text:
How are germ cells not reduced in number?
If germ cells produce haploid daughter cells by meiosis and are thereby "consumed" (where there was a germ cell there are then 4 daughter cells), where do the germ cells come from?  I asked my biology teacher if they undergo mitosis prior to meiosis, but she said they don't and proceeded to give an unclear answer.  Is this true?  If so, are they regenerated from somatic cells elsewhere in the body?
My question basically is - if the germ cells of, say, the testes are dividing by meiosis to produce sperm, where are the germ cells coming from so that the testes don't shrink and ultimately disappear as they're converted completely into sperm?

In case of gametogenesis (let us talk about spermatogenesis) gametes are formed from meiotic division of Primary spermatocytes.
In Primates Primary spermatocytes are cells that that are formed from mitotic division of B spermatogonia (which is another class of germ cells) which inturn are formed from mitosis of Ap spermatogonia which arise from mitotic division of Ad spermatogonia.  Ad spermatogonia are inturn formed from Primordial germ cells (see below for details).
Ad spermatogonia are dark A type spermatogonia, reserve stem cells  which occasionally divde to renew itself and Ap spermatogonia are pale A type spermatogonia, renewing stem cells.

Why the testis doesn't run out of germ cells? (adaptation of your key question)

The reserved  Ad spermatogonia and renewal of both  Ad and  Ap spermatogonia are responsible for the continuous cycles of spermatogenesis.

This process starts at puberty and usually continues uninterrupted until death, although a slight decrease can be discerned in the quantity of produced sperm with increase in age. (wikipedia)

The process of spermatogenesis in human:

In non-primates like mice it is little different, the following diagram should explain it:

Note:

Germ cells are cells that give rise to gametes ( present at any level of gametogenesis).
Primordial germ cells are embryonic cells that originate from a different location (outside the gonads) and migrate into the gonads during the course of embryonic development to divide into germ cells.
In females, oogenesis also involve production of germ cells (cells of primary follicles) from PGCs through mitosis but the primary follicles produced is fixed, doesn't increase after birth so at a definite age of 40-45 gametogenesis stops.

Further reading:

Stem Cells in Reproductive Medicine by  Carlos Simón, Antonio Pellicer, Renee Reijo Pera
A paper

Edited the answer making it specific to Primates which is relevant to your question. Thanks to @JayCkat.

"How are germ cells not reduced in number?"
It does happen. Germ cells do eventually run out. It is called menopause in women. And age related infertility in men.
As for your question of where do germ cell come from? Much like were do muscles cells come from?, you have to be specific. Germ cells comes from the gonads (ovaries and testis) would be a simple answer.
EDIT:

They are coming from Spermatogonial stem cells (SSCs), cells that for the most part are immortal, and can replicate endlessly (well ~60 years anyway).
https://www.ncbi.nlm.nih.gov/pubmed/23784829

any resources to add?


text:
What is the incentive for plants to add rich nutrients to food?
As we know fruits are good sources of vitamins and minerals. What is the incentive for plants to add so much of vitamins and minerals to fruit pulp. My thought is that  seeds would need is some protection, and why waste rich nutrients and vitamins by adding it into pulp?

What research have you done before asking it here? I think you should start with "what is the use of fruits?"

I think i found answer. It is for reproduction, so that when animals and birds eat fruit, seeds will be transported and it'll help plants to go to new regions and of course  for protection of seeds.....

Yes. And the point here is that when an animal will get more nutrients from a fruit, it will prefer that fruit over others, which will increase the chances of the fruit's seed's dispersal. Now, you should close/delete this question as it is likely to be closed as off-topic.

Not sure why it's off-topic. At any rate, OP, first separate minerals from vitamins - minerals are absorbed from the ground (see here and note p. 784) while vitamins are usually synthesized by the plant's cells (see this as an example). Also keep in mind that plants have no "incentive" to do anything - all reactions happen according to energetic considerations. Seek and you shall find.

Thank you. I'm kind of newbie for biology.  I was asking from evolution point of view, wondering why would they put so much effort in producing fruits..

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What does "melanistic phase" mean in regards to black jaguars?
From Black Jaguars in Belize?: A survey of melanism in the jaguar, panthera onca by John R. Meyer:

There occurs in jaguars, as well as in leopards (Panthera pardus), a melanistic phase which has been much sought by zoos for exhibition purposes. This color phase was relatively difficult to acquire until the 1970's, by which time a few zoos, among them the Jacksonville Zoo, had begun to breed them regularly.

And likewise on the Wikipedia page for Black Panther:

This "black cougar" was most likely a margay or ocelot, which are under 18 kg (40 lb) in weight, live in trees, and do have melanistic phases.

I don't understand this term "melanistic phase", which makes it sound like the jaguar has a period of time in which it is black.  However, it looks like it means something else, i.e., along the lines of What does phasing mean?, but I don't really understand that.
What does "melanistic phase" mean in regards to black jaguars?

I think it is coming from color phase (see meaning 2: https://www.merriam-webster.com/dictionary/color%20phase or meaning 1: http://www.dictionary.com/browse/color-phase)

In this context, "phase" means the same thing as "color phase". Here's the definition from Merriam-Webster:

1: a seasonally variant pelage color
  2: (a) a genetic variant manifested by the occurrence of a skin or pelage color unlike the wild type of the animal group in which it appears (b) an individual marked by such a variant

So it sounds as if "phase" originated in the case of animals that spent a season with a particular pelage (meaning "fur, hair or wool"), such as the snowshoe hare, which is brown in summer and turns white in winter, and the term then began to be used for animals that might be a different color from other individuals of that species. If the alternate color was caused by a recessive allele, most offspring of that individual would have the wildtype color unless bred with another double-recessive individual, and alternate offspring might spontaneously be born to wildtype heterozygous individuals, so pre-Mendel biologists might have seen it as a "phase" between wildtype generations.
As you can see from the illustrations on the snowshoe hare Wikipedia article, "morph" is much more commonly used today for this kind of visible variation within a species. Wikipedia has a fuller description of the nomenclature of this and related terms.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Mosquito vs Human: Swapping the roles
Is there a known mosquito-specific lethal (for some relevant species of mosquitos) virus that you could safely (for the humans) put into the blood of living humans? Is it technically possible to engineer humans to produce such a virus?


text:
Why is living on land beneficial?
When fish started developing the stronger limbs needed to walk(Slither?) onto land how was this beneficial? I cannot think of any form of food that would be helpful that would not be plentiful in water, but it must have been so as from what I can tell most beneficial mutations tend to be either a better way to either survive or obtain nutrients.

No competitors, no predators, lots of new niches to conquer. Isn't this enough?

Welcome to Biology.SE. What have you found so far? There are a large number of hits that talk about the role of the serosa when insects came out of the water but I am not sure this is what you are looking for. Maybe @JayCkat answer is what you are looking for but it sounds a bit like common sense and will be hard to find any peer-reviewed paper on the subject.

https://www.newscientist.com/article/2124873-these-fish-are-evolving-right-now-to-become-land-dwellers/

Related: How many times did terrestrial life emerge from the ocean?

Insects were the first animals to conquer land. Vertebrates followed later. So there may not have been an absence of a food supply. Also, the ability to leap to land for safety to avoid a predator is useful if said predator cannot follow. similar in manner to flying fish.

Also lots of plants to eat.

Walking developed before fish moved onto land. Fish that live in shallow water crawl along the bottom instead of swimming, because it is easier to sneak up on prey and hide from predators that way and it disturbs the water less than swimming. There are several modern fish that do this.
Like many brackish water fish they also could already breath air. Brackish water tends to be low on oxygen while air is always high.
Resources may have been plentiful in water but so was competition and predators.
For vertebrates there were no predators on land, there was food that no other fish were eating, there was access to new pools of water, etc. It was a completely open environment full of resources that had not evolved alongside them (thus had few defenses), no competition (the advantage of being the first vertebrate on land) and it was completely free of predators that is the like eden for an organism. There would be a huge selective advantage in exploiting it. You may want to familiarize yourself with adaptive radiation in general if you don't understand this.
Further reading:
https://academic.oup.com/icb/article/53/2/192/806098/Vertebrate-Land-Invasions-Past-Present-and-Future
https://en.wikipedia.org/wiki/Vertebrate_land_invasion


text:
Will you stop sweating if you exercise in a cold enough room?
It's common knowledge that you will sweat from being in a very warm room. And you will also sweat from exercise, presumably because it raises your body temperature.
But if you exercise in a cold enough room, which magically adjusts its temperature to counteract your body temperature, will you then not sweat at all? And is it therefore possible to exercise without sweating... And not even have to take a shower afterwards?

Well, if you define "cold enough room" as outdoors in the winter, and the exercise is cross-country skiing, then it is perfectly possible, as long as you adjust your clothing layers appropriately.  Indeed, you do not want to sweat much - enough to wet your clothing - as that exposes you to a risk of hypothermia when you stop.

Apparently you can sweat even in a cold enough room, without even doing exercise! The main causes of sweating include, among exercise and high body temperature, stress and anxiety. This condition is called cold sweating. See this article:

The body normally produces sweat as a way to help keep cool. Sweating normally occurs with exertion such as when exercising or in high temperatures. However, there are other reasons for sweating. Sweating can be triggered by fear or anxiety, and this is often referred to as a cold sweat. It comes on suddenly and results in cool, damp skin. It is the body's reaction to stress as part of the "fight or flight" response that helps us to react in a dangerous situation.

So, even if you just think about doing heavy exercise, you might get sweat in hands or feet.
But cold sweating is not the only cause. It may also be caused by a more severe condition known as hyperhidrosis. See this article:

Normally, your sweat glands produce perspiration that’s carried to the skin’s surface when the air temperature rises, you develop a fever, you’re exercising, or you’re feeling anxious, nervous, or under stress. When those factors are no longer an issue, the nerves that signal sweating are put on hold. For the 2% to 3% of the population who have hyperhidrosis, however, the sweat glands don't shut off. They sweat even when the circumstances don’t call for it: when they’re in air conditioning, or while they’re sitting and watching television. Some people even tell their doctors that they sweat in a swimming pool.

So, one might start sweating even in a cold enough room, if not because of body heat, then because of anxiety, hormones or medical conditions. Also, this condition does not work the way you are speculating. When the surrounding environment is very cold, the body prefers to shut off blood supply to skin than to cool it down through skin i.e. sensing cold environment, the body shuts off blood supply to skin and diverts it to core of the body. This is what causes more urination in cold environment and is called cold diuresis. Have a look at this answer for more information on this point.

Why the downvote? Anything I missed or said wrong?

I believe many at times people would have experienced this. I have had sweat drops even on a very chilling evening.

It wasn't me, but it might have been because you didn't actually provide OP with the information they were looking for. At least, according to the way I read the question. You go into other things that can trigger sweat to conclude "it is possible to sweat in the cold," but "Is it possible to sweat in the cold?" isn't the question that I see, rather it is "I start sweating when I exercise, but would that still happen if I exercised in a cold room?" Read: all other things being equal, am I likely to sweat... not is it possible to sweat. Note the "Is it possible to exercise without sweating"

... However, an answer about people who have a condition that makes them unable to sweat likewise would not answer the question, even despite the "Is it possible to exercise without sweating," as the context is (again) "Normally I sweat when I exercise. Could doing it in the cold stop the sweating." Still, interesting information and relevant to the topic, even if it doesn't get OP to precisely what they were after.

@another'Homosapien' I do understand your perspective, and your answer was a good read. And if you try to pick out a single sentence from the question and answer it directly, and you pick the part that says "is it possible to exercise without sweating", then your post has answered that very directly, and quite well. I'm merely responding to your (1.5yr old) comment asking for criticism because of a down-vote. Although you have answered one of the specific questions contained within OP's post, I would suggest OP did not get the info they specifically were after based on the question's context.

That is, it appears that the asker is interested in avoiding sweating while exercising. If you set aside the specific words the asker used, and just look at what their end goal is, the answer you provided hasn't helped them with that. At least, if my assumption about the asker's intent is correct. This is one of the issues with the format of StackExchange... if the asker asks the wrong question, even a perfect answer might not help them. And we aren't supposed to have a lengthy discussion about it.

@aaron oh I get your point now! I will surely try to make some edits to make the answer better


text:
Counter Staining with Safranin
After Gram Staining,
We use counter staining to find out that is there any gram(-) bacteria present on the prepared slide.
My question is-
What component in the cell wall of gram(-) bacteria is responsible for the retention of Safranin dye?
Like the Techoic Acid is responsible for the retention of CVI complex in gram (+) bacteria.
As I have just studied the staining process,any additional useful information is appreciated.
Thanks!

I find it hard to find actual literature on this, so this is just my reasoning. Safranin is a basic dye (ie positively charged). I suspect electrostatic interactions with negative charges on phospholipids in the inner membrane are responsible for its retention.

@canadianer- thanks! Your explanation helped a lot. If you can find any literature related to this, can you please post it? :)

Safranin is retained, very much like Crystal violet, by the peptidoglycans in the cell wall. However, the main difference is the thickness of the peptidoglycan layers in Gram positive and Gram negative bacteria.
Gram positive bacteria, due to their thicker peptidoglycan layer, have a higher affinity to and retention rate of crystal violet. On the other hand, Gram negative bacteria, due to a thinner peptidoglycan layer cannot retain crystal violet as well and are more likely to retain safranin.


text:
Definition of Ancestral Eudicot?
I am wondering what are examples of ancestral eudicots which can be purchased from an aquarium store, and or grocery flower store.

Have you tried googling this?

yes. that would be my first go to ...

and what did you find? Tell us a bit, so we can help elaborate!

All I found was the definition of ancestral (in terms of a cladogram). I mean, there are several plants which can be purchased from aquarium and grocery stores. However, since I am not a plant biologist it is hard for me to even guess how to go about figuring which ones are ancestral eudicots

If someone could tell me the answer, and how to go about figuring something like this in the future, I would really appreciate it.


text:
How to design a ChIP-exo experiment with controls?
Does anyone have any ideas on how to run a control/input sample for a ChIP-exo experiment?  Is it even necessary to run a control (similar to input DNA for ChIP-seq)?  I'm looking for any references or forums that discuss this issue and experimental design?
This video (https://www.youtube.com/watch?v=8qLRI9Bqtso) briefly touches on this issue (t=32.45), indicating NOT to use an Input sample due to the Exo digestion.  However, I don't know how the community (or reviewers) feel about this?
Thanks for any help!

There is a recently published paper addressing the lack of input controls for ChIP-Exo procedures. https://doi.org/10.1093/nar/gkw741 Hope this helps


text:
How symmetrical can an organism be?
The majority of living things have some form of symmetry.  Many mammals and fish have bi-symmetry, and anemones, starfish and jellyfish (among others) have radial symmetry.  However, there usually are many small or major differences that make them not perfectly symmetrical.  Is it possible for something to evolve to be 99% perfectly symmetrical, possibly even spherically?
Edit: I'm talking about something big, maybe as large as a cat or dog, not something tiny (ie. cocci bacteria).

Is there a specific scale you're interested in. Cocci bacteria are pretty spherical.

In short, no. As soon as you have a chambered heart, you have asymmetry.

Perfect spherical symmetry is impossible (at least, cellular organelles aren't spherical) but some organisms are way more symmetric than us. A lot of bilaterians doesn't have large asymmetrical organs like our liver, stomach or hearth.


text:
Does the Plasma Membrane have a hydrophilic interior/exterior/contain vesicles?
I am very new to the study of biology, and have been unable to find information in other sources which could tell me whether the plasma membrane has the following traits:

has a hydrophilic interior
has a hydrophobic exterior
contains vesicles

Thank you!

Where did you look for sources?

The plasma membrane is a lipid bilayer. Plasma membrane lipids have a hydrophilic head group and hydrophobic tail groups. Since cells are usually in an aqueous environment (and are filled with aqueous cytoplasm), the hydrophilic head groups is face both the exterior and interior of the cell. Between these head groups facing the interior and exterior, the hydrophobic tail groups of opposing lipids associate with each other to create a hydrophobic core within the membrane.
Vesicles are also made of lipid bilayers. Vesicles can exist within cells or be released by cells.

Please add some references to your answer.

The plasma membrane typically refers to the double lipid bilayer, which has a hydrophillic exterior and a hydrophobic interior.  In your case, the only thing I can think of is a layer/mixture of inverted micelles, which would fulfill your three criterion.

Image is from "Lecithin-based nanostructured gels for skin delivery: An update on state of art and recent applications"

Please add some references to your answer.


text:
Are there venomous plants?
There certainly are poisonous plants, but I was wondering, whether there are venomous specimen, too?
First, I thought the stinging nettle could be one such. After all, it's common knowledge it "applies a toxin upon touch". However, reading about the mechanics it seems that the injection is actually a much more passive procedure, which would render the plant poisonous, wouldn't it?
So what are some venomous plants?

By venomous, do you mean plants with parts, such as leaves or thorns that sting you with a toxic substance if you touch or get pricked by them?

By definition, the word "venomous" can only technically be applied to animals.  The most "poisonous" plant would be the gympie gympie tree, but if you want something "venomous", you might be able to find something similar within some species of carnivorous plants.

That's interesting. I thought "venomous" simply meant the toxin is applied proactively, rather than passively by being ingested or such.

Please add references to your answer to support your claims.

Yes, venom typically uses some form of injection, and doesn't need to be eaten to harm or kill you.  The gympie gympie tree uses silica tipped hairs to put a toxin into your flesh, much like how jellyfish do.  This tree is naturally found in Australia, because of course it is.  But it isn't only australia.  Stinging netals, definitely, and poison oak debatably are also venomous, since you don't have to eat them to take some form of chemical harm.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Is Phenylalanine hydroxylase gene biallelic?

Since the PAH gene is biallelic, and there are many disease causing mutations, most PKU patients are compound heterozygotes.
  (paper)
Compound heterozygosity in medical genetics is the condition of having two heterogeneous recessive alleles at a particular locus that can cause genetic disease in a heterozygous state.
  (wikipedia)
More than 400 disease-causing mutations have been found in the PAH gene. (wikipedia)

Why is Phenylalanine hydroxylase gene considered biallelic when PKU is also caused by the presence of two different mutant reccesive alleles at a locus with more that 400 types of mutations occurring in nature?

I've edited the link.

In this context I would guess the "biallelic" was just meant to indicate that the gene is on a somatic chromosome (not X or Y), so that there is always two alleles of PAH in an individual.

@Roland Not only in this context but in many books(Principle of Genetics by Snustard for e.g) PKU is considered an autosomal recessive trait controlled by biallelic gene. Many times in other books too PKU has been mentioned in Pedigree analysis and Hardy Weinberg sums (taking only p and q the involved frequencies).


text:
What is the point of toxins without remarkable coloring?
As far as I know, some toxic species (eg: some mushrooms) have no remarkable coloring. Therefore, what is the purpose of their toxins?
Toxic species often have colorful appearances to warn predators. Therefore, if a species has toxins but no vibrant coloring, this seems to me to not be beneficial for either this species or potential predators. But still, some toxic mushrooms (for example) have plain coloring.
What is the point of being toxic without vibrant coloring?

I think you got it wrong. Vibrant colors often attract animals (just think, would you like to eat a red apple or a green apple?), so plain color can be considered as that fruit (or anything) as not edible. That is (partly) why not many animals have pretty much no interest in eating sand as it doesn't have vibrant color. Obviously, sand itself is not alive ;)

why warn them, must mushroom are only a tiny fraction of the fungus's mass and dead animals make for good fertilizer. Also consider that toxic to humans or mammals is not the same as toxic to everything, there are still lots of critters that will eat toxic mushrooms without harm. so you have to weight dissuading some predators vs attracting others.

Also, the toxin might be incidental - e.g. it performs some role in the species metabolism.  Or it might have evolved in response to species with different visual capabilities, the way some plain to human eyes flowers have dramatic patterns when seen in UV, which the flowers' insect pollinators can see.

This is a really great question. To take a specific example, let's consider Amanita phalloides, the death cap mushroom. It doesn't advertise its poison; in fact, it resembles several edible species of mushrooms, including Caesar's mushroom and the straw mushroom. It contains alpha-amanitin, an extremely potent poison that inhibits RNA polymerase, shutting down protein synthesis. The estimated minimum lethal dose is 0.1 mg/kg or 7 mg of toxin in adult humans. The poison has a delayed effect, taking between 10-24 hours for significant effects to appear, so it's not like a poisoned animal can learn to avoid the mushroom in the future. None of the amatoxins appear to have any purpose except as a mammalian poison. They aren't specific to humans, and are capable of poisoning dogs. So what's the evolutionary advantage of this poison?
According to an essay written on the California Native Plant Society blog by John Chesnut, a horticulturist, the answer might lie in where the mushroom grows -- on tree roots as ectomycorrhiza (emphasis mine):

Death cap is an ectomycorrhizal symbiont. This means it forms connections on the root-tips of forest trees; in California, its typical (but not exclusive) partner is coast live oak. [...] Ectomycorrhizal (EC) fungi collect major nutrients, nitrogen and phosphorous, and exchange these with the host tree for sugars. Delicate hyphal strands extend outward from the root tip mass into the surrounding soil and mulch. EC also allows efficient active transfer of macronutrients, micronutrients, and soil water to the tree. The chronic phosphorous limitation in serpentine soils makes the EC symbiosis especially important for local forest types on this soil. Studies in Norway discovered up to 50% of a birch tree’s sugar is exchanged at the root tips with EC symbionts.

So the poison might not be intended as a way of preventing itself from being eaten, but as way of defending the tree it lives with from nematode pests (emphasis mine):

So why are Amanita so poisonous? It is an unlikely deterrence to vertebrate predation of the fruiting caps, as the effect is slow-acting (36-72 hours before the toxic crisis in humans) and the toxin is not concentrated in the cap. Evidence supports the hypothesis that the fitness obtained from synthesizing the toxin is secured within the hyphal network. Perhaps toxic Amanita obtain nitrogen from poisoned nematodes, or protect themselves (and their symbiont hosts) from plant parasitic nematode predation.
Perhaps the toxin suppresses the growth of competing fungal webs. It seems clear the toxic effect of death cap is intrinsic to its invasive success worldwide.

Interestingly, he points to some research suggesting that some mushroom flies might have co-opted this mechanism to keep themselves parasite-free (link and emphasis mine):

An evolutionary entomologist working in New York State, John Jaenike, has discovered four species of mushroom flies in the genus Drosophila that lay eggs in the gills of fruiting Amanita phalloides. The fruit fly taxa are related to ones that inhabit rotting skunk cabbage, but in New England have recently transferred to the recently introduced Amanita fruitings.
Jaenike discovered that Amanita phalloides is toxic to the damaging parasitic nematodes Howardula that reproduce in the stomach of fruit flies. The toxicity of the death cap to the parasitic nematodes results in much greater egglaying (fecundity) by the fruit flies. The fruit flies are affected by the toxic amanitin, especially the males, but the poison is more than offset by the increase in reproduction.
Janike also discovered that most other insects using mushrooms as egg laying sites (craneflies and forest gnats) shun use of the Amanita (due to its toxicity).

(in response to post by Gaurav) The concentration of toxins in Amanita phalloides IS highest in the cap and is basically zero in the hyphae (mycellium). This was found in 1996 and verified separately in 2015. Mycologia8, 8(6), 1996, pp. 909-921. Toxicology and Industrial Health 2015, Vol. 31(12) 1172–1177


text:
Absorbable stents
Stents are tubular scaffoldings, which are used to expand blocked arteries. Absorbable stents dissolve after few years. Shouldn't the blood vessel become narrow again once the stent has dissolved?

Blood vessel by that time gets remodelled.

"Restenosis" is a problem with both absorbable and non-absorbable stents.


text:
Is some of the energy of food lost during digestion?
I know that chemical energy of food is converted to heat energy to be used by the body in many metabolic reactions. Specifically, I know that the breaking down of bonds is what releases energy.
Does that mean that some of the energy of food is lost during digestion as enzymes breakdown large food molecules into smaller soluble ones? Or is it the common concept of losing energy during digestion because not all the food is absorbed and some are egested?

How do you know that energy is required for digesting food? Enzymes are biocatalysts i.e. they just enhance the speed of digestion of food. Without enzymes too, all your food will get digested, but will take more time.

THere is plenty of overhead cost from digesting food. It takes energy grind up that food into small bit so that it can be digested and absorbed. To move food bolus through the digestion system via pertaltic contractions. And it takes energy to make those enzymes. And it take energy to maintain the immune system to control any parasites that came with said food. It also takes energy to breakdown anti-metabolites (compounds that prevent digestion and absorption) that come with most living tissue.

virtually all of the food is digested, most of your poop (that isn't water) is actually dead gut bacteria, chemically resistant fibrous material makes up most of the rest.

@another'Homosapien' Enzymes aren't free, and they aren't the only contribution to digestion.

@bryankrause certainly they are not free, but they are not made from energy lost from digestion (if any) and I don't think any of such contributions is paid up through that energy (if any) either. My point was that though body spends energy on digestion, yet that energy does not come from the food being digested.

Good question. But it is not true that heat energy is used by the body to drive other reactions. Heat is the portion of energy that is lost.

Typically, catabolic reactions such as the hydrolysis of food stuffs into their monomers is an exothermic process. This includes conversion of proteins into amino aids, starchs into monosaccharides and fats into fatty acids plus glycerol. As an example, hydrolysis of a peptide bond linking the amino acids in a protein liberates 8-16 kJ/mol of energy.
https://en.wikipedia.org/wiki/Peptide_bond
So, that means a certain amount of the energy in food is liberated in the gut. But this is very minimal compared to the amount yet to be liberated, and harvested, as the many other bonds in the monomers are further broken down during cellular respiration.
A bit of research from a few different sites suggests the gut temperature is not meaningfully higher that the core body temperature measured in, say, the anus or vagina. https://en.wikipedia.org/wiki/Human_body_temperature  Any heat liberated from digestion in the gut must be slow enough to be absorbed into the bulk of the body without accumulating in the gut.

Also, this release of some heat is what makes digestion spontaneous, otherwise (if $\Delta$G is 0 too) enzymes would require ATP for digestion to provide activation energy to the molecules. Anyways, nice answer, +1!


text:
How are colors outside the standard RGB color scheme perceived?

I found this image in a German book about biology. It's called DIN 5033 and represents the RGB color scheme.
What colors are outside the RGB scheme, i.e., in the black areas of the picture?

DIN 5033 covers wavelengths 380nm to 780nm along its edges. Everything in that space not on the edge varies only in spectral purity. Anything outside those wavelengths would be not covered by this color space (e.g. ultraviolet). Anything in the black area makes no sense (light consisting of nothing but precisely X nm light can't be any more "pure"). Human visual range varies but roughly covers that same spectrum. Outside the range is more towards infrared (higher wavelength) or ultraviolet (lower).

Note also that the bottom right edge (magenta) isn't on the visible spectrum, it's a blend of red and blue. Also the black area isn't light outside the 380-780 range, it simply isn't defined, just as (x,y)=(1,1) isn't a possible solution for x^2+y^2=1. If you wanted to modify that colorspace to add infrared/ultraviolet, you would simply increase its perimeter, inserting ultraviolet in the bottom left, infrared on the right, thus shifting magenta more towards the center and the bottom edge becomes a gradient of ir/uv mixes.

If you mean "perceived" by something other than human eyes/brains, I would also love to know if cameras/devices that are sensitive to the full spectrum of light have been used to map "invisible" chromatic territory (i.e. by having a machine that can measure frequency)

This question is both biology and physics I think (I guess it's biophysics! :) so I feel it's worth answering here.
First, we must recognize the difference between wavelength, which is just a physical property of light, and color, which is by definition a human visual perception. The color "red", for example, is a particular visual sensation humans have when encountering light of certain wavelengths. A color cannot be described by a single wavelength number, because the light we see in nature is never monochromatic; it's a complex mix of photons of all sorts of wavelengths.
As John's answer also pointed out, the human eye has three types of cone cells which responds to wavelenghts differently, determined by their absorption spectra (see picture below; R represents the rod cells, which I ignore here). Human color perception can be described as a mix of signals from the L (long wavelength, red), M (medium wavelength, green) and S (short wavelength, blue) cone cells. Mathematically, this is a linear combination $l \cdot f_L + m \cdot f_M + s \cdot f_S$ of the three spectra $f_L$, $f_M$ and $f_S$. The coordinates $(l,m,s)$ generate the LMS color space, which by definition contains all colors humans can perceive.

Now for your question: what colors are outside the RGB scheme?
This depends on precisely what you mean by "the RGB scheme" and "color". The picture you posted is actually not an RGB scheme but a two-parameter color model known as CIE 1931, which is roughly the same as the LMS color space, minus a light intensity parameter. If by "color" you mean the human visual perception, then by definition there are no colors outside the LMS space.
On the other hand, there are many kinds of light that humans cannot perceive correctly: you can imagine from the figure above that there any many cases where two different wavelength mixtures give the same response. For example, a mix of "red" and "green" light may result in the same $(l,m,s)$ values as "yellow" light, even though this is physically different. And of course, some wavelengths our eyes don't register at all, but we usually don't consider such wavelengths as "colors".
Finally, if by "RGB model" you mean the types of light that RGB devices like your computer screen can produce, then the answer is that there are many colors outside RGB. This because RGB devices use light sources for R, G and B with different wavelength profiles than those of the cone cells. Therefore, a typical RGB device generates only some subset of the LSM space. For example, in the figure below, the triangle represents the colors generated by mixing three monochromatic R, G and B light sources in the CIE RGB space, one of many possible RGB spaces.

the colors we humans with our trichromatic eyes cannot see.

.Color for us is produced by a combination and comparison of cell activation. We can see every wavelength between about 4-700nm, we can't differentiate well near the ends or at all for that matter compared to non-mammals. for most of the RGB  one wavelength activates more than one cell the comparison of activation creates a color, by activating more than one type of cone cell by different amounts. example activate both red and green but red more than green and you see orange, activate both the same and see yellow.
The deep purples or magentas however are weird and can be activated in two ways. Our red cones actually also pick up light in the 400nm range. so light  close to 400nm activates both blue and red but not green (if our red cones did not have this bleed over it would normally be impossible to active red an blue but not green), but you can also trick the eye by using both red and blue light together which produces the same result of activation. that's why you have that purple smear across the bottom of the color chart.

But there are also wavelengths below 400 and above 700, Other animals can see part of these wavelengths as colors. There are animals that see colors in what we see as white light. Animals with more than three types of cones or with cones that are activated by different areas of the spectrum see different colors.

Well ...  The RGB model is certainly designed to create colors that we humans can see, but it's not the same color space, since the R,G and B primary colors of RGB devices have different frequency envelopes than our cone cells.

if you look at the OP's graph you can see the same plot our eyes are stuck with, a smooth spectrum from blue to red and purple is when the ends of the spectrum are active without the middle. past that you get into the infrared and ultraviolet.

I think you need to distinguish between color and wavelength. Colors are properties of human biology; wavelengths are just physics.

If you look at the OP's chart it is graded by wavelength, Color for us is produced by wavelength or a combination of wavelengths. we can see every wavelength between about 4-700nm, we can't differentiate well near the ends or at all for that matter compared to non-mammals. But there are also wavelengths below 400 and above 700, Other animals can see part of these wavelengths as colors. There are animals that see colors in what we see as white light.

This answer is incorrect. The black area does not contain "colors we cannot see". The black area is undefined because it would represent signals with more than 100% spectral purity (if a signal is already precisely 750nm wavelength with no other components, it can't be more pure than that). IR and UV, if you wanted to add them to that space, would go on the right and bottom left corners respectively, expanding the perimeter of the space and shifting magenta towards the center and making the bottom right edge a gradient of IR/UV blends.

In other words, you are correct in your notice of the wavelength gradations on the edges, but light outside those wavelengths is not what the black area represents. The black area is undefined in the same way that (x,y)=(1,1) is not a solution to x^2+y^2=1. The black area doesn't have anything to do with human perception either, only math. The only part of this colorspace related to human perception is the choice of wavelength range it represents, which was chosen to roughly match the visible spectrum. That choice, even though it makes sense, is essentially arbitrary.


text:
How pulmonary vasculature removes embolism?
This book says:

Pulmonary vasculature removes emboli before they reach into systemic circulation.

I can speculate that if the emboli are made of fat or clot then our body could degrade it but how does it removes air emboli?
Wikipedia without any citations just states:

Gas bubbles arising from decompression sickness are generally formed in the venous side of the systemic circulation, where inert gas concentrations are highest, the bubbles are smaller at first and they are generally trapped in the capillaries of the lungs where they will usually be eliminated without causing symptoms.

Could anyone provide a reliable source for it or a satisfying explanation?

Diffusion is the primary job of the lungs, so it's easy to see why this would happen more easily there; size is also a factor. In fact, large air emboli will eventually be removed from the right atrium if they spend significant time there just because gasses diffuse into liquids. (Breathing 100% O2 will help decrease the size of the embolus by speeding up nitrogen diffusion.)

So we can say that the air inside the microbubble will diffuse into atmosphere through alveoli ?

Yes, that is safe to say. It's also safe to say that the gas will simply diffuse into the blood stream (the lungs are very blood-vessel rich) and go the route of all gasses in the blood stream.


text:
Is there a map of the individual motor axons in the limbs?
As of right now, I can only find a map of nerve fibers, but not necessarily the individual neuron axons.
For example, here's a map of the nerves in the arm and hand.
http://www.innerbody.com/anatomy/nervous/arm-hand

Maybe, sort of; can you clarify why you want this information or what type of map you are looking for?

Nerves are somewhat variable (the image on your link shows an idealized version). Axons are even more variable than nerves. Consider that nerves are growing out from the CNS to muscles that are developing from a completely different germ layer. The actual axons reaching individual parts of muscles are not at all conserved.

@BryanKrause Yes. I'm trying to learn more about how biological neurons could be connected directly to computers instead of indirectly through EEG. If that were possible, I could definitely see full motor and sensory capabilities being implemented in bionic arms.

No it is not possible to map axons at that fine of a scale between individuals.
You mention a possible use for controlling bionic arms. There are a bunch of problems with that approach.

Like @kmm says, at the fine level there is a ton of variation.
I think you are failing to appreciate just how many axons there are, even going to a particular muscle; while each muscle fiber only gets input from one axon, there are thousands of fibers in a single muscle.
The EEG-based approaches to prosthetic control are most relevant when there is a problem with spinal function, for example caused by an injury. In this case, there is no connection between the motor neurons and the brain.
Axons often degrade if their targets are damaged. Therefore, if a hand is lost in an accident, for example, the neurons projecting to the muscles of the hand will atrophy.
If the axons themselves are in place, there are already prosthetics that operate based on muscle contractions in existing muscles. It takes some time to train users to use these devices, but most movements you make involve all sorts of muscles you may not realize are involved, and it is quite possible for brain plasticity to allow muscles in, for example, the shoulder, to control a bionic hand after an amputation.

If for some reason the issues I raised don't apply, there is another alternative: mapping. You don't need to know which axons you want information from, you only need to be able to record their activity (which you will need anyways to operate the prosthetic). Record the activity while the patient tries to move their finger, for example: now you know the signal you should transduce into a finger movement. The technical challenge, then, is being able to isolate that signal from all the other signals from all the other axons in the same nerve. This challenge is related to, though not precisely the same as, the challenge of isolating a signal in the EEG.

With diffusion tensor imaging I they're pretty close on mapping fibers, at least in the brain.

@AliceD Source? DTI is worlds away from mapping individual axons, unless some massive new technological leap has totally escaped my notice. It would certainly be possible to use DTI to map the statistical connectivity of different brain regions but that is nothing like what the OP is suggesting. DTI resolution is on the order of mm, axons can be closer to 1 micron.

aha gotcha.  +1 and thanks for clearing that up for me. Perhaps adding your sources may help you get some more up votes.

@AliceD Yes indeed, I'll try to track some down where possible. Possibly of interest to you I did some research on DTI methods and it seems there are some recent works that get the resolution down to 100um and below, but these are with high-strength 7T+ scanners that are sized only for rodents.


text:
Can you freeze an ATP assay sample for later use?
I am going to use adult Drosophila to do an ATP assay (ATP determination kit A22066). The most convenient for me is to freeze the samples and perform the experiment later.
However, the protocol provided by the kit producer keeps saying the assay is extremely sensitive, so I'm not sure if it's okay to keep the homogenized samples under -80°C for a short period of time.

you'll never know for sure unless you run some fresh and run some after freezing - might not be worth the risk

Pure ATP can be stable when stored frozen but I would be worried, perhaps unjustifiably, about storing a homogenized sample. You should try dividing a homogenized sample in half and assaying one half right away and the other half after freezing to see how the signals compare.

Could you elaborate why storing a homogenised sample should be worrying?

@Marzipanherz I would be worried, perhaps not justifiably, about controlling pH and ATPase activity.

I was told that there is no (noteworthy) enzyme activity at -80°C. However, I just took this for granted... Guess it's time to find a reliable source for this :)

@Marzipanherz My supervisor once told me that he was working with a colourimetric substrate that turns from clear to purple during some enzyme-catalyzed reaction. He prepared a stock solution, clear in color, and froze it overnight. The next morning it was purple, presumably due to trace enzyme contamination. There's also the time spent while freezing and thawing it but, again, my concerns may be unfounded.

That's really interesting! Thank you for sharing!

@Marzipanherz Well it's just anecdotal. I found it hard to believe myself.


text:
Does the humeroradial joint move medially/laterally?
The humeroradial joint is a ball-and-socket joint that, if unrestricted, would allow for movement around all possible axes. However (as succinctly stated from Wikipedia):

the annular ligament, by which the head of the radius is bound to the radial notch of the ulna...prevents any separation of the two bones laterally.

As a result of the annular ligament, the proximal radioulnar joint and -- quite honestly -- the humeroulnar joint, the humeroradial joint is considered to be "limited." In other words, the humeroradial joint is typically considered only to be capable of taking part in flexion/extension of the elbow and lateral/medial rotation of the forearm.
However, although no internet/textbook search I've conducted mentions it, I'm wondering does the humeroradial joint allow any movements at all in the frontal plane (i.e., adduction/abduction)?
Here's a visual:

It seems unlikely, but at least a slight "jittering" seems possible.
Although just barely related, the knee (a hinge joint) comes to mind because of its somewhat unexpected (based on classification, not structure) ability to "slightly rotate" when unlocking.

Adduction is highly unlikely because of the restriction provided by the crest in the articular surface of humerus. Also there are no muscles for voluntary abduction and adduction.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Why hasn't life on Earth reached an evolutionary stable strategy?
I heard in some YouTube video that cheetahs only existed 5,000,000 years and according to https://en.wikipedia.org/wiki/Extinction, extinctions are occurring all the time so I assume life on Earth hasn't reached an evolutionary stable strategy. I know some species like ants are in an evolutionary stable strategy and most species are close to their evolutionary stable strategy because the system of the rest of the species is changing so slowly but why hasn't the system of all life on Earth reached an evolutionary stable strategy. Could it be that it's destined to never reach one? That doesn't necessarily mean there isn't one. According to https://en.wikipedia.org/wiki/Evolutionary_game_theory, the side blotched lizard has 3 forms undergoing cyclic evolution so it's destined to never reach an evolutionary stable strategy if the state of the rest of the species on Earth doesn't change. There's another case of cyclic evolution where rabbits outcompete wolves when there are very few rabbits and wolves outcompete rabbits when there are a lot of rabbits? Why are there so many species that have existed for no more than 5,000,000 years instead of the system of all life on Earth being stable with a few species undergoing cyclic evolution? What's causing the current state of all life on Earth to keep on not being evolutionary unstable?

The concept of ESS applies to a population (in a constant environment), not to all of living things on a planet.

Because the environment on earth is not stable on the long run.
Antarctica was on the tropics. However plate tectonics has moved the continent from that location to south pole. And in time the continues will leave the poles and move toward the tropics again.
So a perfectly evolved animal in tropical Antarctica 200 million years ago, would have to continue evolving or it would have gone extinct as Antarctica moved southwards. And the animals living on Antarctica today will have to evolve as the continues continues with its motions.
Also predator-prey relationships... are red queen type relationship. They may appear stable on the outside, but both parties are actually under selection pressure to evolve, to counter the advantages of the other party. They are in an arms races. Pressure to out run the predator. Pressure to outwit the prey. Pressure to better camouflage. Pressure to detect prey from multiple senses (sound, sight smell).
So on the long term, the strategy that a predator uses will change as its prey evolves. And vise versa for the prey.

"are only..." what?


text:
How are neurons / synapses "biased"?
I'm trying to see if I understand this correctly. I've read the question Can the human brain be reduced to a binary system? and one of the answers explains:

While action potentials are usually binary, you should note that
  synaptic communication between neurons is generally not binary. Most
  synapses work by neurotransmittors, and this is a chemically mediated
  graded response that, for example, act on voltage-gated ion channels.

Looking into the graded response article on Wikipedia:

Postsynaptic potentials are changes in the membrane potential of the
  postsynaptic terminal of a chemical synapse. Postsynaptic potentials
  are graded potentials, and should not be confused with action
  potentials although their function is to initiate or inhibit action
  potentials

Ok, so from what I understand, involving what I learned in this video about action potential, and those two quotes, there can be a "bias" in the synapse process of neurons that make them more or less likely to reach the threshold for action potential when they receive neurotransmitters as the result of the activity from axons connected to their dendrites. Basically, I have the idea that somehow, the synapse area between neural connections becomes trained based on past interactions on whether or not to fire "easily" or be "reluctant" to fire or else fires more powerfully or weakly contributing more or less toward action potential of neurons on the receiving end.
Edit: On second thought, I also recall learning about a mechanism enforcing recharge time between firing, so the neurons are throttled if they fire too rapidly, a mechanism which, (iirc) if defected can cause epilepsy. Really not sure about that, but it would sort of be the opposite of "training" it seems to me.
So I have a few questions surrounding this subject:

Are some "actions" or "transmissions" (for lack of the correct terminology, when the neuron fires) more powerful than others, contributing more dramatically to action potentials of neurons receiving neurotransmitters when it fires?
Or if I'm on the wrong track with that question, how does the bias occur / form over time? Is a bias based on short term or long term series of interactions? How many past interactions are significant in the current state of the bias at any given time?
Is there bias at all?

The term that most scientists use to describe a synapse's "bias" is synaptic strength. The strengths of synapses depend on their "history".  The change of synaptic strength is called synaptic plasticity. This topic is closely related to memory formation and is a very broad question to answer (groups of wikipedia/scholarpedia pages and tons of reviews, not single publications).
Generally, the strength of a synapse, i.e. the size of the effect of a presynaptic stimulus on the postsynaptic neuron depends on presynaptic and postsynaptic factors. To name just a few:

the number of vesicles released from the terminal,
the expression levels of the neurotransmitter reuptake and/or breakdown enzymes,
the expression level, location and posttranslational modifications of postsynaptic receptors and
uncountable other factors.

Although there have been decades research and a nobel prize (to Eric Kandel) on the topic, there is still a lot to find out.
For a start, you might want to look up
Synaptic plasticity and/or
Spike-timing dependent plasticity (long term potentiation and long term depression).
LTP is also a good example to answer all three of your questions (if I understood them correctly).

third question: yes.
second question: LTP (and other mechanisms).
first question: Different frequencies of spike trains are more or less effective at triggering LTP, making them more or less powerful to the change in synaptic strength, affecting the response of future input to the same synapse.

Nice answer, +1! I have added some more details to your answer as my own answer. Feel free to improve/criticize :)

@a tiger has given a nice answer, but to me it seems too summarized. So I just want to elaborate it by giving some more details. Also, let me tell you at first that it is a very broad topic, so covering up everything in anything less than a book is pretty much impossible. I'll only add points enough for an introductory answer. I will answer your questions one by one.

Are some "actions" or "transmissions" more powerful than others, contributing more dramatically to action potentials of neurons receiving neurotransmitters when it fires?
Yes, that is why they are called graded potentials. Graded potentials are actually different from normal action potentials in that action potentials follow the all or none law whereas the strength of a graded potential can vary depending on how many ion channels it stimulates. You might better understand this by the equations they follow.
Normal action potentials follow Nernst Equation i.e.
$E_{eq,K^+} = \underline{RT}\times \ln \underline{[K^+]_{out}}$
$\hspace{20mm}nF\hspace{12.5mm}[K^+]_{in}$
On the other hand, graded potentials follow the Goldman Equation i.e.
$E_{m} = \underline{RT}\times \ln \underline{P_K[K^+]_{out} + P_{Na}[Na^+]_{out} + P_{Cl}[Cl^-]_{in}}$
$\hspace{14mm}F\hspace{14.5mm}{P_K[K^+]_{in} + P_{Na}[Na^+]_{in} + P_{Cl}[Cl^-]_{out}}$
which is significantly different from Nernst equation. The biggest difference is that as per Goldman equation, the net potential depends on the concentration of more than one ion, meaning that it can attain a range of values, unlike that from Nernst equation. This directly answers your question that Yes, some graded potentials can be different from others in strength and time, thus giving different contributions to action potential on the following neuron. Yes, time too. It is so because different ion channels remain in different states (open, close, inactivated) for different times and take different times for transitions. You might understand this by this diagram:

How does the bias occur/form over time? Is a bias based on short term or long term series of interactions?
Generally, bias is formed by continuous strengthening of a synapse based on its activity over recent time, a process known as LTP or Long Term Potentiation. LTP can lead to a long-lasting strengthening of a synapse and is hence considered to play a major role in formation of memories in brain. When a synapse is repeatedly stimulated over time, the following neuron creates more dendritic receptors so that more effective potential can be generated. Over time, the first neuron starts releasing more and more neurotransmitters whenever it is excited. These two factors, when combined, lead to stronger synaptic connection i.e. formation of bias. You can see the following images for better understanding:

In fact, a bias results from both short term and long term potentiation. The former i.e. STP is a transient increase in synaptic strength of two neurons usually due to increase in synaptic vesicle release probability. It can also be caused by diseases such as tetanus. So, if you look at the big picture, then yes, a bias is the result of both short term and long term interactions between two or more neurons.

How many past interactions are significant in the current state of the bias at any given time?
Bias formation is a long process which requires many steps, including gene expression and protein synthesis. That is why, LTP has been divided into two (and sometimes three) different phases: E-LTP (early phase or LTP1) and L-LTP (late phase, further divided into LTP2 and LTP3). A schematic diagram of LTP is below:

Thus, in short, we don't know exactly how long it takes for LTP formation, and there probably is no exact time required for its formation.
Is there bias at all?
I should have answered this question at first, but since I do so at last, I will add some more points. Biasing, or synaptic plasticity, is the ability of synapses to strengthen (by LTP) or weaken (by LTD) over time due to change in their activity patterns. Its mechanism has been theorized to be dependent on:

change in probability of glutamate release.
insertion or removal of post-synaptic AMPA receptors.
phosphorylation and  dephosphorylation inducing a change in AMPA receptor conductance.

The third one is a more complex part of the process, while the first two processes have been examined by a mathematical formula for calcium-based model of plasticity as:
$\underline{dW_i(t)} = \underline{\{\Omega([Ca^{2+}]_i) - W_i\}}$
$\hspace{3mm}dt\hspace{22mm}\tau([Ca^{2+}]_i)$
where:

$W_i$ is the synaptic weight of the $i^{th}$ input axon
$\tau$ is a time constant, dependent on the insertion and removal rates of neurotransmitter receptors, which is dependent on $[Ca^{2+}]$
$\Omega$ (the concentration of calcium) is also a function of the concentration of calcium ($\Omega = \beta A^{fp}_m$) that depends linearly on the number of receptors on the membrane of the neuron at some fixed point.

So in short, Yes, biasing does exist in neurons and plays an important part in many important phenomena such as memories.

P.S. I also want to add about relation of synaptic plasticity with epilepsy as you talked about in your question. Though we don't know everything about epilepsy, we know that synaptic plasticity indeed does play a role in epileptic seizures. During epilepsy, seizure threshold i.e. amount of stimulus required for action potential, is lowered. Also, because of factors such as long term potentiation, even a small potential gets enhanced into a larger potential. All these factors, along with some other unknown ones, when combined, lead to a seizure or attack.
Also, epilepsy is also caused due to decreased resistance of neurons towards a stimulus and a decrease in the refractory period of ion channels (what you call recharge time). Due to decrease in this recharge time, neurons are able to generate kind of unnecessary action potentials which ultimately leads to a seizure. As said, refractory period is the time immediately after depolarization of ion channels during which it is unable to transmit another signal. A simple graph shows refractory period like this:

I might be a bit biased here myself (pun intended ;-) ), but IMHO you gave a  specific answer to a broad question. My impression is that you gave details, but not all details that would be necessary to give a full answer (which is almost impossible in this case), underselling the complexity at hand. E.g. you are only talking about AMPA receptors, but there is more to it than AMPA. In answer 4, you mention a few LTP mechanisms, but this is far from a complete list. I think it is very nice of you to have put so much effort into an answer, but I think it gives a wrong impression of completeness.

@atiger I just wanted to give more details for your answer. If you see, our answers are very similar, mine just being a bit longer and detailed. It is obvious that we don't know everything about anything, so giving a complete answer would be just utopia ;) anyways, I'll slowly add more and more details until the answer starts becoming too long.


text:
How many transmissions does it normally take for a neuron to reach threshold for action potential?
This video illustrates and explains how the dendrite connections being activated causes the neuron to be polarized until it reaches "threshold", and firing. My question is how many times might a neuron's dendrites need to receive "fires" from other neurons in order to reach threshold. I think I understand that it isn't a binary matter, so I realize the answer isn't going to be 5 or 5,000 but a general range.
As a related question, how long does it take for polarization to wear off if additional transmissions don't come in, and if the polarization does wear off, is this wear-off mechanic important to the neural system? Is wearing off a significant aspect of the neural process, in other words?

To give a rough idea, according to my calculations it takes 153 inputs (individual action potentials) from CA3 pyramidal neurons to produce a depolarisation above threshold in the CA1 pyramidal neuron. This is of course a very simplistic division that does not consider spatial and temporal summation or any other complicating factor. Also note that each CA3 pyramidal neuron forms a variable number of synapses onto each CA1 pyramidal neuron (~5? according to the hippocampus book), and for each action potential only some of these synapses release a vesicle. Thus 153 inputs = xxx number of activated synapse (activated synapse = synapse receiving action potential).
So how did I arrive at 153?
According to this paper [1], a single action potential from a CA3 neuron produces an average depolarisation of 131 uV, presumably at the cell body, which we can also take, for simplicity, to be the depolarisation produced at the axon hillock. So assuming the threshold is 20mV (I'm not sure exactly but it should be in the 20-30mV range), the number of CA3 neuron each producing a depolarisation of 131 uV required to reach threshold is 20/0.131=153.
Again this is a simplistic division and may not be a good estimate once you take into account all the complicating factors in summation, but hopefully it gives some idea. Also bear in mind that synapses in different parts of the brain can have very different properties, so 153 might not be applicable to them.
[1] The time course and amplitude of EPSPs evoked at synapses between pairs of CA3/CA1 neurons in the hippocampal slice.
RJ Sayer, MJ Friedlander and SJ Redman.
Journal of Neuroscience 1 March 1990, 10 (3) 826-836

How many action potential are needed to cause an action potential in the postsynaptic neuron depends on the strength of the synapse(s) involved. It's not possible to answer this question in general.
It is not just the number of action potentials received but also the firing pattern in which they arrive and the location of the synapse(s) on the dendrites/soma (proximal/distal, on a spine or not, on which kind of spine,...) of the postsynaptic neuron.
However, for some neurons it is possible to trigger an action potential in a postsynaptic neuron with a single action potential. But in this case it is very probable that multiple synapses were involved between the two neurons (example paper).
To your second question: the time until polarization wears off is called the time constant tau of a neuron. It is a property that varies from neuron to neuron and is one of the things that can be measured when recording from a neuron. It is one of the many factors that affects how incoming action potentials are translated into a neuron's output firing.

What would be a minimum number? The smallest number of transfers it can take? 2 or 3? In other words how big do the synapses get in terms of polarizing the neuron? 30%? 80%? 100%? Also is it proper to use the word "synapse" the way you did, to refer to the transfer rather than simply the location of the transfer? That's a topic of confusion for me.

The synapse is the structure that connects the presynaptic to the postsynaptic neuron. The effect on the postsynaptic neuron depends on the activity of the presynaptic neuron, but also on the strength of the synapse (see my answer to your other question: http://biology.stackexchange.com/questions/56402/how-are-neurons-synapses-biased/56477#56477)

Your question about how far in % a synapse can get in terms of depolarizing a neuron is misleading. It depends on so many other factors such as the location of the synapse (look up dendritic integration), the proteins expressed on the postsynaptic neuron and so on. You can't answer this question with a single number. It's more complex than that.

Let me change the question for the OP so that we can get a quantitative answer: In a CNS neuron, what is the threshold for action potential initiation at the axon hillock, what is the typical depolarisation produced by an activated synapse on the dendrite at the dendrite and what is the resulting depolarisation at the axon hillock. I know it varies with different neurons and with different distance of synapse from soma, but something like  ~20mV at the dendrite and ~1mV at the axon hillock will help us get some idea about how difficult it is to excite a neuron.


text:
Aseptic technique: a single technique, or any technique fulfilling criteria, or collection of said techniques?
My friend just used the following sentence in her lab report:

Aseptic technique is used in this step:

I immediately felt something was wrong. She used the term as if it were a specific technique. Is her usage correct, and if so is "aseptic technique" indeed a specific technique with a specific procedure?
Rather, I thought "aseptic technique" referred to any technique that involves complete sterilization of a certain environment or apparatus/instrument. If this were right, then perhaps "an aseptic technique" should be used instead?
Further still, if "aseptic technique" refers to the collection of all techniques that involve sterilization as described above, the perhaps it should have been "the aseptic technique" instead?
Which one(s) is/are correct, grammatically and semantically (hence conveying the concept accurately)?

I bet it means she just used a new pippete

This is more a question about English language and usage than about biology. I vote it be moved to that SE. PS. For what it's worth I think you are wrong, but I'm not going to argue it here.

I'm voting to close this question as off-topic because it belongs on SE English Language & Usage.

Aren't you mistaking antisepsis for asepsis?

@David not sure if I'm conveying it well, but I intended to seek clarification for what the term really means. Is asking for a definition of a biological term that is clearer than what I could find an off-topic question?

@Flo AFAIK you can just sterilize something with fire for aseptic technique, what exactly that means tho is what I'm trying to find out here

I have answered your question. Take note, not only of the answer, but of the way I have supported my conclusions with the results of internet searches for the professional usage of the term. Another time you should undertake research of that type yourself. Although certain scientific terms (mass, current, atom) have precise and unvarying meanings, the meaning of many others — especially when they are in common usage — may vary depending on context. Often the language changes. In English there is no Academy that passes judgement.

This is primarily a linguistic question and I am answering it on the basis that it will be migrated to Stack Exchange, English Language and Usage.
The question is whether, in the context of a report describing (otherwise unspecified) student work, the phrase “aseptic technique” can be used without an article, or whether it requires the definite or indefinite article. This is a question of meaning and usage, and, without using any technical grammatical terms, can be answered by anlysis of scientific publications and by analogy.
“The aseptic technique” (definite article)?
The definite article would normally be used in this type of situation if reference was to one specific clearly defined technique. As an anlogy I would take ‘The Heimlich manoeuvre’ (where ‘manoeuvre’ occupies an analagous position to ‘technique’. Clearly the phrase does not refer to a standard defined procedure like the Heimlich manoeuvre, but merely that the work was performed asceptically (i.e. under sterile conditions). So in this context the definite article is certainly not necesary. In some circumstances employing sterile conditions requires satisfying certain enumerated criteria (example below), in which case the definite article may be used.
“An aseptic technique” (indefinite article)?
I think that this is possible but not obligatory. The use of the indefinite article indicates that the asceptic technique used was one of several possible. Although sometimes this would be used in the context of a limited number of items, this is not a necessary requirement. Analogies with a different adjective would be “she executed the dive with a graceful technique”. Here, the article is (almost) obligatory, but less so in the case of “she showed superb technique in executing the dive”.
“Aseptic technique” (no article)?
As the last example shows (“she showed superb technique in executing the dive”), omitting the article is perfectly acceptable in analagous phrases. I would say it is perfectly acceptable in this case.
The arguments above are only useful to the extent that they reflect actual practice. A quick internet search brought up an interesting example in which both no article and the indefinite article were used in the same text. This is the entry for Asceptic Technique on a website called Healthline.
The second paragraph omits the article:

Aseptic technique is a method designed to prevent contamination from microorganisms.

But when it gets down to specifics:

According to The Joint Commission, there are four chief aspects of the aseptic technique

So unless your friend was referring to ‘The Joint Commission’ (which I doubt) there is nothing wrong with that sentence of her lab report.
Other Professional Examples
ThermoFisher Scientific — no article

Aseptic technique, designed to provide a barrier between the microrganisms in the environment and the sterile cell culture, depends upon a set of procedures to reduce the probability of contamination from these sources

Nuffield Foundation — indefinite article (implied by use of ‘any’)

There are some general rules to follow for any aseptic technique.

ANTT — definite article used in reference to a specific named technique

Aseptic technique is the most commonly performed infection prevention procedure in healthcare; it is also probably the most critical. This article looks at the Aseptic Non Touch Technique (ANTT) model for reducing healthcare-associated infections

(You could argue that the definite article refers to the model, rather than the technique, although I think if you omitted ‘model’ you would be left with an example like the Haemlich manoeuvre. In any case the English in this article is appalling — “infection prevention procedure” gives a foretaste of the stylistic horrors that follow.)


text:
Why do plants flower in different seasons?
I know how it is controlled (photoperiodism), but I wonder why all plants don't start to flower in spring? Is it connected with ecological niche?

This is a really big question, related to niche, evolutionary history, life history, and coevolved species (pollinators, seed dispersers etc). Among many other things.

Plants all have a strategy which takes advantage of their physological strengths and habits, and the time taken to grow fruit and seed. i.e. the first to flower have better cold resistance and can take advantage of the understory before the trees have leaves, and many, many other "strategies and physiological differences" https://en.wikipedia.org/wiki/Plant_strategies ... http://bio.rutgers.edu/~gb102/lab_13/13i2m.html

Why plants evolve to flower at various times depends on several factors. I've taken these from the book chapter Kudo 2006.
1) Climate and other abiotic conditions.
Spring, and the onset of consistent above freezing temperatures, is the first opportunity for many plants to flower, but it may not be ideal for all. For example some locations are still very dry in the spring and plants require water from rain later in the year.
Late frosts, which can damage flowers, is always a risk. Some plants can suffer the occasional frost and loss of flowers, while others hedge against this by flowering later.
2) Pollination competition.
For plants which are pollinated by animals (mainly insects), the finite amount of pollinators results in competition among plants for this resource. If all plants flowered at the same time competition would be extremely high, and no amount of animal pollinators could successfully visit every plant. Thus some plants have evolved to start flowering later in time and potentially have less competition. Note that other strategies to increase pollination from animals could also be to have larger and/or more numerous flowers.
3) Herbivory
Flowers eaten by animals are a waste of resources for the plant. For example if an insect preys heavily on flowers, and is most active during a certain part of the year, plants would evolve to flower outside of that time.
4) Seed maturation and dispersal
The ultimate purpose of flowers are to reproduce, and the timing of flowering can influence that. Plants with large fruit, such as berries, need ample time before winter to mature and this necessitates early flowering so that there is enough time for animals to disperse the fruit.
Constraints
There are many limitations to everything above, and if a plant species evolves one strategy it generally limits itself in other aspects. For example the very first plants to flower in temperate environments may have low competition for pollinators, but they also risk being damaged by late frosts. A viable strategy may be to flower throughout the spring and summer, which some plants do, but they can only grow in environments with year round resources and likely cannot produce large fruit which animals can eat and disperse. Plants which flower in late summer or autumn likely need large roots to store the water and energy to do this.

Kudo, G. (2006). Flowering phenologies of animal-pollinated plants: reproductive strategies and agents of selection. In L. D. Harder & S. C. H. Barrett (Eds.), Ecology and Evolution of Flowers (pp. 139–158).

To add a few reasons, in dry regions (e.g. Death Valley) there are ephemeral plants, which grow from seed to flower only after a rare rain.  Or in deciduous forests, understory plants grow & flower in the early spring, before the trees leaf out and block the light.


text:
Why do hair on head not get pilo-erected?
Whenever we have "goosebumps", there is a momentary piloerection, due to which hair on our elbows and legs get "erected" and "stand" almost perpendicular to the surface of our skin. But why do our "head hair" not get erected ?

This seems to also be true  about facial hair and pubic hair

Piloerection of head hair does happen as often as it occurs elsewhere on the body, but head hair length tends to make it difficult to see. Close observation, especially with short hair, should make it visible.
Piloerection of head hair is something more commonly felt by the person it is happening to rather than seen by others (or in mirrors); when you get that "goose-bump" sensation across your scalp, that will be due to pilo-erection.
(PS added) I haven't provided citations - this is not a phenomena that has had much specific academic research and I have not found any stating it occurs - or stating it does not occur (except in association with balness) despite looking, but is almost universally experienced, often without close examination or reflection about what specifically happens.
Citing references for baldness resulting in absence of piloerection on the scalp is not quite the same as a reference specifically stating it happens, but ... Professor Rodney Sinclair, head of dermatology at the University of Melbourne says - “You can’t get goose bumps on the scalp when you go bald and you can’t regrow hairs either because the follicles can’t regenerate.” ( https://www.futurity.org/goose-bump-muscle-1324242-2/ ) ( https://link.springer.com/article/10.1007%2Fs12565-016-0359-5 )

Many sources say that it does.  See the word "horripilation", for instance.  Or no less an authority than Shakespeare, who tells us
I could a tale unfold whose lightest word
Would harrow up thy soul, freeze thy young blood,
Make thy two eyes, like stars, start from their spheres,
Thy knotted and combined locks to part
And each particular hair to stand on end,
Like quills upon the fretful porpentine

(For those unfamiliar with English Literature, the source is William Shakespeare's play "The Tragedy of Hamlet, Prince of Denmark", Act I, scene 5, lines 15-20, first performed ca 1602, and published in various versions between 1603 and 1623: https://en.wikipedia.org/wiki/Hamlet )

I find Shakespeare a respectable, yet a non-scientific source.


text:
Why oldest trees are all around 4k years old?
In christianity stackexchange I saw someone discussing young earth creationism.
One of the evidence they show is that the oldest tree, if measured by ring counts, are around 4k years.
Which, according to YEC, correspond to the Noah's flood.
Yes there are trees that are 10k years old. However, YEC doesn't believe in carbon dating. I wonder what ring counts do those tree have.
Is there any other reasonable explanation why oldest trees are 4k years old besides some massive catastrophe to all trees 4k years ago?

You might be interested in this.

Actually,   the oldest trees  are  almost 5000  years old. See here

You could argue on the same grounds that the world is only 200 years old. After all, there are no 200 year old people! What they are missing is that trees have natural lifespans too.

You can also use dendrochronology, matching ring patterns in the oldest parts of living wood to dead wood to extend the record back past 10,000 years: https://en.wikipedia.org/wiki/Dendrochronology  Also, if those old trees are supposed to have been around "forever", why do they produce seeds?


text:
Why is the origin (patient zero) required to cure a virus?
I'm not sure if it's just a movies thing but I always notice that the original strain of a virus is required to cure a virus, why is this? is this even true?

Nope. This is a total movie fallacy/exaggeration.
How worthwhile it would be to isolate the original strain is debatable, but certainly not necessary for vaccinology purposes.
On one hand, the inital strain might be interesting to study if its an aetiological agent which has never caused human disease before. It would be the first 'snapshot' of the genomics/transcriptomics of an organism/agent which has been able to jump a species barrier perhaps, or has evolved to survive at our body temperature, evade our immunity and so on.
However, as the infection progresses through a population, in order for it to stay infectious, it must by definition have maintained the molecular patterns that permitted it in the first place, so isolation of the 'zero-th', 10th or even 10,000th infection shouldn't make any real difference from a therapeutic standpoint. It may even be the case that as subsequent infection has in effect, passaged, the organism, that the later strains may even be more dangerous than the initial one.

Oddly enough, we were discussing this at a tea break the other day (I work in a research institute that does a lot of vaccine development).
Firstly (as the other answer notes) this is a complete fallacy, but useful for dramatic purposes. It's basically a "MacGuffin" or "plot coupon".
Secondly, disease-causing agents evolve as they spread. This actually occurs pretty quickly, both because pathogens generally have short lifespans and because our immune systems are adaptive, and "learn" how to fight pathogens they encounter, so they need to adapt to evade that response (continually). This results in what is often called a coevolutionary "arms race" and is why for instance you need to get a flu shot every year.
Mutations may also affect other traits, such as how a pathogen spreads - a well-known example is the appearance of the E1-A226V mutation in chikungunya virus which allowed it to be spread by a different mosquito species.
Lastly, there can be changes that do not affect the ability of a pathogen to spread or to fight the host immune system; for example every time a population passes through a "bottleneck" (for instance if the agent is introduced to a new continent by a single infected air traveller) the new region is populated exclusively by descendants of that small population, and will reflect its genetic makeup.
Now, going right back up to the top you might have already spotted the problem here. Vaccines expose your immune system to a less dangerous (chemically inactivated, thermally inactivated, or otherwise attenuated) form of a pathogen or parts of the pathogen (such as its outer coat) to allow your immune system to recognise it while not actively being under attack. If the vaccine is made from an old strain of the pathogen - let's say, last year's flu - your immune system might learn how to fight last year's flu but won't be equipped to fight this year's.
As the other answer notes there could be research value in having a sample of the original strain (for instance, it might be easier to prove where it came from), but it's much less useful for vaccine development than the latest version.
(We also discussed the frequent fallacies that vaccines are effective within seconds, or work if you already have a disease, but those are separate questions...)


text:
Calculating chromosome number in meiosis: Why is the crossbreed between a fox and a dog (dox) sterile?
Given the following example/question (originally found here):

I worked out the haploid number of the dox to be 29 and the diploid number of the dox to be 58. 58 is an even number, so surely 29 homologous pairs of chromosomes can form for the dox to be fertile. Why is it sterile?
Thanks

Please add the original question as a text and not as an image. Moreover, the image is also not posted in SE and any user has to go to an external site.

I would rework the the title of your question as in its current form it doesn't properly reflect the content of your question.

This is not simply a question of math, just determining if the diploid number is even or odd. If it was that easy, all hybrids with an even diploid number would be fertile, and that doesn't happen. The problem is way more complex, and it has to do with chromosome pairing.
In the question described, we have the following numbers:

Canis lupus (dog): 2N = 78, therefore N = 39;
Vulpes vulpes (fox): 2N = 38, therefore N = 19;

Now, let's suppose, in an exaggerated simplification, that all 19 chromosomes in the fox's gamete find an exact homologous in the dog's gamete (again, this is very unlikely). So, in this oversimplified scenario, we would have 19 pairs of homologous chromosomes in the hybrid's cells.
However, even if that's the case, we still have 20 chromosomes in the dog's gamete that didn't find any homologue in the fox's gamete.
That mismatch, alone, is enough to block meiosis, particularly at the pachitene checkpoint.


text:
Why does V. cholerae produce a human specific choleragen?
V. cholerae secrete choleragen to grow and escape human intestines, however choleragen does not work on other mammals, why so? Why didn't it evolve a general mammal affecting choleragen? This question is a continuation of the last comment on the only answer for my previous question, How does Vibrio cholerae benefit from infecting its host? Kindly refer to the answer and comments in that question as well.

Vibrio cholerae originated in the Sundarbans, a very large wetland at the mouth of the Bay of Bengal. Although it can exist as free living, it is much more fecund when associated with tiny crustaceans called copepods. In 1760, the East India Company settled and sprawled, hewing the mangroves and planting rice. So, that was the first opportunity of note introducing V. cholerae to a major species of land animal, humans. The frequent contact with a sizable population of humans, plus time, allowed V. cholerae to evolve the traits to become a parasite.
For example, a hair-like filament evolved which allowed the cells to clump together forming colonies that could stick to the gut. At that point, perhaps with additional traits, V. cholerae became a zoonosis. That is, a disease we acquire from animals, copepods in this case, but not directly from other humans. Further evolution over time gave it the traits to spread directly between humans making it a true human pathogen.
So, humans were the species that became available and V. cholerae evolved to take advantage.
This is a minute fraction of the whole story as related in the 2016 book Pandemic by Sonia Shah. She is a science writer, the book is extremely well referenced. Since this is your second question on this, I suspect you may well be interested in the book.


text:
phylogenetics and substitution ratios for positive selection
So very new to phylogenetics!. I've been scrambling and reading so much to get this done!!.
I would like to see if one or more of the sequences I have (from a gene family) are under positive selection using the dN/dS ratio. The conceptual parts are clear to me, however, practically speaking i have found several problems/questions along the way.
My most important question would be: I have four related organisms (insects), and their full sets of genes in a gene family. I have reconstructed trees to delineate their evolutionary story (duplications and losses). What would be the input for the calculation of dN/dS ratios when a single gene has several possible orthologs in the other organisms?, like gene A in species 1 has gene B and C and D in species 2 and E, F, G, H in species 3 etc... Do I need to align only the orthologs for each species? all of them?, or just align all the sequences form the subfamily including all paralogs and orthologs?, wouldnt that overestimate the ratio?
I have tried PAML yn00 package and got a result for a small "test" set of sequences, which were not codon aligned. Results are pairwise, how can I interpret this?, do I want to get "overall" omega values instead of pairwise? what would be the most interpretation on each case?
Second question is how I get codon alignments for these sequences?. I saw a couple of free software on th internet but they wouldn't work.
thanks a lot!


text:
Why do we see a different color when we mix two colors?
The compounds responsible for a color do not change when they are mixed with another material. The same compounds are there after mixing. However, when we mix colors such as blue and yellow we see green.
BUT we are able to tell where a color starts and ends in pictures. For example, if we hold a yellow piece of paper up to the sky, we can tell that the paper is yellow and the sky is blue. We can distinguish where the paper ends. And where the sky starts. We do not see a green outline near the paper.
I believe that  how we perceive colors may explain this. But I am not sure how. Is it because how the brain integrates information. Or is it because of how the cones cannot register two signals at the same time. Why do we see green instead of a blue and yellow?

Assuming you're correct (and I'm not sure you are), most likely because of the size of the particles mixed is too small to differentiate with the naked eye. Consider: Mix blue and yellow M&Ms and you'll have no trouble distinguishing the colors. Keep halving their size (pretend there's no chocolate) and at some point, the whole group will look green. They'd have to be quite small, though.

Are you asking why eyes don't have microscopic resolution or how color vision works?

I don't seem to understand the question either. Could you be more specific?

@John  I am asking whether it is the inability of microscopic resolution that makes us see a different color when two colors are mixed OR whether it is how color vision works that makes us see a different color OR something else.

well it depends on whether you are talking about mixing pigments or light. For pigments it is basically resolution. for light is how we see color. here is a great ted talk about color vision research. http://www.ted.com/talks/beau_lotto_optical_illusions_show_how_we_see

I am not sure if this is entirely correct, its just a scientific guess. But it might actually play some role in this phenomenon. This is actually the physics part part of answer rather than the biology part.
Rayleigh criterion for angular resolution is the minimum angle which two bodies should subtend on an object so that they can be viewed as distinct bodies by that object.

Suppose there are 2 bodies, (right now) with same color of wavelength $\lambda$. Now, they are viewed from a lens of aperture $d$. Thus, from Rayleigh's equation, the minimum angle which these bodies should subtend with each other on the lens is given by:
$\theta = 1.22 \lambda/d$
Now I'm not sure if this is correct, but if the 2 bodies have different colors, of wavelengths $\lambda_1$ and $\lambda_2$ then the equation becomes:
$\theta = 1.22\times (\lambda_2 - \lambda_1)/d$
$\theta = 1.22 \times \Delta\lambda/d$
Now, putting values in this equation:
$\lambda_2 = 597 nm$
$\lambda_1 = 492 nm$
$d = 5 mm = 5 \times 10^{-3} m$
Answer comes out as:
$\theta = \underline{1.22 \times 105 \times 10^{-9}}$
$\hspace{15mm}5 \times 10^{-3}$
$\theta = 2.56 \times 10^{-5} rad = 1.4 6\times 10^{-3\circ}$
So, if these 2 bodies subtend an angle less than $2.56\times10^{-5}$ radian, then they will appear as a single object with green color.
Now, solving it by a common formula:
$\theta = a/l$
$l = a/\theta$
$l = \underline{\hspace{7mm}10^{-2}\hspace{7mm}}$
$\hspace{8mm}2.56 \times 10^{-5}$
$l = 390.625 m$
It means if yould hold two 5 cm x 2 cm papers together (i.e. total 10 cm2), one with blue color and the other with yellow color, then you would see a single paper of green color if you keep these papers $\approx$391 m away (if my calculations are correct ;).
This, in part, explains that it is not the fault of only our eyes, but of light and physical laws too.
References:

Angular resolution
Wavelengths of different colors
Resolving power of imaging instruments

The geometry part at the end with theta = a / L ...  is not clear. From the  figure it should be tan (theta) = a/2 / L, to be precise.  But I guess theta = a/2 / L is a good approximation since the angle is so small.

@Roland I don't understand that one, why would it be  a/2? If you take the eye at origin and bottom line at x-axis, then $\theta$ has to be a/l. I suppose a/2l would give $\theta/2$.

My mistake. I read the figure wrong, you're right.


text:
How do birds decide which branch to land on?
What factors do they weigh on? Shape, position of branch within the tree body/structure, fatigue, nearness to current position, etc.
And how fast does a bird's brain and nervous system decide on this?
Narrowing it down to a bird of prey, say the Harpy Eagle.

I think that the question is too broad. There are over 10000 species of birds and the majority of them uses branches to perch. The reasons/ motivation can be so many that your question should be targeted to more specific situation to be able to provide an answer.

I agree it is fairly broad question, but, nevertheless, I'm sure the OP would benefit from a brief discussion (or the very least a list of potential sources to read) examining/reflecting on this question for any species. I wonder myself if anyone has tried to model/determine these behaviors. I vote to keep this question open.

@theforestecologist thanks for the upvote. I understand that the question is too broad in a sense. But my question was directed towards the basic premises of a bird's cognitive decision making. Let me narrow it down to a certain species within the wide classification of birds of prey in that case.

Btw, I found this for a start.
http://asifg.mycpanel.princeton.edu/publications/pdfs/TeufelGhazanfarFischer2010.pdf


text:
RNA isolation- role of pH
Why does RNA alone go into the aqueous phase when treated with phenol-chloroform at lower pH? At a neutral or basic pH, both DNA and RNA would escape into the aqueous phase. So how is DNA held back at acidic pH?

Well, because it is more soluble in water than phenol. Are you asking why DNA does not separate into the aqueous phase at acidic pH?

I'm asking why it happens at low pH and not at neutral or basic pH

You should add that to your question or it may be closed.

RNA gets degraded in high pH.

The purpose of acid phenol extraction is to selectively retain RNA in the aqueous phase while DNA partitions to the organic phase or coalesces at the interphase. I have found many people on the internet say that this is due to protonation of DNA phosphates while RNA phosphates remain ionic, thus giving differing solubility. I do not buy this explanation because:

The pKa of the phosphodiester moiety is several orders of magnitude lower than the pH  used in acid phenol extractions, and so should be largely deprotonated.
Given their similar structures, the drastic difference in pKa between RNA and DNA required for it to be preparatively useful, to me, seems implausible.
I found no such claims in scientific literature.

The properties of DNA and RNA that come to mind and which may explain the differential solubility are:

DNA is denatured in acid due to protonation of the nucleobases, which imparts positive charge. This could facilitate aggregation.
DNA is generally longer.
RNA has a 2' hydroxyl group which increase polarity of the molecule.

Somewhat supporting this is a FAQ from ThermoFisher:

Partitioning of the nucleic acids in phenol is pH dependent. At pH 7.0 or higher, both DNA and RNA partition into the aqueous phase. At an acidic pH (below 7.0) DNA is denatured and will move into the organic phase, but the RNA remains in the aqueous phase.

The exact biophysics escape me. I realize this is not an answer but, rather, more of a long comment. I thought it important to address what, in my mind, may be a misconception. Criticisms are welcome.

But isn't RNA more unstable and hence get affected by low pH? What are the ionic interactions that keep them stable?

I understand that RNA is stable in acidic pH and DNA is stable at basic pH. But why is my question.

@user29995 The phosphodiester of both RNA and DNA are susceptible to acid catalyzed hydrolysis under strongly acidic conditions (ie pH < 1). RNA is less stable in basic solutions due to base catalyzed cleavage of the phosphodiester. RNA is more susceptible than DNA because, under basic conditions, the 2'-hydroxyl is deprotonated and the resulting 2'-alkoxide can nucleophilically attack the phosphodiester.

The main reason acid is used in RNA extraction is, as mentioned, to separate it from DNA and not to prevent hydrolysis.

In this case there are two properties that determine the behaviour of RNA:

Its polarity;
Its acidity.

Because of its polarity, RNA tends to escape the phenol-clorophorm phase; actually, it can go into the aqueous phase even if the pH is neutral [1], but with a lower efficiency than if the pH is acidic. Here comes the second property, RNA acidity. Because of that, when RNA is in a neutral solution, it has a negative charge: the $-OH$s of the phosphate group dissociate to $-O^-$ and $H^+$. However, this does not happen in an acidic solution, where there are already too many $H^+$. Thus, at basic pH the $-OH$ groups are intact and have a neutral charge; this stabilizes the system.
Think about it: if the aqueous phase is at neutral pH and fills up with negatively charged RNA molecules, after a while no more negative molecules can enter that solution. On the other hand, if the RNA molecules that enter the aqueous phase stay electrostatically neutral, the number of molecules which go into the solution will be limited only by the availability of water molecules to dissolve them.
That is why you use acidic* pH, it is simply a matter of efficiency.
Disclaimer: This answer is based upon a comment by the OP under the OQ.
[1] You would never use a high-pH solution to extract RNA because such condition hydrolyses RNA.