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What physics knowledge can be applied to biology of organisms and ecosystems?
In the wiki page of Biophysics:

Biophysics spans all scales of biological organization, from the molecular scale to whole organisms and ecosystems.

But after searching on the internet; the dominant application of physics in biology that I see is at the molecular scale. In the wiki page Mathematical biophysics, there is a lot of interesting information, but it is only about mathematical knowledge applied to biophysics, not physics itself.
What, if any, physics knowledge (based on principles and laws of physics) can be applied to biology in the sense of organisms and ecosystems?

For a non-molecular example, see biomechanics.

This question should provide one example: http://biology.stackexchange.com/questions/11044/how-do-trees-lift-water-higher-than-10-meters/

Thanks, that's organism scale. What's about ecosystem? @fileunderwater

You might be interested in reading about biomimetics.

Brownian motion.. It is used for migrations and dispersal

This question is really asking for examples, and the list of ways that knowledge of physics can be used in biology could be very long. However, here are a couple of examples:

Systems ecology, especially with regard to energy and nutrient flow.
This type of ecology can be strongly influenced by physics. For one example see the book Theoretical Ecosystem Ecology: Understanding Element Cycles by Ågren & Bosatta (Ågren was originally a physicist)
Physical limitations to growth and transport
This can include for instance mechanical contraints on plant growth (see e.g. the book Plant Physics by Nicklas & Spatz), water transport in trees (see e.g. this BioSE question) or the biomechanics of movement (see e.g. Hudson et al (2012) on the speed and movement of cheetahs or Wikipedia: Biomechanics).
Allometric relationships between organisms, e.g. with regard to metabolism
To explain these types of relationships knowledge in physics is useful. See e.g. Kleiber's law for more.
MAXENT as a general approach to ecological patterns or to model species distributions
This is basically a tool lifted from physics that can be applied to ecological problems. There are many papers to look at, but Harte & Newman (2014) (Harte is another previous physicist) and Elith et al (2010) are two good starting points.
Dynamical modelling of populations and communities
This field use many of the same tools for analysis as physics, e.g. systems of differential equations. One of the pioneers in this field (among many) were Robert May (also started with a PhD in physics), and his classical book Theoretical Ecology: Principles and Applications is still a good starting point.
Energy harnessing and conversion by organisms
This can refer both to how organsims convert prey to energy (e.g. conversion efficiencies) and the physics of photosynthesis (which is an interesting intersection between physics and molecular biology). See Jang et al (2004) and O'Reilly & Olaya-Castro (2013) for examples of the how quantum mechanics can inform us about photosynthesis.

Hopefully this will give you a sense of some different ways that knowledge in physics can be useful for biology.

Thank you so much for taking your time writing this wonderful answer :D

I am currently interested in evolution. Does any of your suggestions have it? Does any field in evolution have physics in there?


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What is the importance of urea in mass spectrometry?
What is the importance of urea in mass spectrometry? We use 8M urea to FASP our proteins prior to mass spectrometry.  What is the significance of using 8M urea? and how does it affect the proteins?

What does FASP mean? Otherwise high concentrated urea is used to denaturate proteins.

@Chris filter aided sample preparation

I think that the OP was asking about relevance of using urea with respect to the FASP method. In the FASP method, the primary denaturant is SDS . Protein are denatured with a ~4% SDS solution (buffered to pH 7.5 - 8.0). Then 8 M urea solution is used to replace the SDS. Urea serves two purposes here, first it keeps the protein denatured and in solutions as SDS is replaced/washed off. Second, because urea is a chaotropic agent, it reduces the size of SDS micelles which otherwise would block the pores of the membrane filter.
Read the original article here: http://www.nature.com/nmeth/journal/v6/n5/abs/nmeth.1322.html

One more thing I think should be added: it is important to understand that denaturants like urea, GuHCl, or SDS not only unfold/denature protein, but also keep them in solution thereby allowing their biochemical analysis. Otherwise heating to ~100 ºC or using Trichloroacetic acid can also denature protein, but they render protein insoluble.

8M urea is a denaturant, as @Chris mentioned. Denaturing proteins is important for molecular (aka classical) mass spectrometry. If you analyzed a non-denatured protein, you'd get information not only on the primary structure, but also on noncovalent interaction (2+°):

The classical MS approach, so-called “molecular MS,” analyzes, in the gas phase of the mass spectrometer, individual species initially present in solution after destruction of the noncovalent framework. On the other hand, “supramolecular MS” or “nondenaturing MS” aims at transferring intact noncovalent complexes that preexist in solution into the gas phase of the instrument.
(Sanglier et al. 2008, Methods Mol. Biol.)

Denaturing proteins is important for molecular/classical mass spec because it ensures your analysis only reflects the covalent bonds (primary structure) present in your target protein.

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Protocol for checking pipette calibrations using absorbance readings of a dye in solution?
I've been looking around the net looking for a nice protocol to validate micropipette calibrations using absorbance readings of a dye in solution. Does anyone have one they can share? I'd highly appreciate it!

you mean absorbance?

I just weigh water on an analytical balance and then compare the measured mass to what the mass should have been given the density of water. You should check the temperature of your water to be sure you have the right density.

^ I second this. I don't see why you would calibrate a micropipette using a spectro over gravimetric analysis.

I've never done it, but it seems to me like all you'd need to know is the concentration and extinction coefficient (at whatever wavelength) of the dye.

Thanks for the feedback. We are just trying to come up with the fastest way possible of validating the accuracy of a robot that dispenses into 96 well plates within a given run as well as to check for variations from one run to another over the course of time. We are tight on time and do not have enough trained hands on deck for the gravinometric procedure.  @Chris Stronks, I've edited accordingly.

does the manufacturer of the robot perhaps supply overall error rates and variability measures?

@Yaritza weigh the plate! If you are looking for variations within a plate I would suggest you use 12 or 8 sample strips. good luck, sounds like cool #$%^ your doing.

@Yaritza. Usual spectrometers keep the path length fixed and illumination is done horizontally (to measure conc.). Therefore the differences in volume don't matter as long as the light path is through the analyte. For your experiment you would have to fix a concentration and would need a vertical illumination so that you can measure the level by absorbance (varying path length); you would have to design such a setup and have it built AFAIK there is no setup like that.

To measure dispensed volume you'd have to dispense a small amount of dye into a known-volume container and measure the concentration of dye or something. I'm not sure which technique is better, but you don't have to rebuild your spectrometer. If you're dispensing very small volumes perhaps dye would be better than weight?

I see what you are getting at however this would be a very WRONG way of calibrating such an instrument. If dyes varied among trials it would throw off your calibration. Also, you would need to generate some sort of standard curve to equate absorbance to weight, since true calibration of these instruments is done by weighing the volumes they dispense (1g = 1ml water). The weight of water and the weight of your dye solution will not increase the same in terms of moles/g. Also a scale is far easier to calibrate that the detector in any spectrophotometer. Calibrate pipettes by weighing the volume of water they dispense. It should be done in a chamber that inhibits evaporation and you need a precision scale.
Here's a reliable guide for pipette calibration
enter link description here

A regular 5 place balance with doors and some wet sponges on the edges should help minimize evaporation while you try to take measurements.

I found an article published by Beckman Coulter for measuring the accuracy of their liquid handling automation platforms. It could be used for hand-help pipettes as well

Link-only answers are generally frowned upon on Stack Exchange sites. In time it is possible for links to atrophy (as your's has) and become unavailable, meaning that your answer is useless to users in the future. It would be best if you could provide the general details of your answer in your actual post, citing your link as a reference.

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Is it possible to move your arms above your head when handcuffed in the back?
This move was seen in Pitch Black and i wonder if it is possible at all. Say you are handcuffed to a pole, hands in the back, and the pôle is a little higher than your head. You just want to do a complete loop with your hands, going above your head, so they end up in front of you and you are free of the pole.
Now, putting horrible pain aside, is it possible to perform this move alone?
If not, maybe with a small surface to rely on, for a lever effect?
Would it cause minor / major damage at all or just pain ?
I am also curious if performing this move slightly turned sideways help ( as much as you could at least, considering the situation). In the movie he goes one shoulder at a time.
Anyway, i hope im clear enough !
Exactly what i mean is this video at 1:35

Contortionists do far more painful looking stuff, so I guess with the right training it could be possible.

Sort of like http://youtu.be/lY5V5la5nhU, https://www.youtube.com/watch?v=5bJyXN9EBrk or http://youtu.be/RpV4FHyQTyc?
Depends on the hight of the pole though.

Thanks everyone !
I just saw someone wrote an amazing answer that i was about to validate, but then deleted it. :(

I edited my answer with an exact video if what i saw.

Another very clear example https://www.youtube.com/watch?v=fRcuoLSDTjM, and a contortionist like this: http://youtu.be/sPYU24bauOM could do it without any problems.

yeah my sister can do it and she never said it was painful :P

i can do it. i can put my hands behind my back than over my head many times before. even with handcuffs, i tested myself.

maybe if you can, step through the handcuffs and then it'd also be in front. it's not easy or for everyone, I'll grant you, but it's possible for some

This is not normally possible or would be extremely painful if done. But there are special cases.

Atraumatic dislocation.
  This occurs when the shoulder dislocates with minimal force such as reaching up for an object or turning over in bed. Usually it will 'pop' back in itself or with a little help. Normally this type of dislocation does not need reducing in A&E. It can occur regularly throughout the day and will be associated with certain positions the arm is placed into. This type of dislocation is associated with people that have 'lax' joints, for example people who hyper-extend their knees and elbows and can get the palms of both hands onto the floor with ease.  This joint laxity is normal for these people and the onset of dislocation can be associated with a change in how the muscles around the shoulder are interacting with each other or a change in posture/ position of the arm. This can produce an imbalance in the control of the joint. Referral for appropriate physiotherapy is the initial form of management. The physiotherapist should look at the way in which the muscles and shoulder joint is moving and posture aiming to restore the balance. Treatment can 'cure' the problem as long as the exercises and advice is continued, but in some cases there is only minimal or nil benefit. At this point surgical intervention is indicated.
Positional Non-traumatic dislocations.
  This group of people can dislocate their shoulders without any form or history of trauma. Some may have started out dislocating their shoulder as a party trick; others may have always had shoulders that just 'fall' out of joint. This type of dislocation is usually painless and can be put back in easily. Both shoulders are typically involved. The cause of this type of dislocation is usually a result of what we call 'abnormal muscle patterning' which means the strong muscles around the shoulder joint are not working in the correct order causing them to pull the shoulder out of joint with active movement in the particular direction such as lifting the arm forward above the head or out to the side and above the head.  The main treatment for this is physiotherapy that looks at re-sequencing the muscles in order to prevent further dislocations.  Occasionaly surgery in the form of thermal capsular shrinkage or plication may be neccessary.

Taken from here such people would be able to dislocate then get their hands in front and relocate.
The body can be trained to be quite flexible through training like gymnastics etc...

Depending on the situation (i.e. orientation/rigidity of cuffed hands and the height of the pole), you could potentially escape, but getting your arms flipped around where your hands are in front of you would involve serious damage.
It may be technically possible to achieve alone with some way to continue wedge your arms further, but the pain would probably knock you out before you succeeded.

I thought so, too; see @fileunderwater's YouTube link.


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What is the effect of persistent hypothermia on cardiac performance?
I define persistent hypothermia in this thread about the mechanisms of persistent hypothermia.
The Graph of Katzung et al. in Pharmacology about Heart Failure:

I am thinking which parts here are critical on temperature.
Temperature has a direct effect of reaction rates of chemical reactions here, for instance NE, AII and probably chemical reactions in endothelin such as ET.
Therefore, I am thinking that the relationship between temperature and cardiac performance cannot be linear at all.
Some have said me that low temperature can decrease metabolism and oxygen consumption.
However, I started to think differently when time goes enough far that is when heart cannot anymore supply enough blood with oxygen. Thus, hypoxia can occur and asymptomatic exodus may occur.
Physiological case
Based on physiology, I can propose that the cardiac output curve shifts to the left (CO1 $\to$ CO2), due to less oxygen being supplied to the heart, similarly EDV1 (end-diastolic volume) shifts $\to$ EDV2 and SV1 (stroke volume) $\to$ SV2.
However, the venous return (VR) curve can shift much more, since I propose that the effect of temperature on smooth musculature is relatively bigger than on heart because of proportional size of tissue.
So the VR1 shifts to VR2, so EDV2 $\to$ EDV3 and SV2 $\to$ SV3.
Consequently, SV3 > SV1, while EDV3 < EDV1.
See my draft figure about this:

where EDV (End Diastolic Volume) in the x-axis and SV (Stroke Volume) in the y-axis.
In a healthy person, who have no hypertrophy of ventricles and elastic myocardium, the heart can tolerate this. So such a condition of cardiac failure as in the figure 13-3 is possible.
However, if flexibility of the myocardium, for instance, is not possible, such a pathway may not be possible.
The autonomic nervous system may enter the picture and increase vagus nerve stimulation (PS more).
However, not sure about the exact pathway.
What is the effect of temperature on cardiac performance?
How can temperature decrease cardiac performance?

Many processes are affected by temperature including metabolism and growth rates. Reaction rates increase with temperature but not in case of catalysed reactions where the catalyst can operate at only an optimum temperature. See this related post.

Why is the venous return increasing as temperature decreases? Please label the X and Y axis more clearly

Winter swimming and infarcts
The publication Long-term risks of cardiac and cerebral vascular diseases increased following winter swimming in the cold seawater which came out just some weeks ago shows a link between long-term winter swimming and CVD.
I think this is the best evidence so far about the possible link.
WYSIWYG's comment has some good general idea:

Many processes are affected by temperature including metabolism and
  growth rates. Reaction rates increase with temperature but not in case
  of catalysed reactions where the catalyst can operate at only an
  optimum temperature.

Some related topics

temperature effect on the rate of protein degradation

So further studies

protein degradation in the heart in persistent hypothermia
...

Effect of persistent hypothermia on processes of cAF
[1]
Let's have cAF (chronic atrial fibrillation) here as an target.
Electrophysiological study shows that cAF-related remodeling is typically divided into three categories: 1) electrical, 2) contractile and 3) structural.
They cause respectively

1) shortening of both the action potential (AP) duration and effective refractory period (ERP)
2) possibly a result of impaired Ca2+ intracellular handling
3) changes of cellular level (hypertrophy, glycogen accumulation and modified mitochondrial morphology) and tissue fibrosis

cAF's processes in persistent hypothermia
I cannot say now more anything about persistent hypothermia and cAF by confidence.
Those mechanisms of Koivumäki et al are cellular processes, while the representation of the heart requires integrative analysis in the cellular, tissue and organ levels.
In cellular level

Only some catalyzed reactions can work in persistent hypothermia. TODO consider which enzymes of the heart and body work in low temperature in short-term and long-term cases. Depletion cases too.
Effect of persistent hypothermia on the outflux of Calcium (probably, slows down).

In tissue level

I can say without rigor that electrical coordination is uncoordinated in tissue fibrosis.

In organ level

I say say without rigor that the mean electrical axis should be determined and fixed in the study.
Effect of Arterial hypertension must be fixed. Sokolew-Lyon index can a starting point for the indicator but better indicator is required with higher specificity.

Persistent hypothermia from the extreme side (Sauna)

[2] Regular Sauna is with better hemodynamic function; however, the association of sauna bathing with cardiovascular and all-cause mortality is not known.

so possible effect of persistent hypothermia can be

lower hemodynamic function if no compensation mechanism
better hemodynamic function if some compensation mechanism (genetics; unknown)

Some research topics

Effect of Persistent Hypothermia on the Arterial Hypertension. This may be associated with coagulopathy, especially in the lower limb.
Effect of Persistent Hypothermia on Atherosclerosis. It would be very nice to see long-term study about the effect of regular 4-7 winter swimming on the cardiovascular risk score, SCORE and others.

Sources

In Silico Screening of the Key Cellular Remodeling Targets in Chronic Atrial Fibrillation. Koivumäki et al. Computational Biology.
Association Between Sauna Bathing and Fatal Cardiovascular and All-Cause Mortality Events, here

Please, see the reference of the publication for more better view.

Both pictures you posted show that increased peripheral vascular resistance decrease cardiac output. If you are talking about someone outdoors not properly dressed in a Scandinavian winter, then their cutaneous vasculature would constrict and Also their extremities would get less blood flow. That would increase peripheral vascular resistance and thus decrease cardiac output. These articles were the first to pop up for me (http://circres.ahajournals.org/content/7/3/366 & http://www.ncbi.nlm.nih.gov/pubmed/10215232) and it seems to say that the primary cause of increased vascular resistance is actually caused by decreased cardiac output as well as local control.
This may seem contradictory to therapeutic use of hypothermia, where it is used to decrease metabolic needs (I don't know what is the mechanism for this) to help compensate for hypoxia (in cardiac tissue and the brain?). Cooling the heart would decrease it's metabolic needs (less perfusion, increased metabolic demands resulting from sympathetic input to heart. I guess the same thing probably happens when doctors prescribe a beta-blocker or non-dihydropyridine calcium channel blocker (CCB), the vascular resistance probably increases (except for the CCB diltiazem which dilates blood vessels in addition to it's effects on the heart). But the main thing is the sympathetic output to the heart, which is blocked by these drugs, and cold; this is more important than the increased peripheral vascular resistance. But remember that afterload is not identical to peripheral vascular resistance!!! The decreased cardiac output would probably decrease blood pressure and afterload, I'm guessing.
As for the slowing of reactions related to vasoconstriction (transmission of nervous signal from hypothalamus via pre ganglionic sympathetic fiber, then synapse in sympathetic chain, then transmission via post ganglionic nerve; release of NE, Epi, AT-II; rate of diffusion to receptor; effect of cold on membrane fluidity; effect on the alpha adrenergic receptor; rate of second messenger signalling cascade; effect of cAMP formation by G stimulator protein or breakdown by phosphodiesterase; effect of Ca++ release; effect on PLC mediated IP3/DAG release; effect on NO release and receptor stimulation of guanylate cyclase;  and the various other factors regulating endothelial function and smooth muscle contraction), I don't know. I also assume that an increase in viscosity (a factor included in the calculation of vascular resistance) could be another factor leading to increased vascular resistance, but even if this happens, this is less important than the decrease of the hearts metabolic rate.
Personally I'm not acquainted with the literature on therapeutic use of hypothermia, aside from the ethical debates about using Nazi hypothermia research. I'm just going at it with the same physiology knowledge you have, and relaying your confusion back at you. I'm just as lazy as you and I don't feel like spending hours delving into review articles on hypothermia research, but I agree that it is an interesting question, and it is also relevant to other very important topics in medicine (ie. use of beta blockers, non-dihydropyridine CCBs other than diltiazem).

I am not speaking about someone not dressing adequately for the winter. Persistent. The temperature remains anytime at 36 C.

Okay, then ignore the stuff on viscosity of blood affecting vascular resistance. And ignore, as you already should have, all my info don't knows on factors affecting endothelial function and smooth muscle contraction. Also a shivering reaction would increase the bodies overall metabolic rate, which would likely increase demand for oxygen, but  who cares, probably none of this matters, since we are only focused on the heart. If the heart is cooled, as in cardiothoracic surgery, it's metabolic rate decreases. There are alternative uses for decreasing cerebral metabolic rate.

Btw I suck at the metric system, is 36 degrees normal or low? Really I don't know the definition of "persistent hypothermia".

36.0 C is very slow. Normal is 36.5–37.5 C.

Okay, so my main point is that most of the damage doesn't come from the dilation of the heart and it's reduced contractility (as far as I know), but the increased metabolic demand placed on the heart: the after load and the increased sympathetic output affecting the heart. I think a heart affected by a negative isotope/chronotrope (drugs previously mentioned) or hypothermia is not pumping enough so I think afterload would fall despite increased vascular resistance. Plus it's insensitive to NE/epi. Problem solved. I am not a cardiologist, so I could be wrong.

Okay, now that I read your other question on this forum, I get that I'm not answering your question. Persistent hypothermia is some odd condition that affects "normal" people, not iatrogenic or a polar bear swim. I've never heard of it, so i can't answer.

Please, search for it as described by the condition. It is covered in some places but with emphasis that we do not understand the mechanisms. This thread is the first place in any literature which tries to understand its mechanisms and try to explain it. Some interesting cases, I have found, where asymptomatic exodus, and where even supporting the temperature by external devices cannot keep the temperature in the normal range. There is very likely change in the set point of body temperature, probably pathology related to hypothalamus.

@Masi What is asymptomatic exodus?


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Why did humans become bipedal?
Somewhere in evolutionary history homo started walking upright and became bipedal. You hear these hypotheses that, by walking upright, they could see better across the grassy savannas to escape predators, find food, find fellow humans etc. However, the most parsimonious way to accomplish looking farther across the grassy plains is by growing taller - much less adaptations necessary and hence more favorable from an evolutionary perspective. Other hypotheses say homo freed his hands to carry things. Quite fine, but some apes are known to carry around stuff. Moreover, walking on all fours increases running speed (you don't have to see far if you can escape faster) and apes climb trees better (what's a better place to hide from predators?). Hence my question: Why has bipedalism been favored in evolution?

I don't have a good source for this, but my anthro class in undergrad claimed it was an energetic efficiency thing. I've also heard it was for cooling reasons (less sun cross section during the hottest part of the day).

As already pointed it out, there is no scientific consensus on the answer to this question. This is because it is hard to test proposed explanations and it's likely that several factors interacted.
All of these have been claimed to be the explanation for the evolution of bipedalism:

Freed hands for increased tool use. (Encyclopedia Britannica)
Freed hands for the use of weapons in hunting or the use of containers to transport plant foods obtained by gathering.
There are three variants: the “man the hunter” version which sees male hunting as the key stimulus (Washburn 1967 in Haraway 2013); the “woman the gatherer” version which sees women needing their hands free to carry gathered vegetable foods as the stimulus; and the “man the provisioner” version, which stresses males carrying food (either meat or plants) to provision females and offspring.
All of these explanations are probably flawed because they invoke present utility to explain the origins of bipedalism.
Bipedalism was created by female sexual selection of males with large, visible genitals.
Although unlikely, this may be correct, but it is impossible to test. (Encyclopedia Britannica)
Bipedalism evolved to aid in avoiding predators. Higher head allows you to see longer distances over the grass. (Encyclopedia Britannica)
Bipedalism evolves because it allows energy efficient locomotion between forest patches in an increasingly open environment.
“Radiator theory”: Natural selection favored bipedalism in open environments because it decreases exposure to the sun and helps keep the brain cool. (Wheeler, discussed in Haviland 2007 and Encyclopedia Britannica)
Brain is highly sensitive to heat stress.
This allowed hominins to be active in mid-day, when competing predators are less active. (Essentials of Physical Anthropology, p. 165). Since the same carnivorous animals with which hominins were in competition (both would scavenge dead game) could attack hominins, hominins were probably safer from predator attacks during midday as well.
Terrestrial bipedalism may be a continuation of an upright body posture inherent in a tree-climbing/brachiating adaptation.
Gibbons, the most arboreal of the apes and the best brachiators, walk bipedally on the rare occasions they come to the ground. (Encyclopedia Britannica)

The earliest hominin fossils appear to have been bipedal, with no clear evidence of a transition through a knuckle-walking stage, the principal mode of locomotion of modern African ape. (Kivell and Schmitt 2009, here's a secondary source, and here's a primary source that disagrees, Richmond and Strait 2000)
If this is true, then the modern African ape mode of locomotion (knuckle-walking) is a derived trait, and vertical body posture may be the ancestral trait in the African hominoid evolutionary lineages. In other words, if this is true, the ancestor of all great apes including humans was already bipedal, and modern African apes have evolved to knuckle-walk since then.
Also if this is true, the previously mentioned factors would reinforce and refine bipedal locomotion in the hominin lineage.
It is likely that explanations 4, 5, 6 and 7 all interacted to select for bipedalism. They correspond best to the paleontological and ecological data. Numbers 1 and 2 are unlikely, because bipedalism appears long before evidence of tool use.

Bipedalism does NOT predate tool use, All the great apes use tools. It iso also worth noting there is a prevalent theory that chimps( and bonobo) may be secondarily quadrupedal and our common ancestor may have been bipedal.

The thunder chimp's answer summarized the answer very well.  To try to pull things together a bit, if you have seven minutes, check out this video.  It shows a man chasing down a kudu. They both run for 8 hours, until the kudu literally collapses and the man calmly walks up to it and slays it.  The video shows the evolutionary adaptions that the man has - he sweats all over his body, cooling himself. The kudu needs shade to cool, and sweats only a little.  The man can carry water, to replenish himself.  The animal cannot.
Perhaps more importantly, the man walks upright on two feet, thus shifting his center of gravity in a energetically favorable way.  The animal is restricted to galloping, which is faster for a sprint but not energetically favorable for long distance running.
Here are some articles for further reading:
Evolution of Marathon Running
The Energetic Paradox of Human Running and Hominid Evolution
Endurance running and the evolution of Homo
They say similar things as the video: that we evolved for persistence hunting in an arid environment.  This is an activity that the other primates don't engage in. Our ability to hunt effectively allow us to eat more meat, and thus favored efficient long distance running.

Dogs can trot for days on end. It is the most efficient gait.

The ones that co-evolved with us? Or the wild ones in Africa? Or Both? @nocomprende

Your name doesn't @ for some reason... Anyway: I don't think it makes much difference, but domestic dogs probably don't get as much opportunity to trot for days as the Dingoes in Africa that I was referring to. Someone HAS run a 4 minute mile, that doesn't mean everyone can. No one will ever run a 2 minute mile. It is good to recall that the original "Marathon runner" died.

I doubt you are going to be satisfied with any answer since the authorities on the matter can't test the many hypothesis and don't all agree. Around the time of homo erectus (1.89 million years ago), hominids began walking upright on a more permanent basis but this wasn't the only evolutionary event. Additionally, hominids began growing taller now as well [1].
Charles Darwin hypothesized that upright walking was linked to tool use in 1871 [2]. In 2009, Lovejoy reformalized Darwin's hypothesis and came to the conclusion that upright walking comes down to food and sex [3].

To be successful providers, males needed their arms and hands free to carry food, and thus bipedalism evolved. This scenario, as with all bipedalism hypotheses, is really hard to test. But earlier this year, researchers offered some support when they found that chimpanzees tend to walk bipedally when carrying rare or valuable foods.
At this point, Lovejoy suggests, a mutually beneficial arrangement evolved: Males gathered food for females and their young and in return females mate exclusively with their providers. To be successful providers, males needed their arms and hands free to carry food, and thus bipedalism evolved. This scenario, as with all bipedalism hypotheses, is really hard to test. [1]

In 1980, Peter Rodman and Henry McHenry claimed that bipedalism carries bioenergetic advantages [4]. Then in 2007, another group of researchers validated the energy advantage of walking upright [5].

Raichlen notes that if the same variation existed in our early ape-like ancestors as does in today's chimps, with some finding it easier to walk than others, this could have helped to drive adaptation. "That's what natural selection would be able to work on," he says [5].

Since there is no agreement and testing many of theses hypothesis are impossible since early hominids no longer exist, no one in their right mind can say, "Chris, this is why we evolved to walk." Even if they were correct, it would take some time to cycle through the academic community before it gained enough support to be the consensus.

Someone can be in their right mind and say why even if there is no consensus. Only one person needs to be right for it to be the answer.


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Hamilton's inclusive fitness approach
The underlying intuition of Hamilton's model of inclusive fitness is that we should study social behaviors from the point of view of actors -- rather than the recipients. To build his model, Hamilton expresses the genotype of the actor $j$ in terms of the genotype of the recipient of
the behavior, $i$. The genotype of $j$ is decomposed in two parts,
``genes which are copies by direct replication of genes in $i$; the
other part consists of non-replica genes'' (Hamilton 1970, p. 1219).
Hamilton (1970) further defines $q_{i}$ as the gene frequency of the
replica part, $b_{ij}$ represents the replica fraction, and $q$ is the average gene frequency in the population. From these definitions Hamilton (1970) jumps to the equality:
\begin{equation}
      E (q_{j}) = \frac{1}{1-b_{i}}\left\{ (b_{ij} - b_{i})q_{i} + (1-b_{ij})q\right\}
\end{equation}
where
\begin{align*}
  b_{i} = \frac{1}{n}\sum_{j}b_{ij}
\end{align*}
How did Hamilton derive the above equation?

Here is what I think Hamilton is doing. My impression is that the above equation expresses $E(q_j | q_i)$ as a linear regression on $q_i$. In other words, I think the above equation is equivalent to:
$E(q_j | q_i) = E(q_j) + \beta (q_i - E(q_i))$
$E(q_j | q_i) = q + \beta (q_i - q)$
In fact, this equation is equivalent to Hamilton's equation if the regression coefficient is:
$\beta = (b_{ij} - b_i) / (1 - b_i)$
However, I haven't been able to derive this regression coefficient. Given that $\beta = Cov (q_j, q_i)/Var (q_i)$, I suspect that the way to go is to rewrite $q_j$ and $q_i$ in terms of $b_{ij}$ and $b_i$ and calculate the regression coefficient.

Reference:
Hamilton 1970 "Selfish and Spiteful Behaviour in an Evolutionary Model"
http://www.nature.com/nature/journal/v228/n5277/abs/2281218a0.html

Hamilton's papers are always sooo complicated!

Agreed! I think his 1964 papers are even worse. I suppose the above equation is a linear regression of $q_j$ on $q_i$. But I still don't see how Hamilton arrived at the equation above.

Sad to see that research-level question often don't receive as much attention as basic questions. I hope you'll get some more upvotes and will get someone less lazy than me that will be ready to dive into Hamilton's article.

I can't access the paper so can you provide more detail about the model. Also, $E(q_j|q_i)$ conditional expected value?

@dustin: Hamilton does not use conditional probabilities. I'm the one that wrote that way when I was explaining my question. I changed this now.

@dustin: I also added the relevant portion of his paper. What Hamilton does earlier is to express the fitness from the point of view of the recipient. This is described here: http://biology.stackexchange.com/questions/26396/hamiltons-derivation-of-direct-fitness-from-his-1970-paper

It is not a regression (not at this stage of the paper, a regression will be done latter)
The only complicated thing to understand is $b_i$, which is the 'base relatedness', ie how $i$ is related to a random individual (to be compared to how related it is to individuals with whom it interacts).
To simplify let's first consider the situation where $b_i = 0$:
$E(qj) = b_{i,j} q_i + (1-b_{i,j}) q$ is just the translation of 'the gene frequency of the replica part is q_i' and 'the gene frequency of the non replica part is $q$'; because $b_{i,j}$ is the fraction of the replica part, ie the chances that our locus of interest belongs to the replica part of individual $i$ in individual $j$.
Now let's re-introduce $b_i$. The idea is to compare relatedness of the two individuals $i$ and $j$ to the average relatedness of $i$ with a randomly picked individual in the population (this random relatedness is exactly $bi$). This is important because $q$ already accounts for this 'random relatedness'.
So instead of giving probability $b_{i,j}$ to $q_i$, we give it probability $b_{i,j}-b_i$, which is the chance that the allele of interest is present because of the replica fraction being higher than random. And because now the quantity varies between 0 and $1-b_i$ we normalize it by $1-b_i$

The underlying intuition of Hamilton's model of inclusive fitness is that we should study social behaviors from the point of view of actors -- rather than the recipients

Not exactly, it is saying that we should study social behaviors from the point of view of the alleles causing it, that may be shared between the actors and the recipients. But this paper is not the paper that introduces inclusive fitness, quite the opposite it is the paper that tries to reconciliate kin selection with Price equation.

you say that $(b_{i,j}-b_i) \in [0,1-b_i]$. My impression is that  $(b_{i,j}-b_i) \in [-b_i,1-b_i]$.  $(b_{i,j}-b_i)$ will be negative when the individual $j$ is less related to individual $i$ than average.

I suppose the lower bound of $\frac{(b_{ij} - b_{i})}{(1-b_{i})}$ is $- \frac{b_{i}}{(1-b_{i})}$ (since $0\leq b_{ij} \leq 1$). However, this doesn't seem right because, otherwise, $\frac{(b_{ij} - b_{i})}{(1-b_{i})}$ could assume values in the interval $[0, -\infty)$.

From the limited information, I can provide the following but I am not sure if this is what you are looking for. Also, I still don't see the statement where the author concludes we get the Linear regression model $E(q_i) = Aq_i + C$ which is odd notation since it says the expected value is a linear regression. In fact, if it is a linear regression, it should say $q_j = Aq_i + C$.
$$
A = \frac{\text{cov}(q_i,q_j)}{\text{var}(q_i)}\quad\text{and}\quad C = E[q_j] - \frac{\text{cov}(q_i,q_j)}{\text{var}(q_i)}E[q_i].
$$
Now, we can write the variance and covariance as
\begin{align}
\text{var}(q_i) &= E[q_i^2]-E^2[q_i]\\
\text{cov}(q_i,q_j) &= E[q_iq_j]-E[q_i]E[q_j]
\end{align}
where the expected value of a discrete random variable $X$ is calculated as
$$
E[X] = \sum_{i=1}^Nx_ip_X[x_i]
$$
where $p_X[x_i]$ is probability of $x_i$ and $N$ can be countable infinite.

The mean of conditional PDFs comes up in optimal prediction where the minimum mean square error is $E_{Y\mid X}[Y\mid x]$. This optimal prediction covers linear and nonlinear. For the standard Gaussian PDF, the optimal prediction will be linear since $E_{Y\mid X}[Y\mid x]=\rho x$ where $\rho$ is the correlation coefficient. I am going to short hand $E_{Y\mid X}[Y\mid x]$ to $E[Y\mid x]$
$$
E[Y\mid x] = \mu_Y + \frac{\rho\sigma_Y}{\sigma_X}(x-\mu_X)
$$
where $\mu_i$ $i=X,Y$ is the mean and $\sigma_i$ is the standard deviation. If $X$ and $Y$ are not Gaussian, then the model can be nonlinear. Are there examples of non Gaussian be linear probably.

You're right. Hamilton does not say that this equation is a linear regression. This is something that I assumed (I changed my question to reflect that). My guess is that Hamilton's above equation expresses $E(q_j\mid q_i) = E(q_j) + \beta (q_i - E(q_i))$, where $\beta$ is the regression coefficient.

@falsum what do you mean by $E[q_j\mid q_i]$. I know it has a conditional expected value. Is that what you mean?

Yes. This is what I mean. My guess is that Hamilton is providing an equation that is trying to predict the gene frequency of a random actor (i.e., $q_j$) from a given $q_i$.

@falsum If we use that definition, there is a chance it will be a nonlinear predictor not linear.


text:
Mutation Rate in Multicellular Eukaryotes
I always hear people saying that the mutation rate is around $10^{-6}$ or $10^{-7}$. I don't even know if this number is the mutation rate of genes or of a single nucleotides and I actually (almost) never seen a referenced estimation of the mutation rate.
I know there is an impressive variance in mutation rate depending on the species we look at and depending on the genomic region we look at. Various other factors also influence the mutation rate such as ecological factors (thermal stress for example).
In multicellular eukaryotes, what is a good estimate of the mutation rate per nucleotide, per gene and per genome? How does real values vary around these estimates?

Actually depends on the environment also you see: Mutagens etc. BTW did you see Bert Volgenstein's paper in science last week on cancer prevalence and replication error. You would find it interesting

@WYSIWYG Thanks for the reference. No I haven't read that paper yet. Yes, I actually edited my post right before your comment to add "ecological factors" in the list of things influencing the mutation rate.

The real mutation rate of any organism depends by too many factors both external, like the environment, and internal, like the error rate of the DNA polymerases and DNA-repair enzymes and even from different region in the same genome (the mutation rate of non-coding DNA tend to be higher than the one of actively used DNA).
In general however it is possible to determine an average mutation rate for a given organism and usually it is expressed in mutation per base pair (or single nucleotide) per generation.
If you want to know roughly the mutation rate per gene or per genome you just need to multiply the mutation rate by the number of bases of the gene or genome.
Good papers on the topic are:

Drake JW, Charlesworth B, Charlesworth D, Crow JF (April 1998). "Rates
  of spontaneous mutation". Genetics 148 (4): 1667–86.
Ossowski S, Schneeberger K, Lucas-Lledó JI, et al. (January 2010).
  "The rate and molecular spectrum of spontaneous mutations in
  Arabidopsis thaliana". Science 327 (5961): 92–4.
Nachman MW, Crowell SL (September 2000). "Estimate of the mutation
  rate per nucleotide in humans". Genetics 156 (1): 297–304.

If you want to know about some specific organism you have to dig into the literature...

Hello. Welcome to bioSE. I guess the OP is aware of what mutation rates are. OP is asking information on Multicellular Eukaryotes. I understand it is a broad category. So can you, from the articles that you have listed, paste some excerpt or provide information otherwise about the estimated figures of mutation rates for the respective organisms?

Hello! Indeed, as WYSIWYG said, I am looking for estimates of mutation rate in multicellular eukaryotes and estimates of how the mutation rate varies (variations being caused by a whole bunch of factors as you said). Thanks for the references.

The point is that "Multicellular Eukaryotes" is a huge category... Here are some numbers from the papers cited before http://www.genetics.org/content/148/4/1667/T5.expansion.html the paper "Rates of Spontaneous Mutation" report all the details...

@alec_djinn I understand that it is a broad category. Can you please look more carefully at my previous comment. I'll upvote your answer if you do that :)

Ok...Then, summarizing the data I got from the publications above, the mutation rate per genome per replication span from 0.01 (in C.elegans) to 0.5 (in Mouse).
Mutation rate per base pair per replication (that probably is a more convenient unit to use) ranges from is 1.8 × 10^−10 (Mouse) to 5.0 × 10^−11 (Human) and around 3 x 10^-10 in insects and worms...
So, roughly, the average mutation rate (per base pair per replication) is 10^-11 and it can vary of +- one order of magnitude.
These values seems to be valid for most of the eukaryotes but not for plants.


text:
Aligning multiple sequences in heterogeneous group
I have a list of ~200 DNA sequences, representing probably 50 different genomic regions but they're all mixed up. For example, if I have seq1, seq2.... seq10, seq1 might align to seq3 and seq8, but be completely unrelated to the others.
There are also some differences in the lengths sampled, so the above example might represent:
Seq1-------------------------------------------------
Seq3----------------------   seq8-----------------
Such that seq3 and seq8 don't align to each other, but both align to seq1
So what I'd like to do is go through and somehow generate a list of groups of sequences that align to each other, as well as the alignments. eg:
Group 1
Seq1-------------------------------------------------
Seq3----------------------   seq8-----------------
Group 2
seq2------------------------------------
.       seq6-----------------------------
.   seq7--------------------------xxxxxx
Group 3... etc
Trying ClustalW or MUSSLE to align everything doesn't work (or takes an unreasonable amount of time), I'm guessing because there are so many sequences that don't align at all. I tried making a custom BLAST database and then BLASTed each sequence against it, but then I get multiple hits for the same alignment (with the group 2 example above, seq2:seq6, seq2:seq7, seq6:seq2, seq6:seq7, seq7:seq2 and seq7:seq6 all get returned as 6 unique hits, when they should be grouped together.
My current coding knowledge is fairly basic, but I'm willing to read docs and figure stuff out, I just don't want to reinvent the wheel.
Edit2:
Really, the grouping is the important part - once I have the groups, I can do the alignment separately with little effort. I'd just like to have groups where each sequence is in a single group.

You can try this:

BLAST each sequence to every other sequence (pairwise).
Every alignment (with some defined cutoff) denotes a connection.
Map all connections.
If a sequence is connected to some other directly or indirectly, it falls in a group. Put all the sequences that seq1 aligns to, in Group-1, then go to the alignments of these sequences; put all the sequences that these align to again in Group-1; so keep populating the group like this.

Methodology:

Install standalone blast (if you don't have many sequences then you can run online BLAST as well)
Make a blast database from your sequences using makeblastdb
Align these sequences against the database. If you are using online BLAST use BL2seq (align two sequences). It is much better and convenient to use standalone. You can also mention if you want plus-plus or plus-minus or both alignments. You might in some cases want only either of the two.
In the standalone BLAST you can specify the output format (which fields to include etc- the format you choose just depends on your requirements).

A tabular output format looks something like this:
# BLASTN 2.2.27+
# Query: TCONS_00036712 gene=XLOC_017996
# Database: ../nt_db/nt
# Fields: query id, subject id, % identity, alignment length, mismatches, gap opens, q. start, q. end, s. start, s. end, evalue, bit score
# 1014 hits found
TCONS_00036712  gi|191174875|emb|CU655970.6|    95.54   202 9   0   423 624 16680   16479   8e-85    324
TCONS_00036712  gi|51491599|gb|AC144709.2|  95.02   201 10  0   424 624 28443   28243   1e-82    316

Ignore the commented (#) lines; the first field is query ID, the second is the subject ID and there is an alignment between the two; the other fields provide information about the alignment (You can choose these fields).
For parsing I use a fast and easy scripting language called awk which is included in all UNIX based systems. It is also available for windows in GNUWin32 package.
What you have to do is check the first two fields and update the group.

# MakeGroups.awk

BEGIN{FS="\t"}     # Declaring Field separator as Tab

!($1 in grp){          # Check if the seq is a parent group. If not...
    k=1
    for(i in grp){
        if($1 in grp[i]){    # Check if the seq is part of any other groups
            parentgrp[$1]=i
            if(!($2 in grp[i]))   # Check if the second field i.e subject already present in the parentgroup
                grp[i][$2]        # if not assign the second field to the parent group
            k=0
            break    # stop checking further
        }
    }
    if(k==1)        # There is no parent group with this label and the seq is not a part of any other group
        grp[$1][$1] # Make a group with the query-id as the label and add this query to this group.
}

$1 in grp{
    if(!($2 in grp[$1]))
        grp[$1][$2]    # If the second field is not a part of the group with first field as label then assign it to that
}

END{
    for(i in grp){
        x++
        print "Group-"x"\n----------"
        for(j in grp[i])
            print j
    }
    print "\n"
}

Run this script like this in the terminal:
gawk -f MakeGroups.awk blastalignmentfile.txt
Note: This script contains multidimensional arrays. It will not work with all versions of awk. Use gawk version >4.0.
As swarnbes mentions in their answer, there are faster algorithms which do this kind of stuff and are used for sequence assembly. What many of them do is to make a graph (networks called deBruijn graphs), where each connection is an alignment, and compute an Eulerian Path. See this review by Pavel Pevzner for details. Overlapping sequences form contigs and you can easily trace back which sequence came from which contig (which you can call a Group). Each contig/Group is a disjoint deBruijn sub-graph.

Yes, though if you can even just point me in the right direction, that would be great.

@kevbonham This script should work. If you like some other programming language you can implement this logic in that.

Wow, thank you very much! This seems like it should work... I might attempt to re-write in python (since that's what I'm most familiar with), but the logic is easy enough to follow. I suppose I would add another loop to ignore matches < a certain % match, or would you specify those parameters in the initial BLAST parameters?

@kevbonham you can add that condition along with checking if the second-field is in a group or not no need to add another loop. Basically all those criteria is to be stringent about the relationship between first and second field. Thing with awk is that it stream reads (doesn't load the entire file in the RAM) and field separation is an easy job. Good for text parsing.

Makes sense. Is stream reading equivalent to something like readline() declared explicitly in python?

@kevbonham readline() reads the entire file line by line and stores it as a list. In stream reading one line is read and the code is implemented on it before proceeding to the next line. To implement stream reading in python use for line in file:. See here. Awk by default does stream reading. Awk also has good regex base; in python you have to import re. Having said that Awk is not as versatile as python but good for certain tasks.

@kevbonham in awk you can specify what the record separator is (RS, which is newline by default). You can instead set ">.*" as the RS for a fasta file and each nucleotide/protein sequence will be read in a stream.

@kevbonham Another point: the equivalent of associative arrays of awk (hashtables) in python is a dictionary. Dictionaries are sometimes very convenient and work much faster than lists.

I finally managed to make this work in python, using your script as a template (at least what I understood of the logic behind it). It's probably far more bloated than it needs to be, but it was a good learning exercise. Is it appropriate to post my code as an answer to this question as a reference? I'm still not completely sure about stackexchange etiquette.

@kevbonham Yes you can do it but this should not be about writing codes in general and this is not the right forum to delve into programming details. Code that explains an algorithm is fine. Pseudocode is better. Codewriting comes under the domain of StackOverflow.

Do you really need BLAST?  That is, are the sequences different enough from each other that you need an algorithm that looks for large differences between them?
Maybe you could use something like Phrap, which should put together contigs for you, if the sequences which should go together are very close to identical.

Well, not exactly. Where the sequences overlap, they overlap with >99% identity, but there might be flanking sequences that don't overlap. I changed up the question a bit to clarify (I hope).

Not sure if Phrap itself would work because it's built for sequence assembly, but the related cross_match or SWAT might work... will look into them a bit more


text:
What do biologists mean when they use the term "biological distance"?
Here is its usage.
"there is sufﬁcient genetic control to make nonmetric traits useful in anthropological work, and such variables have successfully assigned individuals from distinct geographic regions to their correct groups (for example, ... As such, nonmetric traits are an appropriate means for studying biological distances"
Source:https://www.academia.edu/5201951/Sahara_Barrier_or_corridor_Nonmetric_cranial_traits_and_biological_affinities_of_North_African_Late_Holocene_populations

Biological distance is pretty much what you'd guess: how closely related are x and y based on genetic (phenotype or genotype) studies?
There is zero biological distance between identical twins. There is extremely little biological distance between family members (for most intents and purposes, none, no matter where they live). It goes on and on in this manner.

Biological distance, or degree of genetic relatedness, will be assessed by a comparison of dental nonmetric trait frequencies.1

The phrase has been used in Theoretical Population Biology for decades. Back then, they had phenotypes to measure the degree of biological distance.2 Today, actual genetic determination of kinship is possible.

Biological distance, or biodistance, is the measure of biological relatedness (or divergence) between and within human groups, living and past, based on human skeletal and dental variation.3

1 Dental Variation of Prehistoric Amerindian Populations
from Eastern Tennessee
2 Kinship, information and biological distance
3 Biological Distance in Bioarchaeology and Human Osteology

You just outran me by 1 minute!

@ChrisStronks - I saw! You gave the better answer, though, I think. :) So you got +1 from me.

Yours is great and to-the-point, +1'ed you back :)

I think this is more of a Biological Anthropology question, and my guess is the question could be rephrased as "What do anthropologists mean when they use the term “biological distance?”
The Anthropology Stack Exchange is still under construction so that is a dead end for now.
Pietrusewsky (2014) gives the following definition, and I quote:

Biological distance, or biodistance, is a measure of relatedness or divergence among groups separated by time and/or geography based on morphological variation (Buikstra et al. 1990).

Pietrusewsky continues with elaborating on Biodistance research:

Biological distance studies, which are undertaken to reconstruct population history and to assess ancestry, dominated bioarchaeological research during the 19th and early 20th centuries. [...] These early attempts were flawed due to limitations of the approach, which included the mistaken belief that humanity could be divided into a finite number of pure races, and the lack of adequate quantitative methods. Advances in evolutionary theory, including quantitative and population genetics, and improvements in computing and statistical procedures in the early 20th century provided a much sounder basis for measuring and interpreting morphological variation within and between human groups.

These elaborations may explain the rather defensive stature the authors take in your cited article to back up their methods, and I quote:

In any case, there is sufficient genetic control to make nonmetric traits useful in anthropological work, and such variables have successfully assigned individuals
  from distinct geographic regions to their correct groups (for example, Winder, 1981; Prowse and Lovell, 1995; Blom et al., 1998; Christensen, 1998; Donlon, 2000;
  Hanihara et al., 2003). As such, nonmetric traits are an appropriate means for studying biological distances among North African populations and the implications of
  the patterning of these distances in assessing the relative role of the Sahara Desert as a barrier to gene flow.


text:
Grafting vegetables onto fruit-bearing trees
There are multi-fruit trees with as many as 40 different fruit, but would it be possible to graft a vegetable onto a tree?
Or maybe something in between, like grafting onto an apple tree a fruits in the botanical sense, but one of those often eaten as savory food, similar to vegetables: tomato, squash, avocado?

Some vegetables are actually fruits (like apples and bell peppers), others like carrots and potatoes are root modifications. You have to clarify what vegetables and fruits you are interested in. The type of plant is also important.

For grafting to "take", the the two plants' vasculatures have to be organized similarly. This is not possible for two such differently organized stems as a pepper and an apple.
This is a cross section of a young woody stem (such as an apple, though this example is a tilia):

This is a cross section of an herbaceous stem (such as a pepper):

You can see there is dissimilarity in organization. Furthermore, herbaceous plant stems die back in the winter.
Even if possible, grafting an herbaceous (non-woody) stem onto a woody stem (e.g. apple) would not confer any advantage for the green pepper, a tender annual, and would be disadvantageous to the woody stemmed tree (pruning for no reason, when the branch would otherwise have produced apples, and the leaves performed their useful functions.

How about a tomato and an apple tree?

@DanDascalescu - how are a tomato and a pepper significantly different? They are both tender annuals in the nightshade family.


text:
Hydrogen Peroxide on Open Wounds
I know that H2O2 is a chemical with high oxidative potential. It can deliver nascent oxygen which can destroy bacteria.
I understand that open wounds have cells that are dividing at a fast rate to effect healing. Is it good to add a substance that can cause damage to cell membrane and possibly cause mutation in the DNA of these fast growing tissues?
Can H2O2 be safely used to sterilize wounds?

H₂O₂ is used only at the time of first cleaning afaik; good against Clostridia. For regular dressing it is not generally prescribed.

There will be few rapidly-dividing cells in a fresh wound (which is the wound to which H2O2 is applied). In general, it is a good idea to avoid applying irritants to rapidly dividing tissue.
Hydrogen peroxide is a weak mutagen. It is produced in many body tissues, ingested in drinks, produced by mouth bacteria, etc. It may well cause some cancers. Some OSHA-mandated literature does warn that it is a mutagen and must be handled with care, but these are warnings to people who work with concentrated solutions.
However, a relatively weak hydrogen peroxide solution, even if it is mutagenic, would need to be left in place and active (or renewed) for a long period of time to produce skin cancer. As it has been a staple of first aid kits for decades, and this association has never been made clinically, my best guess is that the benefit (as a bacterocidal agent) far outweighs the risk in the treatment of minor wounds. As in all things, however, prudence is advised. (I myself don't use it because soap and a lot of water is quite effective. Nor is it used in the care of wounds in Emergency Rooms where it is considered to be detrimental to wound healing. If I were in a country where clean water and soap were in short supply, I might well use it if necessary.)
Because it is an irritant (and many irritants can be considered mutagenic), it is actually used to treat precancerous skin lesions, the finding being that it affects the more rapidly dividing pre-cancerous cells than the rest of the epithelium.
Far more potent peroxides have been used topically, which may increase the risk of skin cancer.
Interestingly, one of the responses of skin cells to H2O2 is the generation of an oxygenase to fight the effects.
Topical sulindac combined with hydrogen peroxide in the treatment of actinic keratoses
Effects of Peroxides on Rodent Skin: Epidermal Hyperplasia and Tumor Promotion
Heme oxygenase is the major 32-kDa stress protein induced in human skin fibroblasts by UVA radiation, hydrogen peroxide, and sodium arsenite
Recent Advances in Wound Care, Michael K. Abraham, MD, MS, and Jason S. Oh, MD

Nice answer. I shouldn't ask new questions, but what about chronic repeated exposure to peroxides via mouth wash, given that epithelial cells in the mouth are quite rapidly dividing?

@ChrisStronks - Almost any irritant has the potential to be mutagenic. One weighs risks to benefits. When there are specific benefits (to whiten teeth, for example), it's unlikely to do more damage than good. But where there's little benefit, I wouldn't do it on a daily basis.

Ahem, I think you may have teased out the self-helpness there.... But yeah. That helps :-)

@ChrisStronks the epithelial cells in your mouth also shed fairly quickly, so even if a cell were to develop enough mutations to become cancerous, it likely wouldn't be around long enough to start dividing into a tumor.

@MattDMo - while it's true that epithelial cells in the mouth have a high rate of turnover, it's also true that oral cancers occur still. 43,250 Americans will be diagnosed with oral or pharyngeal cancer this year, of those, only slightly more than half will be alive in 5 years. Alcohol has long been a risk factor because it is held in the mouth, and it's an irritant. So, no pleasant daydreams about this are helpful. I've seen people with their lower jaw removed due to oral cancers. :-O (Not recently, though.)

@MattDMo - also, hydrogen peroxide is readily absorbed into tissue, which means it can easily reach more permanent cells. I'm not a cancerphobe. I think the risk from using a peroxide mouthwash is lower than alcohol and smoking, but as they have been on the market for far less time, we don't know their long-term safety. The good thing I can say is that it is produced by our own bodies, and we seem to have means to fight it. But, prudence in all things is not bad advice.

@anongoodnurse I completely agree with both of your comments. My thinking was that since H2O2 would only be in the mouth for 30 seconds to a minute once or maybe twice a day, it wouldn't be quite the same level of exposure as would be seen in a smoker, smokeless tobacco user, or chronic consumer of alcohol. I was also primarily thinking of the cells on the inner cheek, which shed rapidly, while other epithelium, such as gums or the roof of your mouth, may turn over less quickly and allow mutations to accumulate (...)

(...) Still, it's a matter of degree as far as risk is concerned - you need to think about the cumulative exposure over time - 1 to 2 minutes of H2O2 exposure/day is nothing compared to a 1-2 pack/day smoker, or a heavy drinker. It all comes down in the end, however, to how much risk you're willing to take.

@MattDMo - I agree completely. I think we are agreeing in principle, and perhaps differing in the details. :)

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


text:
Chemical reactions at the synapse
For my course project, I am thinking of listing out major chemical reactions that occur at synapses, along with their temporal characteristics.
I could not find any textbooks to use as a starting point, and Google did not help me either. I was hoping to receive help in finding a review paper or textbook about chemical computations at the synapse.

Acetylcholinesterase is just one very important example of an enzyme in the synapse. Inhibiting this enzyme is how nerve gases and pesticides work.

If you are interested it from the point of view of "chemical computations", you probably want literature which looks at signal transduction in detail. I would suggest Marks' et al textbook on signal transduction. I have not yet read it through (it is on my list), but I liked the clear writing style of the introduction, and, as you can see from the table of contents, it does have chapters which address synapses and their neurotransmitters specifically.
I doubt that it will contain a complete list (there are several hundreds of compounds which can be considered to be neurotransmitters), but as an introductory textbook, it is likely to contain the major ones.


text:
Using perceptual adaptation for enhancing realism of VR/other entertainment
I am quite a fan of the recent oculus rift VR glasses, but it does have several flaws over normal vision, most notably a much less wide field of view, the so-called screen door effect because of too low resolution (example 1, example 2) and often also a certain latency between head movements and corresponding view angle change.
Could one, in theory, create glasses which have these limitations to wear during everyday life to adapt to them, and later have the benefit of a more "realistic" experience?
I know making the glasses is not trivial, I'm just asking about whether the perceptual adaptation part would even work as intended, what timeframe I could expect to adapt in, and how stringent the wearing of them has to be (is waking up without them ok, or should sleep be blindfolded, etc).
Does anyone have experience/advice/knowledge on the subject, maybe even links to prior applications?

Very interesting question. Just for clarification: What do you exactly mean with: "Could one, in theory, create glasses which have these limitations to wear during everyday life to adapt to them, and later have the benefit of a more "realistic" experience?" This is your primary question right? Are you wondering, in general, if one could adapt to altered visual perceptions after a while? Or are you specifically asking whether electronic glasses exist that use this principle?

Both. I'm wondering whether this principle could be used in such a way, and if yes, whether someone has already done so. In the meantime I've learned that apparently combined nearsight/farsight glasses for elderly occasionally do something like this (left eye nearsight, right eye farsight, for instance), but I've never heard of limiting sight to enhance realism of "fake sight" (television, VR, etc).

Adaptation to altered vision is probably most well-investigated using prism-glasses. Prism glasses can shift the visual horizontally, for example by 20 degrees (Redding et al., 2005):

The use of horizontal shifting goggles has been investigated intensively to treat the symptoms of attentional neglect. Neglect occurs due to unilateral parietal brain lesions. For example, a lesion in the right hemisphere may induce left-sided neglect, where the left part of the visual field is seen, but simply not processed and neglected (Rosetti et al., 1998). Wearing prism goggles for approximately 6.5 hours/day, over the course of 2 weeks has been shown to reduce the symptoms of neglect significantly by as long as 17 weeks(!) after treatment (Frasinetti et al., 2002).
For the treatment of a neurological disorder such as neglect adaptation to prism glasses is great. However, treating healthy controls with comparable methods may induce unwanted side effects. 15 min of prism exposure has been shown to lead to several degrees of error in pointing tasks, for up to two weeks after the adaptation in normally sighted controls (Klapp et al., 1974).
To mention some studies closer to your question: in a virtual reality experiment subjects wore a head-mounted display that shifted the virtual position of their eyes. Their performance on a hand-eye coordination task first decreased by ~40% and then increased again with ~30% after adapting to the display. After taking the display off, there were transient after-effects, that impacted eye-hand performance (Rolland et al, 1995; Biocca & Rolland, 1998). In other studies wearing a head-mounted display longer lasting discomfort was reported in 5% of the subjects (Cobb et al., 1999) as well as binocular stress after removal of the display (Mark Mon-Williams et al., 1993).
Although the latter studies did not report serious after-effects, the more rigorously performed studies with the prism glasses have shown long-standing effects after visual adaptation. Hence, although the performance with virtual-reality head-mounted displays and comparable devices will undoubtedly increase after adapting to them, visual functions in everyday life may correspondingly be compromised.
So although this answer may not be addressing all your practical questions, I would say it is not advisable to let one actively adapt to head-mounted displays, or other wearable virtual-reality glasses that change visual function in the first place.
References
Biocca & Rolland, Presence 1998; 7:262-77
Cobb et al., Presence 1999; 8:169-86
Frasinetti et al., Brain 2002; 125:608-23
Klapp et al., Perception & psychophysics 1974; 15: 399-400
Redding et al. Neurosci Biobehav Rev 2005; 29:3, 431-44
Rolland et al., IEEE Proceedings of VRAIS 1995
Rosetti et al. Nature 1999; 365:166*9

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


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Why do we find some things disgusting and others delicious?
For example, why do I love paprika while my girlfriend hates it? Why do I find broccoli disgusting and she adores it? As humans, there are things we'd all agree on being awful, like rotten meat, for obvious evolutionary reasons - those things are damaging to our body and we should not eat those. But when asked about delicious food, everyone would pick something slightly (or completely) different.
I wonder, is it because our tongues are different and the food does indeed taste different, or is it our brains that interpret the same taste differently? Also, what evolutionary purpose does this serve? To me it only makes planning the dinner a pain without really adding anything to our lives.

Afaik. bowels decide about disgust, and not the brain.

Food preferences are largely cultural (including social). Most people find caviar and oysters, to name a couple of foods, revolting the first time they eat them. It's an "acquired taste" for most. Our tongues are not significantly different.

@anongoodnurse Why not move the previous comment of yours to the answers. I think its bang on. Additionally (although perhaps not relevant) There are also cases of disease that dramatically alter taste, and any degree of anosmia (like a blocked nose) can alter a personal pallet too.

Have a look to the wiki page for Taste Preference

Explaining phenotypic variance
You may want to make sure you have a good understanding of the concepts of the underlying variance of phenotypic variance (discussion linked to the concept of heritability) before reading this answer. In this post, I linked several sources of information on the subject.
Culture (environmental variance)
Variance in food preference is in part (in majority eventually) explained by cultural differences.
Genetic variance
I guess that very few people like the smell of rotten eggs. There is selection on taste and smell preferences. Those who don't like the smell of rotten food increase their chance to suffer from bacterial intoxication and mycotoxins. I remember from my Bachelor degree (can't find the study right now) Nestlé (among others probably) performed a genome-wide association study that showed genetic variance for food preferences.
Adaptation
There are probably many loci that are now fixed (not polymorphic anymore) that were at some point under selection as explaining variance for food preference. In other words, at a given locus there might have no more genetic variance as the current allele is well adapted.
By-products
Also I suppose that a part of the underlying genetic and environmental variance for the variance for food preference might be qualified as by-products. For example, it might be beneficial to appreciate a given smell because the smell when present in the sweat of a partner is associated with greater health. If this odour (or similar odour) happen to be present in food, then we may be indirectly selected to appreciate this food item as a by-product of the selection for recognizing healthy partners.


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Do males of all sexual species have Y chromosomes?
I know for instance some cells are sexual, so, this got me wondering, do the males of all species that have distinct sexes have Y chromosomes?

Very short answer
No, not all males of all sexual species have Y chromosomes. You might want to have a look to the Wikipedia page on sex-determination systems.
Long answer
Diversity among the species that reproduce sexually
Not all species that have sexual reproduction have sexes. Yeasts, for example, have mating types but no sex.
Diversity among the species that have sexes
Sex is determined by both genetic and environmental factors. In some species, genetic factors are more important than environmental factors in other species it is the reverse. Species which sex is mostly determined by the genetics are said to have GSD (Genetic Sex Determination). For example, humans are GSD, as the female is XX and the male is XY. The species where sex is mostly determined by the environment are called ESD (Environmental Sex Determination). For examples, crocodiles are ESD as sex is determined by temperature. It is important to understand however that there is a whole continuum between these two extremes.
Diversity among the species that are GSD
Among the species that are GSD, some have sexual chromosomes some don't. Some have one locus  (locus=position on a chromosome) that determines the sex, some have many loci (loci=plural of locus). Humans, for example, have sexual chromosomes (X and Y) and have only one locus which determines the sex. This locus is called SRY and it codes for a protein called TDF.
Now you can split GSD with sexual chromosomes into two more categories (it is a bit more complex in reality): XY and ZW. XY are those species where the male is heterogametic (XY), while the female is homogametic (XX). In ZW systems, the male is homogametic (ZZ) and the female is heterogametic (ZW). Birds and some plants have ZW systems for example, while mammals (except "basal" mammals) and Drosophila have XY system.
See also the post What determines sex in birds?
Extra Information
Dosage Compensation
In species that have sex chromosomes, there is a difference in the number of copy of genes between the sexes. In eutherian mammals, for example, females have two copies of all the genes on the X chromosomes, while males only have one copy of most of these genes (plus a few Y chromosome genes). The set of methods to deal with this issue is called Dosage Compensation and there is also an impressive diversity dosage compensations.
Comments on this diversity of sexual systems
The diversity in a sex-determination system, dosage compensation and other things related to sex are impressive. It is even more impressive when we look at how many independent origins there are. Below are some other examples.
The Amazon molly (a fish) is a species that have sexual reproduction but there are no males. The females have to seek for sperm in a sister species in order to activate the development of the eggs but the genes of the father from the sister species are not used. (see this article)
There are also hermaphrodites including sequential hermaphrodites (first male, then females or the opposite) in plants and animals. There are also species where populations are made of hermaphrodites and females and others where there are hermaphrodites and males (very uncommon).
In some species, the sex is determined by social factors. In clownfish, the sex is determined by comparing its own size with the size of the other fishers living in the same anemone.
In an ant species (or two species actually), males and females can both reproduce by parthenogenesis (some kind of cloning but with meiosis and cross-over) but they the meet they reproduce together and their offsprings are sterile workers. So males and females are just like two sister species that reproduce sexually to create an army to protect and feed them. See more information in this paper

Here is a nice figure from Bachtrog et al. 2014 that offers an idea of the diversity of sex determination system (thank to @rg225 for pointing out this figure).

Book suggestion
The Evolution of Sex-Determination is a great book that may interest you.

http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001899

You should modify your wording in the beginning of the answer so that gender --> sex for an accurate terminology, see wikipedia: sex and gender distinction

Fixed! Thank you for the comment @fileunderwater.

No. There are many sex-determination systems. Mammals and fruitflies use the XX/XY sex-determination system — except for the platypus, which has 10 sex chromosomes.
ZW sex-determination system is used by birds and some reptiles. It's similar but with the male having two of the same chromosome (ZZ) and the female being the heterogametic sex (ZW). There's several other variations, such as X0 (XX for females, X for males, with no Y).
There are also animals with temperature-dependent sex determination and others use reverse their sex.

another fun fact is that the bird sex ZZ/WZ and the mammalian XY/XX evolved independatly without common origin... also the genes involved in sex determination is mostly the same but the order of the activation of genes is different. For example: birds are capable of sex reversal on stimulation/inhibition of  estrogen, unlike mammals but like reptiles...


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Why can blood vessel contraction be described as a second order system?

Suppose that the x-axis represents time, and the y-axis vessel diameter.
Then this graph is claimed to roughly describe what happens when the blood pressure increases, then decreases.
When the blood pressure first increases, the vessel diameter expands to its maximum radius. Then it contracts. What I don't understand is why it keeps on expanding and contracting after its initial expansion - does this model still make sense after its initial expansion and contraction?
Can anyone explain?

This phenomenon is called damped oscillation. Negative feedbacks sometimes result in such kinds of dynamics. I don't know the physiological mechanism behind it if there is one but I can understand the logic.

In broad terms: pressure causes vessel to dilate, which in turn reduces the pressure, which in turn reduces the diameter, which then leads to increase in pressure. With certain sets of parameters you would get damped oscillation. Can you provide a reference to the model that you mention?

the blood vessels have smooth muscle cells on its walls. One of the property of the smooth muscle cell is that it contracts when stretched. I think this explains the physiology behind damped oscillation

Many systems have this property. The plot you are looking at is the plot of the transfer function for blood vessel diameter vs time. A trick in mathematics or engineering is to understand a system is to sometimes look at at different system with the same properties that you do understand. For instance, a mass springer damper system is similar to a RLC circuit. That is, if we understand the mass spring damper system, we view the RLC circuit as the analog to the mechanical system and vice versa. In the case of blood pressure, we also have a driven force (the heart). Thus, an extremely simple model would be
$$
m\ddot{x} + c\dot{x} + kx = F(t)
$$
As we see below, the mass spring damper model produces the a similar plot of the transfer function. If you understand the mechanical system or RLC circuit, you can look at your plot parameters as an analog to one of these systems to understand the dynamics occurring in the body.

A more interesting question is can we use PID control to manage the overshoot, rise time, and settling time of the vessel diameter in the body?

The differential equation that models this process is probably related to a Bernoulli differential equation.

http://en.wikipedia.org/wiki/Bernoulli%27s_principle
page 15 http://www.physics.usyd.edu.au/~jbryant/Fluids/Fluidslect4.pdf
http://bme.ccny.cuny.edu/faculty/bfu/blood%20flow%20permeability%20in%20microvessels.pdf

A precise differential equation will need to account for pressure (Bernoulli), fluids (Navier-Stokes), and the elasticity of the vessel walls.


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Why is the Trendelenburg position used when placing and removing Central Venous Line catheters in the sub-clavian vein?
The title says it all. Why is it that patients are placed in the trendelenburg position when a catheter is inserted in the sub clavian vein? What would happen if the patient wasn't placed in the trendelenburg position when placing the catheter?
Thanks in advance for the help.

Positioning the patient in Trendelenburg will increase the size of the IJ vein. From http://www.med.uottawa.ca/courses/cvc/Landmark%20Techniques/e_landmark_techniques.html

There are 2 main reasons for using the Trendelenburg position when placing and removing a central venous line catheter into the subclavian or even internal jugular vein.

Exactly what C Rags mentioned-- to increase the size of the vein. This position utilizes the force of gravity to pool blood towards the head from the lower extremities. This makes the vein of interest easier to visualize compared to surrounding structures, to palpate since this increases pressure within the vein, and to ultimately puncture.
To avoid air embolisms, which are particularly more damaging if they get into the brain causing a stroke than if they travel inferiorly to the leg, for example. Air embolisms can be introduced when inserting or removing a line.

Ref:

http://emedicine.medscape.com/article/422189-overview#showall

I'm sorry if this seems to be too picky, but how does being in the Trendelenburg position make an air embolus travel against the flow of the blood (as you state, inferiorly?) Will an air embolus introduced into the subclavian vein go to the leg if a patient is placed in Trendelenberg? If so, how does it navigate back into the superior vena cava -> inferior VC -> etc.?

Great question, it is theoretically possible for an embolism to travel retrograde to blood flow depending on the position of a patient. This paper does not specifically test the subclavian vein, but the authors created a simulation of blood flow through a vein-mimic to determine at which angles an air embolism could flow retrogradely.

Thanks for answering! Your paper states @ angles between 0 - 45°, air bubbles followed fluid flow (these are smaller bubbles, though). Trendelenburg is  <45°. While it's is recommended for insertion and removal (it's always good when an answer sparks my curiosity), I read that it's to create a pressure gradient (blood is more likely to back up into the line than air to enter the vein). Once an air embolus is introduced, however, the left lateral decubitus (sometimes +Trendelenburg) position is recommended to trap the embolus in the R atrium until reabsorbed. Fascinating.


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Why does hair grow after trimming but remains at a constant length after a while?
Some hair especially body hair regrows after trimming but stops growing after a while. What is the mechanism behind control of hair growth and how is the length limit determined?

Hair grows from the follicle; there is no way for the follicle to determine if the hair tip is trimmed or not. This is unlike plant shoot/root growth that happens at the tip. Also there is no signaling from tip to follicle.
Hair growth has four stages: Anagen (Initiation), Catagen, Telogen (resting) and Exogen (falling off). Initially the primary follicle is formed during development of the skin, after that the hair growth continues in a cycle. In other words the old hair shaft is replaced by a new one. The period of the cycle (or how fast it happens determines the final hair length); the faster is the cycle the shorter will be the hair (you may note that certain people have a very short head hair even when they do not trim). This is because the old shaft doesn't get time to grow before it is shed and replaced by the new one.

From: Stenn & Paus (2001)
From the same source

Because there is a limit to the time a follicle stays in anagen, there
  is also a limit to the length of its product, the hair shaft. The
  anagen phase has been divided into six subphases (64, 359). Except for
  the last subphase, anagen VI (the duration of which dictates the shaft
  length), the length of the anagen subphases I–V does not differ
  substantially between follicles from different regions (490, 565).
  […]
   Because the actual length of a hair follicle does not appear to
  dictate the length of its shaft (rather the duration of anagen
  determines hair shaft length), it is tempting to speculate that the
  subcutis offers optimal growth conditions…
  […]Although influenced by environment (light, temperature, and
  nutrition) and systemic (endocrinological factors) parameters, it is
  generally believed that there is considerable innate local control of
  hair shedding; each fiber grows to a specific length, for a specific
  period of time, before being shed

Interesting. I looked at the source, and it seemed to imply that hair length is determined only by the length of time in which the hair has grown, which would assume constant growth speed. This would be a very interesting fact, I'd intuitively assume that hair (within the same animal) grows with different speed depending on body part and the current state of the body chemistry. Do you know if such difference exists, or is it a constant speed growth process? I don't remember an explicit statement from the paper, it was just an impression I got, maybe I overlooked something.

@rumtscho Yes that happens indeed. It is mentioned in the paper. For example head hair and body hair. I also cannot find an explicit statement but it is indicated implicitly. for eg: "Except for the last subphase, anagen VI (the duration of which dictates the shaft length), the length of the anagen subphases I–V does not differ substantially between follicles from different regions"

To be clear, you are implying that the only reason your hair has a limited length is that the skin itself regenerates, causing the hair to fall out?

To be clear, you are implying that the only reason your hair has a limited length is that the tip of the hair "sheds" (breaks and falls off)?

@cowlinator not the tip but the root. It doesn't break. It is displaced by a new incoming hair tip.


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Can humans live without their right atrium?
The right atrium  is one of four chambers (two atria and two ventricles) in the hearts of mammals (including humans) and archosaurs (which include birds and crocodilians). It receives deoxygenated blood from the superior and inferior venae cavae, the coronary sinus, and the anterior and smallest cardiac veins, and pumps it into the right ventricle through the tricuspid valve.
Can humans survive without right atrium? In this condition blood would fill the right ventricle directly, comparable to some animals like  frogs, toads, snakes and lizards. What advantages does the normal human heart have to this anatomy ? If we had this anatomy, where would the best place for pacemakers be, like the sinus node?

I slightly modified your question for clarity. Feel free to roll back.

Since there is no record of a congenital absence of a right atrium (that I can find - there are defects of the pericardium that affect the atrium), I suspect it is incompatible with life.

This is an interesting theoretical question, but several things would need to be clarified:

Does removing the R atrium relocate the SA node to the R ventricle or remove it completely from the picture?
Does the remaining R ventricle have a tricuspid valve?

Technically, the R atrium is the home of the sino-atrial node, which provides natural pacing of the human heart between 60-80 beats/min. Without this natural pacing, our hearts would rely on back-up pacer systems such as atrioventricular node, His-Purkinje systems or the intrinsic but ectopic pacing of individual atrial or ventricular cells.

1
It is possible for humans to survive without the SA node because of these back-up systems. However, our heart rates would be lower, or bradycardic. Although there are many individuals who survive with bradycardia ranging from top athletes to the elderly, this condition could lead to negative symptoms including fatigue, dizziness, lightheadedness, syncope, and even cardiac arrest [2]. Ideally, the SA node would be located at or near the area of blood entry into a chamber (or, put another way, opposite from the side where blood exits the chamber), so that blood is pushed synchronously out of the chamber rather than against a wall or the entry, causing turbulence.
The R atrium also provides a chamber through which venous blood can sit before it is pumped into the R ventricle to be pumped again into the pulmonary vasculature to be oxygenated. This function allows blood to enter the pumping ventricle quickly, a physiologic benefit [3]. In a heart without a R atrium, if the R ventricle still had valves to be able to keep blood from backing up into the vena cava system, then this function of filling and pumping would still be preserved, although it would not be as efficient as if there was a preceding atrium.
In nature, there are three-chamber hearts found in certain amphibians and reptiles. However, usually it is made of 2 atria and one ventricle, rather than 1 atrium and 2 ventricles. In this model, deoxygenated blood and oxygenated blood are mixed (to different degrees, based on the animal), which is not ideal. However, these animals usually have other modes of oxygenation such as through the skin.
In summary, the short answer is- yes, probably, humans can survive without the R atria but it would not be without serious consequences in quality of life.


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Why do flies "rub" their front legs when resting?
I've noted that every time a house fly is resting on a surface, it appears to "rub" or "scrub" its front legs in a repetitive movement. And they do it continuously. Why?

Flies rubbing their legs are cleaning themselves. They can also often be seen rubbing their back legs often. Additionally, flies also often clean their wings, compound eyes and bodily bristles. Legs and wings are used as a primary means of locomotion and means of escape. Eyes and bristles are sensory organs and hence also essential for their survival.
Below a picture of a tachinid fly showing the bristles and compound eyes:

The eyes need to be clean as they are essential for the detection of visual stimuli. The bristles, as a commenter rightfully stated, contain chemoreceptors reminiscent of receptors on the human tongue that sense sweet and bitter tastes. These taste receptors alert the fly for sweet (food) and bitter (poisons) substances. Hence, cleaning of the legs may not only serve hygienic purposes, but may well be important for keeping the bristles and hence the associated sensory organs clean and free of prior encountered substances.


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Why do we experience temperatures below 37 degrees Celsius as 'hot'?
We always prefer to be in 20-25° C, although our core temperature is about 37°? Why is our skin temperature lower than our core temperature?

related to http://biology.stackexchange.com/questions/2955/if-body-temperature-is-37%c2%b0c-98-6%c2%b0f-why-are-most-people-more-comfortable-at-ar?rq=1


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Why do men have a higher hematocrit (red blood cell count) than women?
The hematocrit, also known as packed cell volume (PCV) or erythrocyte volume fraction (EVF), is the volume percentage (%) of red blood cells in blood. It is normally 45% for men and 40% for women.
so,Why do we have hematocrit for men?
First,I thought it might be caused by different hormones but I couldn't find adequate evidence to prove this Hypothesis.Therefore I decided to share it.

I found a nice article that has insights to this matter. As posted before me it is true that only adults, but not juvenile individuals show this difference. Direct and indirect effects of sex hormones on bone marrow erythropoiesis and renal erythropoietin production has been proven, but it works in both sexes the same way. Females are capable to elevate their haemoglobin / red blood cell levels to external stimuli, yet at same conditions (same altitude etc) the difference remains. Also:

Men, premenopausal women and postmenopausal women have similar plasma erythropoietin levels, indicating that women do not attempt to compensate for their lower haemoglobin levels by increasing erythropoietic drive. These observations show that the prevailing lower haemoglobin level in females cannot be ascribed to a lack of bone marrow or renal erythropoietic capability: they indicate that adult females maintain their venous haemoglobin levels at a lower level than adult males as a physiological steady state — they do not try under physiological conditions to maintain the same levels as adult males.

This could be achieved by modulation of the juxtaglomerular apparatus signal (JGA) of the kidney. The JGA has important role in the regulation of the haemoglobin level - it is the main input for erythropoietic red blood cell production by regulating renal filtration and thus regulating the amount of oxygen that gets to the EPO producing peritubular cells.
It is noteworthy to say that similar difference exist in mammals and even there are examples among birds and reptiles.
It is described in the linked paper that both men and women achieve the same or very similar microcirculatory haematocrit level inspite the different mean venous haemoglobin levels.
This implies the very interesting theory / reasoning in the article:

(...) that both sexes set their mean optimum level separately and to some degree independently.(...) the red cell mass is an enormous resource in animals — one third of the body's cells by number in adult humans, and demands enormous effort to establish and maintain.(...)This price must be paid for by increased fitness.(...)The excess red cells over the critical minimum that circulate in the large vessels (and slowly through in the spleen in some species) and that constitute half or more of the venous haemoglobin level probably provide a storage function for the reserve red cell mass for use when the need arises for increased work — fight, flight, food and reproduction. They may also act as reserves for heat exchange and iron storage. It is likely that the return in fitness from this reserve differs between the sexes, and therefore that the optimal size for maximal cost benefit also differs.

This is a very interesting point. It shows that my answer was obviously too simple.
In fact, reference ranges for erythropoietin depend on age but not sex. See http://emedicine.medscape.com/article/2087846-overview for details.
Hemoglobin homeostasis in women seems to adapt to the repetitive loss of iron by lowering its set point. The benefit of this mechanism could be that it saves valuable resources that would only be lost by menstruation.
Thanks again for your valuable answer.

Reference values for hematocrit are identical in male and female children and as well in elderly men and women. Differences in hematocrit between fertile women and men are caused by repetitive loss of blood - and therefore iron - in menstruating women.

Could you maybe add references to support your claim that it is caused by menstruation?

There is an interesting study that investigated menstrual blood loss in filipino women (Cheong RL, Kuizon MD, Tajaon RT. Menstrual blood loss and iron nutrition in Filipino women. Southeast Asian J Trop Med Public Health. 1991 Dec;22(4):595-604. PMID 1820649). The authors found a significant correlation between menstrual iron loss and transferrin saturation index. Interesting information is also available from this site by American Regent, but it is not without competing interests.

Nice. Add them to your answer, so that the statement is supported.

males have testosterone that increase thyroxin secretion.thyroxin is importnat for ATP production,then if there is more energy production more oxygen is needed that directly increase more epo production.

Please could you add some references to your answer

Males have more muscle mass,so they require more blood.Also females undergo menstrution so they lose more red blood cells.

Welcome to Biology.SE! I think this is a good start but we're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations.