry of MuLV and SuperScript? On the face of it I only get the gist that they are for reverse transcription.

Zhao et al. 2018 is one free article (so many other articles are behind a paywall). It‘s interesting since it discusses an RT that‘s not isolated from a virus (like every coomercial RT out there), but actually from a transposon (which are like ancient viral elements in the genome of every animal). It also compares it to SuperscriptIV, which is the pinnacle of enzyme beauty. Have fun reading.

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