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What causes humans to be physically weak compared to animals like gorillas?
Animals like gorillas seem to have a physical fitness and muscle mass that don't depend as strongly on how much exercise they get, compared to humans. E.g. gorillas living in the wild sleep and rest a lot. While they do get quite a bit of exercise (a lot more than the average human), they are not going to exert themselves much more than is necessary. So, they push themselves a lot less than people who exercise very hard. Yet the average gorilla would easily outperform even a well trained human being in bodyweight exercises.
So, there seems to be something fundamentally different about maintaining physical fitness in humans compared to gorillas.

Humans would outperform gorillas on endurance. We evolved with different needs.

@Remi.b: But wolves and most dogs (especially sled dogs) far outdo humans in endurance, at least in colder climates.

And whales far outdo humans in apnea.

Yes, as someone who is into running (an hour per day), I do appreciate that we are have quite good aerobic fitness in the sense that it is relatively easy to acquire and maintain extremely high levels of aerobic fitness. But my experience with strength training is that it is extremely hard to make progress. Perhaps the point @DavidBlomstrom makes about animals walking on all fours is also important for core muscles. A very strong core is needed to do exercises like this that I've tried but failed to do for quite a while now :( .

Finding references for this is difficult (I've tried before), but there are probably three major reasons: (1) Lever attachment of muscles to bones optimizing for strength vs. fine control; (2) Relative muscle mass - Chimps have proportionately more upper body than humans, and human leg strength is probably as good as chimps; (3) Genetic changes - humans lost a muscle-related gene that makes their muscles weaker, although this may be only a factor in masticatory muscles.

Evolutionary tools that are not needed for increased survival rate of offspring of a certain lineage deteriorate with time. The deterioration might have a form of gene expression changes or mutation accumulation. For example, gene MYH16 encodes a protein that facilitates strong jaw muscles in primates, but humans carry a mutated gene that had lost its function (Stedman et al. 2004. Nature). We cannot bite hard, but we can articulate.
With respect to muscle strength, the common ancestor of apes and humans was likely stronger than we are now. Their descendants that formed a lineage diverging towards humans increased their survival by being smarter rather than stronger than their contemporaries.


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Glycoprotein hormones metabolism
Why do the carbohydrate groups in glycoprotein hormones decrease the rate of metabolism? And increase the half-life?

can you give some specific examples of how glycosylated hormones have altered half lives and affect metabolism?

source: Stack Exchange

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

sort: votes


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Did the number of rods changed from ancient time?
Correct me if I am wrong, but I know that rods work under limited light conditions only.
But now we are in a world that always have lights everywhere unlike ancient time when humans had to deal with darkness.
I also know that the humans adapt to its living conditions.
Since our eye only uses the cones and don't use rods often, will the number of rods decrease because of this?

Such evolutionary changes happen very slow - and the availability of light happened very recently in evolutionary terms. So if such a adaptation happens, it will take quite a while to happen. If at all.

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Why did eukaryotic cells develop?
If eukaryotic cells can survive in extreme conditions, then why are their still prokaryotic organisms?

This is essentially the same as another question that was just submitted - have you tried looking at some textbooks?

The question suggests that you might want to have a look at Understanding Evolution (UC Berkeley), a free online introductory course to evolutionary biology.

I am not quite sure I understand the relationship between the title and the content of the post. Also, I suppose you meant "evolved" rather than "developed".

Are you thinking that eukaryotes are so competitive that it seems weird to you that procaryotes would not be outcompeted and get extinct. Do I understand you correctly?

It is like asking if humans are so advanced, then why do gorillas exist. Basically, all lifeforms are different survival strategies and none is "better" than the other (whatever exists is good enough for this environment). Please go through the website that Remi mentioned. It explains the evolution basics nicely and in easy words which even a high-schooler can understand. If you have specific doubts related to evolution then please feel free to ask (but make an effort from your side before asking others). I let your other question be but I have to put this on hold.

As far as I understand your question, the "development" of eukaryotic cells can be linked to the endosymbiotic theory Symbiogenesis.
This diagram only depicts a possible trajectory of evolution which is still unknown.

A cell that respired anaerobically took in a bacterium that respired aerobically, supplying both itself and the larger cell with energy in the form ATP. This created a competitive advantage for the larger cell because aerobic respiration is known to be more efficient than anaerobic respiration. Unhurriedly, the aerobic bacteria evolved into mitochondria and the larger cell into a heterotrophic eukaryote.
A heterotrophic cell took in a smaller photosynthetic bacterium, which supplied it with organic compounds, thus making it an autotroph. The photosynthetic prokaryote evolved into chloroplasts and the larger cell into photosynthetic eukaryotes.

Do we know which aerobic bacteria evolved into mitochondria? Do they still exist?

@CountIblis Ancestors of mitochondria belong the the group of α-proteobacteria. Many free-living bacteria of this clade still exist.


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Why did multicellular organisms evolve when a single cell can survive on its own?
Since unicellular organisms can survive, why would there be evolution of multicellular organisms?

Potential duplicate of Why would a single celled organism evolve to be multi-celled?


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Energy input during ATP Dephosphorylation?
What is the energy input needed to break the phosphor bond during ATP Dephosphorylation? How and when this will occur?
Many thanks for your answers.
Edit 1: I know how much free energy (∆G) is released with the hydrolysis of ATP, but I dont know how much energy is needed to start the hydrolysis of ATP.
Updated Question/s:
To break the phosphorus bond of ATP, must there be some input energy? What is the amount of this energy? Else how can break any bond of ATP without the supplement any energy?

read into https://en.wikipedia.org/wiki/Dephosphorylation and https://www.boundless.com/biology/textbooks/boundless-biology-textbook/metabolism-6/atp-adenosine-triphosphate-71/atp-adenosine-triphosphate-349-12938/

I know how much free energy (∆G) is released with the hydrolysis of ATP, but I dont know how much energy is needed to start the hydrolysis of ATP. To break the phosphorus bond of ATP I think there must be suplied some input energy? What is the amount of this energy? Else how can break any bond of ATP without suplying any energy?

It sounds like you are asking about the activation energy of the ATP hydrolysis reaction. This paper estimates the activation at 35--39 kcal / mol, depending on details of the reaction mechanism. So yes, energy is needed to break the phosphate bond; this ensures that ATP does break down spontaneously (which would make it a rather useless molecule for cells).
Note that this concerns ATP hydrolysis without enzymatic catalysis. Enzymes that break the phosphate bond of ATP to drive reactions lower this reaction energy substantially.


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Why can't we see in low light if staring long enough?
For me it seems reasonable that if I kept my gaze on a fixed point in a room with low light, a progressively brighter and better picture would appear before my eyes, just like a camera can see in the dark if the shutter speed is really slow, e.g. 4 seconds exposure. Why can't our brain do this trick as well (accumulate visual information over time)? Or is it a limitation of the eyes?
edit:
To further clarify what I'm after; I will show a concrete example from the world of photography (images taken from this website).
Here is an example where we have a series of underexposed images - this would be what the brain receives:

Now, combining all of them with a simple add-operation reveals one image that has normal exposure.

This seems like a simple trick for our powerful brain - surely it can add incoming signals?

Calling it a simple trick that the brain should be able to do is really kind of missing the entire point of the answer.

Maybe it would be a simple trick, but what would be the evolutionary benefit to such a trick?  The visual system works quite differently, detecting change/movement (which probably equals threat) far more easily than static scenery.  The human eye has built-in motion - saccades - that allow it to see more clearly.  IIRC (though I can't quickly find a reference) if you electronically compensate for the saccades, so the visual field stays fixed, everything washes out and you're effectively blind.

@jamesqf - Thank you. I guess my answer was too vague, that "not be[ing] able to detect change rapidly [is] something that would be most inconvenient." Your comment adds a lot to the answer.

Also think in terms of evolution.  Say you're a species evolving towards being nocturnal, and "need" to improve your low-light vision.  The easiest route is simply to increase the size of the eye.  You could also add a reflective layer, e.g. the " tapetum lucidum".

out of curiosity - have you tried to add your 8-bit, noisy, underexposed pictures to obtain the exact final image? I bet you can't :)

A point that I missed the first time around: evolution has not had much time to work in dark rooms.  Even though humans are not primarily nocturnal, our low-light vision is perfectly adequate to cope with most natural low-light settings, where there is still light from moon & stars.

For simplicity's sake, let's really reduce this to something like photography.
A camera's aperture can stay open indefinitely, allowing the plate (or whatever is receiving and recording light) to "collect and save the effect of photons" over time, if you want to phrase it that way. That allows a camera to make images that our eyes never can, for example, of "star trails".

The retina isn't like a photographic plate or a digital sensor's photosites (or pixels). It can't "collect and save" like a camera can. There is a "refresh rate", if you will, that disallows a collection and saving of light that doesn't apply to cameras, because cameras don't care if something in their vicinity is sneaking up on them and presenting a danger to their lives. Not being able to detect change rapidly is something that would be most inconvenient to survival.

It is the time sampling with long exposures that really makes the magic of digital astrophotography possible. A digital sensor's true power comes from its ability to integrate, or collect, photons over much longer time periods than the eye. This is why we can record details in long exposures that are invisible to the eye, even through a large telescope.

How Digital Cameras Work

Good answer - I have added an additional example in my question to handle this as well by not relying on a single long exposure.

And for an extreme example of this, consider the Hubble Ultra-Feep Field (https://en.wikipedia.org/wiki/Hubble_Ultra-Deep_Field ), with an exposure time of about a million seconds, or over 11 days (if I did my math right).

I don't feel that this is the answer: it assumes that it would be the retina's job to record data, but that's not necessarily true. The question should be answered with this and why it's not feasible for the brain to record the light as well. A combination of this and some of the answers below that actually address that would be perfect.

@Numeri - I did say it was a simplification.

@anongoodnurse Fair enough :), but I do think you should mention why the retina 'refreshes': our eyes move themselves every so often in order to keep alert (still a simplification, but I feel like it would be more informative). But thank you for your well written answer!

The simple answer is, that eye is not constructed such way.
The eye have much more "pixels" than "links" to the brain and sends in "preprocessed" image. Moreover the the eye is constantly moving and scanning the "area of vision" and the body and head are supposedly also moving (willingly or not - nobody can freeze totally) so longer accumulation of data would lead to big blur.
And the main purpose of eye is to spot danger - something changing, or moving victim - as we human are not nocturnal animals, we are constructed/optimized to work in mode active on light, passive and sleeping in dark. As there is real need for sleep anyway, there is not good reason to develope secondary system for night vision - meaning duplicate the main vision system completely with totally different mode of work (long time collecting data) which would be used only in very little split of time - when predator find us in night sleeping and we survive the first attack.
So only the main system was slightly modified with other kind of pixels more sensitive to light, but less to color, which allows us work to relatively last night and from really early morning when only split of light is accessible. At the price of color and details. But it is much cheaper, then mainly unused secondary system. And covers more time, than we usually use to move in.

The differences at the photoreceptor level have been addressed by others. The mechanical restrictions of the visual system were shortly hinted at by @gilhad et al., but deserve more attention in my opinion.
First off, in darkness we cannot focus on an object and our eyes will move. And even when we focus on a specific point there is always movement of the eyes due to due to tremor, drift and microsaccades. Microsaccades are involuntary small movements of the eye (Fig. 1) that have received quite some attention lately. It is estimated they occur 1 - 2 times per second and they can reach amplitudes of up to 1 degrees of field of view (Martinez-Conde et al., 2013) and last for about 15 ms (Cui et al., 2009). It is thought that these movements prevent adaptation at the retinal level, and prevent image fading. Hence, images on the retina are constantly mechanically refreshed. The brain in turn stabilizes the image by correcting the image at the perceptual level through oculomotor feedback (Martinez-Conde et al., 2013).

Fig. 1. Microsaccades recorded by an eye tracker. Source: Martinez-Conde et al. (2013)
While a camera must be fixated on a tripod stand to allow for overexposure,  our eyes cannot be fixated to the same extent, even when we try. Hence, combining exposures as indicated in the question is impossible and results in image blur. Instead, retinal images are constantly refreshed and when lighting conditions are too dim we cannot integrate photon input in the temporal domain.
Note, however, that photoreceptors do integrate photon input to some extent, given that higher luminance results in brighter perceptions.  However, this operates only in the order of milliseconds and doesn't allow for long-term exposures as necessary to obtain images like the one shown in the great answer from @anongoodnurse.
References
- Cui et al., Vis Res (2009); 49(2): 228–36
- Martinez-Conde et al., Nature Reviews Neurosci (2013); 14: 83-96

I'd like to think, if we just focused on something for even half a second, that our brain could take in half a seconds light, process the directions we were moving in and adjust the images before threading then through to remove blur and then we could see in low light. I just wonder, from a purely technical point of view. Could our brains do this. As of course, half a second, or however long, would have impacts on survival. So again, just technically

There's probably a theoretical capacity to do so.  The brain is amazingly good at signal processing, and could probably pull off such a summation.  However, there is a limit.  You have to hold very very still for it to work.
Go take one of the time lapse pictures, like anongoodnurse's answer posted.  The shutter is open for quite some time (her picture looks like a 30 minute or 1 hour exposure to me).  During that exposure, the camera holds perfectly still. All motion you see is motion due to the objects in the scene moving (or,  if you prefer the technicality, the stars are holding still, and the camera is rotating... really really really smoothly).
The body does not have such an ability to lock itself down.  Try taking one of those pictures while holding the camera in your hands, and you'll see its particularly difficult.  Now consider that your eyes are even more twitchy than the rest of your body, capable of darting this way and that.  We have good control over our eyes, but nothing close to what you need to create an effect similar to that of a tripod.
Thus, if you were to try to use your eyes in this way, almost all of what you would see is your own motion.  Presumably a very well controlled individual might be able to sense that movement and account for it, but there's little reason for the brain to have that ability in "hardware."
Of course we can lock our eyes on to see with incredible accuracy, right?  We can read words on an eye chart at 20 paces.  Those activities are being done in a scene which permits visual feedback.  If its too dark, we don't get enough visual feedback to see where our eyes are pointing and compensate.

What I believe you are referring to, is the phenomenon by which the camera adjusts light exposure by adjusting aperture. We can also do this, but it happens very fast. Go from a dark room to a brighter room and you will be blinded, but that effect soon subsides, and vice-versa.
The pupil opens up in a dark room and production of visual purple or Rhodopsin takes place in the Retina, a pigment responsible for visibility in low light. When you enter a bright area, the pupil contracts and Rhodopsin is photobleached, with production of Iodopsin taking place.
https://en.wikipedia.org/wiki/Adaptation_(eye)
^
Check out the Dark adaptaion and Light adaptation sections
(Sorry I don't have more sources, I had done this from my highschool bio textbook, and I can't find it)

Thanks for your input, but unfortunately that's not what I'm after. You did however send me on the right track to find the correct term I'm looking for: shutter speed.

I think the question's actually referring to a camera adjusting exposure by increasing shutter speed. Increasing aperture would be, as you say, (literally) equivalent to opening the pupils of your eyes, but the question's talking about staring at a scene for a long time, "collecting" lots of light and summing (rather than averaging) that into an image.

Oh alright, got it. Glad I could help!

"adjusting exposure by increasing shutter speed" Er, I mean decreasing shutter speed but you probably all figured that out.

Pretty much all answers which focus on movement of the eye causing blur (something a digital camera does not have to deal with) are wrong. The brain has absolutely no problem processing images in low-light at speed.
The answer is all to do with the fact that the eye is not a camera. Much of the old-school theories which where based on the fact that the eye works like a camera, such as persistence of vision, etc, have been proven demonstrably wrong. The eye does not have a shutter speed - information is constantly being sent back to the brain with no interval delay.
(https://en.wikipedia.org/wiki/Persistence_of_vision)
This means that resolving blur/etc is done in the brain, not by the eye. Think of digital image stabilization that actually works, and works in real-time.
However, the brain does appear to work on chunks of eye-input, at roughly 16-24 chunks a second. Why this speed? Well, liking the brain to a computer, it probably has something to do with the amount of memory the brain can store for unprocessed eye-data. Long-exposure photos require a lot of RAM to store the raw data, then a lot of time to compile it into a single image. The brain could do no doubt do the compilation from raw data to image, but it very likely cannot store more than 1/24th of a second's worth of data in "memory" before it has to compile.
More importantly, doing so would reduce our reaction time significantly. This is important because you do not want an organism that can see a branch clearly at night, but when they try to grab it, miss by 5-10 seconds.

This is more like the kind of answer I was expecting to this question. Makes me wonder if slow moving nocturnal animals already uses this kind of temporal accumulation of visual information to improve their vision.

The brain has absolutely no problem processing images in low-light at speed is true, as rods are built for speed. However, because of eye movements the brain cannot integrate signals barred each frame would be re-positioned over the previous one. That doesn't happen.  Hence, calling out that ...all answers which focus on movement of the eye causing blur are wrong is off, especially because the arguments you pose are based on a lot of 'probablies' and 'likelies'. Show us the references that prove the other answers incorrect, or otherwise you might want to tone down your answer.

I should tone it down because that would just be better - however i cant do much about the references because all the articles I read for this post state that the field itself is unsure how the brain does it. All we really know is that it doesnt work like a camera, which is all I stated. Would be great to get some more info though - I find this really fascinating :D

I wish my computer as capable of sending an illustration of the arrangement of the human eye, versus the hypothetical "camera lens" idea, as organic eyes and camera optics are in NO WAY SIMILAR! Most of you have been in gross error by doing such, in your discussions.
The eye uses a combination of organic optical cells called "rods," and "cones," in order to manifest an image. In addition, there is a "dead spot" on the image perceived by an eye, owing to the insertion-point of the optical nerve. Any discussion of organic vision has to take these facts into account.
Organic eyes MUST go through a variable period of "dark-adaptation" in order to be able to perceive an image,as well. The minimum period is between 50-120 minutes; and even then, even an instant's exposure to "brighter" light will erase all of this adaptation, necessitating "restarting the clock" to dark-adapt the eye, again.
There's an anecdotal tale purporting that pirates had worn eye patches so that they achieved and kept dark-adaptation in one eye. There are many advantages to keeping one eye dark-adapted--- one is going from a brightly-lit deck, down into the very dim below-decks areas of a victim's ship. This is a case where being able to pull off the patch and being able to immediately see the enemy crewman coming in with a cutlass would be very valuable!
Another factor is that the distribution of rods and cones is not uniform, across the eye. Cones deal with colour-perception, and are concentrated at the centre of of the visual field. The concentration of cones rapidly declines, going outward.
Densities of rods in the same eye rapidly increases, going out from about five degrees from dead centre to a maximum of approximately 25 degrees from dead centre. Rods are responsible for our peripheral vision, our "sensitivity" to even seemingly-microscopic motion, AND OUR NIGHT VISION.
Because of the lack of rod-cells at the centre of our eyes' visual field, we are unable to see anything dead-ahead of us, under low-light conditions!
In order to be able to bring the maximum number of rod-cells to bear on an "item of interest" in our visual field, we have to use our peripheral vision and "cheat" off to one side of our visual field by about 25 degrees. This is like watching the front door in the centre of a building by looking "straight" at the middle of the left or right facade.
One would also be able to detect motion far easier than exact shape by looking in such a way. By continually "looking to one side," and by altering our location so as to change the background, it is entirely possible for an astute woodsman (a Native American or a Hillbilly, for example!) to be able to not only spot a raccoon in the top of an oak tree, but also to make out the form of the opossum looking up at him, from a lower limb!
Many animals far better able to operate at night have eyes that are not only better-equipped with rod-cells, but are in fact, much larger than ours! We would see as well as any owl, had only we been born with eyes the diameters of "jumbo" grapefruit!
Plus, watching and closely emulating the owl, with the head-bobbing, the weaving from side to side, and the peering-ahead, we would naturally improve the peripheral-sensitivity and the "looking to one side" conjuring of sharper images of those objects of interest to us!
I am sorry to be critical, as many comments showed great understanding of non-organic optics, as well as great imagination, but it is simply not possible to be able to blythly interchange the principles of non-organic optics and organic optics.


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Wax layer destruction from seed coats
I'm working with some orchid species, and i encounter a specific issue. Some of those species deposits upon their seed coat a wax layer. This layer makes seeds behave in a very hydrophobic way. You cannot dispense them in a pour water.
That behavior has many impacts. One of the most significant is that it does not let water come in touch with the actual seed and then with embryo to make it sprout.
So i tried many ways to remove that layer but nothing actually seemed to work out.
I treated seeds with the following chemicals:
a) 1% NaOCl with some dish soap water solution for 10min. After throwing seeds into this solution you could see that they can be evenly dispensed in it and come in touch with the solution. But if you wash them up with pure water for example 3 times they are getting back their hydrophobic behavior.
b) 1% H2SO4 water solution for 10min. I thought that with this treatment waxes will be removed from the seeds but nothing like that happened. Maybe they had been better dispensed in the pure water comparing to the previous treatment but nothing significantly changed.
c) 93% ethanol solution for 1, 2, 3, ... 30min. results here were also very disappointed. While the seeds are immersed into ethanol, they were very well dispensed into the liquid without any hydrophobic behavior. After three washes with pure water, hydrophobic properties came back.
Treatment time seems not to play any significant role on the results.
My conclusion is that there is no destruction of the waxes with the above chemicals. The only thing that happened probably, is the creation of a Micelle around the seed, which make it for a while (the time that it was in the solutions with soap and ethanol) non hydrophobic.
Finally my question is, if there is any way to destruct chemically, to some grade the waxes. So even when you put the seeds in a pour water not be so much hydrophobic.
Thank you.

Using H₂SO₄ is not a nice idea for dewaxing. Try ether or chloroform. Have a look at this page.

I 'm thinking if it's possible these chemicals to harm the embryo of the seed. Maybe if they are in small concentrations to not harm them. I'll read your page suggestion and maybe there is an answer. Thank you very much.

This paper describes dewaxing of sunflower seeds using various solvents. As you have already shown for yourself, using hydrophilic substances such as bleach and acids do not work well in removing the waxes.
Waxes are highly hydrophobic substances, and must be removed with either hydrophobic solvents (much like washing away acids with water at the emergency eye-shower) or detergents and water. The hydrophobic solvent mixtures used for lipid extractions recommended in WYSIWYG's link will likely work as well.

Try a nonionic detergent like NP-40, it is a very good surfactant.

Waxes look something like this:

ref: http://lipidlibrary.aocs.org/Primer/content.cfm?ItemNumber=39369

So you will never be able to dissolve them with a polar solvent like ethanol or water. You need a detergent or an apolar solvent.
If I were you I would try out gasoline to dissolve the wax and soap + water after that to remove the gasoline remnants from the surface of the seed. They are cheap, but they might damage the seeds. If gasoline would be too strong for the seeds, you can use plant oils, like sunflower oil as apolar solvent too, but you might need to rub the surface with that, because it is very slow otherwise.
Using hexane and ethanol like in the article March Ho linked is somewhat more sophisticated, but chemicals are harder to procure at least in some countries.


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Countercurrent multiplier mechanism
How exactly does the countercurrent multiplier mechanism work in formation of urine in the body? I am unable to find a satisfactory answer to this.

The countercurrent system permits forming a concentrated urine
In the presence of ADH, which increases water permeability, the hyposmotic fluid that enters the distal tubule (DT) from the thick ascending limb (TAL) looses most of its water by osmotic equilibration with the surrounding cortical interstitium along the CNT and cortical collecting duct (CCD). It also continues loosing NaCl through reabsorptive transport along DT, CNT and CCD, until the tubule fluid becomes isoosmotic with plasma, by the end of the CCD.
The relatively small amount of isoosmotic fluid that flows into the medullary collecting ducts losses progressively more and more water to the hyperosmotic medullary and papillary interstitia and is finally excreted as hyperosmotic, highly concentrated urine.
The countercurrent system permits forming a dilute urine
In the absence of ADH, the hyposmotic fluid that enters the DT from the loop of Henle, continues to be diluted by transport of NaCl via NaCl (thiazide sensitive) cotransporters into DT cells and via Na channels (amiloride sensitive) along the CD. Water reabsorption is limited so that the tubule fluid becomes more and more dilute along DT, CNT and collecting ducts (CCD, OMCD and IMCD), until it is excreted as a large volume of hyposmotic urine.
Sources:

Barac-Nieto, Prof. Mario. "Countercurrent System and the Loop of Henle." Countercurrent System and the Loop of Henle. Kuwait University. Web. 08 Feb. 2016.
Wikipedia. Wikimedia Foundation. Web. 08 Feb. 2016. https://en.wikipedia.org/wiki/Countercurrent_multiplication.
"7. Urinary Concentration (countercurrent Mechanism)." 7. Urinary Concentration (countercurrent Mechanism). Web. 08 Feb. 2016.


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How should one interpret heritability? Is it related to $R^2$?
From Wikipedia:

Heritability estimates are often misinterpreted if it is not understood that they refer to the proportion of variation between individuals on a trait that is due to genetic factors. It does not indicate the degree of genetic influence on the development of a trait of an individual. For example, it is incorrect to say that since the heritability of personality traits is about .6, that means that 60% of your personality is inherited from your parents and 40% comes from the environment.

So what is the plain english interpretation of heritability?
Is it supposed to be the genetics version of $R^2$? If so, please explain it to me anyway because I forgot my statistics.

I found this so from what I understand, one might say:

If height is estimated to be 80% heritable, and if we get 10 people, get their heights and then compute the variance, we say that around 80% of that variance is likely due to genetic factors while the remaining 20% is due to other things.

Such interpretation of heritability seems to work for non-categorical traits. What about categorical or binary traits?
Hair and eye colour is categorical (I think?). So what, we assign a number for each colour and then compute the variance?
ADHD is binary (I think?). Do we assign 0 for not having and 1 for having then compute variance?
I seem to recall regressing binary or categorical variables needs some kind of adjustments and hence interpretations of estimates (such as intercepts or slopes) may be different.

Also, the book linked above says

heritability represents the degree to which the variance in a trait is attributable to genetics in the population on average

Combining that with the Wiki paragraph above, I don't think someone saying

Eye colour is around 98% heritable. I have brown eyes. Therefore, around 98% of the reason why I have brown eyes is genetics.

is far off from saying

If we have a million people who near-identically flip a million near-identical coins a hundred times, and we compute the average of the coin flips that turn out to be heads to be 58.6, then the probability that you will flip heads when you near-identically flip this near-identical coin is around 58.6%.

Is it? (Of course 'near', 'around', etc are not always used similarly...lol)
So yeah, technically the 60/40 interpretation in the Wiki example is technically wrong but practically it's around 60% $\pm$ some standard deviation?

Possible duplicate of Why is a heritability coefficient not an index of "how genetic" something is?

@Remi.b $R^2$ is there?

No, it is true that the other post does not explicitly talk about the relationship between heritability and it's measure in parent-offspring regressions... I haven't decided yet how I would deal with that. I might retract my vote close soon but I must read your edit first :)

I would advice that you restrict your question to the regression interpretation of heritability and ask separately about the heritability of a non-quantitative trait.

Heritability (as shown a long time ago by Galton) is the slope of the parent-offspring regression. However, I don't understand it well enough for the moment to formulate an answer. +1 btw

@Remi.b Are you sure it is slope? Since it is a ratio of variances, it sounds closer to an $R^2$, though some manipulations might give you slope

Yes I am pretty sure. I would expect both the slope and the $R^2$ to get closer to 1 as heritability increases. I would vote to close as too broad until you reduced you post t only a single question (currently you talk about the interpretation of heritability as a regression and about the case of non-quantitative traits). Note that you might want to talk about which regression (which variables) you are referring to.

@Remi.b approaching 1 through values from the left? Anyway, go ahead and close for now, I guess. I'll split up and edit later on. Thanks ^-^

What do you mean "approaching 1 through values from the left"? If you agree that the question should be closed, you should probably just delete it (or vote to close as duplicate).

@Remi.b I'll edit it later. I'm asking if you mean for both slope and R2 that we have 0.8, 0.9, 0.99, 0.999, etc rather than 1.1, 1.05, 1.01, 1.001, 1.00001, etc or 0.9, 1.1, 0.99, 1.0001, 0.999, etc

Yes from the left. You should not have a slope steeper than 1 and it makes no sense to have a correlation coefficient greater than 1. You seem to describe the dynamic of a system (especially when seeing to hypothesize cyclic behaviour) though and I don't get it.

@Remi.b R2 and correlation coefficient I get. But why can't we have a slope steeper than 1? Is it a bio thing? I seem to recall slopes steeper than 1 in areas outside bio

Yes it is a bio thing! For a parent-offspring regression, only sampling error could cause slope to be higher than 1. In the whole population the slope is bounded between 0 and 1. We will have to delete all these comments once you've edited your post.

@Remi.b Thanks! ^-^ What am I supposed to do again? Not really into Bio SE hehe

The post Why does the slope of parent-offspring regression equals the heritability in the narrow sense? can help. Otherwise, I would recommend you having a look at the section on quantitative genetics of Gillespie's book.

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


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Anemiaceae etymology
What is the etymology of the name Anemiaceae for a family of ferns? I assume that it's from the name Anemia for one of its genera, but that is equally mysterious. Obviously it has no blood, but what fern does? I have been unable to find an answer by searching the internet.

That one is Greek origin from aneimon or "naked, unclad, without clothing" which is to refer to the panicles of the sporangia.


text:
Was there originally a non-ribosomal way of synthesizing proteins?
Proteins are synthesized on ribosomes from mRNA copies of regions of the DNA. But ribosomes themselves are made up of proteins (and RNA). So how could the first ribosomes have arisen? Was there previously some other way of making proteins other than by ribosomes and mRNA?

Although I am of the same opinion as fpdx and the majority of scientists — that there was an RNA world in which the genetic material and the catalytic molecules were RNA (rather than DNA and protein, respectively) — there are some quite respectable scientists who hold a different view. As there is no proof for either viewpoint (and hence no correct answer to the question), it is important to present this alternative.
In brief, the alternative viewpoint is of a "proteins-first" world: i.e. the first proteins were made without ribosomes from chemical reactions in the "primeval soup". Only later did the contemporary and template-driven ribonucleoprotein machinery for making proteins evolve.
I do not know of an online source of arguments in favour of the protein-first viewpoint — an article by C. Kurland in Bioessays 32: 866–871,(2010) requires library access or purchase. However there is an on-line article discussing the objections to the RNA-world viewpoint, which, even though it argues against these objections, gives one an idea why the question cannot be considered settled. This is available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495036/#B57.

(A quick answer to a question that will be likely closed being not well focused on the physics of all this)
First: the ribosome translates mRNA into the chain of amino acids that eventually will become a protein. The ribosome is a huge complex, made of both proteins and RNA. RNA can have enzymatic activity like a protein: the ribosome is a Ribozyme.
This chicken or the egg problem has puzzled biologists, chemists and biophysicists for a while. The structure itself of the ribosome was the "smocking gun" for the model we have today: the RNA world. In few words: because RNA can act as a protein and it is so similar to DNA, probably our DNA-world (i.e. information stored on the DNA, work done by proteins, RNA between the two) emerged from a fully RNA-world, where RNA was responsible for both protein activity and information storage.
How in detail all this happened by evolution, is probably the subject of several nobel prizes to come.


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Are these lovebugs?
I used to see these insects frequently in Chennai and Bangalore (South India). I just would like to know if this is a kind of lovebug. The lovebug as mentioned in the Wikipedia page is, however, different in appearance, although they too are walking as pairs.
Why are they always walking as attached pairs? It also seems to me that the bigger one drives the motion and decides the direction. Is that true?

I believe this is a member of the family of Phyrrocoridae also called firebugs. A more detailed identification would require a more high resolution image of the head and also an image of the ventral (belly) side. However, they are certainly not lovebugs.
Edit: As PhilipC pointed out, they are probably from the genus Melamphaus.

Taking a more high resolution picture is only necessary if you need to know to which subfamily or species of phyrrocoridae this bug belongs. However this classification will require a lot of detailed information (there are more than 300 species in the family of phyrrocoridae world wide), maybe even about the larval stages and thus a lot of work on your side and on the side of an expert doing the classification. Thus if you are satisfied with the information that this is a firebug, the picture is perfectly fine.

There's a pretty reasonable chance they are Melamphaus looking at the picture on Wikipedia, and that Bangalore is mentioned on that page.

As to them 'always' walking in pairs:
I had a different firebug (Pyrrhocoris apterus) living around my previous house. They do not always walk in pairs, especially early in spring i've often seen them walking alone. In summer pairs become more common indeed.
You will probably have guessed that the pairing has to do with sexual reproduction. The question however is why they stay together so long, as mating in insects usually takes no more then a few minutes. This is called mate-guarding, the male wants to make sure that the female deposits eggs with his sperm and stays with her until she has layed her eggs, as shown Shöfl & Taborsky 2002 (thanks to @fileunderwater for this reference.)
This behaviour is not uncommon for insects, and is also well documented for dragonflies (odonata, e.g. Corbet 1962).

Indeed so, see e.g. Schöfl & Taborsky. 2002. Prolonged tandem formation in firebugs (Pyrrhocoris apterus) serves mate-guarding

I agree with Phillip C's comment – this pretty much seems to look like a melamphaus

Melamphaus Stål, 1868
kingdom Animalia
phylum Arthropoda
class Insecta
order Hemiptera
suborder Heteroptera
superfamily Pyrrhocoroidea
family Pyrrhocoridae

Descriptive features

Body large (15–30 mm), elongate oval. Colour usually dark with different pattern on dorsum and venter; abdominal venter never with alternating black and light transverse stripes. Integument dull, covered by very short but distinct, dense pubescence. Head (Fig. 25) triangular, as wide as anterior margin of pronotum, postocular part gradually narrowing posteriad, eyes medium-sized, not stalked, remote from anterior margin of pronotum. Antenna relatively long, second segment distinctly longer than third. Labium long and gracile, surpassing posterior margin of metasternum, first segment surpassing base of head. Thorax: pronotum (Fig. 25) subtrapezoid, relatively elongate, lateral margins not explanate and reflexed. Metathoracic scent gland ostiole with well-developed peritreme (Fig. 20). Fore wing: apical angle of corium narrowly rounded. Abdomen: intersegmental sutures between abdominal sternites 4/5 and 5/6 laterally strongly curved anteriad. Legs: fore femora with small denticles ventrally.

Sources:
http://psybugs.biota.biodiv.tw/files/biota_psybugs/fig.1-2.jpg
http://psybugs.biota.biodiv.tw/pages/598


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Crossing over and exon shuffling?
Campbell Biology 10e, in discussing the functions of introns, writes:

The presence of introns in a gene may facilitate the evolution of new and potentially beneficial proteins as a result of a process known as exon shuffling. Introns increase the probability of crossing over between the exons of alleles of a gene—simply by providing more terrain for crossovers without interrupting coding sequences. This might result in new combinations of exons and proteins with altered structure and function. We can also imagine the occasional mixing and matching of exons between completely different (nonallelic) genes. Exon shuffling of either sort could lead to new proteins with novel combinations of functions. While most of the shuffling would result in nonbeneficial changes, occasionally a beneficial variant might arise.

Hitherto, I had perceived crossing over as the shuffling of alleles between two homologous chromosomes, not of parts of alleles. That is, breaks in the DNA during synapsis would occur in between loci, not within them. Am I wrong to think that? My books tell me that, with regards to evolution, sources of genetic variation include mutations and genetic recombination. Genetic recombination includes random fertilization, independent assortment of homologs, and crossing over, yet it is only mutations that can produce new genetic material. If exons were crossed over, then new alleles would be formed, would they not? Is this a type of mutation? (I do not recall studying such a specific case of mutations.)

Crossing over primarily happens because of homologous recombination (HR). From the molecular point of view, it can happen between any homologous regions and it is not necessary that an entire allele has to be crossed over. During the process of HR, a DNA double strand break occurs. This is followed by resection (exonucleolytic degradation of one of the strands — 5'→3', from the break-point) by the MRX complex which leads to formation of ssDNA ends. The length of these ssDNA ends dictate the total length of crossover region.

 Taken from: Branzei, Dana, and Marco Foiani. "Regulation of DNA repair throughout the cell cycle." Nature reviews Molecular cell biology 9.4 (2008): 297-308.

This length can be from around 1.5kb to over 10kb depending on the repair kinetics with possibly an average of 3kb (more than half the cases) [1, 2]. Therefore, the author speculates that the probability of intra-gene crossover would increase with increase in intron length. However, in my knowledge, there are no recent reports to validate this hypothesis.
Edit:
Going back to the original question. It is not necessary that entire alleles are crossed over. Generally the genome has some recombination "hotspots" flanked by what are known as LD (linkage disequilibrium) blocks. An LD block need not cover an entire gene, as observed by Twells et al. (2003)[3] :

LD breaks down in the region LRP5 g.5257T → G–LRP5 g.28149C → T, in
  intron 1 of theLRP5 gene. A second block of very strong LD
  (‖D'‖ > 0.9) is observed, LRP5 g.28149C → T–LRP5 g.45704G → A,
  spanning 17.6 kb of intron 1 to intron 3 of the LRP5 gene.

References:

Chung, Woo-Hyun, et al. "Defective resection at DNA double-strand breaks leads to de novo telomere formation and enhances gene targeting." PLoS Genet 6.5 (2010): e1000948.
Zhou, Yi, et al. "Quantitation of DNA double-strand break resection intermediates in human cells." Nucleic Acids Research (2013): gkt1309.
Twells, Rebecca CJ, et al. "Haplotype structure, LD blocks, and uneven recombination within the LRP5 gene." Genome Research 13.5 (2003): 845-855.

1) Does crossing over occur between gene loci, or can it occur within them?
The cross-over events can happen within genes in introns and/or exons and still lead to viable gametes.  The text is stating that it's the increased length from introns that increases the probability of a cross-over event there, which is basically true.  This is simplified, and there are hotspots for crossing over and low probability areas.  The exon shuffling between completely different genes would not occur by crossing over; there are other mechanisms that would lead to these kinds of structural rearrangements in gametes.
2) Would a new allele be formed by a cross-over between exons, and is this a type of mutation?
A new allele could be formed if one arrangement of exons is allele1, another is allele2, and the cross-over involving 1 and 2 is uniquely allele3. If this happens by a cross-over event, it is not a mutation.  Also, there is no "new" genetic material in allele3 even though it could be considered a new allele; it is only a new combination of sequence that existed in 1 and 2.


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What separates gene loci?
Introns are sections of noncoding DNA that separate exons within a gene locus. However, between different gene loci, I also would assume there to be noncoding regions of DNA. What are these regions called? (And if my assumption is wrong, then please correct me.)

These regions, if unannotated, are simply called intergenic regions.
Sometimes, if a large section of chromatin is regulated by an enhancer/silencer/locus control element, then there are boundary elements that demarcate this chromatin region and prevent the spread of the chromatin state to neighbouring regions.

It would be valid to call them "intergenic regions", but this is just another way of saying that they are the regions between genes. I don't think you can do much more because they are not homogenous in nature. Some may be short and perhaps lack any other function than that described by @WYSIWYG, others may be very long and have enhancers and regulatory elements for proximal or distal genes, simple repeated sequences, pseudogenes, replication origins etc. etc.


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Distinguishing Father from Brother
Given the (non-identical) DNA sequences of two men and the knowledge that the second man is either the father, brother, or son of the first man, is the DNA useful in determining which of these three he is?  Even the slightest probabilistic indicator would be useful.

I will clarify your question a little. We start with two men, Dave and John. We know Dave and John are related, either as brothers, or parent-child. Can we use genetics to work out their relationship?
If Dave and John are brothers they will have the same mtDNA, the DNA in the mitochondria, because mitochondria are maternally inherited. They should have the same Y chromosome, because they have the same father (the Y comes from the father, and males have one Y to pass on, therefore they each received the same Y).
If Dave (John) is John's (Dave's) father, then they should have different mtDNA because they have different mothers (assuming that Dave (John) didn't have a child with his mother or sister, and that mtDNA is variable within the population). They would have the same Y chromosome, because that is paternally inherited.
If Dave and John have the same X chromosome it would be indicative of the same mother (there is a 50% probability that two male siblings will have the same X chromosome, while the probability of a father and son having the same X chromosome would be determined by variability of the X chromosomes within the population).
For the autosomal part of the genome, each parent carries two copies of each gene. This means that, in each gene, there is the potential for four different alleles, with two of those being passed to the offspring. For example, at gene $A$ the mother may have alleles $A_1$ and $A_2$, while the father has $A_3$ and $A_4$. The offspring receives one copy from each parent, with equal probability. The probability that a son receives $A_3$ from the father is 50%. The probability that a second son receives the same $A_3$ allele is 50%. Therefore, both father-son and brother-brother relationships have a coefficient of relationship of 0.5.
In summary, the mtDNA will liekly be the best indicator, but it is only indicative, it is possible (but highly unlikely in most modern societies) for father and son to share the same mtDNA.

You could, in principle, work out whether Dave is John's son or his father. For example (a really over simplified example), look at the diagram below. You first look at Dave's sequence and one chromosome in a pair has the sequence AAAAAAAAAA (Red chromosome) while the other has GGGGGGGGGG (Yellow chromosome). You then look at John's sequence and find one chromosome with the sequence TTTTTTTTTT (Green chromosome) and one with the sequence AAAAGGGGGG (Red & Yellow Chromosome). John could have received the AAAAGGGGGG chromosome from Dave after Dave's red and yellow chromosome recombined, while it is not possible that John is the father of Dave. John's green chromosome came from his mother.

+1 I am not quite aware about this but does Y-chromosome have enough polymorphic loci to differentiate close relatives? Is the variation in Y sufficient for these tests?

Depends really - a lot of the problems are methodological (sequencing the Y is difficult because of heterochromatin and repeat sequences) - and populations should be highly depleted for variation within, it would depend on the specific population and some regions of the Y generate new variation quickly (again, repeat sequences)... The key to the question is really the mtDNA, that's going to be the best indicator. The Y should be the same in both males regardless of the relationship.

@WYSIWYG I made some edits to clarify the points.

Also, perhaps you can add a note on how to differentiate whether an individual, X, is a son or a father of the other individual, Y.

@WYSIWYG I haven't considered whether this actually possible before, here is something that I think should work in theory

Another possibility is to look at imprinted loci.

I think you meant "there is a 100% probability that two male siblings will have the same X chromosome" and that Steve is John, right?

It's 50% - the mother has two X chromosomes, each will receive one of those with 50% probably that they get the same one. Well spotted on the name.

OK, I get it now and see why the mtDNA is the better indicator.  By the way, for bonus points, if I had changed brother to "half-brother from the same father" in my original question, is there a method?

Male half sibs would have the same Y and different mtDNA and X chromosomes - and they'd be related at the autosomal loci with a coefficient of relatedness of 0.25 (differing at the maternally inherited genes inline with population variance, at the paternally inherited genes having 50% probability of identity by descent)


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Can DNA be denatured at acidic pH?
Some say that DNA is denatured only at basic pH. And some say at both acidic and basic pH. So I want to know clearly why and how if DNA is also denatured by basic pH.

Alkaline denaturation neutralize the charge of acids but also cause hydrolysis of bases upon prolonged treatment. Strong bases will raise pH until the H+ shared between the N-base electronegative centers (N-H and O=) is stripped from the H-bond, effectively breaking them.
Organic solvents such as dimethyl sulfoxide and formamide, or high pH, could break the hydrogen bonding between DNA strands too. Low salt concentration could also denature DNA double-strands by removing ions that stabilize the negative charges on the two strands from each other.
Low pH (less than pH 1): both RNA and DNA hydrolyze (phosphodiester bonds break and the bases break off).
High pH (greater than pH 11): RNA hydrolyzes, DNA will denature but the phosphodieser backbone remains intact.
[salt]
Tm is sensitive to Na+ concentration.
Na+ acts to shield the negative charges of the sugar-phosophate backbone from interacting with one another. The repulsion between the negatively charged phosphate backbones is the major force destabilizing the double helix, therefore increasing Na+ concentration increases helix stability and decreasing Na+ concentration decreases helix stability.
References:
http://faculty.tru.ca/dnelson/courses/biol335/335notes/3recdna/4-hybrization/recDNA3a.html
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1367631/pdf/biophysj00681-0002.pdf

So could u please explain how denaturation differs from hydrolysis?

@AungT  As far as i know with the term denaturation is related to the change from a double strand DNA (dsDNA) to a single strand DNA (ssDNA) due to breakage of hydrogen bonds (it could be caused by heat), while in hydrolysis there is a degradation of the strands backbone eg phosphodiesterases enzymes hydrolyse the phosphodiester bond between different nucleotides.

Denaturation is a process in which proteins or nucleic acids lose the quaternary structure, tertiary structure and secondary structure which is present in their native state, by application of some external stress or compound such as a strong acid or base, a concentrated inorganic salt, an organic solvent (e.g., alcohol or chloroform), radiation or heat
The denaturation of nucleic acids such as DNA due to high temperatures is the separation of a double strand into two single strands, which occurs when the hydrogen bonds between the strands are broken.
DNA Hydrolysis is a chemical method of DNA denaturation.DNA hydrolysis is the breaking of DNA through the addition of water. It can be done in several fashions; enzymatic (exonucleases)or chemicals (acid).
In general, hydrolysis is defined as the cleavage of chemical bonds by the addition of water
References:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806061/
file:///C:/Users/user/Downloads/9783540201120-c1.pdf

So hydrolysis is also a kind of denaturation? The difference is just the method used?


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Lifeforms concentrations of the categories of macromolecules, and Lipids
Lifeforms are formed of large, modular, organic molecules called macromolecules, large organic molecules called Lipids, and simpler molecules such as H2O.
Macromolecules are commonly grouped into the following categorises:

Protien
Nucleic Acid
Carbohydrate

The concentrations of these types of molecule by mass, in a dehydrated (therefore dead) "E. coli" are:
Protein: 55%
Nucleic Acid: 23%
Carbohydrate: 0%
Lipid: 9%

From: http://book.bionumbers.org/what-is-the-macromolecular-composition-of-the-cell

Q: Repeating the above table for other lifeforms, for the whole organism if it is multi-cellular, can examples be given of lifeforms that are particular outliers?

I have been unable to find much more useful information, however this data probably exists, I could find nothing for larger lifeforms such an animals. Around 60% of a cells cytosol is proteins, however this is by volume, not by mass.

I hope I was able to better word the question. Knowing more terminology made it possible to search for information more effectively and I was able to find an example. I can continue working on the question if needed, feedback is appreciated.

what do you want to know when you saw "outliers"? I didn't catch that one

Extreme, unusually high or low proportion by mass of one of those four categories. Protein, Nucleic Acid, Carbohydrate, or Lipid. An outlier in these concentrations compared to the vast majority of other lifeforms. From the chat, bacteria have a lot of protein and grains have a lot of carbohydrate, although I think grains are only part of a larger organism.

The values that you mentioned are not absolute. There is certainly a range. If you look at plants, the composition of carbohydrates will be high because of the cellulose cell wall.


text:
amount of tRNA and its extra arm
How much of the total RNAs is tRNA? Some say 15% and some 20%. Those percentages came from my different teachers. Which is correct? And what are the functions of the extra arm (variable loop) of tRNA? My teacher said it was just for classification but an international textbook says its function is unknown.

could you post sources for the claims of 20 and 15%

Total RNA of what? The species? What species? The cell? What cell? Total in terms of what? The number of genes coding for it? Molecular mass? RNA moieties? Please [edit] your question and clarify.

With respect to at least two sources I could find, tRNA is commonly reported as encompassing 15% total RNA in both rapidly-dividing mammalian cells such as HeLa, and in S. cerevisiae (1, 2). To give you an interesting tool to look it up in the same way I did, I used Harvards' Bionumbers webpage to search tRNA.
As for the function of the variable loop, it would seem that it serves to stabilize the tRNA overall structure through three-base interactions, and somehow interfaces with the type II tRNA synthetase (3). I'll try to find more on this interaction.


text:
What causes swelling after impact?
Why does the head swell after getting hit by something hard? What is the liquid that forms after impact?

When physical damage to the cells occur a biological process called inflammation occurs. When inflammation occurs, white blood cells are rushed to the area in order to fight off any bacteria or harmful waste leakage from damaging the cells further. In order to get the white blood cells to the site of damage faster, the body induces a process called vasodialation where the arteries are expanded and blood is rushed to the site. This causes the site of injury to swell and redden, two signs of inflammation. The white puss that forms comes from the white blood cells. The white blood cells release chemicals that kill of bacteria and waste in the area and forms a white pus that will eventually harden or break through the skin to be exerted. If the site of impact begins swelling within a matter of hours, it is likely acute inflammation is occurring and the body is rushing blood to the site. However, if swelling occurs on a more rapid time scale it is more likely that this fluid is from the damage of the impact itself and the cells and capillaries are leaking blood and extracellular fluids (What is Swelling?).
In short, when you bump your head your body is trying to fight off further injury and infection by inducing the inflammatory response. It is also leaking fluids due to the impact and may result in rapid swelling at site of impact. The symptoms you discuss are due to inflammation and are a normal process of your body's defense mechanism. Hope this helps!

I'm not sure you're correct (at least I'd appreciate seeing evidence for your assertions.) Inflammation takes time. The bump that appears after hitting one's head takes moments to minutes. I think this is much more likely to be simple extravasation of serum from damaged cells and capillaries, etc.

Thanks for the rebuttal. The question offered no information when regards to time scale, but vasodilation and rush of blood to the site of impact can occur within a matter of hours (http://www.nationwidechildrens.org/swelling-bodys-reaction-to-injury). If swelling occurs on a shorter time frame, @anongoodnurse 10  is correct in saying it is likely due to the peripheral damage to the capillaries and cellular structure. Thanks for the input, I will be updating my answer!


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Sexing fish from a tissue sample
I am a member of a local fish club, we have a lot of different aquarium fish and would like to trade them amongst us. We all have a few fish that don't form pairs and would like to see if they pair up with someone else's. But as you can imagine keeping track of all the fish would be extremely hard and pointless if they were the same gender, so someone suggested we should buy a microscope and sex them via tissue or blood sample. But none of us has any experience doing that or if that is even possible, so we need some expert advice on the matter.
I wish to know if you can tell the gender of a fish from a tissue or blood sample and what equipment do you need (how much magnification in a microscope)? We work with discus and other cichlids, and countless marine aquarium fish.
For the sake of being specific I restrict my question to Discus fish, however, I would like to know if any general principles of tissue-sample based identification exist, for different species of fish.

I know nothing about ichtiology but if you just google discus fish sexing you get tons of hits (including videos).

But it's not restricted to discus fish, they are just the most common fish with sexing difficulties that came to mind. As for the google results, they are useless copy-paste guesswork.

I might misunderstand your point. Discus fish are maybe just one example but it is impossible to describe sexing generally for all fish. Is it? Or maybe you are asking for a list of methods generally used for sexing without willing to discuss sexing for any specific species? However, question like the magnification will obviously vary between 1X to 500X I suppose.

Well if you have a tissue sample you may be able to do genetic testing (PCR and gel electrophoresis) but it depends on species - sex determination systems are variable in nature. Asking what magnification scope you would need makes it sound like you want it to be a visual inspection method.

Depending on the number of fish, sending tissue to sequencing might be cheaper than buying a microscope. But it only works if the species is 100% GSD (genetic sex determination) and this depend on the species (won't work for clownfish for example). Also karyotyping might be a solution for GSD that have sex chromosomes which also depend on the species. The feasibility of a non-lethal visual inspection (with or without a microscope) depends on the species. So really....it depends on the species

Ironically, assuming 100% GSD, FISH might be a good option :)

As already pointed out by Remi, you can identify the sex from a tissue sample only if there is a genetic (such as chromosomal) sex determination system (by using techniques such as PCR or in-situ hybridization). However, different species of fish employ different mechanisms of sex determination:

Focus on or attachment to genetic systems involving X and Y
  chromosomes must quickly be shed in studies of sex determination in
  fish due to the diversity of mechanisms utilized, and, by doing so,
  the researcher can explore alternative regulatory mechanisms that hold
  important clues for understanding sex determination in general. The
  biology and ecology of fish is sufficiently diverse to provide unique
  examples of sex-determination mechanisms, yet they possess many of the
  same processes and pathways that are used in other vertebrate systems.

 Devlin, Robert H., and Yoshitaka Nagahama. "Sex determination and sex differentiation in fish: an overview of genetic, physiological, and environmental influences." Aquaculture 208.3 (2002): 191-364.

Though Devlin and Nagahama comment (above) that fishes also employ the same signalling pathways as other vertebrates for sex determination, study of these pathways to determine the sex would be extremely difficult as you may be aware that the cell-signalling and the gene regulatory networks are highly complex.
Fishes are highly sexually dimorphic (including Discus) and the sex can be easily identified (with some practice) by visual inspection. Microscopic identification would be both money and time consuming. Morphology based identification can be automated (when the machine is trained sufficiently). You can have a look at this article1 which is about using image analysis to score salmons.

1.    Merz, Joseph E., and William R. Merz. "Morphological features used to identify Chinook salmon sex during fish passage." The Southwestern Naturalist 49.2 (2004): 197-202.


text:
What is the function of the Moderator band?
The moderator band in the right ventricle is a band sorts of muscle which consists of a significant branch of the AV bundle. Does it mean it delivers impulses to the anterior papillary muscle faster? If it does, how does this help? and why only the anterior papillary muscle? What makes it special to have a moderator band?

Does it mean it delivers impulses to the anterior papillary muscle faster?

Yes.

If it does, how does this help?

To facilitate the conduction time thereby allowing coordinated contraction of the anterior papillary muscle.

and why only the anterior papillary muscle?

This is because its chordae tendineae insert into anterior and posterior tricuspid valve leaflets, so only their contraction before systole would be optimum.

What makes it special to have a moderator band?

For effective Cardiac Output because it helps in coordinated contraction of ventricular cells. The ventricles must maximize systolic pressure to force blood through the circulation, so all the ventricular cells must work together.

Could you add some reputable support/citations for your answer? Thanks!


text:
How would one identify cellular transcription factors associated with a viral protein in a treated cell line?
I've been working as the computer guy for a microbiology lab for the past few months. I've always been interested in bench work, but my wet lab experience is rather limited and thus so is my understanding of wet lab techniques.
The PI has expressed his support and given me the opportunity to conduct my own project from start to finish (generation of wet lab data and computational analysis) and write a paper in preparation for my Ph.D school applications.
I realize that coming up with an actual question is a long and thought out process so I want to do my homework before approaching him with a question. I've read quite a bit of literature and have come up with a question i'd like to answer, the computational stuff I can handle and explain in detail, but I'm having a hard time with the wet lab techniques I could use to generate some of the data i'm interested in.
Effectively I am looking to obtain a list of potential cellular transcription factors that are physically associated (bound) with/by a specific viral protein. Is there a lab technique that would allow me to generate such a list?
Links to papers, wikis, your own theories or anything will be greatly appreciated. Also any advice, or "this isn't possible" is all appreciated, as long as you can give me a bit of "this is why".
Thank you! (PS I'm not sure if this type of post is allowed here).
EDIT: It is important to note that I am looking for new binding partners.

Co-immunoprecipitation followed by a western blot comes to mind; you pull out a known TF from lysate with antibodies and then try to detect what you suspect is complexed with it in a western blot with another antibody for the viral protein, or vice versa.

@Kendall this can only be done for TF's that are known or that we believe to be associated with the viral protein correct? What if there is no research on TF's that bind with this viral protein, so I have to actually identify new binding partners (I know this is non-trival and probably an entire paper on its own).

Basically you need to have antibodies to what you are studying, and when you do the actual pull down the hope is your TF is complexed in some way with your viral protein, so that during the western blot if you get detection with the second antibody, you can logically conclude that there is a physical interaction between the two. Co-IP cant discriminate direct/indirect association, however, so if you need to know the direct binding partners, a more complex technique is necessary

If you need to identify new binding partners for some reason, you probably need to do something like tandem affinity purification (basically somehow purify the unknown binding partners) followed by separation and biophysical methods like mass spec.

That second answer is what I was looking for, the viral protein hasn't been studied in the context of binding to host cell chromatin so i'm interested in determining at least one of it's binding factors. Some computational analysis done on another paper my lab has written leads me to believe that the viral protein recruits some regulatory transcription factors in order to bind to chromatin, but there isn't much or anything known about who these TF's are.


text:
Do primate RGCs have overlapping receptive fields?
According to this link,
http://hubel.med.harvard.edu/book/b10.htm
retinal ganglion cells (RGCs) receive input from overlapping receptive fields (RFs). This is also an idea used in convolutional neural networks for deep learning of images.
On the other hand, this one, for the primate retina, states that there is no such overlap:
http://www.sciencedirect.com/science/article/pii/0042698995001670
So do primate RGCs have overlapping RFs? If not, how does the primate visual system deal with this sparse input? How does it fill in the blanks?

Another one that says "no overlap in mammalian retina": http://webvision.med.utah.edu/book/part-ii-anatomy-and-physiology-of-the-retina/morphology-and-circuitry-of-ganglion-cells/
And yet another that says "overlap in cat retina": http://faculty.washington.edu/jpalmer/files/Teller/ByChapter/tellerChapter08.pdf (pg 214, fig 8.14)

A paper with overlap in cat retina: http://www.ncbi.nlm.nih.gov/pubmed/480198

Short answer
Associated ON- and OFF-center retinal ganglion cells can show 100% overlap in their receptive field.
Background
When looking at the elementary neurophysiology of the retina, we can see that a single cone generally synapses onto two bipolars. Because photoreceptor cells hyperpolarize when illuminated, glutamate release from their synapse is inhibited. In turn, OFF-center bipolar cells are hyperpolarized and ON-center bipolars are depolarized. The OFF-center bipolar synapses onto an OFF-center retinal ganglion cell (RGC), while the ON-center synapses onto an ON-center RGC (Fig. 1).

 Retinal circuitry linking cones to bipolar cells (left panel) and bipolar cells to retinal ganglion cells (right panel). source: Washington University.
Then to your question - the basic circuitry shows that the ON- and OFF-center RGCs receive their input from a single cone and hence have 100% overlapping field. In the foveal region, bipolars link 1:1 on cones, as in Fig. 1, so in this example case, they show 100% overlap.
Note that there are an estimated 30 types of retinal ganglion cells, about half of them being not even described yet, as per a 2015 review article (Sanes & Masland, 2015). Hence, this answer is anywhere from exhaustive, but it does show there can be substantial overlap between RGCs.
Reference
- Sanes & Masland, Ann Rev Neurosci (2015); 38: 221-46


text:
How and why do skin tags develop?
WebMD writes:

Skin tags are small, soft pieces of skin that stick out on a thin stem. They most often appear on the neck, armpits, upper trunk, and body folds. The cause of skin tags is not known.

Do we really know nothing about why they appear? Is there research that suggest hypotheses of the causes of skin tags?
It seems to me a pretty well established phenomena for it to be without good research.

Given that skin tags are considered benign, it doesn't surprise me to find very little published research focusing on them. It's unlikely that much grant money exists to answer questions about them.
That said, though, I found a handful of groups that have done some work on them. It seems that they all noticed a statistical relationship between the occurrence of skin tags, obesity and metabolic syndrome. These are the papers describing their research efforts so far:
http://onlinelibrary.wiley.com/doi/10.1111/j.1468-3083.2011.04401.x/epdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740583/
http://www.ncbi.nlm.nih.gov/pubmed/21860156
None of the groups suggest a mechanistic explanation for the occurrence of skin tags, which makes me think that this remains a very open question. However, they all notice a correlation between skin tags and elevated leptin levels.
Leptin is best known as a hunger/satiety regulating hormone. However, it functions through the activation of the JAK/STAT pathway, which in turn activates a number of genes involved in cell survival and in turning off apoptosis, or programmed cell death.

This image comes from this paper in Nature, which, unfortunately, is behind a paywall.
So, my guess based on these data is that increased levels of leptin activate proliferative pathways in cells, leading to the occurrence of skin tags. That this proliferation results in benign cell growth probably has to do with competing tumor-suppressor and related pathways, which I can reasonably assume to be active and functioning, where outright cancer is not present.
What I wonder now, but can't find any information on, is whether skin tags are the only visible evidence of differential cell proliferation, or whether there are other instances within the body. That is, if the leptin-to-skin-tag hypothesis holds, is there something special about skin cells in that response, or are they just the only visible signs of it?

Are there any cases of skin tags forming into cancerous tumors?


text:
Why do denatured proteins tend to be less soluble than the native protein?
Why do denatured proteins tend to be less soluble than the native protein?
In terms of hydrophobic effects, could anyone explain this phenomenon for me?

Put bluntly, soluble proteins have shielded as many hydrophobic residues in their sequence as possible from the solvent (say cytosol, primarily aqueous). As the solvent then has access primarily to hydrophilic residues, the protein is largely soluble. Denatured proteins with large, exposed regions of hydrophobic residues become insoluble because hydrophobic molecules do not dissolve in water. As this is what amounts to a homework question, however, do keep in mind for subsequent questions that this site requires some personal effort to obtain a good answer!

Background information
A native protein has it's hydrophobic amino acids folded inwards, so it has a hydrophobic core. why? Because it's thermodynamically favoured. When a protein is denatured the hydrophobic amino acids won't be longer inside the core of the protein, but instead will be exposed to the hydrophilic environment (assuming you are talking about a protein inside an organism). But this isn't thermodynamically favoured because hydrophobic parts cannot form H-bonds with water and so aren't much soluble in water:

So when this happens, many protein molecules will aggregate like soap micelles (because hydrophobic interactions are favored). This will lower the total surface area of hydrophobic amino acids in contact with the water, thus lower disturbance in H-bonding in water molecules.
Here's my self-made depiction of effect of organics molecule on H-bonding in water (its quite rough, so don't care about fine details).

Summarized
hydrophobic amino acids will be exposed to the hydrophilic environment --> the proteins will aggregate together --> insoluble plaque.


text:
What do proton pump inhibitors do?
I know that sodium azide and 2,4-DNPH inhibit proton pumps. The azide is called an inhibitor and 2,4-DNP is called uncoupler. I want to know what's the difference between the mechanisms of action of sodium azide and 2,4-DNPH in proton pumps. Why is one called an inhibitor and the other an uncoupler?

There's a decent presentation here that basically goes over what you're asking.
As an inhibitor, azides are similar to cyanide in that they inhibit complex IV by binding cytochrome oxidase, resulting in a sort of chemical asphyxiation.
Uncouplers are a little harder to wrap your head around. They embed in the membrane space, and we know that ETC and proton pumping depends on the established proton gradient across a membrane. Uncouplers uncouple the proton gradient from the electron transport chain, allowing protons to diffuse across the membrane, effectively negating the proton gradient.

Isn't OP asking about protein pumps? This answer seems to focus on ATPases. It's just all in the name, but just wondering.

The question is weird because when i think proton pump inhibitor, i think like omeprazole or benzimidazole derivatives which block the ATPase. I think the title is just misguided, because the compounds in the question body inhibit the electron transport chain.


text:
Good pipetting technique?
Good pipetting technique is essential for many biologists, but it can be hard to get right. When I take 1 µl of liquid using a micropipette, I seem to always take less than 1 µl, and that amount is variable/inconsistent. I would like to know what could be wrong.
What is the proper pipetting technique? Could it be that the pipette is inaccurate?

Welcome to Biology.SE. You should try to give more info about the moment at which you realize you did not piped exactly one microlitre. Do you see directly in the pipette that you did not pipette 1 microlitre. Or do you sometimes have some leftover in the pipette and sometimes not. Do you think the pipette you are using might be in cause?

I wouldn't be surprised if your pipette needs some service. Some of the parts (rubber rings) that are important for proper function wear out and need to be replaced every now and then.

I've retracted my close vote, good pipetting technique is essential in a lot of biology. General pipetting technique information would be of use.

This post can be made a community wiki but I'll leave that decision with the OP and @rg255

What pipette did you use? Using a 10-ml one won't help you. Use the smallest one you can find. Also, when you use one single pipette to combine all solutions  and that one pipette has a systematic error (i.e., calibration needed, but not done) then there is no issue, as it is all about relative volumes. If you use multiple pipettes to combine fluids into a reaction mixture, then trouble arises.

Here's some step-by-step advice on good pipetting technique:

Make sure the pipette is set for the correct volume
Ensure the tip is firmly attached
Keep the pipette vertical when pipetting
Slowly and smoothly depress the plunger to the correct point (the first stop position)
Insert the tip in to the liquid to be pipetted. Ensure the tip is properly immersed in the liquid, but not touching/near any surfaces of the container
Slowly and smoothly release the plunger back, keeping the pipette upright, and tip immersed, and making sure no bubbles form - you can try pre-wetting (see video linked below, around 3:00)
Withdraw the pipette from the liquid
Carefully dispense the liquid in to the desired container by steadily depressing the plunger to the second stop position (fully depressed), making sure all liquid is dispensed without spills or splashes.

"Put the tip in a 45-degree angle onto the wall of the container; then
  start pushing down up until the first stop; then push through to the
  second stop; keep the plunger depressed and remove pipette and check
  whether the drop is in the container and pipette tip is empty" -
  Christiaan

Discard the tip using the release plunger

Also check you've got the right size/type of tip, and are using a suitable pipette (e.g. don't use a 10-100 µl pipette for 120 µl)
If this still causes incorrect measures then you could need to get your pipette calibrated.
Test a pipette by taking several samples. If the pipetted volume is consistent but incorrect (e.g. always 10% under the target) it suggests the pipette needs calibrating, it's probably not the technique that's wrong. If it is inconsistent (both under and over pipetting) then it's either technique or the pipette (bad/damaged pipettes can be inconsistent, poorly but good calibrated pipettes will more likely be consistent and only need calibrating).
Try using multiple pipettes, if they are each consistent but variance is among them (pipette 1 is always under by ~10%, pipette 2 is always over by 15%, pipette 3 is always over by ~2%...) then your technique is good, and you need better pipettes. Also get an experienced pipetter to check your technique and try the pipettes themselves.
Calibration can be done internally by lab techs or by external specialists, speak to your lab responsible person.

Also see this video which is well explained.

Additional point: care should be taken while pipetting surfactants and viscous liquids. Surfactant containing liquids should be properly mixed prior to dispensing and mixing by pipetting just before dispensing (with the same tip) should be avoided. Multiple rounds of pipetting creates bubbles inside the tip and leads to picking up of lower volumes. Viscous liquids should be gently pipetted and care should be taken to not let the liquid stick on the exterior of the tip.

It's also a good idea to practice your pipetting with serial dilutions of colored compounds, then measure the absorbance of each one and plot it. If your slope is off, you need to keep practicing, or fix your pipettes.

It's been a long time since I held one, but ref. step 8) - shouldn't you always put the tip in a 45-degree angle onto the wall of the container; then start pushing down up until the first stop; then push through to the second stop; keep the plunger depressed and remove pipette and check whether the drop is in the container and pipette tip is empty? Then give a few small taps to the container to make sure the drop is at the bottom of the container?

first of all i need to disclose i work for Andrew Alliance, but i answer for the sake of providing information and not for commercial purposes. What you experience depends - as we measured with our robot - from the humidity in the environment. if you have 1 nL of liquid water evaporating inside the tip, becasue the environmental humidity is low, it will become 1 ul of water vapour above the liquid level, so your sample will go down by the equivalent of 1 uL. you can verify this phenomenon by extracting the tip from the liquid, recovering air pressure and keeping the humidity inside the tip, and re-aspirating the liquid. This is actually why calibration laboratories work at 70% ambient humidity...

Interesting detail, I have never thought about it.


text:
What is the definition of a mutation?
There are two alleles that determine the sensitivity of a person to Coumadin (a medicine for blood thinners used to treat a stroke etc). Sometimes you encounter the terminology that one has a mutation on both alleles (father's and mother's side). But why is that called a mutation and not just a variation? Does a mutation mean that it changed during lifetime, or is the difference between mutation and variation arbitrarily defined? Or is there really a kind of standard taken where deviations are considered to be mutations?

Good question!
The term mutation can be used with two different meanings. Each definition can further be split into two different more detailed definitions. The reason for this slight mess is mainly historical. In short, a mutation can refer to

An event

narrow sense
broad sense

An allele

definition based on ancestral/derived states
definition based on frequency

Before going into the details of these definitions, it is important to first define a few other terms.
A few other definitions
The terms I want to define here are Locus, polymorphic locus, allele, nucleotide and phenotype.
In short (simplified version), a phenotype is the way an individual look. The variations of phenotypes of the individuals in a population depends upon the variation of genotypes and the variation of environments that they encounter. This concept is very much related to the concept of heritability. You may want to read more about it here.
The DNA sequence is made of four nucleotides. It is the sequence of these nucleotides that affect the phenotype of an individual
A locus is refers to the position of a DNA sequence of arbitrary length. At a given locus different types of sequence can exist, such a coding or non-coding sequence, a gene or just an intron, only a few codons, etc..
An allele is one variant of a sequence (often a gene) at a given locus. If, in the population, more than one allele exists at a given locus, than the locus is said to be polymorphic. Most polymorphic loci have only two alleles. In such case we can talk about bi-allelic loci.
Mutation as an event
A mutation can refer to an event.
Narrow definition
A mutation may refer to the event of a spontaneous change in the nucleotide sequence of an individual such as typically an indel (insertion or deletion of one or few nucleotides) or a substitution (substitution of a nucleotide by another one). In other words, a mutation can refer to the event of changing allele (eventually making up a new one) at a given locus.
Broad definition
The broad definition is similar to the narrow one expect that it encompass more types of genetic changes. In the broad sense, a mutation may refer more globally to any genetic spontaneous change. For example a whole chromosome deletion or a full genome duplication are examples of mutations.
In my experience, most often when the term "mutation" is used, it is to refer to the broad definition of mutation.
Mutation as an allele
A mutation can refer to an allele. Note however that very often we prefer using the terms "mutant allele", "mutant state" or just "mutant" as synonym to refer to this allele. Pretty much the only circumstance in which we would use the term mutation here is in sentences of the kind "Individual A carries the mutation.".
Definition based one ancestral/derived states
A mutation can refer to the allele that is derived from a more ancestral allele. Consider for example, a given locus was NOT polymorphic in the past. A mutation (in the sense of "event") occurs and the locus is now polymorphic. The allele that has been created by the mutation (in the sense of "event") is sometimes called "mutation".
Definition based on frequency
A mutation can refer to the allele that is at the lowest frequency in the population. For example, consider a bi-allelic locus with two alleles A and B. If the frequency of the allele B is lower than $\frac{1}{2}$ (that is lower than the frequency of the allele A), then the allele B can be referred to as the mutation. The reason for calling "mutation" the allele that is at low frequency is that most mutations are deleterious and as a consequence the mutant allele is often at low frequency. As a consequence, using the Definition based on frequency and Definition based one ancestral/derived states is often not important.
To address your question specifically
It is a little hard to directly address your question as it seems to have several misunderstanding on the concept of mutation. In the same time however, it feels like you are turning around the realization that there are several definitions in use.

Sometimes you encounter the terminology that one has a mutation on both alleles (father's and mother's side). But why is that called a mutation and not just a variation?

The term mutation (whichever definition you pick) is intrinsically related to the concept of variation in the population but not so much to variation within a single individual (homozygote vs heterozygote).
If an individual "has a mutation on both allele", refers to the term mutation as an allele (in the narrow sense probably) and not as an event. More specifically it refers to one allele at a polymorphic locus (probably a locus of only one nucleotide) within the allele considered at the larger polymorphic locus considered.

Does a mutation mean that it changed during lifetime

A mutation (in the sense of event) is a change that if often view at the moment of reproduction but the mutation may have occurred anytime in the lineage of the germ cells. Note, one may consider also mutation that occurred (during the lifetime of the individual) but in the soma cells. Such mutation will NOT be transmitted to the offspring.

Or is there really a kind of standard taken where deviations are considered to be mutations?

Well...yes! A deviation is a deviation to a reference. In other words, we can replace "deviation" by "one allele of a polymorphic locus" in your question. And yes, a mutation (in the sense of a given allele) can refers to one allele of a polymorphic locus.

Good comprehensive answer that I generally agree with. However, I think you should add a reference or two to make it more authoritative.

Also, can you comment on what should be the minimum frequency of a mutant allele to call it a polymorph or variant.

@fileunderwater I am not aware of anybody clearly defining these terms (except for broad vs narrow definition of mutation). One could only find examples of cases where "mutation" is used with one or another definition.

@WYSIWYG I do not think there is any minimum frequency in principle. The use of a threshold appears as a result of a methodological problem. Sequencing makes error and to avoid to consider polymorphic a locus that is not but where sequencing error occurred, we use a minimal frequency.

A couple of dictionary entries (containing both mutation as event and new allele vs parental type) and this page from Understanding evolution should be a start. My point is that the current, unsourced, answer might be read as your personal opinion, when most of it could be well-sourced.

Most polymorphic loci have only two alleles. Why? Isn't polymorphic more relate to the population level?

Both the terms allele and polymorphic are meaningful only when considering a group (or population) of individuals.A locus is polymorphic if, there are variants, at this locus, among individuals within your group. Those variants are called alleles.

What I was taught by people in genomics is that "variation" is preferred for an allele that was not private to just one individual or family, but was found in pretty much unrelated individuals, while "mutation" is preferred for a very recently changed allele that is private to one individual or their family.  Sometimes, it seems the "mutation" is preferred when you mean to imply a clinically relevant difference caused by that different allele (as opposed to a polymorphism, which is usually what we call a survival-neutral different allele) I would say that the term "mutation" is being used incorrectly in your case unless the variant just appeared de novo, but maybe they do mean it in the second sense, because this difference clearly has a clinical phenotype associated with it.

I have a hard time to think of any case where one could hesitate between using the term mutation or variation as one refer to either an event or an allele and the other refers to the existence of polymorphism.

Sometimes you encounter the terminology that one has a mutation on both alleles (father's and mother's side). But why is that called a mutation and not just a variation?

To answer this question, we first need to define a few terms:

What is a Genetic Mutation?
A genetic mutation is a permanent modification to the DNA of an organism, such that the modification causes differences in the DNA that are not "typically" found amongst other members of the organism's population. These mutations can be classified into two major categories, and are defined by the means in which the organism obtained the mutation(s): hereditary mutations, and acquired (somatic) mutations.

Inherited mutations are prevalent throughout virtually every cell within the organism's body, and are most commonly referred to as
germline mutations. The primary causes of germline mutations are
cell replication errors, cell age, and environmental factors;
however, there is still little data on this, and as a result, it is
still widely debated as to which of these is most to blame. An
example of an inherited mutation is Sickle Cell Disease.

Acquired mutations are located only within affected somatic cells, and are caused by environmetal factors, such as UV radiation (see
Xeroderma pigmentosum), or by DNA replication errors during
mitosis.

The fundamental difference between inherited and acquired mutations is that inherited mutations are passed down from parent to offspring, whereas acquired mutations are not.
With both inherited and acquired mutations, they can occur in any of the following ways:

Missense mutation
Nonsense mutation
Insertion
Deletion
Duplication
Frameshift mutation

See here (page 7) for a brief description of each.

What is Genetic Variation?
Genetic variation is a descriptive term that encapsulates the comparision of a DNA sequence belonging to an organism with respect to the composite, genetic "profile" of the population that the organism is a member of. For each expressed (phenotypic) trait of an organism, and of a population, there are a collection of possiblities with respect to how that trait is in fact expressed. Examples of variation for a given trait, when considering humans, are:

Ear lobe shape - free; attached
Hairline - widow's peak; straight
Hair color - black; brown; blonde; red/orange

It's important to note that genetic variation is not (commonly) brought about by the occurrence of mutations, but in fact, is caused by polymorphisms.

So, how do the two differ?

Does a mutation mean that it changed during lifetime, or is the difference between mutation and variation arbitrarily defined?

A genetic mutation occurs after a normal allele has been transferred from parent to offspring, and then that allele is altered into an "abnormal" state. Implicitely speaking, a mutation is referencing a single individual.
Conversely, a polymorphism is a DNA sequence that is acquired (inherited) from the parent, remains unaltered, and is commonly found within the organism's population. Again, implicitely speaking, genetic variation maintains the perspective of the population, and not of a single individual.

Or is there really a kind of standard taken where deviations are considered to be mutations?

The cutoff for if an allele is considered to be a polymorphism or a mutation is 1%. Which is to say that 1% or more of the population must carry that variation of the allele for to be considered a polymorphism; otherwise, it's a mutation (see here and here). Note though that this cutoff is completely arbitrary.

Now, to answer your overarching question...
The reason why an allele may be described as a variation or a mutation is due to the kind of cell that the allele is contained within (germ vs somatic) upon aleration, when the allelic DNA sequence was defined (before/after inheritance), and how prevalent within the organism's population that allele is (cutoff).
In the case of Coumadin (Warfarin), according to the National Institutes of Health, it would seem that a person's sensativity to Coumadin is dictated by autosomal dominant polymorphisms, and so, the alleles involved would be considered a variation, and not a mutation.

Many genes are involved in the metabolism of warfarin and in determining the drug's effects in the body. Certain common changes (polymorphisms) in the CYP2C9 and VKORC1 genes account for 30 percent of the variation in warfarin metabolism due to genetic factors. Polymorphisms in other genes, some of which have not been identified, have a smaller effect on warfarin metabolism.