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What is the genetic difference between two cone branches?
As we can see on this larch, male and female cones are sometimes directed to grow on the opposite side of the branch. We were told in school that this mechanism works against self-fertilization. Also they flower in different times, so they are mostly fertilized from the other conifers.
When I saw this picture, I got that idea, that maybe they face the branches on above by design: To decrease the genetic uniformity at least a little.
But how important this effect actually is? And how big is the genetical difference between two branches? Are there any other factors taking effect in the tilt of the cones?

I don't understand your hypothesis. But the number of pairwise differences between two cells assuming neutrality ($\pi$) in the two different branches in $\pi = 2 \mu L t$, where $\mu$ is the somatic nucleotide mutation rate (around $10^{-11}$ on average), $L$ is the length of the sequence of interest (eventually the whole genome). $L$ can therefore be of the order of $10^9$. $t$ is the number of cell generation since the two cell lineages split. $t$ depends on the relative positions of the two branches but it could be $10^4$ cell generations. With these very quick approximations, we can estimate the number of pairwise differences as
$$\pi = 2 \mu L t \approx 2 \cdot 10^{-11} \cdot 10^9 \cdot 10^4 = 200$$

My hypothesis was it is a significantly better for the branch to be polynated from another branch than from the same branch, This number seems really huge if 2 is a significant genetic difference in Tajima's D, doesn't it? Question is, wheter this could play a role in the evolution of the branch structure.

This number should be verified with better estimates (typically the mitotic mutation rate might be way too high) should probably be compared to the number of pairwise differences in the population. The number of pairwise differences between two randomly sampled indivdiuals in the population is $2 N \mu$.

I am not sure why you are talking about Tajma's D. If I remember correctly (am too lazy to make the calculations now), Tajima's D compute a standardized comparison between the number of pairwise differences  number of segregating sites in a sample of size $k$ divided by $\sum_i^{k-1} \frac{1}{i}$ as both should equate under the infinite site model (coalescent theory).

Oh, sorry. But is it possible that this effect could play a role for example in the evolution of scape stem branching

Intuitively, I would think it is negligible but I am not sure.

Having separate male and female cones reduces self-fertilization just by the physical separation (the greater distance for pollen to travel gives pollen from a different tree a larger chance of successful fertilization).  A much larger effect is from the timing of flowering, since on an individual tree the female cones will be receptive at a time when the male cones on that tree are not releasing pollen.
Another reason for the different orientation of the cones is probably gravity.  The male cone, hanging downwards, can have its pollen fall out of the cone into the air where wind can transport it.  The female cone, pointing upwards, can capture settling pollen into its upward facing structures.


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Did not understand a small excerpt from a research paper
Was going through this paper, among multiple things that i did not understand, I came across this part:

Each amino acid residue of a single
  window was encoded into a unitary bit string of length 20, where a
  bit was set (value = 1) if its position in the string corresponds to the position of the amino acid residue and zero otherwise

Did not understand this line. Someone please explain what position they are talking about

The paper's description is poor, but they seem to be describing an encoding where each of 20 possible amino acids are associated with a position within a string of 20 bits, e.g. alanine with offset 0, cysteine with offset 1, etc.  With that representation, one amino acid residue within a window is encoded by a string of 20 bits, 19 of them being 0 and the other a 1; the single 1 bit occurring in the place corresponding to the residue.
This interpretation is supported by the paper's citation of  Qian N, Sejnowski TJ (1998) "Predicting the secondary structure of globular
proteins using neural network models." J Mol Biol 202: 865–884.  Qian's paper says:

Each group has 21 units, each unit representing 1 of the amino acids (or spacer). For a local encoding of the input sequence, 1 and only 1 input unit in each group, corresponding to the appropriate amino acid at each position, is given a value 1, and the rest are set to 0.

+1 good answer although do not agree with "The paper's description is poor" part. The sentence quoted in the OP's question seems confusing but reading the entire paragraph in the paper puts things into context nicely.

@ddiez, I did not mean to imply the paper was poor (or the surrounding paragraph), but that the quoted sentence did a poor job of describing the representation, which was essentially the sentence's only job. The surrounding paragraph I don't think makes up for that, although it does provide necessary context.  The problem is that nowhere does it convey that there is a defined bit position within the bit string for each kind of amino acid.  It says "corresponds to the position of the amino acid residue" where it would be better ...

(cont'd) if it said something like "is the one defined for that type of amino acid".  Once one understands the bit-for-residue-type representation, one might be able read the sentence as communicating something like that, but if one has not yet thought of that approach, the sentence does not put the idea across well (IMO).

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Why do birds move their heads abruptly?
When we humans look around, we pan smoothly from one side to the other. Birds on the other hand seem to point their head in one direction for a while, then abruptly point their head in another direction and stay in the new position for a while. Then they continue with the abrupt movement. Why is that?

Was exactly my question.

Most species of birds have 2 foveas, the temporal fovea and the central fovea.

temporal fovea, which is like ours in the sense that it looks straight
  ahead and offers binocular vision (i.e. the temporal foveas of both
  eyes point in the same direction). But birds also have a central
  fovea, which points sideways and is, obviously, monocular (i.e., the
  central foveas of both eyes look in opposite directions).

So the bird has a choice of which fovea it wants to look through.

It can look straight ahead with its temporal foveas, to the left with
  the central fovea of its left eye, or to the right with the central
  fovea of its right eye. And this is not a hypothetical possibility:
  Birds actually do switch between foveas all the time! This is why they
  tend to swing their heads erratically in turns of about 90° (reference).

Do you have any more references to back this up? An unreferenced answer from another Q/A site (Quora) can hardly be seen as a reliable source.

@fileunderwater changed the whole answer and added a proper reference. Hope that helps.

If the bird can look sideways,why move it's head at all?

Many birds, especially birds of prey and owls, have eyes that are proportionally much larger than that of similar-size mammals. Most birds are only capable of limited orbital movement, typically 10—20°, as with larger eyes there is little or no room for the required musculature.
This, in addition to having two foveae as @The Last Word mentioned, necessitates that a bird move its head to change viewing angle. The relatively rapid movement of a bird's head is analogous to that of the more subtle, but still rapid movement of your eye as you view different subjects within a frame of vision without moving your head.
Birds have more vertebrae (13-25) in their neck to provide additional flexibility, which provides for their quick head movements. Some birds, such as owls, can turn their head 270 degrees. Other birds have a wide field of vision because their eyes are located on the sides of their head. This degree of flexibility or field of vision provides birds with good compensation for being unable to move their eyes.
These characteristics, combined with the physiology of two fovea, make the abrupt, seemingly unusual movements of birds' heads more easily understood.
For additional insight, consider the book Bird Sense: What It's Like To Be a Bird by Tim Birkhead or Manual of Ornithology: Avian Structure and Function by Noble S. Proctor and Patrick J. Lynch; both of which I own and can recommend.

As i understand it:
Birds can't move their eyes around the way we can (excepting cormorants and maybe some others), and the result is that they don't have stereoscopic vision when they don't move their heads. More than that, their field of focus is very small if their heads are kept still. That last is also true for us.
The chickens we raised have their eyes even more on the sides than pigeons. They would look at us with one eye ---- then the other eye, then the first eye again, etcetera. This gave them a wider field of view and a stereoscopic view of us and their environment.
Try: Look at a letter somewhere near the center of your screen. Without moving your eyes or head, how many words can you make out up, down, left, right of your point of focus. If you can't move your eyeballs (as birds can't) you can only get the wider view by moving your head.
Plus, pigeons are prey animals and therefore have eyes on the sides of their heads which lets them see movement a lot further behind than we can. (https://en.wikipedia.org/wiki/Field_of_view) We have a horizontal field of view of about 210 degrees and "Pigeon FOV is around 340-degrees horizontal and about the same 135-vertical degrees as humans, but their vertical field is even more asymmetrically oriented toward the ground."(https://www.quora.com › What-does-a-pigeons-field-of-view-look-like)

"We" don't, always.  In addition to the factors in other answers, there's a simple matter of size and inertia at work.  If you look at small mammals like squirrels or mice (and presumably small monkeys, though I've never observed one for any length of time), you'll notice that ALL their movements seem to be quick and "jerky", because their heads and other limbs are small, and so have little inertia.  (It's a matter of scale that's not limited to animals.  Consider how small engines or fans can spin much faster than large ones - motorcycle vs diesel truck, computer cooling fan vs wind turbine, &c.)
Larger animals like humans (and dogs, horses, &c) CAN move their heads quite quickly, as when they're startled by something, but it takes effort and is rather uncomfortable.  (Try it!)  But virtually all familiar birds have small heads, though it'd be interesting to look at something like a pelican or toucan that has a large beak.

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Did the Great Oxygenation Event also cause a mass extinction?
It's usually assumed that the Great Oxidation Event around 2.3 billion years ago caused a great extinction of anaerobic life on earth. However, I was reading Nick Lane's book, The Vital Question, and he writes the following:

The 'oxygen holocaust', which supposedly wiped out most anaerobic
cells, can't be traced at all; there is no evidence from either
phylogenetics or geochemistry that such an extinction ever took place.
On the contrary, anaerobes prospered.

Is there really no evidence of such a mass extinction?

The proposed mass extinction due to Great Oxidation Event is actually an elucidation by scientists.
After reading many articles online, although there are evidences of GOE, every article states the extinction of most anaerobes as something that should have happened as a fact (Because $O_2$ is considered poisonous for obligate anaerobes). To better understand this, imagine if there was a spike in Carbon Monoxide in the atmosphere, for Oxygen dependent organisms like us, inhaling $CO$ is harmful and therefore a spike in $CO$ would be toxic and lead to death.
Here are some excerpts, which state the extinction of anaerobes being factual more than anything else:
From Arizona State University, Origins Project >>

In a relatively short amount of time, Earth went from having very
  little oxygen to what may be the highest levels of atmospheric oxygen
  it has ever had. This event had wiped out most of life on the planet
  to which the oxygen was poisonous. Some of these anaerobic organisms
  were though to have survived by burrowing into the earth where oxygen
  levels were survivable.

From Slate.com - Bad Astronomy Blog >>

At some point, though, as cyanobacteria flourished, the minerals and
  other sinks became saturated. They could no longer absorb the oxygen
  being produced. It built up in the water, in the air. To the other
  bacteria living in the ocean—anaerobic bacteria, remember—oxygen was
  toxic. The cyanobacteria were literally respiring poison.
A die-off began, a mass extinction killing countless species of
  bacteria. It was the Great Oxygenation Event.

From Imperial College London >>

The permanent introduction of oxygen into the atmosphere fundamentally
  changed the ecology of the planet. The first impact was on anaerobic
  organisms, which didn’t need oxygen to survive. The rise in oxygen
  levels was poisonous to them and led to most them becoming extinct.
  Some managed to survive, but they retreated deep into the subsurface
  where there is no oxygen.  This was one of the first mass extinctions
  in the history of our planet, and it was also the catalyst for the
  evolution of oxygen-based life – us!

As a result, based on what I have read so far, we really dont have any stone cold proof that rise in oxygen lead to mass extinction of anaerobes. The mass extinction is what scientists consider should have happened as we know $O_2$ is poisonous for strict anaerobes.


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What is the highest pressure at which plants can survive?
Inspired by this awesome question, I'm looking for the corresponding maximum: what is the highest air pressure at which plant life can survive?
For example, Venus's atmosphere is about 90x as dense as Earth's.  Aside from the other obvious factors, like sulphuric air and boiling temperatures and otherwise resembling hell in every possible way, can plant life survive in such a condition?
Additionally, are some types of plant life more adaptable to high pressure environments than others?  (I'm assuming an air environment, and excluding deep-sea life, etc.)

See Effect of very high pressure on life of plants and animals (2012).

Judging from the fact that all the living creatures we have examined, both animals (tardigrades and Artemia) and plants (Ptychomitrium, Venturiella and white clover) were alive after exposure to 7.5 GPa, it was suggested that most of the proteins of those creatures which unfolded at the early stage of the compression remain principally unchanged after exposure to the very high pressure of 7.5 GPa. It was also suggested that the unfolding of proteins was completely reversible up to 7.5 GPa.
The maximum hydrostatic pressure applied to all the living specimens investigated in the present experiments corresponds to that in the upper mantle, at the depth of 180 km from the surface of the earth.

So survival of plants at 75,000 times atmospheric pressure is possible. In this experiment the exposure times were 30 minutes and 1 hour for the plants and 13 hours for the animals.


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Doesn't meiosis form two pairs of similar cells and two pairs of opposite cells?
I am learning about meiosis in biology. I've learnt that the crossing-over in metaphase I only exchanges small portions of DNA at the tips of the chromosomes. Doesn't this mean that:

After meiosis I, there will be two cells that will be almost opposites (for each chromosome, if one cell has the mother's chromosome, then the other will have the father's chromosome), except for the parts where crossing-over happened
After meiosis II, each cell produced in meiosis I will produce two similar cells (the only differences will be where crossing over happened in one but not both of the chromatids)

This means that there would be a rare chance of two of the sperm cells produced by a single meiosis fertilizing two eggs, in which case we could have:

Almost-identical twins
Very different twins, which would have less than the normal 50% of DNA in common

Am I right about this?

Great question - I think there are two misconceptions in your question that are interfering with your understanding.
First, crossing-over occurring at just the "tips" is just for clarity in textbooks so you can easily follow the different pieces of chromosome.
Although crossover events tend to occur at particular sequences, these don't have to be at the tips. There can also be multiple crossovers on the same chromosome, or none at all. See this link for some estimates of recombination rates for different species.
Second, gamete diversity doesn't depend only on crossing-over during meiosis, it also depends on the incorporation of just a single chromosome from each pair. Humans, for example, have 23 pairs of chromosomes. There are therefore 2^23 = 8388608 different combinations of chromosomes - with NO crossing over! Therefore, even without recombination, the odds of two genetically identical sperm fertilizing two genetically identical eggs are incredibly small.

But doesn't this random splitting of homologous chromosomes only happen in meiosis I? If there was no crossing over, then each meiosis II would produce two identical gametes.

Even with no crossing over, each pair of chromosomes splits randomly, not according to parentage. Imagine you have only 4 chromosome pairs, where each pair has one from the Mother (M) and one from the Father (F) - note, these will eventually be the 'grandparents' after fertilization - they could split MMMM, MMMF, MMFM, MMFF, MFMM, MFMF, MFFM, MFFF, FMMM, FMMF, etc etc etc - a total of 2^4 = 16 possibilities. If you have 23 chromosome pairs, like, humans, it's over 8 million. And that is still with NO crossing over within the individual chromosomes.

Then you add in crossing over and suddenly not only is the segregation of homologous pairs random, but now the individual chromosomes are random too, and you get an incredible potential for diversity.


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Why do people perceive blood pressure as the force that moves the blood forwards (see details)?
For example "Veins contain a lot of valves because the blood pressure inside them is low.". This wouldn't make any sense unless if blood pressure was perceived as the force that drives the blood forwards. But in reality blood pressure is the force exerted by the blood on the inner walls of the blood vessels so can someone explain to me why low blood pressure results in increased likelihood of back flow of blood ?

In the vascular system, pressure is what moves blood forwards, at least in an analogous manner to voltage...just like voltage, pressure itself doesn't move things, but a pressure gradient does. You are correct that the pressure applies in all directions, but the resistance of the blood vessels means that the pressure can only be relieved by flowing in one direction: down the pressure gradient.
Although blood pressure is often medically reported at a single site(i.e., 120/80mmHg), this is only the pressure in the larger vessels. The pressure originates from the heart forcing blood out into the major arteries, and the compliance/elasticity of those vessels keeps a sort of "reservoir" just like a capacitor would in an electrical circuit. The pressure drops over time from systolic to diastolic as that reservoir drains out into the body.
Importantly, and most relevant to your question, blood pressure also drops significantly through space, through the arterioles and capillaries, down to near zero in the venous system:

(from https://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/APIINotes5%20cardiac_equations.htm)
This pressure drop occurs for the same reason that you get a voltage drop over a resistance in an electrical circuit: the rules of Ohm's law for electricity are analogous to the Poiseuille's Law for fluids.
Sidenote: there are some exceptions to the pressure drop over space in the arterial system because of hydrostatic pressure (i.e., the pressure from gravity, for example see this question, though the better answer is definitely not the accepted one or the one with the most up-votes). However, that hydrostatic pressure difference is offset by gravity in the same direction, so you can effectively ignore it. It is also much less significant once you get to the smallest vessels.
I'm not sure where you got the quote in your example:

Veins contain a lot of valves because the blood pressure inside them is low.

..but I would say this statement isn't really false, though it could be stated better and the full causation is missing. Veins use valves because a lot of the pressure in the veins is coming from muscle contractions that squeeze the vessels from the outside, not from a pressure wave caused by forced blood volume from the heart. Venous valves ensure that the flow caused by this external pressure travels in one direction.
The Wikipedia page on hemodynamics may be helpful, though I noticed some poor wording in a couple places; any physiology textbook from a major publisher should be a good reference as well.
For a more "ELI5" answer, if the concepts I discussed so far are foreign, try this: In the arteries, blood is moved because the heart fills the big vessels with lots of blood, and the only place it can go is through the vessels into the capillaries. However, because the capillaries are all so thin and skinny, it takes a lot of pressure to push through them, and all the pressure is lost by the time you get to the veins.
So how do we get blood back to the heart? Well, we could try a vacuum, and have the heart "suck" blood back the way it "pushes" out the other side. However, this would collapse the veins. You can suck through a plastic straw because its rigid, but if you make it less rigid, such as by crushing a section, when you suck it will collapse, and sucking harder won't help the situation. Not good!
Okay so it's better to pump, but all the vessels are so small it would be hard to have them each have their own pump. So instead, the veins go through and around various muscles, and when those muscles move, the veins get smushed. Imagine you have a hose full of water, and you jump in the center...oops! Water goes out both ends! Okay, what if you put your hand over one side? Now it only goes out the end you want. That's essentially what a valve does: only lets the flow go one way when things are squeezed. Then the blood stays in the next compartment and over time works its way back to the heart.

I am sorry to say this now ; I am just a high school student so there are some things which you mentioned that i have never heard of before. Hydrostatic pressure is an example. Also i never understood electricity so i wasnt able to understand your analogy. I was also supposed to write my quote in a better way ; "Veins contain lots of valves to prevent the back flow of blood. Blood is liable to flow back due to the low pressure inside the veins." So here it is. I am not understanding how  low pressure in a vein can cause a back flow of blood

I understood the pressure gradient thing but that itself raised another question. If the pressure in the capillaries is higher than the pressure in the veins and blood flows from areas of high pressure to areas of low pressure, why isnt the pressure difference alone enough to make the blood flow towards the heart ? Sorry for wasting your time.

@Sam19KY Try reading over my edits and see if that clarifies things at all. No problem being a high school student, your question is a good question for even college-level physiology. For your question about why the blood doesn't just flow back to the heart, it actually isn't as much of a problem to get blood back to the heart from things at it's level and above: the vein valves are most important in your legs and lower body, and in your arms if they are at your sides, but of course this all depends on posture so there are valves other places too.

@Sam19KY There is also the issue of flow rate with pressure; if you look in the graph, about 80% of the pressure is lost by the time you get to the venous side. At those pressures, you would need really big veins to move the same amount of blood that moved through the earlier stages (in fact, veins are bigger than related arteries), otherwise you would get pooling of blood in the veins. You can't get around this problem by just pressurizing the veins either, because that would slow the flow through the capillaries, so then you need more arterial pressure - hello hypertension!

@Sam19KY And about hydrostatic pressure... sounds fancy but it's all in the roots of the words: hydro, as in water, and static, as in not moving: the pressure that would be there if everything just held still, ignoring the flow. Hydrostatic pressure is the pressure you would feel at the bottom of a swimming pool or lake just from the weight of water above you. The blood in your legs feels the hydrostatic pressure of all the blood on top of it.

SO here is the thing : I got it but what i want to say is that the whole problem arose because i was overthinking it. I literally lost my reasoning skills as i did that and that was making me look stupid. I really should start dealing with my real problem which is overthinking everything. Thank you a lot for helping me.

@Sam19KY I am glad you are understanding better now, and yes sometimes it is possible to "overthink" something and miss a simpler solution, but please don't be so hard on yourself: you haven't lost any reasoning skills, you don't look stupid, and you don't have a problem. My advice is to try to enjoy learning and the complexities that come with it: the things I read in a textbook and "got" right away aren't the things that stick with me; instead, the problems that didn't make sense, were hard, or needed explanation are the opportunities to really understand something better.


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Why is blood pressure different in different parts of our blood vessels?
Why does it change throughout our circulatory system ?

Blood pressure changes throughout the circulatory system because the blood vessels (both veins and arteries) have different radius throughout the body. Also, the further you go from the heart, less pressure it will have. This is physics. Fluid Mechanics, specifically. Check out the Navier-Stokes for more insight on the subject. https://en.wikipedia.org/wiki/Fluid_mechanics#Fluid_dynamics https://www.boundless.com/biology/textbooks/boundless-biology-textbook/the-circulatory-system-40/blood-flow-and-blood-pressure-regulation-227/blood-pressure-855-12100/


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I am not understanding how water passes through root hair cells
Why do people say that water moves into the cell because the water concentration of the cell sap is low ? the cell sap is surrounded by a membrane so if any water moves into the cell it must be because the concentration of water in the cytoplasm is lower than the surroundings. I am thinking that water from the cytoplasm moves into the cell sap solution and as a result , the concentration of water in the cytoplasm decreases so water moves in from the surroundings.

Maybe people use a bad shortcut of what https://en.wikipedia.org/wiki/Osmosis is?


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What is the smallest difference in light wavelength that the human eye can detect?
Is there a lower limit to the difference in wavelength (colour) our eyes can detect? If so, is this consistent between individuals? Are there any other traits correlated with precise colour vision?

Here is an insane article that suggests that humans can't differentiate colors very well unless there are words for them... https://www.sciencealert.com/humans-didn-t-see-the-colour-blue-until-modern-times-evidence-science

The eye really on can sense 3 colors, or to be more precise it only has three types color sensitive each of which detects a large range of wavelengths with no way to distinguish between them within the same cone. We only determine color by the different levels of activation between the different cone cells. This means we need a lot of light to see color and our ability to detect differences in color really depend greatly on where on the visible spectrum that color falls.

As for more precise color vision. The greater the number of types of cones cells the more color sensitive the eye ,birds and reptiles can see far more colors than use becasue they have 4 types of color sensitive cells as opposed to the human 3. More widely spaces base colors will give greater sensitivity. This is why even among trichromats human color vision is poor becasue two of our base colors are close together and overlap greatly.  That is because humans (and primates) are secondarily trichromats, gaining a third base color from a recent mutation. wiki on the subject

Is there a lower limit to the difference in wavelength (colour) our eyes can detect?

The average human can detect differences in color as low a 1 nm depending on color subject to:

minimum spot size - "Mapping the Perceptual Grain of the Human Retina", by Wolf M. Harmening, William S. Tuten, Austin Roorda and Lawrence C. Sincich in the Journal of Neuroscience 16 April 2014, 34 (16) 5667-5677; DOI: https://doi.org/10.1523/JNEUROSCI.5191-13.2014
background color - "Sensations from a single M-cone depend on the activity of surrounding S-cones", by Brian P. Schmidt, Ramkumar Sabesan, William S. Tuten, Jay Neitz and Austin Roorda in Scientific Reports volume 8, Article number: 8561 (2018) DOI: https://dx.doi.org/10.1038%2Fs41598-018-26754-1
location of cone, proximity to blood vessels - "Selective Stimulation of Penumbral Cones Reveals Perception in the Shadow of Retinal Blood Vessels", by Manuel Spitschan, Geoffrey K. Aguirre, and David H. Brainard, in PLoS ONE 10(4):e0124328 (April 2015) DOI: https://doi.org/10.1371/journal.pone.0124328

The following graph shows the minimum and maximum discrimination values at various frequencies:

Figure 13. Mean wavelength discrimination curve. (From Davson, H., The Eye, vol 2. London, Academic Press, 1962)
Source: Color Perception by Michael Kalloniatis and Charles Luu

Source: Computation of Cone Fundamentals (Color Matching Functions) in Terms of Energy for Various Field Sizes and Ages Based on CIE 170-1, Spreadsheet Prepared By Mark Fairchild (mdf@cis.rit.edu), RIT Munsell Color Science Laboratory (mcsl.rit.edu), from Rochester Institute of Technology, Program of Color Science: Useful Color Data.

If so, is this consistent between individuals?

No.

Individual variations in photopic sensitivity
Results for 52 individuals, based on heterochromatic step by step brightness matching; "The visibility of radiant energy" Gibson, Tyndall and Kasson (1923)
A newer study, "Individual Differences in Scotopic Visual Acuity and Contrast Sensitivity: Genetic and Non-Genetic Influences" (Feb 17 2016), by Alex J. Bartholomew, Eleonora M. Lad, et al., PLoS One. 2016; 11(2): e0148192. DOI: 10.1371/journal.pone.0148192
PMCID: PMC4757445, offers a different variance plot (without nm):

Fig 1. Test-retest assessment. Four data sets are depicted: Visual acuity (left panel) and contrast sensitivity (right panel) at photopic luminance (green triangles, near top left and at scotopic luminance (blue discs, near bottom left). Result of the first test on the abscissa, second test on the ordinate. Grey 45°- line is the identity line, next to it the ± limits of agreement (photopic, dashed; scotopic, dotted). Visual acuity in logMAR units have an inverted scale, and contrast sensitivity is in logCSWeber units, meaning that better performance corresponds to the top right for both graphs. As expected, photopic measures of VA or CS are markedly better than scotopic ones. The 95% limits of agreement are remarkably similar. All in all, there is no marked deviation from a normal
distribution, and the reliability is good for the range measured.

Are there any other traits correlated with precise colour vision?

For your third question, above the one question per post limit, I'll offer these links (I may come back to this as time permits):
The website Handprint has these webpages:

Measuring Perceptual Discrimination
Individual Differences in Color Experience
Color and Language

See also:

"Color naming across languages reflects color use", by Edward Gibson, Richard Futrell, Julian Jara-Ettinger, Kyle Mahowald, Leon Bergen, Sivalogeswaran Ratnasingam, Mitchell Gibson, Steven T. Piantadosi, and Bevil R. Conway in PNAS October 3, 2017 114 (40) 10785-10790; first published September 18, 2017 https://doi.org/10.1073/pnas.1619666114
Human Color Vision
Teach the Correct Color Theory in School

Briefly: Precise color perception is not only the capability of the eye but the training of the brain (seeing different similar colors and having a need to differentiate between them) and the teaching of the vocabulary, the learning of the differences, and learned application of this in practice.

I am unable to answer the first question.
But yes, there is an upper ad lower limit to what frequency of light the human eye can detect. This is why you cannot see microwaves, infra-red, ultraviolet or gamma rays. Given the light cones humans have, the limits is consistent within the species. However given that the exact number of each light cone (red, blue, green) varies between individuals, sensitivity to a particular colour will vary between individuals. So both of us can see blue. But my blue maybe bluer than yours.
Should be noted that there are two variants of the green light cone in the human population. One has a sensitivity that is slighted to the red. And the gene for the green light cone is on the X chromosome. So about 2-3% of the women in the world have both variants and thus better colour discrimination.
https://en.wikipedia.org/wiki/Tetrachromacy
PS: Yes.. there are colour blind people. And if you include colour blind people then there are some people who have a narrower range of colour perception than most of the human population.

The question asked about the smallest difference in wacelength, not about the wavelength bounds of the parts of the EM spectrum visible to humans.

First, it depends a lot of the brightness. And also, of the part of the spectrum: we have high accuracy between red-green (since 2 of the cone have close sensitiveness), and very few in deep red and violet (were mostly a single cone reacts).
As always, you do have differences between individuals. Small ones, + big ones related to the variations in cone peak sensitiveness (or missing or extra cone).
In addition, it seems that there is a cultural factor: some cultures are more trained to pay attention to differences within blues, or reds, or greys.

that is a good point.. I recall reading an about an idea in psychology.. if you have a name, a word for  a thing, you can more easily recognize it and distinguish it. So if your language/cultue has more words for the different shades of blue, you are better able to recognize those shades. (Other examples include types of snow, clouds and  waves)

About 2 nm wavelength difference. The human eye can detect about 150 different hues in a rainbow, which for us consists of a visible light 380-700nm. About 300nm/150hues = 2nm per smallest detectable difference between two hues. I guess that's the answer you were looking for?

Welcome. Can you add sources to your claims?

Yes I can but why should I? There are many sources on the internet claiming the hue discrimination skills of normal and color deficient vision. It's a well known fact. The average is about 2nm in cyan-orange range, while at the ends of the spectrum (violet-blue and orange-red) it starts to decrease toward 10+nm for each hue to be discerned.

Because it's the convention of this site, that's why. -1


text:
What is the difference between alarmones and riboswitches
An Alarmone is an intracellular signal molecule that is produced due to harsh environmental factors. They regulate the gene expression at transcription level. A riboswitch is a regulatory segment of a messenger RNA molecule that binds a small molecule, resulting in a change in production of the proteins encoded by the mRNA, it works as a way to sense eviromental changes.
I've been reading some papers ("ZTP 5-Amino 4-lmidazole Carboxamide Riboside
S-Triphosphate): A Proposed Alarmone for 1O-Formyl-Tetrahydrofolate  Deficiency" , Bochner 1982; "An Ancient Riboswitch Class in Bacteria Regulates Purine Biosynthesis and One-Carbon Metabolism" Kim 2015) which study how ZTP can bring changes upon 10f-THF deficiency. Bochner (1982) through several experiments proposes ZTP as an alarmone for 10f-THF; some assumptions of Bochner might not have been entirely correct and a later paper fails to replicate some experiments. Later Kim (2015) propose ZTP as a riboswitch.
I'm not fully aware of the differences between the concept of "alarmone" and "riboswitch". Seems to me that both Bochner and Kim propose virtually the same thesis.

I don't really consider myself qualified to answer, but sounds to me like alarmone is a functional category whereas riboswitch is a structural category. Thus, they're not mutually exclusive - a riboswitch can act as an alarmone but not all riboswitches do, and vice versa an alarmone might be a riboswitch but not all alarmones are. At least that's my impression.

Your first paragraph answers it!

First time I actually hear the word alarmone so bear with me okay?
"An Alarmone is an intracellular signal molecule that is produced due to harsh environmental factors. They regulate the gene expression at transcription level" <- this probably refers to activating/inhibiting transcription factors and stuff like that. Looking at bit further into the wikipedia article from whence you copied the description, we see that ppGpp is considered an alarmone.
According to the wikipedia article on ppGpp (https://en.wikipedia.org/wiki/Guanosine_pentaphosphate) we see e.g. this line "When (p)ppGpp associates with the promoter it affects the RNA polymerase enzyme's ability to bind and initiate transcription", so this alarmone can act by inhibiting RNA polymerase's ability to bind to the promoter.
A riboswitch on the other hand is a structural element INSIDE an RNA molecule that causes a conformational change upon binding a ligand. This conformational change then has an effect on transcription or translation etc. Thus, an alarmone could probably bind to a riboswitch to exert its effect, but a riboswitch is a quite specific thing.
You can read about some of the mechanisms in the wikipedia article https://en.wikipedia.org/wiki/Riboswitch
So basically, think of alarmones as signalling molecules and riboswitches as structural elements in transcripts that regulate gene expression upon ligand binding.


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What's the real meaning of "brain shrinkage"?
It is known that some pathologies cause brain shrinkage, for example, it is said that depression causes shrinkage in the hippocampus.
My problem to understand the statement, is that I don't undestand exactly how a brain region shrinks, or what they mean when they say that some pathology causes a brain region to shrink. Does the neurons and everything in them become smaller? Do the cellular membranes become shrink somehow and make the intracellular space smaller? or is it just that a large part of neurons stop firing and they say the brain has "shrinked" because the activity region has become smaller.
Basically, I want to know what happens or what is required in order to have a brain region shrink.

You are trying to get a specific mechanical answer for an observational descriptor that can have multiple mechanisms. Imagine asking the same question about the phrase " tissue damage" There is no single mechanical cause. the brain or an area of the brain is smaller than it was prior, that can have many causes, especially given many contextual uses.

Brain shrinkage = brain atrophy, which means a decrease in volume of the brain tissue, which involves different types of degeneration on the cellular level.
Here is a Wikipedia article about cerebral atrophy with a list of ~30 causes, such as Alzheimer's disease, stroke, cerebral palsy, malnutrition, AIDS, etc. Mechanisms can involve: loss of cytoplasmatic proteins, loss of complete neurons or connections between them, etc.
Alcohol consumption and frontal lobe shrinkage: study of 1432 non-alcoholic subjects (BMJ):

The brain tends to shrink physiologically with age. Heavy alcohol
  consumption seems to exaggerate this shrinkage in social drinkers.
  Moderate alcohol consumption does not seem to affect brain volume.

Vitamin B12, cognition, and brain MRI measures (Neurology):

Methylmalonate, a specific marker of B12 deficiency, may affect
  cognition by reducing total brain volume...

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


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What are "feeder cells"?
What exactly are "feeder cells"? A paper I'm reading says they harvested the cells and then plated them onto feeder cells. What is the purpose? Is in order to promote growth?

Cultures of growth-arrested feeder cells have been used for years to promote cell proliferation, particularly with low-density inocula. Basically, feeder cells consist in a layer of cells unable to divide, which provides extracellular secretions to help another cell to proliferate.

From this paper's abstract:
Feeder Layer Cell Actions and Applications


text:
Congenital deafness: can cochlear implants always improve hearing at any age?
People with congenital deafness may acquire a cochlear implant at a later age and be able to hear. Given that it seems there is a curve for synaptic plasticity of different circuits:

(1) Cochlear implants are used in older children (age 3-8) with moderate success. How can we explain the fact that they developed hearing despite not receiving any auditory stimulus in early age?
(2) Can auditory circuits be formed at any age, or is there an age in which the use of a cochlear implants will not be useful anymore?


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Triune brain model
I have heard about the triune brain model in biology class, but my teacher does not know much about it. What I'm curious about, is this model accepted by most of the neuroscientists, or is it just a mere hypothesis? And should I learn more about it? Although I think it's an interesting topic, I won't put efforts in finding all the info on the net, if not necessary.


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Does Science Say That We Should Die?
Excluding situations where you die from accidents, the main reason for death is -generaly- diseases.
And usually it is about an organ which becomes "tired" after many years. These results are all from experience and statistics:

But I've never heard of any study that said: "people can't live longer than x age because the heart can't live longer than that".
From my point of view, I think it's us who control the way we live and consequently someone can live longer than the other. For example, smokers die at an early age.
But even the oldest person in the world, lived for 122 years and 164 days. For me this isn't enough. It seems that someone can't control his age after all.
Basically my question is: Does science provide any limit that a person isn't able to live more than it? For instance can someone live more than 1000 years?

Note: I don't think someone is able to do this because simply even our healthiest habits are not "so" healthy. But imagine someone who doesn't live like any of us as humans, i.e. Can have a very healthy and natural life

Quoting a great biologist Peter Medawar :

It is by no means difficult to imagine a genetic endowment which can
  favor young animals only at the expense of their elders; or rather at
  their own expense when they, themselves, grow old. A gene or
  combination of genes that promotes this state of affairs will, under
  certain numerically definable conditions, spread throughout a
  population simply because the younger animals it favors have, as a
  group, a relatively large contribution to make to the ancestry of the
  future population.

From Why We Get Sick :

Imagine that there is a gene that changes calcium metabolism so that
  bone heals faster, but the same gene also causes slow and steady
  calcium deposition in the arteries. Such a gene might well be selected
  for, because many individuals will benefit from its advantages in
  youth, while few will live long enough to experience the disadvantage
  of arterial disease in old age. Even if the gene caused everyone to
  die by age 100, it would still spread if it offered even minor
  benefits in youth. This argument does not depend on the prior
  existence of senescence. Other causes of death—accidents, pneumonia,
  and all the rest—are sufficient to reduce the population at older
  ages. Nor does the theory depend, like Haldane’s, on cessation of
  reproduction.

The message I am trying to get across is that - As organisms are like vehicles which carry DNA and DNA just "madly" wants to replicate itself and pass itself from generation to generation, Natural Selection will favour those traits that maximise reproductive success. These may be traits that provide maximum benefit in youth but cause gradual damage and lead to senescence and death.
You could also think like this - Every machine has wear and tear and must be thrown away after it is irreparable. Same is with our body, it is the most beautiful machine in the world but it is also subject to the same wear and tear.
Also there is the end replication problem. See telomeres if you dont know what I am talking about. There is a limit to number of times a cell can divide.
So all in all I would say that there is a biological limit - a certain age up to which a person may live.

If you want more examples of such traits see this where the chapter on  ageing from the book Why We Get Sick is available.


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If not intelligent design, what is an alternative scientific theory to evolution?
In the popular culture, Intelligent Design is often portrayed as trying to be an alternate theory to evolution.  However, as the following question points out, it is not scientific, and so cannot be an alternative theory.
What is the viability of Intelligent Design as a supplement to chemical abiogenesis and Darwinian Evolution?
But, this also puts evolution in a tight spot.  Science progresses by competing theories.  Yet, there is no competing theory to evolution as a whole, only variations within the theory (e.g. Neo-Darwinism vs Punctuated Equilibrium).  So, if there are no scientific alternatives to evolution, does that make it unscientific as well?  If there are no proposed alternatives, how do we know evolution got it right?  And finally, what would a non-ID alternative to evolution look like?
Full disclosure: I am quite interested in ID, and do believe it is scientific and testable, but that is not what I am addressing with this question.
UPDATE: For those downvoting this question, how do you suggest I improve it?  Is it not a valid question?
To use an evolutionary analogy, without a diversity of theories our understanding of where we came from will not evolve and remain fit.  Shouldn't evolutionary theory apply to evolutionary theory itself?

I am quite interested in ID, and do believe it is scientific and testable : How do you propose to test it ?

That's material for another question.  Does it interest you?

No. It doesn't interest me- I think it is a deliberate neo-creationist approach. With a premise that is based on religious belief, no test can be unbiased.
Why downvote: Evolution is an active field of research. You should read about it (not necessarily too deeply) and understand its principles before proposing a new theory or to test the validity of a theory that lacks a scientific premise.

Shouldn't evolutionary theory apply to evolutionary theory itself?: Hmm.. That's what research is :)

There have been alternatives, but they're all silly and ridiculous and were quickly debunked.

Too long for a comment: You have a misconception about scientific theories: They are not competing what is wrong or right. They are set up, tested, corrected if necessary or discarded if they can not be proven. Science (or more Scientists) has no problem with rejecting a theory when no other is available. There are always things which can not be explained with the current knowledge, but this is the way this process works. And scientists have no problems admitting this.
BTW: It is not theoretical because it is called a theory. Darwin's theory has been proven quite a number of times and works pretty well - but it has its limitations because of findings he couldn't know of, but this doesn't make it wrong. It is a bit like Newton's theory of gravity and Einstein's general theory of relativity. The first cannot explain certain phenomena that the later can, which doesn't make Newton wrong.
The other thing is, that ID is in fact no scientific theory. A theory makes a prediction, has some foundation on earlier work and can be falsified/proven. It will be corrected if it has minor loopholes and discarded if completely incorrect (For example, see Lamarck's theory of evolution, that was once discarded but is being revisited in the light of the recently discovered phenomenon of transgenerational epigenetic inheritance).
ID is built just on beliefs and is nothing but a refined form of creationism; it doesn't make predictions and can not be falsified or tested (because it is just a belief). This makes it completely unscientific.

Well, if we don't have any alternatives, how do we know we have the right theory?  For example, see Popper: http://en.wikipedia.org/wiki/Conjectures_and_Refutations  All other fields of science would be nowhere without being put up against alternative theories and refuting them.

Darwinism and Lamarckism are both different evolutionary mechanisms.

Additionally, even in the case you mention it is debatable that Darwinism has completely won out over Lamarckism.  For example, see the Baldwin effect.

@yters. there is no war between Darwinists and Lamarckists and there are no fanatic groups that support either of these so called factions. Darwin's theory fits in almost all situations. The neo-Lamarckists are just evoking the term Lamarckism to generate some melodrama. Lamarck himself was not aware of transgenerational epigenetic inheritance. Darwin's theory was more complete than Lamarck's, when they were published. What we, as scientists, are trying to proceed towards is a more comprehensive and complete evolutionary theory- that will explain everything. ID is just a hindrance to this.

@yters A theory is not proven right but competition. It is proven more right when the theory is able to make prediction that matches reality. If the prediction of the theory does not match reality, the theory is wrong, it is either revised or discarded. It does not matter if there is competition. If two theories failed to predict reality, both theories are wrong and we have a situation where no known theory works.  There are no competitors to evolution theory, because nobody is able to create a theory that can encompass all known facts and make better predictions,

@yters there's no alternative to gravity therefore gravity isn't scientific by your logic.

@Praearcturus before the theory of gravity Aristotle claimed everything sought its rightful location in the universe.  Newton's theory worked better.

@yters okey then
https://en.wikipedia.org/wiki/Alternatives_to_evolution_by_natural_selection

@Praearcturus great, that's exactly what I am asking, what are the alternatives.  Your page and a bit of description about how they are alternative theories to evolution would be an acceptable answer to this question.

I try to avoid getting involved in these debates, but I feel the need to point out that if you are going to debate these issues you must make sure that you use terms correctly. Here is the first paragraph from the WP entry for Evolution:

Evolution is the change in the inherited characteristics of biological populations over successive generations. Evolutionary processes give rise to diversity at every level of biological organisation, including species, individual organisms and molecules such as DNA and proteins.

None of this is theoretical - it is observable. In my opinion the term Theory of Evolution is so broad as to be meaningless.

This is a good comment but I think when someone shows up and their first act is to set up a soap box they may not be in receiving mode. +1


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Does ale give less of a hangover than a lager?
I got into an argument surrounding beer type and hangover. Apparently there is a opinion that ales give you less hangover than lagers do (considering same alcohol content consumed).
My understanding is that a hangover is nothing more than dehydration caused by alcohol. More alcohol per unit of mass - more dehydration.
Is there any biological evidence to show that the same amount of alcohol consumed (with a different type of yeast) per same body mass would have different effects?

Is there evidence other than the assertions by the posters that they do in fact cause a greater hangover? The question cannot be answered if the effect does not in fact exist.

@MarchHo that is essentially what I am looking for, some scientific explanation (or thesis or source) that would confirm it or dismiss it.

Not a direct answer to ale vs. lager, but there certainly is evidence that different alcoholic beverage types have different hangover effects, although the effect size is probably small

@oreo I am not sure if that study would qualify since it is purely subjective. The researchers asked the participants how they feel. The same feeling in the bourbon drinker to the vodka drinker may have been rated weaker since we don't know if it is true or just different tolerances to discomfort. Maybe the vodka drinkers could handle discomfort better so rated all hang over effects weaker.

@dustin Yes, you're totally right about "Hangover Intensity" as  subjective measure, but the study that Wired refers to gave participants vodka vs. bourbon vs. placebo randomly, so I don't see any reason to think that tolerances to discomfort would be different among the subject groups.

@oreo it is like sensitivity to pain though. Some people are total fine when they receive a 2 inch laceration and others going into shock over the site of blood. With the alcohol drinkers, I would like to see the vodka drinkers be giving bourbon and the vice verse a. If they then say it isn't worse or is worse depending on the group, one could then say it is plausible that dark liquor is worse.


text:
Is there an evolutionary advantage associated with migraine?
I have read Wikipedia article on Genetics of migraine headaches and I don't buy it

Because genetics influence susceptibility to migraine, it can be
  shaped by evolution. Fitness-impairing disorders, including severe
  headache, tend to disappear as a result of natural selection, and
  their frequency decreases to near the rate of spontaneous
  mutation. However, migraine has not
  diminished over millions of years of evolution. Its prevalence has at
  least been maintained at a high level, and has even been shown to be
  increasing.
  This phenomenon suggests that a central nervous system (CNS)
  susceptible to severe, intermittent headache has been linked to an
  important survival or reproductive advantage.

the argument in wiki is equivalent to since we know that evolution is correct - it means that headaches must benefit us somehow otherwise we wouldn't have it so let's think of some reasons - which is in my opinion is a fallacy.
I could believe that this is a bad side effect of some more efficient to survival trait like being smart, (which is partially covered in same article)

Finally, migraine may be a component of imperfect central nervous
  system design. Evidence has suggested a dysfunction of pain-inhibitory
  pathways in migraine and discordant interaction between the ancient
  brain stem design and the more evolved neocortex.

EDIT:
I have read the meta post and answer from WYSIWYG, and I agree that they do partially answer my question in regard that a mild 'badness' can get past. I would argue that my question is different in a way that I am referring to specific point The trait might have a tradeoff which essentially makes no change to the overall fitness
The way I understand it is that one gets some 'perk' that is beneficial in some situations and disadvantageous in others and they cancel each-other out. (I just don't see how without some huge benefit migraines would get past). What I am asking is what so advantageous we must have gotten - that such horrible thing like migraines got through.
Are there any studies done - that incapacitating migraines are coupled with an evolutionary trait?

There is no need for a benefit from a trait to stay - it is necessary that it is not selected against this trait.

@Chris Hi Chris, I see what you are saying, don't you find it hard to believe that incapacitating migraines would not get selected against? I can't think where whey would not reduce performance be it mental or physical.

We don't know the exact genetic basis for migraine as far as I know (might be wrong). Unless we do, we cannot decide, if migraine is the backside for some other, much more beneficial trait also connected with these genes or gene variants. The classic example for this is sickle cell anemia - not beneficial unless you live in an area where malaria is endemic.

@Chris Thanks Chris, there is this article on twins with migranes, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2779399/pdf/10194_2007_Article_427.pdf  At present, several loci 4q21-q24, 5q21, 6p12.2-p21.1, 11q24, 14q21.2-q22.3 and 15q11-q13 linked to common forms of migraine with evidence of linkage have been reported.

See this.

@WYSIWYG Hi WYSIWYG, I have read the meta post and answer you have linked, and I agree that they do partially answer my question in regart that a mild 'badness' can get past. I would argue that my question is different as it is referring to specific point in your answer, The trait might have a tradeoff which essentially makes no change to the overall fitness.. What I am asking is with which trait did we get migraines (that was so great that even such incapacitating thing like migrenes got past). If you think I should change the wording, please just say so. Thanks.

@WYSIWYG edited the question.

I've updated my answer here - it should answer your question -  see the last bullet point in particular

I have altered your title, correcting the grammar and phrasing it in a scientific manner.

smart apes stayed on the cave with his migraine, while the dumb ones were killed hunting, and that's why we have migraine today.

@montelof and he died from starvation....

no, in that case migraine would not exists, he probably discovered agriculture.


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Phylogenical differences with nuclear and mitochondrial DNA
This is a textbook question, I would like to verify my answers. According to the textbook it is possible to construct a phylogeny using nuclear and mitochondrial DNA and these trees to be different, I should give reasons why this might occur.
Here's two that I think might be valid
(1) Mitochondrial DNA is maternal, while nuclear DNA comes from both parents. It is possible to have a (female) hybrid C between species A and B, and if C cross with an individual with genotype (A), the offspring could show some genes from the species B. I consider this to be a phenomenon of introgression, and genic flux would be in these case shown in the nuclear DNA, but not in the mitochondrial.
(2) Mutations might occur. mtDNA has a higher mutation rate than nucDNA. If the phylogeny is constructed looking at a gene, more recent mutation could should in the mtDNA.
This is what I could think of, I would like to know if they sound acceptable, and if there are more possible reason to find different phylogenies using mtDNA and nucDNA.


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Can IPSPs produce an action potential?
This picture was taken from Purves' Neuroscience, chapter 5:

Image (C) shows a inhibitory postsynaptic potential whose reversal potential "goes"  to the action potential. If two or more IPSPs occur, will temporal summation cause an action potential?

What do you think, based on the other information in C?

@BryanKrause I would say yes, but this seems to contradict the "inhibitory". Also, why is this "homework"?

This is exactly how I would write a homework or exam question for a basic neuroscience course. We don't allow answers to those sorts of questions, because the whole point is to work through it yourself. There are 2 other lines besides the IPSP voltage trace drawn in panel C. What do they mean? Also, have you looked at panel D? What is it telling you?

@BryanKrause Well, it isn't homework... It's a question I come up when reading Purves. I see that Panel D say say if the reversal potential is below the threshold the postsynaptic potential, and according to Purves, this is inhibitory because the change in V will be "pushed" toward the reversal potential of the specific synapse (GABA in this case). But if many inhibitory occur by definition, why can't the temporal summation of IPSPs be enough to reach the threshold value to fire the AP? this sum I'm thinking of can occur by different receptors.

What is the meaning of the reversal potential for a given ion or type of channel?

@BryanKrause The reversal potential is the equilibrium point given by Nerst's equation that separates two opposite directions of flux for the ion, this is to say that if a ion has a outward/inward flux, in the reversal potential the flux is zero, and past the reversal potential becomes inward/outward flux. Is this correct?

Yep. So what happens if you open a chloride channel when the cell is resting near the reversal potential for chloride?

@BryanKrause I think the voltage will be pushed towards the chloride reversal potential, because the flux of chloride will itself move towards its equilibrium potential.

So can IPSPs sum past their reversal potential?

@BryanKrause I feel the answer you expect is "no", but I'm not sure if I can give an argument for it. Would an explanation like this be valid? - If two channels X and Y are open, but with reversal potential lower than the threshold voltage, the SP are added as long as they are below the reversal potential (same direction of flux), and are subtracted if they are past the reversal potential (because the ion flux has changed direction). So the general answer is no.

Don't think of IPSPs/EPSPs summing necessarily. Opening conductances pushes the membrane potential towards whatever their reversal potential is (weighted against all the other open conductances). For excitatory conductances, summation is an okay approximation only because the difference between rest and threshold is small compared to the difference between rest and the reversal potential for typical excitatory receptors. I'll reopen and possibly write my own answer because I feel like you've done enough thinking now, but it would be best to edit your further thoughts into the Q.


text:
Circadian clocks in enzymes
I'm aware of the existence of circadian clocks, but I don't understand exactly how circadian clocks regulate other circadian mechanisms. For example, if an enzyme is found to have a circadian rythm, how is this rhythm produced? Is it because of one or more clock genes?

If i am right, i think that all circadiam mechanisms regulations by circadiem clocks is highly discuss theme in chronobiology. So i dont think that you will get sufficient answer. Anyway can you be more specific about what kind of enzymes would you like to know because still it is too broad.

I think more details about what you're interested in would be helpful here. You seem to have two questions: 1) how the biomolecular clocks generate rythms, ie the fundamental nature of the biological oscillators, and 2) how they transmit that information to other biological elements like genes etc.

Molecular feedback mechanisms create rhythmic patterns. The circadian rhythm is driven by a handful of genes, which in turn can regulate a number of downstream factors.
Here is a very nice explanation of the Drosophila circadian clock, which gives you an idea how this works. The video shows the same animation adding more factors every time to guide you through how the system works on the genetic/protein level.
A brief summary: The genes period and timeless are transcribed over night. Their proteins stabilize each other and build up in the cell. At the same time they block their own transcription, limiting the amount of proteins.
Other factors destabilize the proteins and evoke their degradation. One of them is the light activated protein Cryptochrome. This helps entraining the clock and results in the removal of Period and Timeless protein during the day. The negative feedback of their blockage is removed and transcription starts anew at night, when Cryptochrome is inactive.
These clock genes do not only regulate themselves but can also activate or deactivate other factors resulting in daytime-dependent transcription of genes or protein activity.
The whole picture is of course a bit more complicated and involves a lot of additional factors. But also in humans and other mammals you find very similar mechanisms.


text:
Glia/Neuron ratio
Research seems to indicate that the further we go up the evolutionary ladder, the higher is the glia/neuron ratio, to the point that in humans glial cells conforms 90% of the brain.
Now, if the glia/neuron ratio is somehow related cogntive capabilities (considering it is higher up in the evolutionary ladder), and since the ideal of a brain made solely of glial cells and no neurons seems absurd, how high can the ratio glia/neuron get before it starts to be detrimental?

TL;DR The glia-to-neuron ratio is not sufficient in order to distinguish humans from other primates or mammals.

The figures of the glia-to-neuron ratio (GNR) being 10:1 come from old studies that either used guesstimates for the number of cells in either category or used methods that have since been improved. The newest estimates range about a 1:1 ratio for the whole brain as reviewed in von Bartheld et al. 2016. These authors comment on the evolution of the GNR:

[Comparative studies have] shown that brain size does not scale universally
  with neuron number, that different mammalian species
  such as primates and rodents scale differently, that cell
  numbers in cerebral cortex and cerebellum evolve in a
  coordinated fashion, and that glia density and sizes
  vary much less than neuronal density and sizes. The
  GNR is highly conserved between structures and species,
  pointing to an important and close regulation of
  glia numbers (scaling) in response to, or regulated by,
  neuron density and neuron sizes.

At least in the cortex, cell numbers and size are kept to a minimum, as they take valuable space from what really matters, dendrites and axons (Chklovskii et al. 2004).


text:
Where does the fate map of a human embryo end?
I'm confused about the fate map of a human embryo. Is it just a particular part of the embryo development or does it include everything, from the conception (germinal stage) to the day the baby is born?

Are you talking about projects like this: http://embryo.asu.edu/pages/fate-map?

@Chris Yes, but it doesn't give any information about the fate map of a human

Ok, I will answer this later today.

In the developing embryo you have the three germ layers: Endoderm, mesoderm and ectoderm. From these layers all cell lineages of the body develop and can be traced back through their differentiation and migration to this three layers.
Have a look on the image below, which illustrates this pretty nicely:

The figure is part of this PhD thesis, which also seems worth reading when you are interested in this topic.

Great figure!  The thesis (p20) cites the image as "adapted from Gilberts Developmental Biology, Fourth edition, Figure 9.1."

That is right. I don't have access to the Gilbert, so this should be ok.


text:
What is the difference between chloride shift and Bohr shift?
Does anyone know the difference between chloride shift and Bohr shift?
Is it that Bohr shift happens in respiring tissues when CO2 concentration is low, and that Chloride shift happens in the blood as a buffer?
Sorry for asking such a trivial question and thank you in advance. And sorry for any wrong tags or title (new to the community and is seeking to improve)


text:
How does vasoconstriction retain heat?
I am reading on vasoconstriction on wikipedia. The article states that:

When blood vessels constrict, the flow of blood is restricted or decreased, thus retaining body heat or increasing vascular resistance.

Why/How exactly is the heat retained when blood flow is decreased? Isn't it the case that when things slow down they generally get colder?

Did you read the next sentence after the one you quoted?  It says "This makes the skin turn paler because less blood reaches the surface, reducing the radiation of heat."

@mgkrebbs I did read that, but I thought it was an extra reason and somewhat distinct from the quote. The part "thus retaining body heat" implied that the reason was already mentioned and this is just the consequence.

Think of the body as a heat-sink. We can let off heat by using our fluid exchanges – namely, blood and sweat. When we exercise, sweat cools us off through evaporative cooling. When we’re not exercising or in warm weather, we’re generally not sweating, but we’re still exchanging heat with our surroundings – after all, the metabolism is still active, we’re still “burning energy,” and our skin never reaches air temperature nor does our core cool to the temperature of our skin (so some kind of heat exchange has to be happening). How can that be, when there’s no obvious mechanism to carry away our heat as in the case of sweating?
The answer to this lies at the heart of your question. Human thermoregulation is largely thanks to our blood flow and vasodilation:

“Skin blood flow in adult human thermoregulation: how it works, when it does not, and why.” Charkoudian. N. Mayo Clin Proc. 2003.
Cutaneous sympathetic vasoconstrictor and vasodilator systems also participate in baroreflex control of blood pressure; this is particularly important during heat stress, when such a large percentage of cardiac output is directed to the skin. Local thermal control of cutaneous blood vessels also contributes importantly—local warming of the skin can cause maximal vasodilation in healthy humans and includes roles for both local sensory nerves and nitric oxide. Local cooling of the skin can decrease skin blood flow to minimal levels.

In essence, your core “wants” to stay warm. If the air around your skin is comparatively warmer, cutaneous blood vessels will dilate to accommodate a higher flowrate, allowing more blood to engage in heat transfer. The opposite is true for air that is comparatively colder, and the relationships between cutaneous blood flow, sweating, and local skin cooling can be tested experimentally:

“Skin blood flow and local temperature independently modify sweat rate during passive heat stress in humans.” Wingo et al. J Appl Physiol. 2010.
In protocol I, two sites received norepinephrine to reduce skin blood flow, while two sites received Ringer solution (control). All sites were maintained at 34°C. In protocol II, all sites received 28 mM sodium nitroprusside to equalize skin blood flow between sites before local cooling to 20°C (2 sites) or maintenance at 34°C (2 sites). In both protocols, individuals were then passively heated to increase core temperature ∼1°C. Both decreased skin blood flow and decreased local temperature attenuated the slope of the SR to mean body temperature relationship (2.0 ± 1.2 vs. 1.0 ± 0.7 mg·cm−2·min−1·°C−1 for the effect of decreased skin blood flow, P = 0.01; 1.2 ± 0.9 vs. 0.07 ± 0.05 mg·cm−2·min−1·°C−1 for the effect of decreased local temperature, P = 0.02). Furthermore, local cooling delayed the onset of sweating (mean body temperature of 37.5 ± 0.4 vs. 37.6 ± 0.4°C, P = 0.03). These data demonstrate that local cooling attenuates sweating by independent effects of decreased skin blood flow and decreased local skin temperature.


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Why haven't land animals evolved beyond urination?
It occurred to me (while urinating) that this would seem to be selected against because water is a scarce resource.   Why are we constantly losing water we don't need to through urination?   What is it about the chemistry of urine and the waste products eliminated that make urination necessary as opposed to eliminating them through defecation and recovering the water on the way out?

Actually this process (in the kidney) helps saving a lot of water. The primary urine is concentrated about 200x before it is excreted into the urinal bladder.

I would hardly call water scarce in the natural world…

Many have, see birds and most reptiles, what white stuff in bird poop is their nitrogenous waste. please do a little background research before asking a question.

It is probably true that toilets and other resting-ish area are always a great place to think about biology, I agree $\ddot \smile$.
Why do we urinate?
In short, urine contains the waste from our blood while defecation is just the stuff that we haven't digested. Kidneys are the organs responsible for draining wastes (mostly nitrogen-containing, or nitrogenous, wastes) from our blood.
Trade-off: energy cost vs. water loss
You're correct that the loss of water through urination is a considerable cost for an organism (especially those living in dry environments). But the amount of water used to excrete nitrogenous wastes is negatively correlated with the energy it costs to perform this excretion. In other words, there is a trade-off between water and energy loss during nitrogen excretion. Also, the question of toxicity is important.
Three ways to excrete nitrogenous wastes
Animals basically have three choices to excrete nitrogenous wastes:

Uric acid (excreted by uricotelic organisms)

Solid (crystal) with low water solubility
Low toxicity
Little water is needed
Lots of energy is needed

Ammonia (excreted by aminotelic organisms)

Highly soluble in water
High toxicity
Lots of water is needed to dilute it because of the toxicity
Not much energy is needed

Urea (excreted by ureotelic organisms)

Solid but highly soluble in water
"medium" amount of water is needed
"medium" toxicity
"medium" amount of energy is needed

What method is most beneficial for a given individual?
The amount of energy and the availability of water are very important aspects to understand whether a species is ureotelic, aminotelic or uricotelic. Another developmental constraint must be considered too. For example, birds are uricotelic (uric acid) probably because during the development of the embryo the wastes cannot be excreted outside the egg and therefore, excreting uric acid allows to greatly decrease the toxicity of the embryo's environment. In short, we must consider

Water availability
energy loss
developmental constraints

Note: This domain is not at all my field of study and I have no reference, typically for what concerns the toxicity, water amount and energy amount. One should not take my words for granted!

This is an interesting answer.   But it doesn't explain why nitrogen can't be excreted in solid or gaseous, rather than aqueous, form.

@ThePopMachine Well, Amonia is a gaz, Urea is liquid and Uric acid is solid (it makes cristals if I'm not mistaken). So, yes it can be excreted through solid form but it cost lots of energy (ATP). But you're right that my answer does not explain why it is more costly. But I know nothing about physiology and I can't give this answer $\ddot \smile$ I'll let someone else to give info about that if you're waiting for them.

@ThePopMachine You might want to create another post and to ask a more specific question about the physiology of Nitrogen excretion and why different solutions (Ammonia, Uric acid and Urea) are differentially costly in terms of energy. Consider this post as it had answered the evolutionary part of the question.

Yes, okay this has been here a while, so I will accept.   But this answer can be improved further by talking about nitrogen chemistry.   Any takers?

Are you asking why is amonia gazeous while uric acid is solid? If so, you may want to make another post on Chemistry.beta. I personally know very little about chemistry and won't be able to help you further with that.

As I have already mentioned in my other post, the most important role of urea synthesis by humans is blood pH regulation and urine concentration, so it is not just about excreting a waste product. I don't think human body is very special in this case, so I think most of the urea excreting mammals use urea for the same purposes.
The urea is created from NH4+ and HCO3- in the liver (mostly) and the kidney because of blood pH regulation purposes. It neutralizes the HCO3- created by the lungs from CO2 and OH -.

The urea cycle (also known as the Ornithine cycle) is a cycle of
  biochemical reactions occurring in many animals that produces urea
  ((NH2)2CO) from ammonia (NH3). This cycle was the first metabolic
  cycle discovered (Hans Krebs and Kurt Henseleit, 1932), five years
  before the discovery of the TCA cycle. In mammals, the urea cycle
  takes place primarily in the liver, and to a lesser extent in the
  kidney.
In chemical terms, urea synthesis is an irreversible, energy driven
  neutralization of the strong base HCO3– by the weak acid NH4+, and the
  average daily excretion of 30 g of urea is equivalent to the disposal
  of about 1 mol of HCO3– per day. Thus, a major function of hepatic
  urea synthesis is to effect this neutralization, without which the
  body would otherwise be confronted by a major load of alkali.
Urea is excreted by the kidney, and is normally present in plasma and
  body fluids at a concentration of 3.0–6.5 mmol/L.

wikipedia - Ornithine cycle
Textbook of Hepatology - Ammonia, urea production and pH regulation - Dieter Häussinger
1984 - The role of ureagenesis in pH homeostasis

The kidney reabsorbs urea in order to concentrate the urine

2007 - Critical Role of Urea in the Urine-Concentrating Mechanism

Evolution is reactive, not proactive. While clean water may be becoming scarce, it wasn't previously. Having to pee had no negative effect (probably positive ones) on being able to reproduce, so people that do urinate reproduced.
Now let's imagine a world where we get to people evolving to not having to urinate.
First, water has become extremely scarce, and most of the human race and other animals have died of dehydration. But some people who are very effective at retaining water (who urinate less) make it through the lack of water. They have kids who carry this water retention gene, and some probably have slight mutations that make them even better at it. Since the slight mutation group is better at retaining water, they can live longer and have more kids that may also have a slight mutation that allows them to live longer and have more kids, and so on and so forth until eventually, you might have a human that doesn't pee.

Water scarcity is now and has been forever an issue for land animals, this is not something "new". Different animals handle this challenge differently, as described in the existing answers. I fail to see what new value this answer adds, it seems not up to the standards of this site.

Welcome to Biology.SE. We're looking for answers that provide explanation, context, and include references to reliable sources. Don't just give a short opinion or speculate — instead explain why your answer is right with appropriate citations. Answers that don't include explanations may be removed especially when they are a poor duplicate of an already existing answer. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then delete or [edit] your answer accordingly. ——— Also note the question was not about humans ...

authors: მამუკა ჯიბლაძე


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Question about mutation of multiple nuclei?
If an organism with multiple nuclei, such as the slime mold Physarum polycephalum, was to be exposed to a mutagen, such as 5-bromouracil, what would be the effect (besides death)? Especially if multiple nuclei were effected differently by the exposure.


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Biology Experiment Data (Hodgkin-Huxley)
I'm doing research into the Hodgkin-Huxley Model from an electronics/mathematics perspective and I'm looking to find actual numerical results from experiments on squid axons. I want to compare the results of the experiments to the curves produced by modelling the equations in MATLAB.
My problem is, that while there are an abundance of resources discussing the equations and methodology of the experiments, I am having great difficulty finding tabulated experimental data (not just numbers generated from modelling the equations).
As I am coming from outside the field of biology I would like to know are there sources of quality numerical data for these types of experiments? In particular I am looking for the data for Potassium Conductance vs Time, here is the plot from the 5th paper in their series of publications that earned them a Nobel prize:
Hodgkin AL, Huxley AF. A quantitative description of membrane current and its application to conduction and excitation in nerve. The Journal of Physiology. 1952;117(4):500–544.

You are looking for raw data? I suspect that none of these has been published. You could try to contact the authors and see if you can get hands on them. But I wouldn't be too optimistic.

There are various programs that can help to extract numerical data from graphs, I'd try something like this on the figure you posted. It is very unlikely that numerical data is easily available for such old experiments. The other option would be to look for very new papers about the subject, it is much more likely that such data is available for new papers.


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What caused the Mesozoic-Cenozoic radiation?
The Phanerozoic eon has had 5 major extinction events and 3 major radiation events. After the Cambrian and Ordovician radiations came all five of the major extinction events, the last of which (Cretaceous-Paleogene) occurred during the last major radiation event (Mesozoic-Cenozoic). This timeline suggests the freeing of previously occupied ecological niches isn't the primary driver of major radiations. (However, the Cretaceous-Palaeogene extinction freed niches during the Mesozoic-Cenozoic radiation, and this may be part of why it continued for so long rather than being a purely Mesozoic event.) Although Wikipedia generally gives a good account of suggested reasons for major extinctions, and also for the Cambrian and Ordovician radiation events, it provides no real such detail for the Mesozoic-Cenozoic radiation. What are its conjectured causes?

I'm confused. I always thought that the impact separating the mesozoic from the Cenozoic, which killed the non-avian dinosaurs, and many other lineages freed niches for mammals and birds to fill. Is this no longer the explanation?

@KarlKjer I thought so too, but to quote Wikipedia, "The Mesozoic–Cenozoic Radiation began in the mid-Mesozoic and extends through the Cenozoic". So it seems that, however much the extinction event may have helped the radiation event continue, it started somewhat earlier.

Oh yes. For example, pterosaurs were on the decline. There were a variety of non-impact-related causes. But the impact finished the deal, and it was (as far as I know) mostly the opening of new niches made possible by mass extinction.

@KarlKjer In which case, I suppose, it was some minor extinctions that started the radiation.

There is no real start to a radiation event.
First there are many mass extinctions and many radiation events, what you are referring to are just the most notable ones. also the big five do not occur after the odrivian the first occurs directly before.  Radiation events happen after every mass extinction even minor ones, the amount of radiation corresponds well with the severity of the extinction. The big five and the big three are just the ones we find the most interesting, not the largest, note graph below). The ordovician radiation event happened directly after the cambrian–ordovician extinction event for instance. And there was a massive diversification after the P_T extinction, it just does not get as much press because almost all the major players become extinct in later extinction events and becasue there are  fewer fossils from that time period. Every extinction event is followed by a radiation event. the Mesozoic-Cenozoic radiation is a large radiation because of the KT mass extinction otherwise it would just be the normal background biodiversity turnover.
Essentially radiations are always happening, there is always some radiation going one in some clades.  But if you suddenly wipe out a large number of species and organisms, many of those what survive will be the ones that were radiating simple becasue they were small fast breeding generalists which is also the group that radiate a lot. Small fast breeding generalists are what what best survive mass extinctions and a group that does a lot of radiating. There is also a large anthropomorphic component to this, if you take the tree of life and make a radom slice across it anywhere it sill look like many of the groups that survive are radiating becasue all the other radiation events are cut off, while we ignore stable groups becasue they are stable. You can even notice that the radiation of different groups start at different times but then explode after the event. Almost as if our artificial lines between groups is not a great predictor of diversification events. Radiation events are not one off occurrences with clear cut beginnings and ends but a prolonged uptick in an ongoing system with a lot of variation. there is no clear cut start to radiation events imagine trying to pick the exact second summer or winter begins using nothing but temperature data, there is just to much noise due to local and daily condition to make any such point anything but arbitrary.
So the large scale radiations is still caused by the extinction event, it however will almost always look like it was happening earlier becasue on a small scale it never really stops, and where we draw the lines for groups does not correlate well with radiation events, yet we still use it to decide which "groups" are radiating.
Sources

If you look at this paper and its graph you can see this effect in angiosperms. The group originates and begins to diversify before the KT but a massive upswing in diversity happens after (actually fairly long after, once the climate/extinction has stabilized)

The Big 5 are OS, LD, PT, TJ and KT, so they do all occur after the Ordovician began. You're right that extinction events drive radiation to some extent. But that leaves open the question of which extinctions encouraged MC, and overlooks the possibility other factors drove it too. Explanations of the Cambrian & Ordovician radiations are much broader than then-recent extinction.

And those five are not the largest just the ones we pay the most attention to.

Is it your contention that extinction events are the only causes of the Mesozoic-Cenozoic radiation? Because while extinctions may have contributed to earlier radiation events, they were often not their only cause.

no if you read my post I mention that radiation is always occuring they become major eents when extinction clears a wide swath of niches.Radiation events are not one off occurrences but a prolonged uptick in and system with a lot of variation. there is no clear cut start to radiation events.


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Is this panspermia mechanism feasible?
One episode of Cosmos: A Spacetime Odyssey describes a mechanism by which microbes could travel between planetary systems. As a star's orbit takes it around the galaxy, it occasionally passes through dense interstellar clouds. Rocks thrown into space at that time from the surface of a microbe-harbouring planet could carry life to temporarily nearby planets of another planetary system, before cosmic radiation would sterilise such rocks.
It's an interesting idea for TV; but scientifically, how plausible is this mechanism? My main concern is whether the average number of "infected" planetary systems per passage through an interstellar cloud is estimable as non-negligible.
Note: the use of "panspermia" in the title refers only to the question of whether an occasional interstellar transfer of microbes is tenable, not whether Earth's life originated outside this planet. As I understand it, the mechanism described above is lithopanspermia.

Unfortunately I think this may fall neatly between the expertise of Space.SE and here, but I think the key variable here is the time for which such propagules would remain viable. I suspect the sheer time and distance likely to separate compatible planets would exceed this period by a very significant amount. However, if we can show extensive 'cross-pollination' of planets within our own system then that gives us better data to estimate this likelihood.

The theory is staggeringly improbable. However, so is life. The probability of life emerging from non-life is the basis of the misguided idea of intelligent design (a thinly veiled repackaging of creationism). Bear with me: the probability of life on Earth is 1. It is here, and this is the only observation of Earth we have. But the thought of complex life appearing out of some molecular soup by chance (abiogenesis) is also staggeringly improbable. But as I said, life is here. How did it get here? There are only three possibilities: Abiogenesis, divine creation, or from panspermia (which kicks the can down the road, because it had to have begun somewhere). God is no explanation at all, because even a mystical imaginary creator would have needed some mechanism besides waving a finger. So in terms of probability, both abiogenesis and panspermia would be astronomically improbable, but since life is here (probability of life is 1), then one of these two is the source of it. We have no hard evidence to choose between them.

You've missed the point of the question. I'm not asking whether panspermia should replace terran abiogenesis as an explanation for life on Earth (it probably shouldn't); I'm asking whether it's plausible to claim planetary systems "contaminate" each other in the manner Tyson discussed.

No, I have not missed the point. Since it is one of only two possibilities, AND we have no evidence between either, then it is plausible, because something happened here. My point is, that there is no way to answer questions that estimate probabilities that are extremely unlikely, and have no data to directly support them. Thus Tyson's discussion is plausible.


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How does hibernation reduce risk of radiation-induced mutation?
A recent documentary (skip to 58:20) discusses the possibility that hibernation, if it could be induced in extrasolar astronauts, would reduce damage from cosmic radiation. The obvious reason this could happen is the shielding of hibernation chambers, but the documentary reviews evidence that even hibernation in the wild (e.g. bears) reduces radiation damage due to a slowed metabolism.
I would assume the connection is that reduced need for enzyme synthesis keeps DNA coiled up most of the time so its nucleotides are less exposed to radiation, but even if this is true it raises the question of how coiling shields radiation. (For example, is it less able to penetrate histones or the phosphorylated deoxyribose backbone?) Adding to my confusion, the documentary claims the mechanism is rooted in hydrogen sulphide, but doesn't explain either why this is more concentrated in the cells of hibernating animals nor how it reduces mutations.

This is still an area of active research, and there doesn't appear to be a single definitive answer for the mechanisms behind the reduction in radiation-damage during hibernation.
A recent review by Cerri et al. (2016) covers a lot of the known biology behind hibernation and resistance to radiation damage.
A few select quotes from this review:

At the cellular level, it is well known that cells irradiated in
resting state, and left undisturbed for 24 h after irradiation, are
more resistant than cells re-plated immediately after exposure. This
effect is known as delayed plating, and is generally attributed to the
potentially lethal damage repair (PLDR) in resting phase.
...
The oxygen level during hibernation may contribute to the enhanced
radioresistance. Hypoxia is a well know protective mechanism, and is
arguably the main reason of local control failure in radiotherapy.

Rockwell et al. (2009) discuss the underlying reason behind reduced radiation sensitivity in a hypoxic environment:

Molecular oxygen (O2) is a potent chemical radiosensitizer. This
radiosensitization does not result from any of the metabolic or
physiological effects of oxygen, but instead reflects the fact that O2
is an extremely electron-affinic molecule that participates in the
chemical reactions that lead to the production of DNA damage after the
absorption of energy from ionizing radiation [21,22].

My personal take would be that the reduced risk of radiation-induced damage is probably not due to the structural arrangement of DNA, but rather the overall cellular environment. This is perhaps linked to an enhanced ability to repair damaged DNA, but is also likely to be highly dependent on cellular oxygen levels.


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Neurobiology of tantrums
As mentioned here, tantrums are primarily observed in young children and often involve a loss of self-control, both physical control and the ability to calm after a demand has been met. What changes in neurobiology reduce the propensity for this as children age? (The cause may be partly neurochemical, partly structural.)
I am especially interested in whether the vulnerability to tantrums in the young brain are at least partly due to positive feedbacks. A self-enhancing mechanism for the distress could explain why self-control sometimes suffers. (Positive feedback is also consistent with a colleague's claim, for which I have no source, that the risk of loss of self-control is low if a demand is met quickly.)


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Examples of chromosome fusions
One of the best "smoking gun" pieces of evidence of humans' close relation to chimpanzees, gorillas and orangutans is that human chromosome 2 is a fusion of two primate chromosomes, with a double telomere in the middle and a centromere on each side. This fusion, which occurred some time after our MRCA with chimpanzees, was an accident with no evolutionary importance, but it happens to provide extra support for our common ancestry with other African apes. In theory, such fusions could be so commonplace that they can be used to infer much of the family tree of life on their own. I'm sure they're nowhere near that common, but this got me thinking: are there any other examples of species with chromosome fusions (or splittings?) that betray their closest relatives?

Related: https://www.quora.com/Is-there-any-evidence-of-chromosome-fusion-in-any-other-species

See https://www.physicsforums.com/threads/chromosome-fusion.312786/
for answers and several points of discussion on what are called Robertsonian translocations. https://en.wikipedia.org/wiki/Robertsonian_translocation

My question concerned intraspecific cases (a topic of your link 1), not variation in humans (viz. your link 2). I'm glad for both as I learned much about the effects of translocation besides "it needn't matter because loci can line up in a way that lets meiosis work", which explains why natural selection tolerated the fusion in us but was the previous limit of my knowledge. The RT case reveals how acrocentric chromosomes can introduce complications.

You can go to ensembl.org and look up synteny between closely related organisms, like rats and mice.  Below is one example: rat chromsome 1 is made up of all of mouse chromosome 7 and 19, plus parts of 17, 10, and a smidge of 13
https://uswest.ensembl.org/Rattus_norvegicus/Location/Synteny?db=core&r=1%3A126594509-126694509&otherspecies=Mus_musculus


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Why are fairyflies so small?
The Mymaridae are the smallest insects. This video explains their numerous adaptations to being as small as 140 microns yet still complex, such as smaller cells with as little cytoplasm as possible, denucleated neurons, loss of several body parts (including eyes and hearts, depending on the species), and parasitism as an alternative to insects' usual level of nutrition in eggs. My question is why natural selection would favour their being so small in the first place.
Since few extant species have been extensively observed, this question may require some "just so story" speculation, hopefully informed by other examples of organisms becoming unusually, almost prohibitively small for their taxa. On the other hand, their fossil record covers about 100 million years, so perhaps the time and place of shrinking intermediates would suggest specific explanations.

Fairy flies can be so small because they mooch off other insects' eggs, this is one of the reasons why they need to be small, then after that, they don't need to eat as they will die in only a few days. Information can be found on the "how do they manage to be so small" section of this PDF: https://www.cell.com/current-biology/pdf/S0960-9822(18)31343-5.pdf

This poses the chicken-egg problem (no pun intended) of whether they became small due to such parasitism or need such parasitism to be small. It wouldn't surprise me if the parasitism is older, and the host eggs shrank c. 100 Mya for some reason, as is likely if the host species also shrank or adapted to reduced food supplies. But do we know any of that?