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A colony of humans are sent to an alien world, at what point would the descendants evolve to be genetically incompatible with Earth humans?
I recently heard about the evolution of the London Underground mosquitoes, and how they have changed genetically enough that they almost can no longer reproduce with above ground mosquitos. Since this change in the mosquitos occurred over a relatively short time frame, how many years/generations would it take for a similar process to happen with humans?
The thought experiment that comes to mind is this. Assuming we sent a colony of humans to a distant planet and didn't have any physical contact with them for x number of years, how many years would it take for the colony of humans to branch off enough genetically to be no longer be able to reproduce with Earth humans? This is assuming the planet is habitable but different enough to change the course of human evolution.
In other words, what would be an expected minimum number of years it would take for this colony's descendants to be removed from Earth humans to one day again be reunited and not be able to produce offspring between the now different species?
In other words, what would be an expected minimum number of years the would need to pass before they are reunited and are no longer enough of the same species to produce offspring together?

Welcome to Biology SE! Very interesting question! Although I am not an evolutionist, and I may be wrong here, but I think this question will likely yield only speculative answers. Perhaps it could be rationalized by stating the question as "how long did it take our earthly homo forebears to evolve into species that were genetically incompatible with their predecessors?"

Chris, good point! I realize it is very theoretical, and I assume that the past evolution of our species would be a good indicator of how long this process would take. I suppose the difference here is that it would be an instant separation of the species, rather than a slow migration like our past homo forebears. And there also would be no cross-breading during this time, like it has been expected to have happened with various homo species of the past (slowing down the branching of evolution).

Ah, I understand your point now. Interesting addition to your question.

If Australian Aborigines are any indication, it would take a long time. They arrived in Australia on the order of 50,000 years ago and were still genetically compatible with other humans when settlers arrived within the last 500 years. Prior to exploration in the last few centuries travel to and from Australia would have been pretty negligible.

I think there are 2 solutions to answer this question. If we assume that the environment did not change, one can calculate the number of mutations that accumulates through drift in both lineages. ....

... I am not sure how from this info we can infer any level of reproductive isolation. Eventually, this can be done based on observations of slight level of outbreeding depression in humans today (assuming this exists, see this post) or with known past reproductive isolation in the human history and their genetic distinctiveness (assuming we have these informations).

Better on Skeptics.se?

There's an interesting question (yes hypothetical, but is that bad?), and an interesting upvoted answer. Why close? Astrobiology is serious business!

but it's impossible to answer without using a great degree of speculation

and is that bad? In this field (Astrobiology) I would definitely allow it, as of course no one knows the answer, since no one put a population outside earth's confines. This is a well-thought question and science is there to ponder about and explore the unknown.

that would mean answers would tend to be almost entirely based on opinions, rather than facts, references, or specific expertise

@ChrisStronks I think it need to be narrowed down to be suitable, even though it would still be based mostly on speculation. Whole books have been written on the mechanisms of reproductive isolation. Some relate to differences in environments (selection pressures) while others do not (drift). Some take place prebreeding and others postbreeding. Other mechanisms are behavioural, and in this human scenario these would only be based on speculation. I agree that a narrowed down version that builds on e.g. the average time to reprodutive isolation in mammals could be interesting.

@fileunderwater: that is indeed a valid and very acceptable reason for closure (although I still vote for re-opening :-). However, the closure because of speculation I still disagree with. It is just that I think, in general, too many questions are closed on questionable grounds. But that's probably something to discuss elsewhere. Thank you!!

@ChrisStronks about closing questions on questionable grounds. Chris and I had discussed this on chat that this is same as cleaning the lab fridge. Lots of junk is cleared but sometimes a somewhat important stuff is also gone. That is one tradeoff. We can have meta discussion on deciding whether to reopen those questions or not (as such those questions are not that common). It took quite some effort to clean up the site.

@WYSIWYG - And you guys did a wonderful job! I don't want to undermine your efforts, but it's just that in some (indeed not too common) cases I think babies are thrown away with the bath water. This is one of them. The closing should be balanced and even unanswerable questions deserve the right to exist, let alone answered and upvoted answers like this one (!!). Thanks again.

@ChrisStronks I voted to reopen.

I don't get the votes to reopen, since it hasn't even been edited after it was closed (besides a retag). At least give the original poster a chance to respond to the suggestions/criticism and maybe clarify before voting to reopen. What's the hurry?

I appreciate the honest meta discussion on the nature of this question. I don't think it's necessarily unsolvable, but understand that it seems difficult for one field to give a real answer without some speculation or hand-waving. I can see that genetics are needed to determine the rate at which our genes would change given the environment. Astrobiology would provide that data on the environment to determine the effects it would have (change in gravity, planets rotation, solar energy, etc). Applied mathematics to work out the models. Biology to use past knowledge on evolution. And so on.

I can imagine this would be a very real question if we were to send an "ark" of sorts to another planet, without guarantee of being reunited in any given timeframe. Of course our civilization has never been this concerned with future generations more than 100 years out, I mean just look at global warming and how difficult of time some people have caring about that. But being able to model how [human] life would change in a different isolated environment over thousands/millions of years could be invaluable to many different scientific fields, no?

I do understand (as fileunderwater mentioned) that perhaps this question needs to be narrowed down. There are a lot of variables, and some we may need to resort to hypothetical models or deep speculation. This is an answer for many fields, but biology/astrobiology seems to be at the core. Given my inexperience in the field, I'm mostly curious whether the branching off of the species would even occur (with or without a drastic change in environment). Even if it would take millions of years, it'd still be a fascinating realization given that is a relatively short time.

That's an interesting model, because mosquitoes are vectors for serious illnesses, so are pretty well studied.  One team of scientists are working on genetically altering mosquitoes in Africa to make them unable to transmit the parasite that causes malaria. As the mosquitoes breed, it spreads through the population. In an interview, the lead researcher stated:

In the lab, we saw the mutation spread to more than half the population of mosquitoes we had living in cages. This happened in a time span of 12 to 16 generations of mosquitoes (each generation being between 18 to 30 days in the wild). So it's quite efficient.

12 to 16 generations for one mutation to spread to half of a contained population. In human generations, 16 = 320 years, and that doesn't take into account fertility rates, miscarriages, etc. (Not a problem for mosquitoes, I presume).
How many mutations would it take to make two humans incapable of reproducing without endangering their own health or fertility? Excluding all of the harmful mutations that might just result in disease or decreased fertility? And add to that that the males need to change as well as the females? No one knows.
Imagine a cystic-fibrosis type mutation (one gene) that increased the viscosity of cervical mucus such that normal sperm could not fertilize the egg. There would need to be another mutation in males that would make sperm stronger, or secrete an enzyme that breaks down mucus, or something to that effect. However, look at Cystic Fibrosis. People used to die before adulthood. Most men with CF are sterile. Women with CF, living longer now because of better care and treatment, are getting pregnant, but many have a decreased lifespan post-pregnancy, and almost all the babies are premature. You can't predict "when" a series of beneficial mutations so dramatic as to change a being so dramatically. The answer might be never.
Try to give me a single or a few mutations that would prevent the ability of people from one population and another to mate. Say one mutation led to a smaller pelvis. Most women with that mutation would die in childbirth before a mutation arose to make smaller babies (which would most likely be a deleterious mutation as well).
I am not a geneticist (which is really the person who should be answering this question) but I think the odds of this scenario ever occurring are very low. I just can't imagine mutations making reproduction impossible between two populations being beneficial and selected in one population rather than harmful. Keep in mind that different humans from populations that were isolated for many thousands of years have no problem reproducing.

just out of curiosity - why answer and vote to close?

@ChrisStronks - ethical standards. :D


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What virus transforms full grown plants?
I read an article by a gardener describing how a virus had transmitted a negative trait to his plants. It rather shocked me, because I hadn't realized that a virus could transform an adult plant. I was aware of dipping arabadopsis flowers in agrobacterium tumefaciens, but the concept of non-reproductive structures being transformed seems fascinating. What kind of virus is capable of that?

You're asking for a specific virus?

@canadianer Any information will be appreciated. A category or specific type is what I had in mind.

These are just a couple of short examples, but Witch's broom structures in trees can sometimes be caused by viruses - see Wikipedia: Witch's broom (fungi is maybe the most common cause though). In rose species you also have the similar Rose rosette disease (also called witches’-broom of rose), which is caused by a virus. The same webpage from Missouri Botanical Garden also includes a list of other plant viruses that you might find interesting.
Plant viruses that infect non-reproductive structures are common though - a overview can be found here: The American Phytopathological Society: Introduction to Plant Viruses, the Invisible Foe. More indepth information can be found in Plant Pathology (Agrios, 2012) (see ch. 12: "Plant diseases caused by viruses").

Viruses can infect just about any living thing, so that it could infect a plant is no surprise.
Your article describes how a small virus-infected part of a plant had been cloned and consequently the entire cloned plant was infected, and it infected plants grown hydroponically in the same water. No surprise there either.
Plant viruses have been known for centuries. One of the earliest recorded descriptions of a virus-infected plant can be found in a poem written by the Japanese Empress Kōken (718–770), in which she describes a plant with yellowing leaves in summer. The plant (a Eupatorium) was described as "autumnal".
The top 10 plant viruses (in one paper) in molecular plant pathology were listed as:

(1) Tobacco mosaic virus, (2) Tomato spotted wilt virus, (3) Tomato yellow leaf curl virus, (4) Cucumber mosaic virus, (5) Potato virus Y, (6) Cauliflower mosaic virus, (7) African cassava mosaic virus, (8) Plum pox virus, (9) Brome mosaic virus and (10) Potato virus X, with honourable mentions for viruses just missing out on the Top 10, including Citrus tristeza virus, Barley yellow dwarf virus, Potato leafroll virus and Tomato bushy stunt virus.

Some plant virologists even care enough to argue about it.
One paper describes how a plant was improved by a viral infection:

In all cases, virus infection delayed the appearance of drought symptoms. Beet
  plants infected with CMV* also exhibited significantly improved tolerance to freezing. Metabolite profiling analysis showed an increase in several osmoprotectants and antioxidants in BMV**-infected rice and CMV-infected beet plants before and after drought stress.

*Cucumber mosaic virus
**Brome mosaic virus
Aetiology: The earliest recorded plant virus disease
Top 10 plant viruses in molecular plant pathology
The REAL Top 10 for Plant Viruses

Introduction to Plant Viruses, the Invisible Foe

Virus infection improves drought tolerance

I was killing my brain on the answer. This is it!

source: Stack Exchange

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

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Real Time PCR Test Chemistry
I am working on building a real time PCR machine. Is there any chemistry set that I can purchase online to:

Identify if PCR amplification was successfully done.
Test fluorescence dyes that could be used to validate if the fluorescence detector optics worked; i.e. something I could excite with a specific wavelength and monitor for fluorescence.

I am looking for something that is not dangerous and only serves the single purpose of validating the real time PCR machine.
Mods please advise if I need to move to Chemistry StackExchange

Are you asking for specific and proven techniques ? or information on something like a thermocycler? Other than that, I have no idea what a pcr "machine" is.

I am asking for two things 1) Something that will confirm that PCR occurred (ie color change after 30 cycles of PCR). 2) Something that will fluoresce at a specific frequency when excited by an excitation frequency.

What level of accuracy do you expect for the identification of the PCR product?

If you're looking for a simple fluorophore just to make sure your detector is working, Auto parts stores carry fluorescent dyes to track oil leaks. Probably won't be useful for measuring amount of DNA though.

I just remembered that I used to extract fluorescent dyes from highlighters by breaking them open and passing ethanol through the marker. That would be another easy source of dyes to test your detector.

There are two different ways to detect PCR product in real-time PCR: dyes which bind to DNA in general, such as SYBR Green I, or probes specific to your PCR product. There's a summary of the benefits of each here, with the following table:

You can buy either online; they'll be fairly expensive but I can't think of an obvious way to get them cheaper if you're interested in high-confidence validation.
[edit] forgot to mention that you will also need to normalise the reporter signal against a reference dye such as ROX (https://www.thermofisher.com/order/catalog/product/12223012).

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Why is leucine amino acid used the most in proteins and tryptophan the least?
The amino acid leucine, is used in proteins more than others. Leucine with 9.1 percent (its average in more than 1.150 different proteins) is used most and tryptophan with 1.4 percent is used less than all other amino acids.
Why is leucine used more than tryptophan?

Are you talking in humans, animals, plants, single celled critters? My comment under @WYSIWYG 's answer depends on that as plants can synthesize Trp de novo and we can't

This is a guess.
Tryptophan is a bulky amino acid. Having a lot of if would make the protein bulky. It is anyways hydrophobic and cannot be present on protein exteriors; high tryptophan may distort hydrophobic core possibly because of its bulkiness and ability to form pi-stacking interactions.
However, tryptophan is an essential amino acid and cannot be made de novo in humans. Indeed, it has only one codon perhaps because of its limited usage.
Nonetheless, tryptophan, despite its low abundance, is important in stabilization of protein structures such as β-hairpin [1] and it is also required for synthesizing serotonin.
Leucine is present in the hydrophobic core and β-regions. It also surrounds active sites which causes exclusion of water; this in turn facilitates catalysis by allowing polar residues to bind to the substrates [2].
I don't have any comment on why not isoleucine or valine instead of leucine.

@ChrisStronks yes.. and it also has only one codon perhaps because its usage is less. Trp is also essential for making serotonin.

@ChrisStronks it looks better but I don't think it is the availability that restricts its usage. Even other species do not use Trp much. Leu is hydrophobic.

maybe you're right and we cannot make it because we don't need it.... feel free to ignore my additions. Interesting thoughts!


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Do people grow shorter as they age, how common is it, and what triggers it?
Is it true that people become gradually shorter as they age?
If it is, is it more common in one gender than the other?
And is it known what triggers this? (Considering that the "shortening" probably does not start immediately after the person stops growing?)

Short answer: Yes, we do shrink with age.
The most important reason is that the cartilage in the joints between our bones gets worn out and thinner, as well as disks between the vertebrae of the spine. This results in a compression of the spine and also to a loss in height. Shrinking bones due to osteoporosis can also play a role, as well as muscular atrophy due to ageing.
According to "The Baltimore Longitudinal Study of Aging" (reference 1) adults start shrinking by the age of 30 by 5-8mm per decade. This is relatively short after you completely stop growing. This process gets faster with increasing age, the study says it goes faster after 70.
Men and women do not shrink equally, men loose around 3cm between 30-70 and a total of 5cm by the age of 80. Women loose about 5cm between 30 and 70 and a total of 4.5cm by the age of 80 (these are average numbers from reference 1). Reference 2 also has a nice summary of this original article.
This effect can be attenuated by regulary excercising as the study listed in reference 3 shows.
References:

Longitudinal Change in Height of Men and Women: Implications for
Interpretation of the Body Mass Index: The Baltimore Longitudinal
Study of Aging
Yes, You Are Getting Shorter
Role of physical activity training in attenuation of height loss
through aging.

Muscular atrophy is also a factor

@WYSIWYG Good point, I have added this as well.

What about fat accumulation? Will that affect the height?

@CRags I haven't found evidence for that. But severe adipositas will cause wearout faster.


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What happens when someone is stung by a jellyfish?
What happens in the human body when someone is stung by a jellyfish; namely a box jelly. Judging by what I have heard about the stings I'm guessing that they involve a neurotoxin.

But what is actually happening? What are the symptoms and what happens after the sting (treatments and survivability)?

Someone else should pee on it

The problem is that box jellyfish doesn't specify one jellyfish but a group of different jellyfish. Some of these are highly venomous - I pick here Chironex fleckeri, as this is often called "the most venomous jellyfish in the world".
Chironex fleckeri has long tentacles which are covered with millions of explosive cells called Cnidocytes which inject a dart with the very powerful toxin upon touch. It is therefore very dangerous to touch the tentacles with bare hands to remove them.
The toxin is a mix of different bioactive proteins which have cytolytic, cytotoxic, inflammatory or hemolytic activity. Case reports (you can find information in reference 3 about it) show that the tentacles "burn" though all skin layers causing immediate strong pain and lasting scars (if the victims survive) which tend to show signs of necrosis. The toxins itself paralyze the muscles of the heart and the respiration and also causes hypokalemia by hemolyzing red blood cells (one of the toxin acts as a membrane pore in the blood cells). This causes further problems and often a cardiac arrest. See reference 1 and 2 for details on the toxins. Especially 2 is interesting, as this is a PhD-Thesis on this topic with a lot of references.
Treatment depends on how severe the injury is - in severe cases an antivenom can be used. Besides this typical measures are CPR, giving oxygen and removing the tentacles (with appropriate protection). See reference 3 (good overview) to 5 for details on this topic.
References:

Chironex fleckeri (Box Jellyfish) Venom Proteins: Expansion of a
Cnidarian Toxin Family that Elicits Variable Cytolytic and
Cardiovascular Effects
The molecular and biochemical characterisation of venom proteins
from the box jellyfish, Chironex fleckeri
Chironex fleckeri (Multi-tentacled Box Jellyfish)
Jellyfish stings and their management: a review.
Cytotoxic and cytolytic cnidarian venoms. A review on health
implications and possible therapeutic applications.

Oh, I didn't know that there are different types of box jellyfish XD

You've misspelt venomous twice here, once as "venomenous" and the second as "venemous".. SE's silly 6 char minimum won't let me change it.

@FaheemMitha Ups, thanks for the notification.


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If higher levels of atmospheric oxygen can lead to larger animals, can it also lead to larger plants?
According to some information, in the ancient past (at least some) animals grew larger due to a higher levels of oxygen in the atmosphere. So for example there is this study regarding dragonflies.
Can higher levels of atmospheric oxygen also lead to larger plants? For example, would it be possible to grow gigantic strawberries in a hermetically sealed greenhouse that maintains a higher atmospheric oxygen concentration?

Remember that plants utilize carbon dioxide to grow, and give off oxygen as a byproduct. A higher partial pressure of oxygen in the environment may actually decrease plant growth by inhibiting respiration.

@MattDMo - respiration, if anything, is enhanced by increased O2

Oxygen is good for animals because our basic metabolism is this:

High energy carbon molecules + O2 → energy + H2O + CO2

Plants do that too at night, but during the day, they mostly do this:

High energy photons + H2O + CO2 → High energy carbon molecules + O2

Rubisco, one of the most important enzymes in photosynthesis, can bind to O2, leading to less efficient photorespiration, instead of photosyntheis.  Rubisco is often a bottleneck in photosynthesis, in large part for that reason.  So high oxygen isn't helpful to plants.  In fact, C4 plants and CAM plants have evolved more complicated physiology to minimize the effect of O2.

enzymes merely catalyze a reaction, thereby establishing equilibrium more swiftly then would be the case without. Therefore, Rubsico does not carry out a "wrong" chemical reaction, the equilibrium is just pushed to the other side

The last parenthesis is not uncontroversial (also, bad in what way?) - I think you should back this up with something (or remove since it's not relevant to the question).

@ChrisStronks The one posting the answer.

The already given answers are correct, but I think explaining basic metabolism does not answer the problem of how big organisms can grow.
The argument about metazoan body size and the growing athmospheric O2 levels is that this latter process makes the diffusion of oxygen through animal tissue faster (because of the growing partial pressure of O2). This, in turn, made it possible for metazoans, which at the time had no elaborate body structures and no developed respiratory apparatuses, to actually grow larger, since it was possible for cells further away from the surface of an organism to respirate as well. Or, to put it differently, cell masses could grow bigger without risking anoxy in deeper parts of the tissue.
The problem with plants is not a very easy one to tackle, and I don't think there's a clear answer to this based on current knowledge. One must experiment with this and see what happens.
My guess is that the response of a plant lineage to grown O2 levels would be very dependent on the exact habitat the plant lives in, since for an evolutionary change to happen fast, there must be a clear evolutionary-ecological adaptive value it provides, and that is very dependent on environmental givens. Also, in recent (current) plants, respiration is a solved problem, so I'm not sure a plant would benefit in any way from elevated O2 levels. It would surely affect the working of RuBisCO as mentioned. Maybe an immediate response would be the spread of C4 metabolism within plants.


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How much energy does a lion contain?
I was looking into the following problem:

Obviously, the solution lies in how much energy either can output per unit of time.
The total energy output of the sun is $3.8×10^{26} \frac{J}{s}$.
The number of lions alone pales in comparison ($10^{12}$).
However, I'm now trying to figure out how many lions it would take to have an output equal to the sun, but I seem to be having a hard time finding good data.
What's the peak energy output of a lion per second (or where/how can I find such information)?

How do you define energy output? Its capacity to move an object, like horsepower? How much energy its cells produce? How much energy it would produce if completely combusted?

According tho this websote, a lion needs to eat from 5 to 7 kg of meat per day (with lots of variance from day to day going up to 50kg per meal). How much energy can a lion take up per kg of red meat? If someone find out this information we can easily answer the question by equating energy uptake and energy output (which totally makes sense for adults).

@MattDMo While it would be fair to compare combustion energy (since that's what the sun is doing), I would prefer the actual energy output of a lion itself in J/s (which is equivalent to Watts or ratio equivalent to horsepower, if you prefer that).

I assume that you mean "used" when you ay "output". Because of course there is tons of energy in matter that lions cannot access although this energy get through their body. Because input = output (when growth does not occur), there are two solutions available to us to answer this question: 1) How much do they eat and 2) How much carbon dioxide do they breath out

Peak energy output or average energy output? How long is this contest? Do we need to take into account rest/sleep/lifespan of lions? All important questions.

@Resonating To help the lions, I phrased the original question with peak output. But any data is appreciated, as I couldn't find anything reasonable myself.

Speaking of hypothetical scenarios - did you see the excellent and somewhat related A mole of moles from "what if?"?

Do you expect the lions to remain alive as they generate energy?  If not, do you assume infinite oxygen is available to burn them?  Is nuclear fission of the lions in scope?

If you burn the lions they're no longer lions, are they?

I think this would be a better fit for [physics.se]. I don't see how this is a question about biology. Fun question mind you, just off topic.

This question appears to be off-topic because it is about physics, not biology. It just happens to use a living organism as an example.

@terdon Mind you, I originally asked this question on Physics.SE, but they said it was more fit for Biology.SE. So vote to migrate if you think it's appropriate, but I would say it isn't.

@Nit oh, damn. I can't vote to migrate (we have no path to Physics) only close. I think this is a cool question I just don't see anything biological about it. You could ask exactly the same thing replacing lion with stove.

The interest doesn't seem to have to do with metabolism anymore but with physics. I therefore vote to close this question. The question might as well be flagged to be migrated to physics.SE

@terdon This is definitely borderline, but I think it should stay because of 3 reasons: 1) the quality of the answers, 2) as the answers show, the answer depends on how you interpret the energy output of lions and these discussion belong to biology, and 3) it's fun.

@fileunderwater I quite agree with points 1 and 2. However, the answers clearly push it into the realm of physics in my opinion. I don't see any biology in any of them. Which is not to say they are not fine answers, just not biological ones. I don't see how this can be answered by biology, it is pure physics.

@terdon The thing is that it was apparently deemed off-topic at PhysicsSE as well. It would be a shame and kind of sad to close such a fun/interesting Q at both sites, just because it is interdisciplinary/borderline at both. I think it should stay, just to define exactly where our line is drawn...

Wow, as an astrophysicist who has just logged into biology SE for the first time, I didn't think I'd have a question I could immediately answer.
You are correct about the Sun's output, so what about the lion.
If the lion is in its usual passive state, i.e. lying around as shown in your picture, then you would not go far wrong in treating them as black body radiators (well this will give you an upper limit, though the emissivity of human skin is quite high, so it should be a reasonable approximation.). To estimate a power I need a lion's temperature and its surface area.
According to this site the body temperature of a lion is 311.33 Kelvin.
I found a calculator that used the DuBois formula for surface area (for humans) and put in 440 pounds and 7 feet 10 for the weight and "height" of a (male, adult) lion - this returned a surface area of $3.6\ m^2$ (about twice a, male human, so sounds roughly ok).
Now using the Stefan-Boltzmann formula $P = \sigma A T^4$, I get the power output of a "black body" lion to be about 2 kW.
Thus $10^{12}$ lions have a power output of $2\times 10^{15}\ W$, which is 11 orders of magnitude less than the Sun.
But now take the question at its most basic. Compared to the Sun, the lion is a pretty effective power generation unit. The Sun only generates $2\times 10^{-4}\ W/kg$, whereas a lion-based power source weighs in with a massive $10\ W/kg$!
EDIT: Note that the calculation just assumes the Lion can produce this kind of power output whatever environment it is in. In practice a Lion absorbs a large fraction of this power from its surroundings and its internal metabolism does not need (and probably cannot) supply 2kW. Thus the 2kW should be reduced to some extent, though I'm not sure a simplistic $T^4 - T_{\rm env}^{4}$ calculation can be correct, unless one of you biologists tells me that a Lion's metabolism shuts down once the ambient (African) temperature approaches 311K (I guess in a human a lot of it goes in evaporating sweat?) Whatever, the order of magnitude of the answer is unchanged.

This offers some interesting insight, thank you very much for your answer.

But it probably wouldn't a useful power source, remember that those lions need 10W/kg worth of food.

You've accounted for the heat radiated by the lion, but not for the heat absorbed by radiation from its environment. So unless the lion is floating in deep space, you've dramatically overestimated its power output. Assuming an environment at 295K gives a much more modest power output of ~370W.

@David As lion is a warm blooded animal, regardless of external radiation, the surface temperature will more or less be constant

@CRags I doubt that a lion can hold its body temperature in a 0K environment. Unlike the sun, that can hold its body temperature in a 0K environment, the lion will just die.

I was not talking about surviving in 0 k

311.48K, please :-)

@David I am well aware of that. I placed the lions and the Sun in a similar environment.

@RobJeffries I'd say it explicitly in the answer that you calculated how much power the body of a lion would emit if it was suddenly placed in 0K environment (before the body started cooling rapidly and the lion would die), not how much power output a lion can maintain in passive state.

@JiK Well, I would, but I'm still thinking about it. The intrinsic power output is that given by the Stefan-Boltzmann law. The environment simply affects in what way this energy was supplied to the Lion (either absorbed through its skin or eaten). To me it makes no sense (even for a crazy question) to subtract the power input from an external source (absorbed heat/radiation) in the same way that I do not subtract the power due to the rate at which the Lion is eating antelope. They both supply energy to the Lion, which it then radiates away at the approximate rate I've calculated. I'll edit.

The sun will win until you have enough lions to form a star sized mass.
Assuming that your lions have an average mass of 200kg, which is probably pretty close, 1 trillion lions has a mass of 2×1014 kg, which is pretty close to the mass of Remus, a moon around the asteroid Sylvia. The mass of the sun is about 2×1030 kg.
So your lions would have enough mass to become gravitationally crushed into an object, but probably not enough to become rounded. Once crushed they won't be able to carry out any metabolism.
Even if we considered the sum of 2 trillion individual lions the sun would still win because nuclear fusion completely outclasses chemical reactions in terms of energy released, and the mass of the sun is still much much much larger.
However, if we somehow converted the lions into energy by E=mc2, we get about 1.8×1031 J. So if you managed that you could release more energy than the sun for a very short time.

I am not sure this was what the OP was after. He may have meant "energy consumption / metabolism" of a lion rather than the actual energy stored in its matter. But I missunderstand the OP's question.

@Remi.b It really doesn't matter, by the time you have enough lions for their normal metabolism to compete with the sun, you have more than enough mass to make a sun.

Ha ha yes I got this point. Well... but still I guess he would expect to know what is the ratio of the lion metabolism over the sun energy output. But the question might be better suited of worldbuilding.SE I guess

Relevant: https://what-if.xkcd.com/4/

I'm going to work this from the angle of power the animals could produce for an extended (e.g. 1 hour) time. I'll assume that a lion produces power somewhere between that of a human and a horse, since the typical weight of a lion (180 kg/400 lb-ish for males) is between that of a human (80 kg/180 lb-ish for males) and a horse (850 kg/1800 lb-ish for draft horses).

Human: 100 W
Horse: 746 W ("1 horsepower", or 746 W, is based off of how much work a draft horse can do for an extended period of time)
Lion: 200 W?

So you would need 3.8×1026/200, or 1.9×1024 lions. That's not a trillion, but about 2 trillion trillion lions. The exact amount of power produced won't change this too drastically, e.g. if our lions produce 800 W instead, it'd be 475 billion trillion lions.

Just a side note: this is an international website on science. Please use the SI system, i.e. kg instead of lb.

Just as another side note: the definition of a horsepower was taken off James Watt's marketing materials and is not a good guide to how much work a real draft horse can do even over a period of a few hours. Also: feel free to use lbs; this is an international site after all.


text:
Pasteurisation of orange juice and Vitamin C
In the UK at present, one of the examination boards has set a "controlled assessment" (an experiment that pupils do at school under exam conditions) that involves testing a hypothesis that vitamin C is removed from fruit juice by heating it (i.e. in the pasteurisation process).
I am massively skeptical about this. The teacher guidance suggests "Treating fresh orange juice in boiling water for between 10 and 30 mins gives an easily measurable decrease in vitamin C levels". Leaving aside that this hardly represents a simulation of the pasteurisation process(!), does anybody know of any solid, academic studies of the effect of pasteurisation on the vitamin C content of fruit juice? I have tried (as a scientist, but non-biologist) my usual routes to reliable information and they fail miserably - the www is full of crackpots on this one.
As a follow-up to that, is it not the case anyway that the oxidation of the orange juice when it is boiled in this experiment, plus simple exposure to light could also be responsible for any decrease in vitamin C observed?

Orange juice is pasteurized!? That's unheard of (for me, at least).

Hodgins AM, Mittal GS, Griffiths MW. 2002. Pasteurization of Fresh Orange Juice Using Low-Energy Pulsed Electrical Field. J Food Sci 67(6):2294-2299
This is a study of non-thermal food preservation, but it cites two studies that measured ascorbate loss from pasteurisation. I can't cite the studies directly because I can't find them online. According to these authors, they reported losses of 7.0-15.0% and 18.0% after 95°C for 15s. This is high compared to the pulsed electrical field method.

Yeom HW, Streaker CB, Zhang QW, Min DB. 2000. Effects of Pulsed Electric Fields on the Quality of Orange Juice and Comparison with Heat Pasteurization. J Agric Food Chem 48(10):4597-4605
This study compared ascorbate loss during storage after PEF or thermal treatment. While no difference was observed when stored at 22°C, PEF treated orange juice maintained significantly higher ascorbate concentration than thermally treated orange juice when stored at 4°C. The authors attribute this to the "higher processing temperature".

They also say (and reference other studies):

Ascorbic acid is a typically heat sensitive nutrient. High temperatures during processing and storage cause loss of ascorbic acid.

Thanks for this. The comment at the end is a bit puzzling. Table 3 appears to show that even pasteurisation at temperatures higher than normal (95 vs 72) does not decrease the vitamin C content by more than 20%. I am going to follow this up on Chemistry SE and see if I can find out what is going on.

@RobJeffries Does 20% hold some special significance?

No, I was just rounding up 18% from Table 3. I suppose if I was writing the paper I would argue this demonstrates that it is not especially heat sensitive. I also see from the graph that there is very little difference (none at 22C) between the Heat and PEF curves until you get beyond 40 days storage. So whilst the storage temperature seems important, the processing bit seems much less so.


text:
Eye strain using 3D screens
I don't know if this is a physics or a biology question but this might be better orientated around the element of how the human eye works in a 3D visual situation than physics.
Given the rise of 3D virtual reality headsets such as the Oculus Rift. I have a question about eye strain relating to these.
Often on a computer, eye strain comes from staring at the monitor for too long of which is the same continuous distance that your eyes have to focus on... thus causing computer vision syndrome (as well as lack of blinking). Meaning you should look at an object far away every X amount of minutes to rest the eyes.
How ever in a virtual headset, although the monitor is much closer, it is in 3D (or a fake 3D). So i wondered, does the eye muscles adjust based on this trick of fake 3D. Or will your eyes still focus on the fixed distance to the screen display regardless of the fake 3D perception, meaning you still get eye strain either way?
If you imagine looking through a 3D VR Headset, staring at a 3D object in the distance, is that going to create the same change in muscle adjustment in the eye as looking at a physical object in the real world of the same distance.
Essentially - 3D VR headsets could reduce the amount of eye strain. Because the eye is busy adjusting all the time for these "fake" distance illusions, rather than forced to focus in one way for a long length of time such as a 2D monitor. It might help people who struggle with computer vision syndrome perhaps?
Has any studies been done on this?

I think all illusions are based on certain drawbacks of our own eyes.

Most likely but thats a rather different topic entirely :P


text:
What is the human ear's temporal resolution?
What is the smallest sound duration that the human can hear? In other words, what is the lower duration limit for a sound to be translated into electrical signals by the ear?
Suppose the human ear can discern or distinguish between 18 kHz and 20 kHz sounds, this would mean that, if a single wave could  be processed at 20 KHz, the sound duration would be 1 / (20KHz) = 0.00005 second, which would be next to incredible (and probably impossible).
I am particularly interested in the lower duration limit as depending on frequency.
I am expecting something like this (I am not sure)
 Freq   Duration needed to be aware of the sound
 20KHz  0.05S (50 mS)
 10KHz  0.04S (40 mS)
  5KHz  0.03S (30 mS)
2.5KHZ  0.02S (20 mS)

Yes, it is the question. The duration depends on frequency How? Thank you...

I am an engineer too. Take a machine and hit it with a Dirac delta impulse of the frequency you wish to test and see if you can hear hear the frequency. The impulse will be less than 0.00005 secs.

@ChrisStronks I don't think you understand what I mean but my last comment then.

@dustin What OP wants to know is what would be the minimum duration of the stimulus that can generate a stable action potential along the auditory nerve

@chepelucho This study says that minimum duration for an auditory perception is 120-170ms. Note that this is not the physiological duration that elicits a stable nervous signal. This study was done on human subjects who have to report the onset of a sound stimulus. I think you are interested in the mechanistic aspects. Let me search; I'll get back

It would surprise me alot if this wasn't also related to the amplitude/volume of sound, similarly to how our vision works, see "Is it a limitation of the eyes, or the brain, that we can't see a moving bullet?". I also think that you should clearly separate hearing (a subjective impression) from the sensitivity of the ear (e.g. threshold for electrical impulses in the vestibulocochlear nerve).

Our sensitivity is also highest between 2-5 kHz (http://en.wikipedia.org/wiki/Equal-loudness_contour), and this will probably also interact with the temporal resolution of our ears.

@WYSIWYG - I looked at your linked article, interesting! But from my understanding they investigated minimal perceptual duration, which is different from the physical stimulus duration threshold

@chepelucho - I re-worded your question, based on your comments, to improve clarity. Feel free to roll back.

@WYSIWYG Thank you!!!, Please put your link (minimal perceptual duration) in your comment doing the clarification!!! and you have reason: One thing is the sensivity (or resolution) that the brain "knows" about of this stymulus in the ear by sound, and Other thing "Me" be aware as a person.

I will provide an answer in 2 parts. The first part is a theoretical approach based on the absolute possible minimum (my original answer). The second part focuses on experiments in the peripheral auditory system (added edited answer).
PART I: Absolute theoretical minimum (original answer)
As you inquire about electrical signals in the auditory human system I have to say that electrophysiological data at such a fundamental level is scarce in humans. That having said, we can start off by looking at auditory clicks, which are generally the shortest possible well-defined auditory stimuli. The shortest auditory click I was able to find, and which was used in a psychophysical context (i.e., audible to a human) was 10 microseconds (Leshowitz, 1971).
Now, (1) assuming 10 microseconds is the lower duration limit of a click (it may well be lower), and (2) assuming this click duration is representative of the lower limit of a tonal burst duration limit (it may well not be), and (3) assuming you indeed wish to know about/use auditory tones and not clicks, and finally (4) assuming we need at least one wavelength of a tone to fit in this window, then we could present a frequency of 100 kHz, or higher. As 20 kHz is the upper frequency limit of the human ear, we would need at least 50 microseconds for one wavelength, i.e., basically what @Dustin concluded, but it does not end here:
Frequency splatter (Fishbach et al., 2001) limits the lower limit of tonal stimuli. To prevent spectral splatter one needs to incorporate rise and fall times (ramps) onto the tonal stimulus. Hence, again assuming you do want tonal stimuli, an onset and offset ramp of one wavelength each would be advisable (at the very least) and hence 3 wavelengths are needed, increasing the duration of a 20 kHz tone to 3 wavelengths, i.e., 150 microseconds (spectral splatter may not be prevented, but at least reduced).
On top of this theoretical approach, it has to be noted that I started off with taking a click as a starting point. A click, being an impulse signal, basically stimulates the entire cochlea (the inner ear), and hence represents the most powerful auditory stimulus. Pure-tone bursts are, as a consequence, weak stimuli as they stimulate a small proportion of the available hair cells. High sound levels may therefore be necessary for short tonal stimuli, in turn degrading the frequency resolution in the cochlea as excitation spreads away from the characteristic frequencies. Mostly, several milliseconds are used as tone bursts.
Moreover, taking 20 khz is kind of an upper limit, and many folks are not even able to hear 16 khz. An upper limit of, say, 12 kHz would be advisable when grownups are used. This means a wavelength of 83 microseconds and for 3 wavelengths (for ramp times) that means 250 microseconds.
If lower frequencies are needed, this number would increase further.
EDIT: PART II. Phsyiological experiments.
As you are also interested in electrical signals, we might take another approach and start looking at experimental (animal) data. The temporal limits of the auditory system are generally assumed to reside in the ribbon synapse that is situated between the inner hair cells and the auditory nerve fiber (Parsons, 2006):

This synapse is considered to be the limiting factor in the temporal characteristics of the auditory system (Khimich, 2005). By analyzing this synapse using very short tone bursts, it was shown that the vesicles of glutamate (the neurotransmitter activating the auditory nerve fibers that lead the signal to the brain) were released as shortly as 2 ms after tone onset. Tone bursts were 8 - 16 kHz, 10 ms plateau, 1 ms
rise/fall (Khimich, 2005). Note the tone burstduration and rise fall times mentioned in answer PART I.
Indeed, when first spike times in auditory nerve fibers were determined, spikes with the shortest latency occurred just under 2 ms (Heil and Irvine, 1997).

SR in the figure means spike rate, showing that higher spike rates are accompanied by shorter latencies. A1 means auditory cortex neurons, which obviously have longer latencies.
Hence, from these experiments I dare say that 2 ms would be sufficient to elicit at least one spike.
Why then leave part I of the answer? The problem is that the experimental data do not show that a spike wouldn't have been generated at shorter stimuli. The data merely show that with an ongoing stimulus the first spike appears at 2 ms. It does not show whether 2 ms of temporal summation is necessary, and that is why I have left part I of my answer in place, as a theoretical lower bound.
As a side note: the spike rates are highly dependent on loudness levels. Lower sound levels result in longer latencies. Specificaly, acceleration of the stereocilia on the inner hair cells in the cochlea is the primary parameter. The faster the cilia move, the faster the spike response.
References
- Heil & Irvine. J Physiol 1997; 78:2438-54
- Fishbach et al. J Neurophysiol 2001; 85:2303-23
- Khimich et al. Nature 2005; 434:889-94
- Leshowitz et al. J Acoust Soc Am 1971; 49, Suppl 2:462-6
- Parsons. Nature 2006; 444:1013-4

This and other answers use the 20 kHz upper limit as a reference. But to the best of my knowledge (used to teach audio engineering) the hair cells in the cochlea do not discharge at such rate. Rather, the highest rate of discharge is around 12-14 kHz. Perceived frequencies higher than that are the sum component of intermodulation caused by non-linearities.

@Izhaki - discharge rates follow acoustic tones 1:1 only up until 2 kHz at max. After that the auditory nerve still fires in the same phase as the stimulus, but individual fibers skip one or more cycles and fire only in response to one in so many peaks. Overall, the 16,000 fibers do reproduce the stimulus perfectly though. But then, acoustic pitch is primarily a place-code and not so much a rate code.

The average human auditory range is between $20$ Hz to $20$ kHz [1]. How this relates to time is by the definition of frequency.
$$
f = \frac{1}{\text{time in sec}} = \frac{\omega}{2\pi}
$$
where $\omega$ is angular frequency. So if a human can hear a sound frequency of $18$ kHz, then
$$
(18\cdot 1000)^{-1} = 0.000056\text{ sec}
$$
where $18$ kHz is $18000$ Hz.

Abel (1972) reported duration DLs ranging from approximately 0.4 to 80ms for stimulus durations of 0.2 and 1000 ms, respectively. The lowest frequency on average is $20$ kHz but all people are different and some people may hear at a lower frequency.[1]
A different type of auditory temporal resolution can be assessed by measuring the minimum detectable duration of a gap in a continuous sound. The gap detection is in the order of 2 to 3 ms for tones at moderate and high sound
  pressure levels (Exner, 1875; Ostroff et al., 2003; Plomp, 1964). Zwicker and Feldtkeller (1967) reported values of 1.5 ms and 5.0 ms for gap detection in tonal signals and noise, respectively.[1]

Reference:

http://www.usaarl.army.mil/publications/HMD_Book09/files/Section%2019%20-%20Chapter%2011%20Auditory%20Perception%20and%20Cognitive%20Performance.pdf

You calculated the wavelength of an 18 kHz tone. OP wishes to know how long a tone needs to be for it to be audible. The fact that hair cells can discriminate frequencies doesn't mean one wave length is enough to hear it. 20 kHz is not a duration, but a frequency. And you mean 20 Hz.

@ChrisStronks according to Georgia State Universities Physics department, "the threshold of hearing corresponds to air vibrations on the order of a tenth of an atomic diameter."

@ChrisStronks Hz as units 1/time. If you want time, you invert.

Yes that is auditory threshold level. Then there are frequency limits and OP inquires about duration threshold.

@ChrisStronks and at that limit, some people will pick it up.

In your edit you mention difference limens (DL: duration difference) and gap detection threshold (shortest noticeable interruption in a burst), but both are irrelevant for OP's question I'm afraid (which is on minimal duration threshold). It's is all just basic psychophysics.


text:
How can we measure cardiac output?
I could find a way which could find it by body oxygen consumption and there is another way to measure it by injecting drugs — measuring cardiac output by the so-called “indicator dilution method,” a small amount of indicator, such as a dye, is injected into a large systemic vein or, preferably,into the right atrium.
I read about it but didn't understand it very well.
Can you explain it and Which one is mostly used in clinics to measure cardiac output?

I think this is a pretty broad question. Can you narrow it down to something that would take less that a book chapter to cover? There are more ways than you list. There is no one best method. It depends on a lot of factors. Have you checked Wikipedia? It's not perfect by any means, but it will give you the scope of what you're asking (which is very broad).

@Chris stronks Blood volume is different with cardiac output in order,we measure cardiac output in time.

@anongoodnurse "Indicator Dilution Method"for measuring cardiac output.

Please change your question to reflect the newly narrowed scope, and can you explain what, exactly, trips you up about dilution studies?

@Madscientist I didn't know about it at all, when i read about it.I edited my answer as it is acceptable.

Drs. Swan and Ganz developed a direct method of measuring cardiac output by thermodilution. They invented a multilumen catheter with a thermal resistor on the end (a Swan Ganz catheter) which could be advanced into the pulmonary artery. Through another lumen, a cold saline solution of known temperature and volume is injected into the right atrium. Using a computer model, the temperature of the blood at the catheter tip is used to determine stroke volume. Stroke volume x heart rate = cardiac output.

The injectate mixes with the blood as it passes through the ventricle and into the pulmonary artery, thus cooling the blood. The blood temperature is measured by a thermistor at the catheter tip, which lies within the pulmonary artery, and a computer is used to acquire the thermodilution profile; that is, the computer quantifies the change in blood temperature as it flows over the thermistor surface. The cardiac output computer then calculates flow (cardiac output from the right ventricle) using the blood temperature information, and the temperature and volume of the injectate. The injection is normally repeated a few times and the cardiac output averaged.

The same principle is used with a dye study but measuring the concentration of dye downstream.
Although this is considered to be the "gold standard", because it is so invasive and carries a serious risk of complications, it has largely been replaced by echocardiography and Doppler techniques.
Measurement of blood flow by thermodilution
Measurement of Cardiac Output
Invasive and non-invasive methods for cardiac output measurement

I read in wikipedia that Ficks method of measuring cardiac output using oxygen saturation difference is the gold standard.

http://www.derangedphysiology.com/php/PAC/Ficks-principle-of-cardiac-output-monitoring.php check this out

https://www.google.co.in/url?sa=t&source=web&rct=j&ei=N363VI3pJMuMuASlkYDQDQ&url=http://www.iars.org/assets/1/7/12_RCL_Mackensen.pdf&ved=0CCcQFjAD&usg=AFQjCNHtDfVMtbUadLWJXH08hp0ErhpKdw

http://www.atsjournals.org/doi/abs/10.1164/ajrccm-conference.2010.181.1_MeetingAbstracts.A3392 this article claims both methods must be followed in case of pulmonary hypertension as there is no gold standard


text:
Is the molecule nitric oxide responsible for healing blood vessels?

Is the molecule nitric oxide responsible for healing blood vessels?
How does nitric oxide heal the blood vessels?

I watched a documentary about the healing effects of nitric oxide. In the video I saw a cardiologist show an X-ray picture of one of his damaged heart blood vessels, and then another X-ray picture showing the same heart blood vessel completely healed. He claimed it was due to a radical change in his diet of consuming lots of nitrogen rich vegetables which the body in turn converted to nitric oxide. Is this possible?
Sources :
The original source was the youtube video Forks Over Knifes, however it was recently taken down. I have provide the following links which provide a little bit of information :
http://www.happyhealthylonglife.com/happy_healthy_long_life/2010/06/esselstyn-session.html
http://www.happyhealthylonglife.com/happy_healthy_long_life/2010/12/no.html
Dr. Caldwell Esselstyn was the one who made the statement about heart health and nitric oxide, also showing the xray pictures of one of his colleague cardiologists in the documentary.

Can you provide a link to that documentary? NO causes vasodilation, I have not heard of its role in regeneration. And simply eating nitrogen-rich food will also not increase NO (its synthesis is not limited by the availability of nitrogen)

@WYSIWYG The documentary is called Forks Over Knives. Thanks for the response.

Here's a review published in Nature, about the regenerative role of NO, followed by an application in 2012 to wound healing.
http://www.nature.com/aps/journal/v26/n3/full/aps200541a.html
http://www.nanomedjournal.com/article/S1549-9634%2812%2900090-1/abstract


text:
How does trees know to balance themselves so that they never fall down
Well i was flying kites today I saw a tree and its branches were spread around in random directions... I would like to know that how do these trees know to nourish their branches in some direction so as it doesn't fall off due to gravity. I know it can get its strength from the roots inside the soil so that it does not fall. But if this strength were not enough the tree may fall due to weight of its own branches. Can this happen??
I am new to this site I don't know much about the rules here. Feel free to edit if I have done any mistakes(especially about tags)

tree's do fall down, there may be a benefit, in terms of stability, to growing in a more "balanced" spread of branches but other factors also influence the direction the branches grow e.g. prevailing sun and wind conditions

I think the strength of the tree's roots are more of a factor in holding it up than the symmetry of its branches


text:
Why do the size of the phase 1 notch vary among cardiac cells?
The size of the phase 1 notch varies among cardiac cells. It is prominent in myocytes in the
epicardial and midmyocardial regions of the left ventricular wall  and in ventricular Purkinje fibers. However, the notch is negligible in myocytes from the endocardial region of the left ventricle.
What's the reason?

Between at least the endocardial and epicardial regions, I believe the transient outward current is facilitated much more in epicardial cells. This article demonstrates the differences in Ito between the two cell types in dogs.
I'm also recommending the following article about Ito phenotypes: "Transient outward potassium current, ‘Ito’, phenotypes
in the mammalian left ventricle: underlying molecular,
cellular and biophysical mechanisms"


text:
What effect does the Barr body have, in relation to female Turner syndrome?
Why do persons with Turner syndrome have  developmental abnormalities, when normal XX-females do not, even though they only have 1 active X chromosome? From what I know, one X-chromosome is inactivated into a Barr body in normal XX-females, but these obviously don't show the symptoms of Turner syndrome. What function does the inactive chromosome have?

The reason is that X-inactivation is not complete (Carrell & Willard, 2005; Ahn & Lee, 2008), and as many as 15-25% of X-linked genes escape silencing (Carrell & Willard, 2005; Cheng et al, 2005). This means that some genes on the Barr body are expressed in XX-females, although often at lower levels compared to the active X-chromosome, and this is part of the normal gene dosage. The "purpose" of X-inactivation is usually dosage compensation, so that genes are expressed equally in males and females (and then actually upregulated in both sexes to balance autosomal genes, see e.g. Dementyeva et al, 2009). However, this is not true for all genes, and the ones that normally escape X-inactivation will be expressed in the incorrect dosage in X0 females. Some of these genes are thought to contribute to the symptoms of Turner syndrome.
It is also likely that the genes that escape silencing are involved in sex-linked traits, as stated in Carrell & Willard (2005):

Such genes are potential contributors to sexually dimorphic traits, to phenotypic variability among females heterozygous for X-linked conditions, and to clinical abnormalities in patients with abnormal X chromosomes.
  ... ...
  However, as many of the genes that escape from inactivation do not have Y-linked homologues, strict dosage compensation may not be necessary for all genes on the chromosome. Such characteristic genomic differences should be recognized as a factor for explaining sex-specific phenotypes both in complex disease as well as in normal, sexually dimorphic traits.

Cheng et al (2005) also point out that the expression of the genes that escape silencing is tissue-dependent, which suggests that the role these genes play in the symptoms of Turner syndrome is also tissue dependent.

Very interesting question!
And I don't think either that the linked Wikipedia article answers the question.
Unfortunately I do not know the answer for sure, but I might have some relevant information to add. So, from my studies I know that Barr-bodies are not totally inactive, they, in fact, do have some very limited transcriptional activity. It might be low in intensity, but still vital? I'm just guessing.
My other guess is linked to the development of a Barr-body in a cell with two active XX chromosomes early during fetal development. So this happens via a process called X-inactivation in which a gene called Xist becomes active on both X chromosomes, then another gene, the Tsix also becomes active on one of the chromosomes and suppresses Xist on the other. The one with the suppressed Xist remains active, the other becomes the Barr-body (the process of selecting which chromosome becomes the Barr-body is random, hence female mosaicism). So, the point is, that for correct X-inactivation, the interplay of two X chromosomes are needed, and people with Turner syndrome have only one. That might be the problem, e.g. the Xist becomes active on the one X they have and starts interfering with the normal functioning of the chromosome, and there's no Tsix to suppress it.
But, again, I'm just making educated guesses here.

Thank you for your concern. Your question fits; however, it doesn't expain the case of Triple-X female, they also express some different symptoms, it means the Barr body really plays some role but not just in early fetal development. Today I see fileunserwater's that satisfies me the most. Hope you would agree if you were interested in this issue too.


text:
Why don't myopic people see the world upside-down?

I found this image while reading optical instruments in physics. If we look at the uncorrected rays, we see that the image they outline gets inverted. So why don't people with myopic vision see images as inverted representations?

Could that diagram be exaggerated? Maybe the uncorrected ray in a real eye is focused just in front of the retina rather than in the middle of the eyeball.

@user137 even if that's the case then still it would be inverted, right?

@LucyferZedd - I slightly modified your wording. Please feel free to roll back, it's just a suggestion.

You have misinterpreted the nature of the light rays shown in the diagram in the question.  The two rays are representing light coming from the same (distant) point in the environment, that is, some small feature on an object is reflecting (or emitting) light in slightly different directions and reach the eye separated by a small amount (less than the width of the pupil).  The rays are almost, but not quite, parallel.  The two rays, coming from the same point, should be focused on the same point on the retina (as are the red rays corrected by the external lens).  The spread of the uncorrected rays in myopia or hyperopia sends them to different places of the retina, causing the image to be out of focus, not upside down.
The path of light from an entire scene can be illustrated like this:

As this diagram shows, the image is upside down for all of us, in focus or not.  That the image top is at the bottom of the retina is not especially important -- the cells doing the interpretation could have been located physically located anywhere as needed.

seems, it's not the light rays coming from different parts of the object reflecting the light, but rather the light rays reflecting off of the same part or closely adjacent part of the object but going to different parts of the eye, "misaligned rays"... a quote from opthobook: "punch a small hole in a paper card, and have your patient reread the eye- chart while looking through this pinhole. This technique can actually improve vision by several diopters. It works because the paper blocks most of the misaligned rays that cause visual blur, and allows the central rays to focus on the retina."

Overview
Myopia does not cause image inversion. @mgkrebbs provides an answer with a clearer diagram than the one you have provided that illustrates how only the focussing ability, not the orientation, of an object changes.
However, an image can be inverted by special inversion glasses. Furthermore is that the brain can convert the image to the right way around.
Although myopic vision can't cause the inversion, the answer you're looking for is probably that perceptual adaptation, a phenomenon that occurs to correct our vision, comes into play in cases of inversion. The brain "gets used to" inverted images and what you visualise becomes the correct orientation. So lets say myopia did cause inversion, the person with naturally inverted vision wouldn't experience anything unusual.
Experimental Evidence
The below text from the wikipedia entry describes an experiment with inverting glasses. These glasses contained prisms that flipped the real world image before it reached the eye. Note the experiment was carried out in the in the late 1800s.

On a later experiment, Stratton wore the glasses for eight whole days. By day four, the images seen through the instrument were still upside down. However, on day five, images appeared upright until he concentrated on them; then they became inverted again. By having to concentrate on his vision to turn it upside down again, especially when he knew images were hitting his retinas in the opposite orientation as normal, Stratton deduced his brain had reprocessed his vision and adapted to the changes in vision.

A more recent study by Linden et al., 1999 confirmed the same thing happening with more up to date inverting glasses. The subjects reported slightly different results. Rather than the image being inverted, it was more the case that the subject felt their reality became inverted to match the inverted image. I can't see someone suffering with myopic vision being able to make this distinction since they would only be used to one orientation.
Figure 1 from Linden et al., 1999
On removal of the glasses, the world becomes temporarily re-distorted, but normal vision and perception returns.

How myopic do you need to be to invert the image? I don't notice any problems taking my glasses off, so the image either isn't inverted or my brain adapts within the half a second it takes to remove the glasses.

Undoubtedly interesting, but not relevant to the question; myopia does not cause image inversion.

@user137 I had doubts that myopia would cause inversion except in extremely severe (possibly only hypothetical) cases, but mgkrebbs explains why this wouldn't happen. Here I am just answering a hypothetical about the brain correcting an inverted image.


text:
Why do some cells like myofibrils have multiple nuclei?
I see that myofibrils (muscle cells) contain not one, but multiple nuclei.

Why is this so?
Do all the nuclei participate in cell division?

Is your question about "how it happens" or "what is the importance of such a phenomenon"

@WYSIWYG The first question particularly - more towards a reason why this came about in evolution. Could an equally efficient mechanism as the myofibril come about that didn't require multiple nuclei. Benjamin Markus did answer my second question.

First Myofibrils are not muscle cells. Many myofibrils (essentially long strips of the muscle cell) make one muscle cell, which is known as a muscle fibre. And it's the muscle fibres that have multiple nuclei. And they have multiple nuclei because they were formed from the fusion of multiple myocytes. Why? Probably because the muscle cell is quite a large cell(because it is long) so multiple copies of DNA are required to produce the proteins required to maintain the muscle cell. Also muscle fibres do not divide, so no the nuclei do not participate in cell division. About other cells I am not sure. I am only aware that some cardiac muscle cells also have multiple nuclei, for similar reasons.

Osteoclasts can also have multiple nuclei, usually around 5.

In the case of myofibrils this is the case because of the syncytial nature of that given structure. It means that in developing muscle tissue after a certain stage the cell divisions become somewhat different in that the final step, being separation of the daughter cells via invagination of cell membranes, does not happen. The nuclei though keep dividing after that. In the end what we have is a big membrane coated structure (basically a cell), with lots of nuclei in it.

What you are describing is a coenocyte (nuclear division without cytokinesis).


text:
Why can't we defibrillate the heart within 1 minute after ventricular fibrillation by electroshock?
We mostly can defibrillate the heart before 1 min of ventricular fibrillation by electroshock.Then we often can't do defibrillate it with electroshock.
What's the reason and What's the best way to defibrillate heart within 1 min after ventricular fibrillation?

This edit changes your original question a bit. The best way to defibrillate a heart within one minute of VFib onset is with electric shock. In fact, short of certain drugs in certain instances, it's the only way to defibrillate Vfib, regardless of the amount of time that has passed. I don't want to edit your question because it has the appearance of impropriety. But the truth is, the heart can be defibrillated with shock alone after one minute. After 4 minutes, the brain is negatively affected, therefore CPR is recommended before then.

down voter! Can you explain it for a down vote for below answer.

Unless defibrillated within 1 minute after fibrillation begins, the heart is usually too weak to be revived by defibrillation because of the lack of nutrition from coronary blood flow. However, it is still possible to revive the heart by preliminarily pumping the heart by hand (intermittent hand squeezing) and then defibrillating the heart later. In this way, small quantities of blood are delivered into the aorta and a renewed coronary blood supply develops. Then, after a few minutes of hand pumping, electrical defibrillation often becomes possible. Indeed, fibrillating hearts have been pumped by hand for as long as 90 minutes followed by successful defibrillation.
A technique for pumping the heart without opening the chest consists of intermittent thrusts of pressure on the chest wall along with artificial respiration. This, plus defibrillation, is called cardiopulmonary resuscitation, or CPR.
Lack of blood flow to the brain for more than 5 to 8 minutes usually causes permanent mental impairment
or even destruction of brain tissue. Even if the heart is revived, the person may die from the effects of
brain damage or may live with permanent mental impairment.

I thought a few minutes (say 2-3 instead of 5-8 min) was already pretty devastating to the brain?

This answer would be greatly improved if you could add references supporting your claims.

Some references are some physiology books,for instance guyton and hall physiology and bern and levy physiology book which I read these books before.

To say that there is a cutoff of one minute at which time shocking becomes ineffective is incorrect. The best way to defibrillate a heart within one minute of VFib onset is with electric shock. In fact, short of certain drugs in certain instances, it's the only way to defibrillate Vfib, regardless of the amount of time that has passed.
If the one minute cut-off were true, survival rates of out-of-hospital arrests would be more dismal than they are. Even with the availability of automated external defibrillators (AEDs) to treat out-of-hospital arrest, the collapse to response time is well over a minute. Someone has to notice a collapse, feel for a pulse, and call for a defibrillator (or get it themselves), expose the chest, apply the paddles, wait for the monitor to display the rhythm, clear the area and shock. If you were told that this usually occurs in under a minute, you were misinformed.
Seattle is the best city in the US (probably the world) in which to have a heart attack.[1] The population has a high rate of training in CPR, a highly trained corps of paramedics and EMTs, and a quick response time. So it's logical to do studies about factors affecting survival of out-of-hospital arrests in Seattle.
A study published in 1999 found that CPR did not have any effect on outcomes of out-of-hospital arrests unless the interval time (from arrest to defibrillation) was greater than 4 minutes.[2] (In other words, shocking without CPR was no different in outcome than shocking preceded by CPR; both resulted in cardioversion to a stable rhythm and a return of of spontaneous circulation in the same percentage of patients.)
However, that is not to say that CPR (chest compressions +/- respirations) are unimportant. A 2003 study found an unacceptable level of CPR was performed when AED paddles were connected (i.e. there was an over-reliance on shocking).[3]
The new Advanced Cardiac Life Support guidelines call for CPR to be initiated immediately, regardless of witnessed or unwitnessed arrest (i.e. down time).[4] It needs to be noted, though, that this recommendation does not rest on defibrillation with the aim of return of spontaneous circulation(ROSC), but on improved neurological outcomes.[5] This, not ROSC, is what the new ACLS recommendations are based on, because ACLS is not considered highly successful if the patient leaves the hospital only to be hospitalized elsewhere in a persistent vegetative state.
[1] King County may be the best place to have a heart attack
[2] Influence of Cardiopulmonary Resuscitation Prior to Defibrillation in Patients With Out-of-Hospital Ventricular Fibrillation
[3] Interruption of cardiopulmonary resuscitation with the use of the automated external defibrillator in out-of-hospital cardiac arrest
[4] VF/Pulseless VT
[5] Delaying Defibrillation to Give Basic Cardiopulmonary Resuscitation to Patients With Out-of-Hospital Ventricular Fibrillation A Randomized Trial

according to below answer, We absloutely need to have electroshock after pumping the heart by hand.

@Thirdkidney - if you like that answer, up vote it. But please don't compare one answer to the other like that. If you have a question, ask it. Be clear. In physiological studies, dogs could be shocked out of VFib successfully for 7 minutes without CPR. Look at the studies, not just the answer if you need evidence.

Absolutely there wasn't any comparison,just some notes which I thought, can help answering this question.

@Thirdkidney - I answered it well, with references, and am completely fine with it, thank you.

@Thirdkidney I am surprised you accepted the other answer. It makes a lot of claims with absolutely no evidence to back it up. It is, essentially, the opinion of some random internet user. I'm not saying it is wrong (I don't know and cannot judge), just that there is no reason to think it is correct. This answer, on the other hand is supporting its claims with references so if the two answers disagree, I would believe this one. Incidentally, I also happen to know that Medica is a practicing physician, yet another reason to rethink your acceptance.

@terdon - lol, I'm not medica here. :D (It's a long story.)

Oh, bugger. Sorry! Anon, good nurse then.

@Majid that's fine, you should always accept whichever answer you prefer. I just found your choice surprising, that's all. I did not mean to pressure you to change anything. It is completely up to you.


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Mean and standard deviation of human bone density?
Are the human bones about equal in density? Or is there any published data on the mean + s.d. density for a given bone available?

Interesting question that I'd not considered before.
Bone density is commonly measured by assessing the bone mineral density (BMD) using dual-energy x-ray absorptiometry (DMA), literally the g/cm2 of minerals in the bone.
Having had a search I can only find values for a small number of bones commonly measured when testing for osteoporosis (characterised by reduced BMD). Unsurprisingly the age and sex of the individual has a large effect on BMD; after puberty males have higher BMD (1) and during ageing this then declines, sometimes dramatically (2).
These values are from a Vietnamese study (3) show that the hip and the spine are different.
Men [ mean (SD) ]

Femoral neck: 0.85 (0.13)
Total hip: 1.00 (0.13)
Lumbar spine: 1.05 (0.12)

Women  [ mean (SD) ]

Femoral neck: 0.80 (0.11)
Total hip: 0.95 (0.12)
Lumbar spine: 0.96 (0.11)

There must be other reference values for other bones in different populations but I don't have time to look them up now! Good luck in your own research.
I found this website by the US National Institute of Health and this PDF by the World Health Organisation immeasurably enlightening.

Bonjour JP, Rizzoli R. Bone acquisition in adolescence. In: Marcus R, Feldman D, Kelsey J, eds. Osteoporosis. San Diego, CA, Academic Press, 1996:465–476
Cummings SR, Kelsey JL, Nevitt MC, O’Dowd KJ (1985) Epidemiology of osteoporosis and osteoporotic fractures. Epidemiol Rev 7:178–208
Ho-Pham, et al. (2011) Reference Ranges for Bone Mineral Density and Prevalence of Osteoporosis in Vietnamese Men and Women. BMC Musculoskeletal Disorders, 12:182  doi:10.1186/1471-2474-12-182


text:
Do bacteria with multiple flagella move faster than bacteria with a single flagella?
Do bacteria with multiple flagella move faster than bacteria with a single flagella? Assuming the flagella are at the same length.

Note: in the following I'm going to focus on E. coli, which is the best understood system for bacterial flagellar movement. It would be interesting to compare uniflagellate bacteria and bacteria that have a fixed number of flagella. However, I know about E. coli and I think there is something interesting to be learned just from them, so I'll continue.
You're in luck that you asked this question when you did: a very cool paper (1) was published just last year addressing your question. They find that the number of flagella has only a small effect on bacterial motion, but to understand why requires some background (A lot of the following background comes from this paper, which summarizes it pretty well).
I would argue that E. coli movement is one of the best-understood examples of cell movement we have, with excellent, high-resolution, quantitative data being generated for over 40 years now (the king in this field is Howard Berg at Harvard, if you want to learn more just read a recent review from him).
E. coli have a variable number of flagella, from one to ten or so. They operate in a bundle, but this bundle is highly dynamic due to the way E. coli moves. Rather than proceeding continually a straight line like a car, E. coli moves by a series of starts and stops called a run-and-tumble: the bacteria moves in a straight line for a short amount of time (a run), and then it stops in its tracks and changes direction (a tumble) before starting off again (2). At a first pass this run-and-tumble behavior is essentially diffusion, the bacteria covers a lot of ground without going anywhere on average unless there's some food nearby, in which case the run-and-tumble is slightly biased so that the bacteria drifts toward the food.
As I said, during runs the flagella are bundled together and all turning counter-clockwise. A tumble happens when the bacteria sends a signal to the flagella to start turning clockwise. This breaks apart the flagellar bundle and sends all the flagella in different directions. Up until the paper I mention above, it was still not clear exactly how many flagella need to start turning clockwise before the bundle breaks up and a tumble commences.
Now you can see why having more flagella might not necessarily be a good thing: you might be able to move faster during the run (though this is not obvious to me, given the sometimes unintuitive nature (3) of low-Reynolds number fluid dynamics) but at the same time the flagellar bundle will be more sensitive to break-up because with more flagella come more opportunities for one to start moving counter-clockwise and mess things up.
As the authors of the above paper (1) find, it turns out that there are correlations between the actions of different flagella in a bundle, so that a bacteria with many flagella effectively acts like a bacteria with fewer flagella. The result is that the overall pattern of run-and-tumble is not much affected by the number of flagella; you might argue that number of flagella has a minor effect on bacterial movement.
On the other hand, you might be interested not in the net movement of a bacteria, but just on its speed when it's moving forward, in the run phase. Unfortunately I wasn't able to find any good measurements of the run velocity of a bacterial cell as a function of number of flagella. But hopefully given this recent paper, maybe such measurements are on the horizon!

(1) Mears PJ et al. (2014) Escherichia coli swimming is robust against variations in flagellar number. eLife 3:e01916.
(2) Turner L et al. (2000). Real-time imaging of fluorescent flagellar filaments. J. Bacteriol. 182(10): 2793-2801
(3) Purcell EM. (1977). Life at low Reynolds number. Am. J. Phys. 45: 3-11.


text:
Safety of using industrial water for hand washing
Industrial water taps are present in most biology laboratories I have been too. There are accompanied by a sign stating "do not drink". So obviously it is not a good idea to drink it.
However I could not find any information or reference concerning its safety for body use. The only indication I could find is that eye wash stations are using potable water instead of industrial water, suggesting that industrial water is not suitable for eye contact - at least.
My question: is it safe to use industrial water available in labs for hand washing, multiple times per day over the course of several years?
I am looking for a precise answer about the possible long term harm of industrial water in this context, if possible with references.

You should ask this question of your university's Environmental Health and Safety department (or the equivalent). They will know the answer and are the only ones qualified to answer in your specific case.

The water from taps labelled "Industrial Water, Do Not Drink" comes from the same potable water line as domestic taps. The line should be split somewhere in the building, with the industrial line containing multiple backflow inhibitors to prevent cross contamination of potable or domestic water. Based on that fact, the water should be safe for hand washing, however, should be tested in the case of objective concern.

Thank you for clarifying: the appellation "industrial water" confused me, I thought it was coming from nearby industries... So I guess that it is in general safe to wash hands with such water - depending on the potential contamination sources that could backflow within the lab/building network.

Right, I made a hasty generalization myself but then I realized it was a tap in an indoor lab.. The documentation is a pain to hunt down, but in the following resource from WHO they make the assertion:
"All the water piping downstream of backflow protection devices is normally
classified as an industrialized water system. To protect workers from taking this water for domestic use, each outlet in such industrializedwater systems should be clearly marked “Industrial water – do not drink”"
http://www.who.int/water_sanitation_health/hygiene/plumbing15.pdf


text:
Does the nervous system have "routers"?
Does the peripheral nervous system have a system of routers that decide where a message is meant to go based on some kind of address, or does a signal from the brain follow a single, unbroken chain of neurons that starts at the brain and ends at one destination?
For example, let's say my brain wants to send a message to my left pinky, telling it to contract. In the first model, a series of action potentials travel down my spinal cord, reaching a node in my chest. The action potentials encode the "contract" command as well as an address. The node in my chest reads the address, and routes the signal down my left arm. It reaches my left hand, where another node reads the address and sends the signal to my left pinky, where the signal reaches the appropriate muscle, telling it to contract.
In the second model, every single muscle in my body has a particular chain of neurons that runs in parallel to my brain. If my brain wants to send that signal, it doesn't have to specify an address, it just sends the "contract" command down the path that says "Leads directly to left pinky and nowhere else".
If the second model is true, does that mean that the large, visible structures that we call "nerves", such as the vagus nerve, are actually bundles of point-to-point connections?
Anywhere I can find more information about this would be awesome. I'm a comp sci/biochem double major, and really love reading about the body as an information system.

while the second model is correct, at many points along the chain there is a choice of whether or not to proceed (sort of address)... example, the sensory pathway going from the body to the brain, the thalamus is a relay that decidedes whther or not to permit a signal (spatial or temporal summation) that is determining further access up into the cortex... not sure what exactly is coded within the signal and how the cortex communicates with the thalamus to say how strict the gate keeping should be... I suppose the same occurs in the descending sensory pathway that is involved in pain gating...

The second model is the one. No tags, flags, or routers, just a 1-to-1 system.
A striking example of this is are the different effects of spinal cord injury, which depend on the place where the injury occurs.

And I quote from the apperalyzed website:

Spinal Cord Injury Overview
When a person suffers a spinal cord injury, information traveling
  along the spinal nerves below the level of injury will be either
  completely or partially cut off from the brain, resulting in
  Quadriplegia (Tetraplegia) or Paraplegia.
[...] The brain will still be trying to send messages downwards to the
  muscles in the body, known as motor messages. These messages however,
  will be blocked by the damage in the spinal cord at the level of
  injury. Nerves joining the spinal cord above the level of injury will
  be unaffected and continue to work as normal.
Quadriplegia / Tetraplegia [occurs] when a person has a spinal cord injury above
  the first thoracic vertebra. Paralysis usually affects
  the cervical spinal nerves resulting in paralysis of all four limbs.
  [...]
  Paraplegia [occurs] when the level of spinal cord injury [is] below the first thoracic spinal nerve [and leads to] paralysis of the legs and abdomen up to the nipple line, [but] paraplegics have full use of their arms and hands

This example shows that there are strict one-to-one connections (2nd model) and that messages are not simply flagged and routed to their destination via the shortest or quickest route available among a bunch of redundant, ill-defined pathways (1st model). Hence, there is only one way from the brain to the periphery; once severed the message cannot be simple re-routed via parallel lines.
Another example is the make-up of the sensory-motor cortex:

The picture shows that the motor cortex (muscle control/motor output) as well the sensory cortex (sensory input) contain a complete image of the body. Each part of the motor cortex and sensory cortex is devoted to the control or sense of one specific part of the body, respectively.
Nerves are indeed typically bundles of 1-to-1 fibers. For example, the optic nerve contains fibers that carry info from one, and only one well-defined and localized pixel from the retina to the brain.
Principles of Neuroscience by Kandel and Schwartz is a great book with a wealth of info.


text:
How long can the brain survive during ongoing cardiac arrest?
There was this interesting discussion on CPR and defib in response to the question "Why can't we defibrillate the heart within 1 minute after ventricular fibrillation by electroshock?".
Now I was wondering "How long can the brain cope without O2?".
And to specify this question to a realistic situation: "How long can the brain survive a cardiac arrest without (gross) neurological symptomatic consequences?"
I would define "gross symptomatic consequences" as "noticeable and debilitating" in one way or another to the subject. This opposed to minute changes in, e.g., motor response latencies measured in a laboratory task designed to pick up the slightest results of asphyxia.
As background: I did these CPR and defib courses and the first thing they tell you to do is (1) call 911 / 000 whatever alarm number and (2) arrange a partner in crime to help with CPR;  or in case of a defib situation, (call alarm nr), make your way to the defib, unpack, apply electrodes, look at the manual, casually wait for instructions/warning lights etc. But..but... there is a person here without oxygen supply to his brain! And I know professional staff should be brought to the scene, but what struck me most is that starting up the defib (which inherently takes time) is more important than CPR (which is immediate)? In other words, loosing precious minutes is advantageous over diving straight away into CPR and pumping blood around?

Fibrillation is very hard to detect clinically. It can be confirmed only on ecg (as far as my knowledge extends). So unless the patient is at high risk of fibrillation, generally cpr is the first aid done

From Boron and Boulpaep textbook of Medical Physiology, second edition, p.289:

Because of falling ATP levels in the brain, consciousness is lost within 10 seconds of a blockade in cerebral blood flow. Irreversible nerve cell injury can occur after only 5 minutes of interrupted blood flow.

If conscious is lost within 10 seconds of blockade in cerebral blood flow, I guess a person will not be conscious to do any action in only 10 seconds!
Brain ischemia is divided into

Focal ischemia which signifies stroke.
Global ischemia which occurs in cardiac arrest.

Permanent neural injury means that once perfusion is restored, the symptoms don't relieve as the part of brain which caused those symptoms becomes dead irreversibly.
For a list of symptoms check this page.

If we consider another case, there is blood flow, but no new oxygen is coming into the system, the brain cells may begin to die after about four minutes [1]. However, this depends on the person not the amount of time. Consider free divers and more specifically Tom Sietas. These men and women, in this sport, can go well beyond the 5 minute mark with no debilitating brain damage. Now, Tom Sietas holds the world record for static apnea with the time of 22mins and 22sec under water without air and yes he survived. Here is a news article about Tom but it goes on to say Pearl divers go about 7mins without air.

@ChrisStronks I would guess, with these people (free divers), since their body is trained, they could go into cardic arrest and last longer than 5 mins but this isn't a testable scenario.

Interesting answer, +1. However, I think we are indeed talking about exceptional, trained cases here, which would make an interesting new question as to how they exactly cope!

@ChrisStronks I know they are exceptions but we can't say 4-5mins is a hard limit. It all depends on the person. In the case of Tom, I could die four times before him.

I think such training will enable the lungs to retain more oxygen (well developed lungs that expand fully) and the circulatory system is better adapted by increasing hemoglobin concentration (this increases the blood carrying capacity). It has nothing to do with cerebral perfusion. Cut blood supply to brain no one can stop symptoms from occurring.

@CRags I said let's consider a case with blood flow and no new oxygen.


text:
How much of the weight of yoghurt is due to bacteria?
I recently started making all kinds of bacteria-processed foods by myself (such as yoghurt, but also Sauerteig and so on), and I found myself wondering how much of the weight of these products is actually due to the bacteria themselves in the end. But I couldn't find anything useful on the internet.
So, specifically for yoghurt, how much of its weight is due to the bacteria, i.e. dead and/or living bacterial cells, but not including the products of their metabolism outside the cells?
I would also be happy about numbers on other bacteria- or fungi-processed foods, but I wanted to keep the question simple.

I've asked myself a similar question for fermented stuff you don't want to eat: http://biology.stackexchange.com/questions/7251/is-1-g-l-living-biomass-for-a-biogas-fermenter-plausible

I'm voting to close this question as off-topic because it is about food analysis rather than biology in the terms of SE Biology.

Interesting question and it will only be possible to do some estimation. The problem is to know the exact bacterial composition as well as the mass of the bacteria. To start, it is necessary to know the number of bacteria in a defined amount of yoghurt. There are scientific publications on this topic, but the numbers in fresh produced yoghurt are in the area of 108 bacteria per gram yoghurt and declines over time. Based on the numbers in  reference 1 and 2 I use 2x108 bacteria per gram fresh yoghurt.
The other number we need is the mass of one bacterium. This is complicated, as bacteria are very light due to their size and cannot be easily weighted. There are some numbers available (we imply here that all bacteria weight the same, which is of course not the case), and according to them, one bacterium weighs about 1x10-12 grams.
Mutiplying both numbers gives the amount of bacteria in one gram of yoghurt, around 0.0002 gram or 0.2mg. One typical sized yoghurt of 150 gram therefore contains about 30mg of bacteria. The weight of the bacteria can thus be neglected against the total weight.
References:

Survival of Yogurt Bacteria in the Human Gut
Handbook of Food and Beverage Fermentation Technology
Mass of a Bacterium

Thanks for the analysis and for pulling out the references! As far as I understand the second reference, the number there seems to be for living bacteria. Do you know any estimates about dead bacteria? Do they just not die as long as they're producing the yoghurt, so that freshly produced yoghurt contains all the bacteria that ever lived in the yoghurt and they start dying afterwards?

I think the number is highest in the beginning (when the conditions are optimal) and then the bacteria die. Since they are not removed, the number should still fit.

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