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Why would a mother reject her offspring if it has been "interfered" with by humans?
There was a recent incident at Yellowstone National Park in which tourists placed a bison calf in their vehicle, and that eventually led to the calf being euthanized.
The National Park Service issued a statement in which they said:

In addition, interference by people can cause mothers to reject their offspring. In this case, park rangers tried repeatedly to reunite the newborn bison calf with the herd. These efforts failed.

Why would a mother reject her offspring if it has been "interfered" with by humans?

Several ungulates and other species such as seals and primates are known to initially use odour to discriminate their offspring. Most relevant work to study this has been done in sheep; sheep are ideal for studying attachment because there are ethical and logistic difficulties that limit laboratory and research use of most other species known to develop selective mother-young social relationships. In addition domestic sheep are common worldwide, easily bred and handled, and well-understood in terms of behavior and natural history, providing a solid base for more intricate study (more information here).
According to this paper ewes are attracted to amniotic fluid for a few hours after birth, which stimulates nuzzling, sniffling and licking behaviour; after a relatively short time she becomes familiar with the lamb's unique odour. Thereafter, lambs without this odour are almost always rejected. After some time the ewes learn to use visual and auditory cues to identify their lambs and smell becomes less important. The Wikipedia article on the subject gives some information about the neurobiology of the process.
From a selective advantage point of view, I would speculate that this would evolve to reduce the risk of being exploited by 'free-loader' genotypes that engage in behaviour similar to brood parasitism in birds (i.e. leaving their offspring to be cared for by other ewes).
This can work both ways; in addition to the risk of disrupting the smell of a lamb by excessive handling, shepherds have recognised for centuries that lambs which are rejected by their own ewe, or whose ewe has an inadequate milk supply, can be fostered by other ewes who have lost lambs using a technique historically called skin-grafting, where a dead lamb is skinned and the skin tied around the foster lamb. The odour is thus transferred to the foster lamb for long enough for the ewe to accept it and become familiar with its visual and auditory identifiers, after which the odour is no longer important. The paper I cited above above describes a study that found that cloth 'stockinettes' could be used in place of a skin to achieve the same outcome.
edit: Interestingly, the responses to this question at skeptics.SE suggest that the popular notion that odour-based attachment results in abandonment following human interference with birds is probably untrue.

I know that in at least some species  of birds it is untrue.

Actually, once humans or any other animal touches the infant, especially before the mother has recognized it as its own, the scent of the "foreigner" stays on the infant/offspring. Thus, the mother does not recognize the infant or believes it to be "tainted". This is true for a lot of birds as well as wild animals. If anyone "disturbs" the bond- forming during parental care of the newborn, the newborn is often abandoned by the parents.


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If DNA is the input, what is the output?
How does cells use the DNA inside them? I am looking on DNA as a strip of tape of Turing machine, but with machines its easy. I can read the tape and calculate the behavior of that machine. With cells its different we don't really understand the language of DNA.
So instead of trying to understand the language I was wandering if there are any particular behaviors of cells that we can associate to different "outputs" of the DNA tape.

DNA changes to RNA, which can either effect the behaviour of DNA itself through non-coding RNA or changes into proteins, which can also affect the DNA.

We actually really do understand DNA...

the analogy with the turing machine is correct I think, but there is still much and more research to do in biology order to make ideal cell-computing models

@canadianer really? That's news to me. We understand a lot about it but not everything. Not even close to everything.

You might find this article interesting: http://www.ncbi.nlm.nih.gov/pubmed/11504843.

@terdon Who said everything?

@canadianer well, you claimed "we actually do understand DNA" and I'd argue that we understand very, very little. Especially when it comes to complex questions like how "different outputs" are chosen (think alt. splicing/choice of splice site/cis+trans regulatory elements/% of genome transcribed/methylome and epigenetics in general etc, etc). We understand the basic mechanics but are still very very far from understanding the regulation.

@terdon Well, you make a good point.

but with machines its easy.

It's not that easy...the Turing machine can't interpret the tape without knowing something about what the 1s and 0's mean.  A complied C++ program is gibberish if read through a Perl interpreter.
DNA isn't as abstract as that, anyway.  A DNA molecule interacts with other molecules based on its shape, which the sequence of letters defines.  There are thousands of molecules in a cell which the DNA strand can interact with, and those molecules are affected by other molecules.  Think about it...for the most part, all the DNA in your cells is the same, but obviously the cells in your liver are doing different things than the cells in your skin.

With cells its different we don't really understand the language of
  DNA.

That's not the problem.  We just don't understand ALL the relevant interactions, because there are so many of them.  There is not one thing reading through the string of DNA once.

I was wandering if there are any particular behaviors of cells that we
  can associate to different "outputs" of the DNA tape.

The outputs would be proteins, but you can't just look at the DNA sequence and know what proteins will be made when and in what quantities, not without having empirically learned a lot about those proteins.
Look, there are lots of people who know a lot about computers and a lot about biology.  If thinking about DNA as a simple string of information was fruitful, people would be doing that.  We don't, because biology is more complicated than that.

The central dogma of molecular biology states that DNA encodes the information for building proteins, the information is copied to messenger RNA through transcription, and messenger RNA is used to build proteins through translation. DNA is also copied through replication.
So while it's true that DNA contains the information needed to build a living organism, I don't think it can described as "turing tape" If I understand turing machines correctly, you have a string of 1s or 0s, and a machine reads this string. Based on rules provided by an instruction set the machine can set positions on the tape to 1 or 0. The analogy with DNA fails because DNA does not have a separate instruction set and cannot be written to. DNA produces RNA and DNA with the help of many many proteins and other molecules, all tightly regulated to coordinate replication of the genome and to produce the right amounts of RNA and protein at the right times. DNA can mutate when replication makes an error, but this is accidental, not comparable to turing machines.
If you're interested in how DNA might be used like a computer, there are several articles on DNA Computing, though you'll have to sort through those papers because many look like they just used a computer to analyze DNA.

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Identification of small fuzzy flying insect (pic)
These critters were flying around the neighborhood on an autumn evening in Seattle, WA, USA. Their most notable feature was the small amount fuzz on them. They were quite slow in their flight compared to similar-sized fruit flies.
Any ideas?
Here are two close-ups:

One one for size comparison:

I'm having trouble counting the wings. In your image on the right, I can't tell if there is a second wing on the lower edge of the right wing. The left wing is even less visible. If this only has 2 wings, then it's a diptera. But I'd also believe this is a hymenoptera if it has 4 wings. Not familiar with pacific northwest insects.

To me, it looks like a male Aphid (males are winged, and have four wings) from the genus Eriosoma (wooly aphids). The white feathery substance is a wax secretion.
Have a look at Bugguide: Eriosoma, InfluencialPoints: Eriosoma and this page from the Uni of Minnesota for some more info.
A picture of a species from the genus:

I'm with you, and tempted to delete my answer.

+1 : decisive is the wing venation pattern - it's definitely an aphid. By the way, females can also be winged

@har-wradim True that also females can have wings, but my impression is that winged males are more common. I cannot say about this individual though. Females have an ovipositor and males claspers (and often slightly different body shapes), but hard to see in the pictures.

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Are there any multicellular forms of life which exist without consuming other forms of life in some manner?
The title is the question. If additional specificity is needed I will add clarification here.
Are there any multicellular forms of life which exist without requiring the consumption (destruction) of other forms of life in some manner? Thus purely on inorganic material.
I do understand that the definition of life is a semantic distinction, so for this discussion I will assume the one Wikipedia provides:
"Life is a characteristic distinguishing physical entities having signaling and self-sustaining processes from those that do not, either because such functions have ceased (death), or because they lack such functions and are classified as inanimate. Biology is a science concerned with the study of life."
I am open to considering alternative suggestions.
Thank you.

Closely related to the question can humans survive without eating life

Many of deep sea organisms eat dead bodies. They do not catch other organisms alive.

Please include the question in the question. The title may or may not be the same, but the question should read coherently without reference to it.

Yes, plants for example!
Autotrophs vs. heterotrophs
Plants are autotrophs while animals and fungi are heterotrophs. Have a look at the Wikipedia articles. In short, autotrophs organisms are organisms that synthesize their own compounds from inorganic compounds. Heterotrophs organisms are organisms that synthesize their own compounds from organic compounds.
Therefore, any multicellular plants are multicellular organisms that "exist without consuming other forms of life" (with the exceptions of carnivorous plants).
Consuming nonliving organic matter
Of course, many life forms feed on organic matter but only on non-living organic matter. Such life forms do not kill to feed. It is the case of all detritivores (such as earthworms) and decomposer such as fungi.
Competition vs predation
As @TechZen said, not consuming other organisms doesn't mean that the existence of an individual of this species is not causing the death of another individual (competition and parasitism that does not involve consuming the other individual).

Aside from blocking out light, how do zooplankton cause the death of other individuals?

Why do you want to take the "light blocking effect" out of the discussion? Zooplankton (by definition) are heterotrophs and therefore they eat other individuals. Zooplankton probably have tons of impact on their environment too (I am not an ecologist as you can tell) that likely affect other species.

Because what do they gain? Are they gaining resources because their numbers are high enough to smother other forms of life? Do they decompose the dead organisms and use them for energy like other plants do if there are dead organisms beneath them?

I don't quite understand your point. Maybe you want to make sure to have a look at the wikipedia entry for zooplankton.

There are multicellular organisms which do not actively eat other organisms, however, there are no organisms who do not kill other organisms, period.
Trees and other vertical plants evolved in the first place in a competition for sunlight. For plants, being in the shade is like smother or starving a human since they literally use sunlight to create and create food and oxygen. Plants carry out complex chemical war against a wide range of other life forms from microbes to other similar plants.
Plants don't eat other organisms, save indirectly, but they do kill.
All multicellular organisms have an immune system that wages and unrelenting slaughter against microbes which in turn are constantly assaulting multicellular organism.
Lastly, every individual organism and probably all strains and species, displace other individuals, strains or species just by existing. No energy is wasted in the biosphere. If something is living in one place or niche and then dies, the energy it was living on becomes available for something else. Conversely, while it lives it prevents other organisms from evolving to fill the niche, or as an individual moving into the physical niche.
Just by our very existence, we kill.

Though there are saprophytic plants which "eat" dead organisms, parasitic plants (like this one: https://en.wikipedia.org/wiki/Sarcodes ) which feed off other plants, and even carnivorous plants that eat animals.

@jamesqf - Doesn't matter, what they eat or were, they displace something else and kill. All multicellular organisms have to constantly kill microbes to prevent being eaten by them.

No, there are no known multicellular organisms that depend exclusively on inorganic material.
Plants have been put forth as examples of multicellular organisms that do not "consume life", but that does not mean they don't depend on organic matter. Plants depend on nutrients found in the soil, and these nutrients come largely from decomposing organic material.
It is now early spring here and the local farmers have started spreading manure on the fields. That manure consists largely of dead plant matter digested (mainly) by cows.
Of course, a plant can live exclusively on inorganic nutrients, if you grow it hydroponically and exclusively give it inorganic fertilizers. Ammonia can be produced from nitrogen in the air through the Haber-Bosch process, and the rest, phosphates, potassium, sulphates etc. can be taken from mineral deposits, but this is rather artificial. Plants are, by and large, completely dependent on organic matter.

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How does the new discovery that mitochondrial dna is inherited from both parents change population genetics and other dates?
This new study seem to have pretty much proven that mtDNA is inherited from both parents. I assume that this would lead to most age estimates of ancient human populations that heavily depending on mtDNA, being discarded. Is this right?
What other things would be affected by this discovery?

What you refer to is just a (non-peer reviewed) vulgarization of an original (peer-reviewed) article. This original article is Luo et al. (2018). I only read their abstract and wants to highlight this sentence: [..] there are some exceptional cases where paternal mtDNA could be passed to the offspring. I will need to read more (I currently don't have access to it due to a paywall) to have an opinion as to whether that might affect our molecular clock estimates.

The authors also write the following: Clearly, these results will need to be brought in agreement with the fact that maternal inheritance remains absolutely dominant on an evolutionary timescale and that occasional paternal transmission events seem to have left no detectable mark on the human genetic record, indicating the opposite of your assumption.

@Astrolamb How is it figured out that "occasional paternal transmission events seem to have left no detectable mark on the human genetic record" independently of whether mtDNA is inherited or not?

@Daud I don't have access to the entire article, so I don't know the author's reasoning. However, considering that so far only 17 individuals in 3 families have been identified who have paternal mtDNA, statistically speaking the impact of a very few compared with the billions on the planet is insignificant.

I should also add that due to decades of study on mtDNA, the vast majority of which followed expected maternal inheritance, we have a pretty decent understanding of what is expected with maternal inheritance, and almost all cases follow those predictions, so unless it were more widespread, paternal inheritance hasn't had a big enough impact to be noticeable.

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If a DNA letter is one of A,T,C and G, and there are 3 billion base pairs, why don't we say that there are 6 billion letters in the genome?
A DNA letter is either one of A,T,C or G. Human genome is supposed to have 3 billion base pairs coming from each parent. But these are pairs - a combination of A-T or C-G. So, doesn't that make the total number of DNA letters from a single parent, equal to 6 billion ?

It's more common to say there are ~3.6 Gbp (Giga-basepairs). What you're asking is equivalent. You only need to know one of the letters in a given strand to know what the other is too.

A, T, G and C are abbreviations for the deoxynucleosides of DNA and often, more loosely, for corresponding bases. They are not letters. 'We' presumably refers to the scientific community, which includes me, and I certainly never talk about 'letters' in relation to DNA. This may appear technical pedantry, but it is important in science to refer to things precisely without adding unnecessary implications. The implication of letter is that it helps to spell a word — presumably in relation to a protein. In many cases that is not so. If you use the correct terminology, your question does not arise.

For all those who have voted to close this question as off-topic (or are willing to do so), please at least read the reason you are chosing. This is certainly not a homework question, and does not show lack of research either, IMO. This is just misunderstanding of the terminology, as @david says. This is what downvotes are for, there is no need to vote-to-close this question.

In response to the comment from @another'Homosapien', I should explain that when questions are voted off-topic under the category ‘homework’ it is not necessarily because they are considered homework in a literal sense. As I pointed out in a post on meta, ‘homework’ includes “A question that addresses a basic biology concept that may seem trivial to biology professionals”. I argued there that it would be better if this were separate category because of the ambiguity. Any takers now?

If a DNA letter is one of A,T,C and G, and there are 3 billion base
  pairs, why don't we say that there are 6 billion letters in the genome?

It is a convention, and stating the actual number of bases would not add any information, but would actually lead to more confusion. It's like saying

I have six pairs of socks

vs.

I have twelve socks.

It means bascially the same, but now one could assume that these twelve socks are not from actual pairs (e.g. twelve left socks). The same goes for DNA. Saying we have pairs of bases emphasizes the redundancy of the DNA double strand.

You can refer to the Human genome as haploid or diploid. The haploid genome is around 3Gb, the diploid one is 6Gb. Usually, the bare term "Human genome" refers to the haploid one. The first picture on this Wikipedia article makes it clear.

If a DNA letter is one of A,T,C and G, and there are 3 billion base pairs, why don't we say that there are 6 billion letters in the genome?

We do.
Just like English has 26 letters while this post has 522 letters (not counting numbers and punctuation), the genetic alphabet has 4 "letters" while the human genome has 6 and a half billion. The thing is people tend to stop using the letter analogy after talking about the 4 or 5 naturally available nucleotides. After that, we tend to go back to calling them nucleotides and base-pairs.
Whenever you have a question about something that doesn't seem to make sense, the first thing you should ask is if your premise is even right.


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What is bilateral symmetry in "bilateria", an actual symmentry
Wikipedia defines bilateria as :

animals with bilateral symmetry, i.e., they have a head ("anterior") and a
  tail ("posterior") as well as a back ("dorsal") and a belly
  ("ventral"); therefore they also have a left side and a right side.

By symmetry, I understand that divisions of the body along some plane be similar. Now, if you have a head and tail, isn't the horizontal symmetry lost (head and tail look different) ? Similarly, for a vertical division, a different looking belly and back also destroys symmetry along this axis.
An organism whose head and tail are exactly the same (you can't even make out if something is head, and the other, tail), is perhaps "actually" bilaterally symmetrical (along the horizontal axis).
What am I missing here ?

You are missing that "bilateral symmetry" does not mean "the divisions are the same on some arbitrary plane" it means "the divisions are the same on one specific plane".
That specific plane for animals with bilateral symmetry is on the mid-saggittal plane that divides the body into left and right. You won't get symmetry if you bisect in any other plane. If you do get symmetry in a different plane, then you are no longer talking about bilateral symmetry but rather some other type of symmetry, such as radial symmetry, spherical symmetry, or biradial symmetry.
Note also that although many animals do not have perfect bilateral symmetry in their internal organs (humans, for one), they are still considered to be bilateral symmetrical, because the bilateral symmetry is the main organizing feature of the whole animal.

Horizontal axis is a meaningless term.
Bilateral literally means bi=two Lateral=side, so one plane (two halves) of symmetry comparing sides, the symmetry is in comparing right to left.
having a front and back create alone (no top and bottom or left and right) would create something like radial symmetry.  add a diffrence in top and bottom and you get bilateral, in which left and right are the only plane in which one side mirrors the other. Consider this image. An organism where you can't tell one end form the other would be a sponge things with no symmetry or spherical symmetry, symmetric across all possible planes.
Horizontal axis could mean anything, it could mean three different things(symmetrical top to bottom, symmetrical front to back,  or symmetrical left to right) that's why we use terms like bilateral. So you need to qualify what you mean by horizontal. Horizontal is not an axis it is a plane, and I know of nothing symmetrical along that plane (top vs bottom).


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Detecting UV by humans
From my experience humans can detect UV - not by seeing it but by pain in their eyes. Many people (me too) feel pain when looking at UV lamps. When looking at sun through clouds I still can feel pain very often even if the after -all-image is not very bright (because of the clouds) but when I look at a light bulb or when I look at sun through sun-watching lenses (which cut all UV) I don't feel that pain despite of them being much brighter than the cloudy sun. I also have read about it once or two.
So, can this be true (I mean humans can detect UV with their eyes) or that's just a coincidence? And if it's true, how it happens?

Related question: Are there specific conditions that allow humans to see ultraviolet wavelengths

I've read that before but this is about seeing UV in specific conditions. I ask about feeling UV with normal conditions.

Well, UV damages your eyes and damage is often expressed as pain. I'm not sure what else you are looking for.

Surely, but is only about damaging eyes and if so, which parts? But this sounds a bit weird for me... UV doesn't hurt (I mean just pain) our skin and eyes of course something different but they... well doesn't see UV.

I am not sure which parts of the eye are being damaged, but I would imagine that skin is much more durable than your lens, retina, etc, which can cause it to be less sensitive to UV. Your skin was meant to take abuse, your eye not so much

Anecdotal comment: Similar to your experience, I also feel pain in my eyes on certain cloudy days, if I stare at things outside. I always suspected it was due to UV, but never measured anything.

First to address some of the comments:
Concentrated UV damage does hurt your skin, it's called sunburn.  Lighter amounts of UV damage can cause cancer over time.  UV damage can be "felt", as can photonic pressure in extreme cases.  The issue at hand is "what is detection."
Back to your eyes:
As addressed in this answer, the human retina is able to detect UV light if it is not blocked by the lens.
I believe your question, restated slightly, is "can we call the pain experienced by UV damage to our eyes human detection of UV light."  Generically I think the answer is no, because we lack the specificity to determine that it is UV light. Many forms of ionizing radiation can lead to pain, and we would be unable to distinguish between them.  We cannot tell the gradation from UV to gamma, despite the damage they might cause.  Contrast this to the visible light spectrum, where we are quite good at determining the wave length.
Further, you could have similar damage caused by infection, where again you couldn't distinguish between the pain and fuzzy sensation caused by the very beginning of infection vs slight UV damage (though blueberry might help).
Does UV light damage your eyes? Absolutely in large enough doses.  Can it be called detection?  Probably not.  We can deduce UV damage from lots of things, including changes in the color of the pigmentation of your eyes (gold flakes = bad).  When we get to the level of deduction, however, we might as well be using machines to detect UV light and save our eyes (and skin) the trouble.


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What is the strength of human cornea?
What is the difference of pressure a human eyeball cornea (cornea, lens and other elements separating vitreous body from air) can handle? Or asking differently: what the outside pressure should be to "blow up" a healthy man's eyeball?

Normal pressure in the eye1,2 is between 10 and 21 mmHg (somewhere around 1.3-2.8 kPa or 0.01-0.03 atm) with pathology occurring at around 30 mmHg.3  Clearly the cornea can handle that, but how much more?  There's a lot more evidence as far as I could see for how well surgeries hold up, with 150-300+ mmHg (20-40 kPa, 0.2-0.4 atm).4  One source5 from 1998 cites work supposedly showing that the stroma:

gives the cornea 100 times more strength than is necessary to withstand the maximum intraocular pressure under physiological conditions.

So maybe around 200 kPa, for just the stroma?  Interestingly, a new eye layer was discovered earlier this year; this Dua's Layer is incredibly thin - 15 microns - but can withstand pressures of around 100-200 kPa (750-1500 mmHg, 1-2 atm).6,7  The large range there is due to some conflicting numbers in those links; the 200 kPa is the more widely reported one, but again, that's just for one layer.
Then, of course, there is this: a beautiful 2009 thesis by Jill Aliza Bisplinghoff from Virginia Tech which thoroughly examines the issue.  As an answer to your question, it includes the following such gems:

The high rate pressurization of 20 human eyes resulted in a mean rupture pressure of 0.97 ± 0.29 MPa (7275.60 ± 2175.18 mm Hg)... A student T-test revealed that the difference in the rupture pressure between the equatorial mean of 0.93 ± 0.30 MPa (6975.57 ± 2250.19 mm Hg) and the meridional mean of 1.13 ± 0.21 MPa (8475.70 ± 1575.13 mm Hg) was not significant (p=0.16)

and

A pneumatic cannon was used to impact eyes with a variety of projectiles at multiple velocities... The projectiles selected for the test series included a 6.35 mm diameter metal ball, a 9.25 mm diameter aluminum rod, and an 11.16 mm diameter aluminum rod... A range of internal eye pressures were produced that varied from 1256 mmHg (24.3 psi) to 22843 mmHg (442 psi)... [and] resulted in zero globe rupture.

Every time you mean the relative pressure, not the absolute right? Anyway, thanks for the answer! :-)

@Jantomedes Most of these are absolute pressures, internal where appropriate.


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Why aren't we ambidextrous?
It seems so simple that if my brain can tell my right hand to do something, then it should be able to tell equally well to the left ? This seems like a pretty major evolutionary advantage. Why haven't we evolved so during millions of years ?

Also see: http://biology.stackexchange.com/q/160/107

It seems evolution has gone the other way. The smarter the animal the greater the handedness. I believe there is a cost to being smart. By breaking symmetry, (ie handedness) you get more brain tissue that can be specialized. And you only need to pay once, rather than having double of everything. Lastly something maybe a major advantage but evolution work on the principle of good enough to have babies.If spending twice as much energy does not mean twice as many babies, it isn't worth it. Also evolution is blind, so if it does not stumble onto an amazing discovery it does not happen.

Having a dominant side is advantageous. Instead of seeing it as the brain influences our fine motor skill, think of it the other way round. The way we use our hands or any other part of our body sends feedback to the brain to increase the portion of the brain devoted to that region of the body and of course with disuse the reverse occurs. The more you do a certain task the more that portion of the brain gets better and coordinating the movement. The portion I talk about is the primary and supplementary motor cortices. So basically we are specialising. In the same way a heart doctor is better with treating conditions of the heart than a foot doctor. So we can either devote our experience to the one hand, or both or the other hand. If we use both hands equally our brain adapts so that we are ambidextrous, if instead we use just the one hand our brain develops just that side. But if you do focus on both you are using your dominant hand less so overall same amount of development just over both sides of the brain rather than just one side. You can probably see the benefit of having this plasticity of improving only what is used because why improve what we don't use and waste resources? And you may also see the benefits of higher specialising of one hand rather than having two slightly specialised hands. There are few tasks that require both hands to be very specialised, but if that were the case then the body would go ahead and do that but in spending time training your hands you are probably training your legs or something else less.
///
Why not have a switch between the two hemispheres to give the hand currently being used the fine motor skill located in the other hemisphere? (from comment)
I see. In my answer I only talked about one aspect. The brain doesn't have to learn skills for each hand completely independently. For example imagine if you learn to play a musical piece with your right hand only. If you try it with your left you won't be amazing but you'll definitely be better than a complete novice. Our brain can learn how to do by seeing which is vital for development. But there's a limit to that, your hands aren't completely identical so there's still a portion that needs fine tuning. Your muscles have different stregth, fatigue, resistance, recruitment patterns, places they innervate. Your hands are mirror images. The weight of your hand is different. And not only that but these variables aren't fixed, there's lots of them and they are different for different tasks. So to use your analogy, the more expensive remote can be used but it wasn't bought for use with the black plane. It'll give more control to the black plane but it still won't be the best ever until it learns what the muscle strength is etc. then it will be just as great.

Maybe I need to explain my thinking better. Consider this analogy: you have two small airplanes that are identical except for their color. You want to use them for spying, so the green one is a better during the day, and the black for the night. You use the green more, so you buy an expensive remote control for it, and a cheaper for the black. Sometimes you use both at the same time, so you need two remotes. Wouldn't it make sense to have a switch on the expensive remote to guide the black plane if that's the only one is use? Isn't it wasteful that I need to teach a skill to both of my hands ?

I see. See my answer above in a moment or two.

The answer seems to be mostly speculation. Could you add some references?

A simple answer to this is that at some point our brain's architecture was wired to have a dominant side, at which point it became too expensive evolutionarily to have drastic brain re-organisation or size changes.
Another answer to this is that the two sides have many different specialisations and functions. While having similar bodily control from both sides might seem to be an advantage, that would mean that one of the hemispheres would have to dedicate more neural circuitry to finer motor control. This means less neural material will be available for other tasks. Alternatively, if you want to be able to do other tasks equally well like now (and keep the specialisation of the hemispheres) , but have ambidextrous ability, you'd possibly need a bigger brain.
So, while it might seem like a good idea to be ambidextrous, it would probably come at a high cost on other brain functions or brain size.

My point is that the extra cost would be minimal if there was a switch in the brain that would just say "do with your left hand what you'd do with your right, and vice versa". At least coming from the direction of computer science, that's a trivial change.

This answer seems to be speculation. Could you add some references? -1


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Why is cisplatin a very potent antineoplastic for testicular cancer, but not necessarily for other cancers?
Cisplatin (structure below) is a platinum-based chemotherapeutic agent which is very effective in the treatment of some cancers. Its introduction was responsible for improving the cure rate for testicular cancer from 10% to 85% according to the wikipedia page on cisplatin.
However, it is not very effective for other types of cancers; interestingly, ovarian cancer does not respond well to it (Siddick, 2003).
Does someone know why cisplatin is so specific to testicular cancer? I haven't found any sources explaining this.

From the Wikipedia article you cited: "Cisplatin combination chemotherapy is the cornerstone of treatment of many cancers".

I slightly edited the question to stress the sources of your claims. If you'd rather revert to your original question, please feel more than free to do so. It's just a suggested edit, mainly because of the wikipedia page providing quite deceptive data.

From the dedicated cisplatin website and Drugbank it appears its use is quite diverse and not confined to testicular cancers. Further, your linked (Siddick, 2003) paper mentions on the first line of its abstract that cisplatin has clinical activity against a wide variety of solid tumors.
Cisplatin.org mentions that cisplatin finds use as chemotherapy against a range of cancers:

Cisplatin is a chemotherapy drug which is used to treat cancers including: sarcoma, small cell lung cancer, germ cell tumors, lymphoma, and ovarian cancer. [I]t can be a valuable part of a combination chemotherapy regimen. Look at the regimens given to patients and you will often see cisplatin as one of the drugs.

Moreover, cisplatin is explicitly used to treat ovarian cancer:

Treatment of ovarian cancer involves putting the cisplatin into the peritoneal cavity rather than a blood vessel. The type and extent of a cancer determines the exact dose and schedule of administering the drug.

As to your comment that cisplatin has "magical powers" I can say that it does not. The article that your linked cisplatin wikipedia page refers to (Einhorn, 1990) is a review paper that describes the efficacy of  combination therapies with cisplatin. The high cure rate of 75% was reached when cisplatin was used in combination with etoposide plus bleomycin. The last 10% was theorized to be achievable with 'salvage chemotherapy'. Hence, it is not cisplatin on its own.
In general, it is common practice to use various chemotherapeutic agents in consort, preferably with differing modes of action to reduce the dose of each and hence lessening the side effects.
References
- Einhorn, JCO (1990); 8(11): 1777-81
- Siddick, Oncogene (2003); 22: 7265–79

This doesn't explain cisplatins nearly magical powers to treat testicular cancer (tc) specifically. When used for other tumors, it does benefit patients but not nearly as much as for tc.

@Daniel - Please check my added last two sections in my answer. Thanks for adding this notion.

Very interesting! Thanks for the addition! :)

This is an striking example why wikipedia without the primary literature as a reference can be deceiving. Thanks so much for asking this question. Excellent.

As a clinician, I can confirm that cisplatin has a very wide range of indication in cancer treatment.

Any apparently "magical" powers of cisplatin in testicular cancer have more to do with the disease than the drug.
Unlike the similarly male-specific prostate cancer, testicular cancer is generally seen in young men in their 20s or 30s (click on "number of new cases and deaths"). This paper suggests, as is generally thought to be the case for earlier-onset types of cancer, that the affected individuals thus had some predisposing mutation or change in gene regulation prior to 10 years of age. As a result, it takes fewer sporadic acquired mutations to lead to this early-onset cancer versus a late-onset type like prostate.
This difference in incidence pattern is important because a late-onset tumor has had more opportunity to develop a broad range of cancer cells having different mutations within the tumor. Such intra-tumor heterogeneity has been recognized for over 30 years as a reason for resistance of tumors to cell-killing therapy like chemotherapy. For example, a heterogeneous tumor might be more likely to have cells that have mutated in a way that happens to make them resistant to cisplatin.
Also, testicular cancers develop in an accessible part of the anatomy that typically receives a lot of attention from men of the ages of peak incidence, so they are much more likely to be caught at an early stage than are prostate, ovarian, or colon cancers within the abdomen.


text:
Blood circulation - How to expand blood capillaries?
Do blood capillaries expand? If yes, through what means can it be done? And can warm water also be used to expand blood capillaries?

It's considered a requisite on biology.se that at least some reading/research is carried out and presented with your question. For example, have you read about vasodilation and capillaries? Otherwise it will be closed as homework. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here

@paul What do you mean by "expand"? Do you mean "increase the number of capillaries by angiogenesis" or "vasodilate"? Given the warm water example, I'm guessing it is the latter?

Capillaries are the smallest blood vessels. They are unique in that:

They don't have any muscular component like arterioles or venules do.
They are lined by a single layer of endothelium  (cells lining blood vessels are called endothelial cells) overlying the basement membrane.

Due to these reasons the capillaries are very permeable facilitating nutrient and gas exchange.
The capillaries don't expand as they do not have muscular or elastic components. However exposure to heat do increase the circulation. This is due to the following facts:

Exposure to heat dilates the pre-capillary arterioles - this would inevitably cause improved capillary circulation in capillaries that are already open.
Increase in pre-capillary flow opens up collapsed capillaries. In the human body roughly only one-fourth of the capillaries are open during rest1. As the pre-capillary arterioles dilate, the collapsed capillaries open up thus further improving circulation.

To improve capillary perfusion:

Temporary improvement can be achieved by activity (exercise), exposure to warmth, emotions (flushing is due to vasodilation), even exposure to cold causes vasodilation after the initial vasoconstriction
Permanent improvement of capillary circulation can be achieved by increasing capillary density. Capillary density refers to the number of capillaries present in 1 cm2 area. Capillary density can be increased by consistent anaerobic (isometric and to some extent isotonic) exercise.

References:
1: Boron and Boupaep text book of medical physiology, 2nd Edition, p.467
For more:

http://corporate.dukemedicine.org/news_and_publications/news_office/news/6597
http://www.ncbi.nlm.nih.gov/pubmed/8852622

Yes, some blood vessels change their diameter, they dilate or constrict. This is termed 'vasodilation' and 'vasoconstriction'. Large and mid-sized vessels contain smooth muscle in their walls. The walls of arteries tend to be stiffer than those of veins, to withstand high pressure coming from the heart.

Smooth muscle, when stimulated by the nervous system, can sustain contractions for long periods of time, and often with fine control. When smooth muscle in the walls of your blood vessels relaxes, those vessels will dilate.
Small capillaries do not have smooth muscle in their walls, but the flow of blood through them can be controlled by the larger vessels that feed them. When arterioles constrict, the capillaries they feed can have reduced flow.

Our nervous system takes in a lot of signals relevant to controlling blood pressure and flow, and controls these smooth muscles. Flow can be increased or decreased to individual organs when needed, like the intestine (after a meal), the muscles (during exercise), the skin (for heat exchange).
The question about warm water is actually quite interesting. Placing your arm in warm water will cause vasodilation in your other arm (the one not in the water), in order to lose some heat to the cold air and maintain your core temperature. Normally, the blood vessels in our 'extremities' (our hands and feet) are kept quite constricted to reduce heat loss with the cold air.
If we exercise or take a hot bath our core temperature will rise, some people will notice their skin gain a red hue after these activities, due to vasodilation.

Very little of this answer addresses the OP's question. Can you expand on what, exactly, increases capillary flow and how?

OP asks "by what means [can capillary expansion] be done?". As C Rags says capillaries don't have muscular or elastic components to their walls, but I (and he) have answered that the flow through them is controlled by contraction and relaxation of the smooth muscle of the arterioles that feed capillary beds. Flow resistance is inversely proportional to the diameter to the power 4 - decreases of diameter increase resistance steeply.
Are you asking what environmental stimuli & nervous input causes increased capillary flow? I can't answer that - there's many (google), and OP didn't ask that imo.

As I said (I did not miss the above), very little of your answer was a direct response to the OP's question. That remains a fact.

You're right. Honestly, I don't see much point in improving it: OP ought to read a textbook, as you commented. I tried to give some background since it can't be assumed from the question.

On 2nd thought, I disagree with you. All paragraphs of the answer contribute, having assumed OP knows little:
-Larger vessels have smooth muscle
-This smooth muscle changes their diameter
-Precapillary vessels control capillary flow
-Circulation is influenced by many things
-Warm water is one
The issue is purely that the question lacks any background awareness of vasodilation. I think the answer is an appropriate one for a bad question, but is not a good read for yourself. :)


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Is there a name for this phenomenon described in "Phylogenies and the Comparative Method"?
The figures below are from Felsenstein's paper "Phylogenies and the Comparative Method". I was wondering if there was a specific name for this effect where there is an apparant correlation that is actually the result of the data being structured into two separate groups, where there is no correlation within groups but an apparent correlation between groups. "Phylogenetic non-independence" doesn't seem specific enough.

Is this similar to Simpson's Paradox?

@Oreotrephes Not really, I'm wondering if there is a term for this specific phylogenetic effect

@kmm "Phylogenetic pseudoreplication" is exactly what I was looking for, I just couldn't remember the name of the term. Thanks!

what is X and what is Y? I mean what is plotted against what in the figures? (and no, the answer won't be coming from me ;-)

@AliceD The axes are arbitrary. X and Y don't matter, nor do their units. The point is to show that the apparent moderate positive correlation between X and Y in the upper figure masks underlying structure. When you separate by 2 monophyletic clades (boxes and Xs), there is clear separation and within groups there isn't any correlation.

I've seen this termed "phylogenetic pseudoreplication", but I can't remember offhand where. I'll see if I can find it. Without a tree, the boxes and Xs essentially represent 2 data points. As Remi.b suggests, this is really just high phylogenetic signal.

http://www.biology.ucr.edu/people/faculty/Garland/Phylogenetic_Pseudoreplication.jpg and Garland. 2001. Phylogenetic comparison and artificial selection. Two approaches in evolutionary physiology. I think I've seen it somewhere else as well though.

The fact that species are not independent observations because of their specific phylogenetic relationship is sometimes called phylogenetic dependence (see its use in this paper for example).
Most often though, we talk about the existence of such phylogenetic dependence for a particular trait and we talk about phylogenetic signal for this trait.
I think (correct me if I am wrong) you're searching for a name to describe a situation where two quantitative traits correlate along a phylogeny (when you have one data point per species) but not within any of the species of this phylogeny. If this is the case, I don't think you will actually find a name for this pattern as it it is already quite specific. You could eventually say that there is an inter-species correlation between the two traits but not an intra-species correlation.

Thanks for the response. I'm looking for a term to describe what happens when there appears to be a correlation between two traits when you just look at the extant species, but actually the correlation is a result of having two separate clades, neither of which has a correlation within the clade. "Phylogenetic signal" doesn't really describe this, but it could be that there actually isn't a term for what I'm describing, in which case phylogenetic dependence is probably as close as I'm going to get.

I think I got your question. See edit (which won't be super useful unfortunately).

I think that the answers here are good, and @Remi.b's term is preferable, but the term in the literature appears to most frequently be "phylogenetic non-independence", e.g. here.
I don't care for this term. Why not just "dependence"? But it seems to be what folks use.


text:
Relationship between nerves and axons
I just wanted to get a realistic viewpoint of our nervous system. I understand arteries and veins, but I wanted to know how similar our nervous system is to that?
I understand we have neurons (please correct me if I am wrong) all over the surface of body. Whenever we feel a touch a neuron fires a response, and that response travels through axons (myelin sheath).
My main question is what a nerve exactly is. Is it a long axon? How many axons (same thing as neuron body?) are in a nerve? I am sure it depends on different nerves.

I vote to re-open - this question is not too broad. On the contrary, it is a set of highly specific questions, basically boiling down to terminology. I edited the question previously when the close-votes were already pouring in, and hence I vote now to re-open without editing any further. I think it is fine as is. Furthermore, there is background info, so there is no ground to 'leave-close' due to homework :-)

I forgot to message you, but I edited your question to make it more compatible with Biology Stack Exchange. At Biology we like clear questions. Nice question +1

Chris, this was my first question on this website. I only knew of one rule and that was to be as specific as possible. I tried. I am not very familiar with the format of this website so I am not sure what "close-votes" or "re-open" you were talking about. I barely found out that my question was answered :) which I really appreciate.

@ChrisStronks I see a number 4 next to my question. What does that mean? Net positive votes I got?
Also, can anyone edit my question? Or do you run this website?

The close-vote and re-open comments were directed to others that close-voted this question. It may help you to read through the help site and see what a good question looks like and what can happen when people not agree with the question content.

The +4 means that 4 folks liked your question. I can edit it among many others. I am just one participant among many others with enough reputation to edit questions.

I will go through your list of questions below:

I wanted to know how similar is our nervous system to [the circulatory system]?
They are very different, but as in every comparison of very complex systems, there is some overlap. The circulatory system carries fluids, the nervous system electrical signals so they are functionally not alike. However, both systems run throughout the body and have a more or less central control unit (the brain and heart respectively). So there is a structural similarity. I reckon they are as much alike as a city's sewer system and electricity grid.
I understand we have neurons (please correct me if I am wrong) all over the surface of body.
That is correct
Whenever we feel a touch (stimulus arises) a neuron fires a response, and that response travels through axons (myelin sheath).
Tactile stimulation may result in firing of one or more neurons, dependent on the intensity of the stimulus. Larger stimuli will, obviously, recruit more fibers. Stronger stimuli will evoke stronger responses (increased firing). Axons indeed conduct the neuronal responses, like an electrical wire conducts electrical current. Longer axons are often myelinated (insulated). Not all neurons related to touch are myelinated, however.
So my main question is that what exactly is a nerve?
A nerve is a bundle of axons that carry related functional information. Typically, nerves conduct information originating from locations closely located together in the body, and generally they convey this information to a localized spot in the body as well. For example, the optic nerve carries information from the photoreceptors (related information) from the retina (localized source) to the brainstem (localized target).
Is [a nerve] a long axon?
A nerve contains many axons. 'Long' or 'short' is rather subjective.
How many axons (same thing as neuron body?) are in a nerve? I am sure it depends on different nerves.
Neuronal cell bodies are typically located outside a nerve. Nerves contain varying numbers of fibers. For example, the auditory nerve harbors the axons of the spiral ganglion cells that transmit auditory information from the inner ear to the brain. It contains between 31k - 32k (myelinated) fibers in normal-hearing humans (Spoendlin & Schrott, 1989). In contrast, the optic nerve, which carries visual information from the retina to the brain, contains some 1.3 million (myelinated) fibers in young human adults (Jonas et al., 1992)

References
- Jonas et al., IOVS 1992;33:2012-8
- Spoendlin & Schrott, Hear Res 1989;43:25-38

Chris, I deleted my answer. Plus this is the source of the picture:http://dtc.pima.edu/blc/182/lesson12/12step6/12step6page1.html

Thank you, Chris for answering the question. I really appreciate it.


text:
How do I find samples/patients in TCGA (the cancer genome atlas) that had radiation therapy?
I want to correlate the expression of a gene (for sample the KRAS gene) with survival and if the patient received radiation therapy using any suitable TCGA (the cancer genome atlas) dataset. However, I have so far been unable to figure out what patients have received radiation therapy.
Any suggestions?

The process is slightly painful but here is how you do it.
Go to UCSC Xena, then launch the browser, hit the Visualize tab, pick your cohort of interest, then in the next menu pick phenotype, and then type radiotherapy in the box and pick the radiotherapy related columns you want. Then, once it has loaded the annotation bar, you can hit download and the downloaded spreadsheet will have this information along with the TCGA barcodes. As for clinical data, https://www.synapse.org/#!Synapse:syn7343873/wiki/412112 is a very good pancancer source.


text:
Can neurons become cancerous?
I've been reading about brain cancer lately, and something I've noticed is that the tumors seem to start in all tissues, except neural tissue. Am I missing something, or is there an explanation?

Short answer
Neuronal tumors are rare, but they do exist. These cancers develop from neuroblast cells, a population of undifferentiated, dividing precursor cells that will eventually fully differentiate into functional neuronal cells.
Background
Most neuronal cell types have lost their ability to divide, because of their progressed state of differentiation. There are but a few regions in the brains that generate new nerve cells in adulthood, for example in the hippocampus where neuro-regeneration is believed to be involved in memory formation. Because of the rarity of cell division of neuronal cells in adulthood, neural cancers are rare.
The point where neuronal cells actively divide is during development. These cells are basically still stem cells. A prime example here are retinoblastomas. These are tumors in the photosensitive part of the eye, namely the retina. During early development stem cells actively divide to lay down a layered structure in the back of the eye eventually forming the rods and cones and other visual cells. If this division process goes out of control, tumors can develop. Retinoblasomas can now be diagnosed in utero (Paquette et al., 2012).
Tumors with a neuronal origin developing post natally are rare, but do exist. Neuroblastoma being a prime example. This is a rare cancer (prevalence of 1:100,000) most commonly found in children younger than age 5. It affects the sympathetic nervous system, which regulates involuntary bodily functions such as heart rate, blood pressure, breathing, and digestion. Neuroblastoma typically begins in the nerve tissues of the adrenal glands but may also begin in the nerves that are located anywhere along the spinal cord, including the neck, chest, or abdomen. The cancer can metastasize (spread) to other organs.
Note that both examples here are called blastomas, those are tumors caused by malignancies in precursor cells, often called blasts, these cells are dividing cells that will develop into a neuron often after a migration phase. Neuroblasts differentiate from neural stem cells and are committed to the neuronal fate. Hence, although these tumors are from a neuronal origin, they are technically not derived from (fully differentiated) neurons.
Reference
- Paquette et al., AJP Rep (2012); 2(1): 55–62


text:
Are blood vessels organs?
Are blood vessels classified as organs? Organs compose of 2 or more tissues and perform a certain function. Blood vessels have 3 different tissues and perform a function (transport blood), yet I do not see them being identified as an organ. Why is this? Are they organs? Or do they hold their own classification?

Did you copy the question from here?

@Cornelius, no need to ask. That is a copy/paste.

@Cornelius - nice find. Wouldn't this issue be a nice one for Meta? It looks like rep mining to me? I retracted my upvote. I might be downvoting if OP doesn't respond.

@AliceD I believe similar issues were discussed on Meta.SE, but I can't find the question now. Anyway I consider we should focus on giving better answers than the ones on Yahoo, where, again, the best answer is a copy-paste from Wikipedia.

@AliceD btw,  ain't hematology a bad tag for this question? The question is not about blood pathology.

@Cornelius - It is a bad tag; I just added terminology and wavered to delete hematology. Thing is there has to be some tag linking it to the vascular system - what about blood-circulation? +1 for your answer btw

http://meta.stackexchange.com/questions/256933/what-to-do-if-a-question-is-crossposted-from-a-non-stackexchange-website

Artery and veins are organs, but capillaries are not.

The cardiovascular system is usually lumped together as an organ. So blood vessels would be included here but you are right in that this is a bit strange being that it includes the heart and the vasculature.

I don't know if they are classified as organs, but basically, blood vessels match the criteria for being organs.
Quoting SIU School of Medicine:

Blood vessels are basically tubular organs found within other organs.

Biology Reference states the same:

Even the glands within the integument can be considered organs; any gland is primarily secretory epithelium surrounded by connective tissue for support and protection. Likewise, the blood vessels and nerves in these organs are organs unto themselves.

Yes blood vessels can be called as organs. They are part of organ system. By definition an organ is one which is made of different tissues and contributes with other organs to a specific function in the body. Here blood vessels are made of different tissues like smooth muscle, epithelial tissue, elastic tissue etc.


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What is this part of blastula called and how is endoderm formed?

Could you tell me what the yellow mass within the blastocoel is called ?
I know that blastocoel is a fluid filled cavity, so are the yellow coloured cells the inner part of blastoderm or are they some other cells ?
If they are the part of blastoderm itself, why is it not in the same colour of light-orange as the blastoderm, or is it the mesoderm, or the inner cell mass  ?
And is it the blastoderm that forms ectoderm , and endoderm pinches  off the ectoderm during gastrula phase? And could you also explain how the orange mesoderm formed ?

@Kaneri the diagram in your question is wrong. See this : http://wikivisually.com/wiki/Gastrulation

The blastocoel, as you say yourself, is a fluid-filled cavity (wikipedia) so it has no cells. Fig. 1 shows cellular and non-cellular regions of the blastocyst.
Your questions on the formation of the three germ layers during germination are nicely shown in the illustration in Fig. 2, right two panels.

Fig. 1. Blastocyst. source: wikipedia

Fig. 2. Formation of the germ layers. source: Class Connection

could you also answer whether the yellow cells within the blastula are cells of blastoderm itself or are they some other type of cells? And also whether purple cells shown within the archenteron are cells of endoderm itself ?

Just wanted to add, OP's image of blastula lacks inner mass so (without any citation) it is likely  referring to Amphioxus blastula.


text:
What is the actual speed of nerve impulses in humans?
For an undergrad assignment I read a biology paper that mentioned the speed of nerve imuplses to be 440 km/h in myelinated fibers. However, our biology teacher told us that this reported conduction speed is not true. So my question is:
What is the actual speed of myelinated fibers?

It would be good if you can tell us what you did to arrive to your answer. And it would be good if you can include any relevant background information. Not everyone who answers questions on this site is a specialist in every field; but a lot of us do have good research skills, and we may be able to review your work to see if it makes sense. But the only way we can do this, is if you provide us with enough information to do so.

I saw in a few books that the speed of the myelinated fibre was 120m/s in human beings but then after sometime I saw the speed of the myelinated fibres was 440km/h in bbc documentary which is similar to 120m/s but one speed is in (m/s) and the other is in (km/h), when I convert the 120m/s into km/h so I got 432km/h therefore I needed to be sure that the error of 8km/h in 440km/h and 432km/h does not matter so I can proof it to my Teacher, I hope that you understand my question.

Short answer
A conduction velocity of 440 km/h is possible in thick, myelinated fibers. However, this number is probably more representative of the upper range of conduction velocities, rather than a conservative average.
Background
First off, there are a heap of variables that affect neural conduction velocities (in myelinated fibers) in complex ways (Waxman, 1980), including but not limited to:

axon diameter;
myelin thickness;
internode distance;
temperature;
axonal milieu;
age of the subject.

Having said that, in humans myelinated, thin A-delta fibers the average conduction speed was established at 19 m/s (Gyberls et al, 1983), or 68 km/h. A range of pain-conducting fibers exist, with different diameters. As a result, they range in their conduction velocities from 0.5 m/s (2 km/h for thin C-type fibers) to 120 m/s (432 km/h for thick A-alpha type fibers).
Hence, the 440 km/h is certainly possible in thick myelinated fibers. Note I just highlighted pain-conducting fibers here as an example, and other classes of neurons may feature even faster conduction in their axons.
References
- Gybels et al., J Neurophysiol (1983); 49(1): 111-22
- Waxman, Muscle & Nerve (1980); 3(2): 141–50


text:
Which tree's root can grow the longest?
In a recent TV documentary it was said that a particular tree root could grow miles long. However, I forgot the name of the tree and I don't remember the name of the TV program as well.
I searched on the internet but I could not get it. Does any one know about this tree and how tall its roots can grow?

Was it Pando? Pando is a single, massive 80,000 year old Populus tremuloides (quaking aspen) individual, that is assumed to have a single, massive root system covering 106 acres.

I suspect it's not.. I heard that the root of this tree can travel many miles

@Learner Since it was a TV production they would definitely state the total lenght of the root system, just like the blood vessels in a human can reach the moon or something like that. It sounds cooler like that.

Possibly yes :)


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Color vision across species
Is it true that color vision is sex-linked for all species with binary sexes? Is there an evolutionary significance to the fact that color vision is X-linked in humans? E.g., only female humans can be tetrachromats.

Welcome to Biology! What exactly do you mean with color differentiation? Note that one out of three cone opsins is coded on an autosome

Thanks!  I just mean having fewer or extra cones in general, I suppose.  Since colorblindness and tetrachromacy are both strongly associated with a single sex in humans, I was just curious whether that was a trend in other species.

The cultural significance of X-linked color blindness would be POB, I would guess.

I agree with @anongoodnurse and have removed the cultural aspect from the question. Please feel free to roll back though.

Thanks for the edits.  But sorry, what's POB?

POB= primarily opinion based.

Short answer
Human females do not benefit much from an extra cone class, as color discrimination is hardly affected in most tetrachromats. In fact, tetrachromats often show increased error rates in their color discrimination. In dichromatic New World monkeys the heterozygous females do functionally benefit from their extra cone as they gain trichromatic vision.
Background
Anomalous trichromats have all of their three cone types to perceive colors, but one type of cone perceives light slightly out of alignment. There are three different types of effect produced depending upon which cone type is affected.
The different anomalous conditions are protanomaly (reduced sensitivity to red light), deuteranomaly (reduced green sensitivity - the most common type) and tritanomaly (reduced blue sensitivity - extremely rare). People with deuteranomaly and protanomaly are collectively known as red-green colour blind and they generally have difficulty distinguishing between reds, greens, browns and oranges. They also commonly confuse different types of blue and purple hues. Red and green cones are indeed coded on the X-chromosome.
One source of variation is the very common Ser180Ala polymorphism that accounts for two spectrally different red pigments and that plays an important role in variation in normal color vision as well as defective color vision. The most common source of variation is the existence of several types of red/green pigment chimeras. The red and green-pigment genes are arranged in an array on the X-chromosome with one red-pigment gene followed by one or more green-pigment genes. Recombination events have given rise to red/green hybrid genes and deletion of the green-pigment genes. Only the first two genes in the tandem are expressed. The severity of red-green color vision defects is inversely proportional to the difference between the wavelengths of maximal absorption of the photopigments encoded by these two genes.
Females who are heterozygous for red and green pigment genes that encode three
spectrally distinct photopigments have the potential for enhanced color vision, as they are effectively tetrachromats (Deeb, 2005, Neitz et al., 1991). However, sensitive color-contrast testing on 43 tetrachromats has revealed that most of these females have no deviating color-discrimination whatsoever. 8 subjects showed relatively small effects, while only one showed a clear increased sensitivity in a narrow range of frequencies. It is believed that the human visual system is not plastic enough to cope with the extra spectral input. In fact, in the group there was an overall increase in error rates on some color tests (pseudoisochromatic plates, and Nagel anomaloscope color matching) (Jordan & Mollon, 1993).
In New World Monkeys, however, the situation is different. Squirrel monkeys are basically a dichromatic species, but two-thirds of the females are heterozygous, and gain trichromatic vision by expressing two of three possible alleles coding for pigments in the middle- to long-wave range of the spectrum. X-chromosome inactivation serves to segregate the alternative allelic products in different subsets of cones. The visual system of the heterozygous female is apparently plastic enough to take advantage of the presence of three classes of cone, because heterozygous monkeys have enhanced color selectivity in the red-green range that are impossible for all males and for homozygous females. This advantage perhaps enables the heterozygote to judge better the ripeness of fruit, or to find fruit or conspecifics (Jordan & Mollon, 1993).
Note that the emergence of trichromacy in humans and some other primates was the result of the red/green gene duplication. Trichromacy in primates was evolutionary selected for likely because of the enhanced capability to discern (ripe) fruits (Lucas et al., 2003). It has nothing to do with sex-differences, because not many human females benefit from tetrachromacy in terms of enhanced color vision.
References
- Deeb, Clin Genet (2005); 67: 369–377
- Jordan & Mollon, Vis Res (1993); 33(11): 1495-1508
- Lucas et al., Evolution (2003); 57(11): 2636–43
- Neitz et al., Science (1991); 252(5008): 971-4
Further reading
- Is our color vision calibrated to sky, vegetation, and blood?


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Is transplantation of neurons between species possible?
Can brain tissue from one species be implanted into the brain of another species? Because the brain is tolerant to the introduction of antigens (it is said to be immuno-privileged), I was wondering whether neurons would be subject to graft rejection?
If neurons from another species survive in their new host, would they create functional connections?

To add on AliceD's comment. You should define a specific trait on which you are interested in. For example, you may ask if mice neurons tend to be shorter than human neurons (yes for many motor neurons) or whether there is more myelin on the mice neurons than on human neurons.

Added information to the question, explaining what i mean by "differences"

@AliceD: it now excludes for example differences in size

Ok, I see now, there isnt an "easy" answer to my question. I dont think, continuing this question will lead to any useful information, due to the topics complexity... the question can be closed

@Mystery -  I have focused the question on your last edit. If you wish, feel free to ask any of the other questions in separate questions. It is interesting stuff!

I know of some papers where neural stem cells (of rats/humans) have been transplanted in mice and there is a change (enhancement in vague terms) of function. AFAIK there is some structural difference too (the size of the processes etc). I can answer your question in a while (a week or two) because I need to dig up these papers. Lots of deadlines at this moment.

Short answer
Neural xenografts can survive and form functional connections in the host.
Background
Across-species (xenogeneic grafting) grafting of cerebral cortex from a fetal rat to an adult mouse brain and vice versa, have shown that immunocompetent hosts can reject a graft in less than 30 days. Rejection results in destruction of  the graft tissue presumably by macrophages. Immunosuppression can be used to prevent graft rejection (Mason et al., 1986).
A review article on this topic shows that in the absence of immunosuppression, neural xenografts (donors were fetal to adult-aged) in a rat host brain survive in 37% of the cases in case of a mouse donor, 16% in case of a hamster donor, 9% in case of a rabbit rabbit, 7% from a pig donor, and 0% when human donor tissue was used. Hence, species-separation seems to be a determining factor in xenograft rejection. Induction of MHC-I and MHC-II expression in the xenograft mediates graft rejection in the brain. Hence, despite the fact that the brain is immunopriviliged because of the relative low expression levels of MHC class proteins, it is still sufficient to reject grafts (Pakzaban & Isacson, 1994).
Xenografts have been shown to generate functional afferent and efferent axonal connections with the host brain when grafts of the striatum, substantia nigra, hippocampus and retina were homotopically transplanted.
Functional (behavioral) studies have confirmed these physiological studies. Rats with Parkinson's disease could be successfully treated with substantia nigra grafting from mouse, hamster, rabbit, pig and even humans. Similarly, retinal xenografts have resulted in functional pupil responses, hippocampal xenografts have restored learning deficits, and suprachiasmatic nucleus xenografts have been shown to restore circadian rhythms (Pakzaban & Isacson, 1994).
References
- Mason et al., Neurosci (1986); 19(3): 685-94.
- Pakzaban & Isacson, Neurosci (1994); 62(4): 989-1001.


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What kind of insect is this?
Found in Russia in the kitchen. It is about 3 mm long.

RelatedTiny dark-colored bug ID in Amman-Jordan

That is a flour beetle, the two most common and likely types are the confused flour beetle and red flour beetle but to identify look at the antennae. I'd suggest it is the confused flour beetle because the antenna go from thin to fat quite gradually, though the pictures may not be good enough for that to be certain.
Other commonly used names are tribolium (the genus name) or flour weevil. They are also used in labs as a model organism, groups in my last two labs have used them. They are a pest and you should probably get rid of them.

"Both types of beetles are often found not only in infested grains,
  but in crevices in pantries and cabinet, as well. Damage to food is
  caused somewhat by the beetles' feeding, but also by their dead
  bodies, fecal pellets, and foul-smelling secretions. In addition to
  creating a foul odor, the beetles' presence encourages the growth of
  mold." - Wiki.

Can we agree that "confused flour beetle" is a fantastic name?

@damien it's because people often confuse the two when identifying them.


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Connection between genes and pathways
I am reading about a paper about inferencing pathway information in cancer cells. Authors refer to ERBB2 as a gene and a pathway. I don't have solid biology background. What exactly means when we refer to ERBB2 as a pathway? Does it refer to activity of a protein encoded by ERBB2?

Which paper is this?

ErbB2 is a receptor tyrosine kinase. This is a class of receptors, which are located in the membrane ob the cell and which pass signals from the outside of the cell into it, so it can for example react to changing conditions.
ErbB2 (which is also called HER2, which translates into "human epidermal growth factor receptor 2") normally reacts when it binds it ligand epidermal growth factor (EGF). Upon binding, ErbB2 changes its conformation, phosphorylates itself (meaning it adds phosphogroups to specific amino acids of the protein) which leads phosphorylation (and therefore activation) of other proteins, which finally results in changed expression of genes, which are involved in cellular proliferation, differentiation, and survival (see this reference: "Review of epidermal growth factor receptor biology.").
This leads to the second part of your question what pathway means in this context: The sequence of different molecules which start at the receptor and finally induces changes of gene expression in the cells nucleus are called pathway. For members of the Erb-family of receptors there are different possibilites, but the picture below shows how this works in principle:

The image is from the Wikipeadiapage on EGFR.
You can see, that the ligand binds extracellular to the receptor, which is then phosphorylated, and then passes the signal downstream for example to Ras-Raf-Mek-Erk and then into the nucleur (in fact, activated Erk enters the nucleus).
This cascade also shows, why these receptors are often mutated in cancers: They are involved in the regulation of genes important for survival, proliferation and differentiation, which is very important for cancer cells. ErbB2 for example is mutated in about 30% of breast cancers. These mutations often lead to a constitutive active receptor which is permanently phosphorylated independent of ligand binding. This leads to a permanent activation of the downstream pathways which is obviously not a good thing, since these genes are normally under a very tight regulation.

ERBB2 appears to be a (tyrosine kinase) receptor; that is, it lives in the cell membrane; with a part that sticks outside of the cell, and part that sits inside.  When the right molecule attaches to the outside part, the inside part changes shape, which alters its function, causing it to start phosphorylating other proteins, which alters their functions.
So the ERBB2 pathway is the set of genes/proteins whose behavior is affected by ERBB2.
Google "ERBB2 pathway" and "tyrosine kinase receptor" for more info.


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Where did the term "vegetative nervous system" come from?
I am interested in the origin of the name. I am aware that Reil coined the term in the 1800s, but want to know why did he choose the term vegetative. I have not been able to find an answer to this question. Today it is called the autonomic nervous system.

"Vegetative" doesn't only mean related to plants, but has other less common meanings.

4 a (1) :  growing or having the power of growing (2) :  of, relating to, or engaged in nutritive and growth functions as contrasted with reproductive functions a vegetative nucleus
  b :  promoting plant growth the vegetative properties of soil
  c :  of, relating to, or involving propagation by nonsexual processes or methods
  Merriam-Webster

So the word "vegetative" refers to the growth/nutrition functions of the autonomic nervous system. The short answer is that he chose that word because, particularly at the time he chose it, that was an appropriate word to use to refer to the regulation of things like digestion. Since the autonomic nervous system has other functions, such as in sexual arousal, and because the term vegetative has other meanings, the term "autonomic" has completely replaced vegetative in this context.

I think its probably not about reproduction: reproduction isn't The most conspicuous work of ANS  the term ANS is supposed to be more general. Vegetative has many meanings. One of which is dull or passively existing. And i thnk the pasaive existence and pasaive cooperation of ANS is the major factor behindnaming it as such

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Thanks for the suggestion about the "non-reproduction" meaning. I have a feeling this is it.