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Could humans theoretically see infrared better than regular light?
I have noticed that in infrared film, people's eyes reflect that light within their eyes much like nocturnal animals (and many other animals for that matter) do with regular light. I know that this is in order to maximize their night vision capabilities by reflecting more light onto the retina.
My question is this: If a human had the nerves in our eyes to process infrared light, would someone with these 'special' eyes be able to see better than someone with 'regular' eyes? What would they see? What about in low-light conditions?

...Infra-red illumination of the eye produces the 'bright pupil' effect

Source: http://www.museumsandtheweb.com/mw2003/papers/milekic/milekic.html
(most of the way down the page)

Although interesting, this question is quite philosophical. It is like asking what if we had an extra pair of hands- would it help us to work better and faster.
Infrared detection goggles are there and are used for seeing in dark. But as we have evolved we cannot differentiate objects just based on their heat signatures. So just infrared vision wont be good.

I was in the military for a bit. There was a guy I met who when the lights were turned off had eyes that glowed in the dark. It was like an animal at night. He showed this to me in confidence, we were alone, but didn’t say it was a secret or anything. He said he had a retinal or cornea transplant. I can’t remember what he said but I’m not sure if that was even the real story. I’m still not sure if a transplant would have that effect without the lining animals have called the tape firm lucid something.....

There are animals that can sense into the infrared spectrum and this seems to help them detect prey.

No, retina doesn't have or has too few infrared receptors.
Practical example: most remote controls use IR LEDs (infra red light emitting diodes) to send commands to a receiver device. So take a remote control, keep pressing a button and look at its front. Do you see any flashing light? Now take a camera (phone camera, photo camera or video camcorder) and look with it at the remote while pressing a button. Now you see it producing white light. The camera sensor detects IR. That is how night vision in cameras work.
What you read in that article is about how light is reflected by the eye (the pupil). There is nothing to do with the retina which is on the 'back wall' of the eye ball.

This just states that humans can't see IR, which we already know. I think the question was more along "If we could choose to see IR, would that be better than seeing regular light?"

Infrared light is emitted by warm things, like our head.  We'd be detecting it ambiantly all the time.  That's why animals that can detect infrared are not warm-blooded.

My eyes are not warm. Air does not reflect infrared light (you don't see an infrared aura around warm objects in infrared captures). Therefore, I could implant infrared sensors into my eyes without seeing myself all the time. And even if, the self-ambiance could still be subtracted out. And cold-blooded animals are not cold all the time, especially not after a sun bath.

Infrared is a very wide spectrum.  The long-wave infrared produced by animal body temperatures is a much different "color" than the near infrared which is part of normal sunlight - and which can be photographed with ordinary digital cameras by removing the IR blocking filter: https://en.wikipedia.org/wiki/Infrared_photography


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Will a Codon result in same amino acid across organisms
Will all organisms with the same 3 nucleotide sequence in the codon produce the same exact same amino acid. I read that the three nucleotide sequence will code for a particular amino acid. I did not understand if that is the case across organisms. Can someone explain this in simple terms.

Yes. One particular sequence of codon code for only and only one amino acid. However, there could be more than one codons for a single amino acid.

@Beginner Please follow the instructions for comments and do NOT use them to answer questions. In this case you also happen to be wrong as I will explain and reference in an answer.

I think it better to not treat this as a duplicate of the mitochondrial question.  This question is even more basic, and one that can be answered straightforwardly and without the confusing twist of context resulting from using that question.

Are you interested in the different codons used across organsims or the different codons used (based on bias, environment etc.) that code for a specific amino acid?

@mgkrebbs OK. I have relented and added an answer focussed at the non-mitochondrial situation.

Although the answer to this question may be found in Mitochondrial Genetic code, because that answer is primarily about mitochondrial genetic codes, I shall give a more directed answer here.
Because the same genetic code that was elucidated in bacteria was found to apply to higher eukaryotes, it was initially assumed that the genetic code was universal, and was referred to as such. Subsequently it was discovered that mitochondria did not generally employ this ‘universal’ code, which is now usually referred to as the ‘standard’ code — indeed different mitochondrial codes were found in different organisms.
However the question seems to be more concerned with the genetic codes of  bacteria and the nuclear genetic codes of eukaryotes. Here also there are deviations from the standard genetic code, which can be found listed either on this Wikipedia page or at NCBI.
Below are some examples from the NCBI list (where references may be found) with the standard coding in parentheses:
 Mycoplasma
 UGA      Trp          (Ter)

 Ciliates, Dasycladacean and Hexamita
 UAA      Gln          (Ter)
 UAG      Gln          (Ter)

 Euplotidae
 UGA      Cys          (Ter)

 Candidate Division SR1, Gracilibacteria
 UGA      Gly          (Ter)

 Pachysolen tannophilus
 CUG      Ala          (Leu)

Finally, tRNAs for the ‘additional’ amino acids, selenocysteine and pyrrolysine recognize, respectively, the UGA and UAG stop codons in specific contexts.

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Blood consumption
Is consumption of blood more "dangerous" compared to meat?
There was a news-article about unnatural chemicals found in the blood of mothers. This reminded me about a question I have pondered upon from time to time. Now, I am not a vampire, but curious as to the nature of blood vs meat in animals. More specifically unhealthy components.
There are various examples of viruses being in danger of spreading by consumption of raw blood like ebola, H5N1 etc. (But then also meat etc.)
Perhaps easier if I throw out some questions to show what I am asking:

Are there more of such in blood then meat?
Are there other things that can be worse in blood even after preparing? Like cooking, conservation etc.
Are parasites etc. more frequently found in blood?
Are there organisms that are highly resilient to heat treatment found in blood?
Are there more heavy metals in blood then meat? (Which I assume cooking does not give much of a difference.)
Other toxins?

Some references:

http://www.eufic.org/article/en/food-safety-quality/animal-health/expid/review-animal-diseases/
http://www.fao.org/avianflu/en/qanda.html

can you reference the news article you have mentioned please.

@potterbond007: I did not include it as it is not in English. Also, I have thought / wondered about this before, the article simply reminded me about the question. The article itself is a tabloid chock piece: http://www.vg.no/nyheter/innenriks/forskere-du-har-gift-i-blodet-ditt/a/10124215/ The particular subject at hand I have read about before and seen some docus etc. about, but my question is in regards to animal-meat/blood, not human ;), and more in general.

The (only) answer is actually irrelevant with the question and very ambiguous. What is high dosage of blood...? You can eat a few blood sausages and you will not get iron overload (which is more often an inherited condition). Although everything is digested in the stomach, raw blood could be dangerous if somehow the hypothetical viruses make it to your blood system.

Is consumption of blood more "dangerous" compared to meat?

Actually yes, a simple high dose of blood is enough to kill. The cause is, though it is most important thing to live when flowing the vessel, it's highly toxic when consumed. There are high chances of getting haemochromatosis or Iron overload.
Source and More on this:
http://www.livescience.com/15899-drinking-blood-safe.html
Composition of Blood

(source: snmjournals.org)

It's the same for menstrual blood?

My question, at least in my mind, was more in the realm of toxins etc. But as there still are no more answers I'll accept yours as it points out a valid point :)

I'm highly dubious of the claim, and I'm not sure livescience.com should be accepted as a definitive source. Haemochromatosis is a real thing, but it seems to be associated with multiple blood transfusions and transfusion reactions, rather than consumption of blood as food. Many cultures include significant amounts of (animal) blood in their cuisine, with no obvious problems.

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Trauma, blood loss and thirst
Back story.
Watched an episode of Arctic Air, (season three episode six), where they are practicing and hoping to become a licensed search and rescue airline.
Anyhow; two hikers gets attacked by a grizzly bear and whilst one get killed the other manages to throw himself off a cliff and ending up with his leg pinched under a rock. He also has big lacerations on his chest from the grizzly. Finally he manages to send a distress signal.
Though not licensed a team travels out to asses the situation. As they find the wounded climber they start to help. First they clean the lacerations by pouring alcohol over them, and then lay some bandages on top. After a while the injured man complains he is thirsty, and they give him water.

TLDR;/Question If I recall correctly one should not give water to a trauma patient. They can have internal bleeding and/or, as in this case big external wounds which likely has caused quite some blood loss.
Liquid will, IIRC, cause some bad effect on the re-production on blood, and might also affect existing blood.
Am I correct in this? If so; what happens and why should one not give liquid to the patient?
Guess there could be some situations where liquid is proper. E.g. patient has been laying in exposure to sun for N hours and dehydration might also cause ill effects... ? (Kidneys, blood-pressure, plasma?) But that might be a negative in any case if one suspect internal bleeding?

If you are satisfied with the answer, please do close the question by selecting it as the answer.

After some general research there are specifically 3 arguments that I came across that people give for supporting this particular theory.
1) somebody seriously injured might be given an anesthesia shot by the doctor or whoever that treats him first up for relief from the pain and distress. This would lead to relaxation of the stomach muscles and the contents of your stomach can travel up to your throat and into your lungs which would be fatal. Read about pulmonary aspiration.
2) the second case is if there is an injury to the gut or the GI tract, then providing water would be counter productive. A layman might not be able to assess the level of injury to someone just by sight.
3) the third is that giving water would increase blood pressure and (sometimes) apparently dilute the scars. This could also lead to chances where sutured wounds might reopen.
There are no real guidelines as to how much water can be given to an injured person. Depends on the situation or how much time he has been bleeding for and the kind of environment that he is subjected to like you pointed out. Some medics have recommended sucking on citrus fruits to prevent dehydration. Also, swabbing the patient all over the body with a cold compress can provide some relief and delay dehydration.
Guidelines for bleeding victims are here.

Thanks. I do not recall where I have it from, but believe it was some first aid course. IIRC the tutor also mentioned some ill effects by giving water but do not recall the reasoning behind it. Believe he also mentioned vomiting -> bad if e.g. neck injury. Your answer gives good pointers. I dug up this discussion, but they seem to be somewhat conflicting in their explanations. http://www.nairaland.com/1460146/dont-drink-water-bleeding-injury . Guess the peristalsis mentioned by Lagusta might have been what the tutor mentioned.

It's the first one.  A trauma patient will likely need an anaesthetic at some point so the aim is to keep them nil by mouth to avoid the risk of airway compromise caused by vomiting.  If they are desperate for water, the advice is small sips or being given an ice chip to suck


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Do axon grows after cutting/damaging of some of its part?
Do axon grows after cutting of some of its part to near original place?
Do axon restores after local damaging of some of its part?
I take https://class.coursera.org/neurobio-001/ classes and learn that axons are very long. So it is interesting if they able to restore connection to far places parts of body...
UPDATE

https://en.wikipedia.org/wiki/Axon_guidance

yes they do.. I'll post a long answer when i get time.. meanwhile you can look for Axonal regeneration. (A lot of experiments have been performed on regeneration of sciatic nerve and DRG neurons)

Well look at this picture from Junqueira histology book:

In an injured or cut peripheral nerve, segments of axons distal to the injury lose their support from the cell bodies and degenerate completely. The proximal segments can
regenerate from their cut ends after a delay. The main changes that take place in an injured nerve fiber are shown in the picture above.
In the nerve segment distal to the injury the axon and myelin, but not the connective tissue, degenerate completely and are removed by macrophages. While these
regressive changes take place, Schwann cells proliferate within the connective tissue sleeve, giving rise to rows of cells that serve as guides for the sprouting axons
formed during the reparative phase.
The axon grows at the rate of 0.5–3 mm/day


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H O N C alternatives for organic life?
Most organic structures built from hydrogen, oxygen, nitrogen and carbon. They are represent 1-,2-,3-,4- bond relations (chemical valence) which allow to build variety of chain structures.
Are there exist some replacements for these elements to create complex structures that theoretically can create life (self-reproduced or be a part of cell as organelle)?
UPDATE

Is there a common chemical model for life in the universe?
Arsenic-eating microbe may redefine chemistry of life
A Bacterium That Can Grow by Using Arsenic Instead of Phosphorus
https://en.wikipedia.org/wiki/DNA#Alternate_DNA_structures
https://en.wikipedia.org/wiki/Arsenic_DNA

For the last two references: These are, nicely spoken, highly debated. Its been a while since I read the paper, but as far as I remember they never showed a direct proof that the DNA from these bacteria contains arsenic instead of phosphorus. They can however grow in the presence of high arsenic concentration which is also interesting and impressive. See this article for example.

Its not scientifically or logically possible to say 'this is impossible' but since this is a speculative question, I'll hazard an opinion.
I'd like to argue that, at Earth standard pressure temperature and atmospheric conditions, C H O and N are not really replaceable.  Throw water into the mix as the most common liquid and replacing any or all of these elements is hard to imagine.
One can think about this by looking at the formation of long hydrocarbon chains.  Silicon can form polymers, but they tend to fall apart. Silcone-oxide polymers [SiR2-O-SiR2-O-] are more stable, but do not resemble hydrocarbon polymers as readily.
Carbon is much more versatile, capable of forming either chain, or including sulfur, nitrogen in stable chains that don't seem to really have any length limitations.
At thousands of atmosphere's pressure, temperatures of 70 Kelvin or in a sea of sulfuric acid, its easy to imagine other sorts of chemistry would dominate - phosphate , arsenic chains or germainium lattices, but on Earth most of these would fall apart.
Even if/when life is discovered elsewhere , it will certainly feature chemistry that will completely amaze us; unlike anything here.  But even so, its hard for me to imagine it being completely exclusive of these four elements.  I just want to point out that by a wide margin, hydrogen is the most common element of the universe.   Nearly all the other light elements like C, O and N are the next most common.  This is simply because they take fewer nuclear fusion events to create.  Hydrogen is pretty useful no matter what chemistry you are looking at.  These four are probably going to be there somewhere - most planetary atmospheres have Ammonia, CO2 and methane in them as well - at least as far as we've seen.


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What is the difference between these terms: clade, monophyletic group and taxon?
Wikipedia definitions for these terms are pretty similar:

http://en.wikipedia.org/wiki/Clade
http://en.wikipedia.org/wiki/Monophyletic_group
http://en.wikipedia.org/wiki/Taxon

They sound like the terms are synonyms. Why there are separate articles for them then?
Is it true that every person is a reptilomorph and an eupelycosaur just like he/she is a mammal?
Bonus question: what is the difference between a cladogram and a phylogenetic tree?
PS Please don't just give definitions and/or quote Wikipedia. Point out the differences, if any. Even better, provide examples that can be considered one but not the other.

A taxon (Plur. taxa) is any (monophyletic or not) group of species. For example the group of yellow flowers is a taxon. The group of primates is a taxon. The taxon of aquatic animals is a taxon.
A clade is a monophyletic taxon or monophyletic group if you prefer. A monophyletic taxon (or a clade) is defined as a taxon that contains only all descendants of a common ancestor and the common ancestor. On the following picture, only the Taxon 1 is a clade.

To cite few examples of clades: Primates, Eukaryotes, Rosacea, Reptilomorpha, Rodentia. (The links yield to tolweb.org. See below for more info about this site)
A cladogram is some kind of reduced evolutionary tree that only shows the branching pattern but the length of the branches does not carry any information. At the opposite on a evolutionary tree the lengths of branches usually indicate the inferred time from the divergence.
I think the best tree you can find online is tolweb.org. You can find here the clade of Reptilomorpha and here the clade of Eupelycosaur. As you can see from these links, the mammals form a clade within the Eupelycosaur which itself is a clade within the Reptilomorpha. So yes, every human being is a Reptiliomorpha/Eupelycosaur/Mammalia. You can have fun going through this evolutionary tree and see what are the common ancestors between human and other mammals, human and turtles, human and jellyfish, human and plants, etc… to cite just a few relationships you might be interested to look at.

+1 But I'd say, taxon is not any possible grouping, but a grouping proposed by someone. It's basically a formalized hypothesis about natural arrangement of  species. (This natural can be understood in multiple ways.) In this respect "yellow flowers" do not make a taxon.

A better example is that Reptilia is a taxon that has turned out not to be a clade because the descendants of the last common ancestor of modern reptiles also include birds.


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Do primitive lymph nodes exist in 12th week embryo?
Someone told me that primitive lymph nodes do not exist during this week.
However, others say they can.
Here is a picture about inguinal lymph nodes from here.
No primary lymph nodes are visible (like circular) at 56th day:

When are the primitive lymph nodes formed?

Have a look at this webpage. I think it answers your question.

@Chris I would like to have some trustworthy source, because the one who claimed that there is no primitive lymph nodes at that time is a smart person. There is something recent research going on by which you can say that those lymph nodes at 3rd month cannot be anymore called primitive lymph nodes. Something new has been discovered by which you can reject the primitive lymph nodes that early. However, I was not told the reason for that. However, this is only research so can be false too; still the claim which I heard today was expressed very strongly.

Then do it the usual way: A person which makes strong claims needs to have strong proofs as well. In this case the original studies. I can have a look later...

@Chris Anything found?


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How much vanilla will kill a person?
I received a gift that is a jug of Pure Mexican Vanilla. Having never dealt with large quantities of vanilla, it made me curious as to what would happen if a person had too much vanilla.
I understand that the alcohol has a higher toxicity rate and is probably more fatal than the actual vanilla itself, but I'm curious as to what ratio of mass of pure vanilla to mass of the human would be considered fatal.
Also, what is the physiological effect of a vanilla overdose as it pertains to inhibiting critical bodily functions? That is -- specifically what about a vanilla overdose would cause fatality?

You get a present and the first thing you do is thinking about how to kill someone with it?

Why do you think vanilla is toxic?

I'm just not used to seeing Vanilla in the "jug-sized" unit of measurement. My friend said not to drink it all in the same place. Naturally that piqued my curiosity about the fatality of Vanilla.

First question: Is it real vanilla extract? Or is it synthetic vanilla? In the first case, it contains alcohol, but that should it be.

As Paracelsus said: "The dosage makes the poison"

@Chris It turns out that most so-called “vanilla” carried back from Latin America is completely fake, and potentially even dangerous.

Vanillin is the chemical that gives vanilla its flavour and smell [1].

Vanillin is pharmacologically active, causing depressed blood pressure, increased respiratory rate & death due to cardiovascular collapse [3].
Non-Human Toxicity Values [4]

LD50 Rat oral 1580 mg/kg
LD50 Rat ip 1160 mg/kg
LD50 Rat sc 1500 mg/kg
LD50 Mouse ip 475 mg/kg
LD50 Guinea pig oral 1400 mg/kg
LD50 Guinea pig ip 1190 mg/kg
LD50 Rat oral 2.8 g/kg
LD50 Guinea pig oral 1.40 g/kg
LD50 Mouse ip 0.78 g/kg
LD50 Rat sc 1.8 g/kg
LD50 Dog iv 1.32 g/kg slow in fusion.

References:

Wikipedia contributors, "Vanillin," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Vanillin&oldid=613429267 (accessed June 26, 2014).
PATTY F. A. 1963. Industrial Hygiene and Toxicology. Volume II Toxicity, page 1696 (referenced from TOXNET, Vanillin - Human Toxicity Excerpts)
TOXNET. Vanillin

Hm that's really interesting. But would humans react similar or differently compared to animals? Plus it would be interesting - considering the initial question regarding the bottle - which would component would be "deadlier"? I assume the alcohol, but would still be interesting to know.

@Mario - The LD50 Rat oral for Ethanol is 7g/kg.
Surprisingly, the vanillin is deadlier.

@MCM In raw form, yes, but I wouldn't expect the mix to be 50% alcohol, 50% vanillin. There's a reason people enjoy alcohol rather than getting killed by it left and right. ;)

@Mario - People overdose on alcohol all the time. Now sugar or water... yeah. Wiki says "pure" extract would be about 35% alcohol and at least 100g of beans per gallon. So drinking an entire gallon of the stuff might be lethal for most people who weighed 65kg or less from the Vanilla. There'd be approximately 1.32L of alcohol - or about 1000g, also enough to probably kill somebody who weighed 150kg or less. They'd be killed by the alcohol before the vanilla.

Out of interest, I've had a look around a bit and it seems like the most dangerous part of that bottle might be the alcohol.
According to the FDA...

The term unit of vanilla constituent means the total sapid and odorous principles extractable from one unit weight of vanilla beans, as defined in paragraph (b) of this section, by an aqueous alcohol solution in which the content of ethyl alcohol by volume amounts to not less than 35 percent.

(Emphasis mine.)

This is not far away from what Whiskey has. Only that vanilla extract will be a bit more expensive...

@Chris So in this case, ordering "Bourbon" might be a bit vague? ;) The EU actually demands 40% or more (for Whiskey).


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Nystagmus drug FDA approval?
Congenital Nystagmus is an eye focusing disorder. It happens in manuals. Wikipedia lists several treatments on its page. Are any of those FDA approved for human use of that disease.

drugs found to be effective against nystagmus in some patients include memantine, levetiracetam, 3,4-diaminopyridine, 4-aminopyridine, and acetazolamide.
  -wiki

googling for the drug name will tell you if it's available. Based on my 4 seconds of research, the first two are.

@MattDMo no sir i think you're mistaken. would you share your keywords so that i can examine the results and validate that nystagmus is an approved condition of treatment.

the links i found said otherwise: Curbside Consultation in Neuro-ophthalmology: 49 Clinical Questions

The mainstay of therapy is pharmacologic and several good options exist for [acquired pendular nystagmus] treatment. Gabapentin has a very tolerable side effect profile a large dosing range and its beneficial effects in suppressing oscillopsia and dampening the nystagmus waveform in APN have been demonstrated in a double-blind controlled trial. (non FDA approved use)

"Available" is different from "FDA approved for this use." Memantine (Namenda) and Levetiracetam (Keppra) as well as gabapentin (Neurontin) are most certainly available to be prescribed for whatever by any doctor, but I doubt any of them is approved for nystagmus. (I don't know for sure, just pointing out this discrepancy in usage.)


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Vegetation density estimation from distance method: random sampling or along the grid?
I am planning to sample the tree regeneration (new ones and advance regeneration, > 2m). I am planning to use small circular points to estimate the counts per area (= density of young trees). I wonder about the sampling design: what is better for following whole area tree density estimation? If the sites would be placed randomly, some might overlap. Is the sampling across the grid a better option, but requires a set number of subsamples: eg. not very scalable?
For any of the metrics, we will then calculate distances to the closes tree. Is any of the metric better in folliwing density estimation from teh distance methods?
Or, what I found, a quadrat sampling, combining both aproaches. Seems however quite challenging to do in the field. What are your thoughts? Thank you.

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Why were dinosaur skeletons so light compared to mammal skeletons?
I was watching a presentation by Dr. Jessica Theodor [1] who discusses (at 38:10), among other things, the skeletal structure of dinosaurs vs. mammals. "Dinosaurs have way lighter skeletons, which means that for the amount of material they can be bigger. If we start to look at sauropods, they have this really interesting set of structures, these big holes in their vertabrae...
it allows you to build a lighter, stronger skeleton. Mammals can't do that. It's not how we build our bones."
Why don't mammals do this? Are there fundamental trade-offs that make our (apparently) weaker, heavier bones better, or is it just chance that we haven't matched this development?
(Of course I'm open to the possibility that I misunderstood the talk, or that it was simplified to the point of inaccuracy on this point.)
[1] Jessica Theodor, Being Giant: Why are mammals not as big as dinosaurs? (2015)

If one wonder about why mammals in general are so much smaller than dinosaurs, I think the answer lies somewhere in that we simply have not gone down the competitional path of pure size. Just in the same way as we generally don't have evolved to use flight (except for bats) or live an aquatic life (except for whales and dolphins). One could say that we don't have bone structure suited for extreme growth and size just like we don't have bone structure suited for flight.

That is because, they have twenty one percent of body mass than minimum skeletal volume.
In Dr.Bill Sellers's journal "Biology Letters", it was said that they laser scanned Brachiosaur as they were estimating it to weigh about 80 tons. But, it actually weighed 23 tons which is relatively light.

@Alex: It's more like "why don't mammals have lighter skeletons, following dinosaur's plans".

@Alex: But also remember that what we know of dinosaurs (and extinct mammals) comes only from fossil remains that have been found.  Until relatively recently, big bones sticking out of the ground were a lot more likely to have been discovered than little tiny ones.  I suspect, though I don't know for sure, that larger bodies were more likely to have become fossils in the first place.

you link to a private video. It's not possible to check your source... found this video which is probably it: https://www.youtube.com/watch?v=whxn9Cc1_Ho

@Frieke It wasn't private when I posted it! I imagine your link is correct, I'll change it.

I have also heard the claim that dinosaur bones were lighter than mammal bones of equivalent  size, and at the moment I do not believe it.  I will not believe it until somebody explains it to me how that is possible.
If you have a structure that you want to add more weight to, to support that weight, you want to ADD structural elements, not subtract them.  If the structure could support itself before adding more weight, then adding structural elements will make it stronger (unless it's already at the absolute limit).  Otherwise, the structure does not stand at all.
If you google about the weight of bird bones, you can find recent research saying that bird bones are actually not lighter than mammal bones.  Their weight is just distributed differently (more densely on the outside of the bone, as opposed to more evenly spread throughout the bone as in mammals) to resist bending and twisting better at the cost of being weaker to impacts.  Birds arguably have a much stronger reason to lose weight than dinosaurs, but their bones are still just as heavy as ours.  Since birds are dinosaurs, I find it very unlikely that ancient terrestrial dinosaurs had magic bones lighter than both mammals and birds.
Also, I'm aware that the internal structure of our bones is very efficient.  As I understand it, the bone on the inside of a bone grows thicker where it is more stressed.  If you train a computer to calculate the ideal lattice structure to support the stresses of a given bone shape, the computer calculates pretty much the exact same lattice as what actually exists in our bones.  So, if the internal structure of our bones adapts to better handle the stresses we experience in life, and if the bones of vertebrates can evolve into any external shape whatever, I cannot imagine how dinosaur bones could be stronger than ours unless they were made of a different material.  I am not aware that this is the case.

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What were the Neanderthal innovations?
At some point the neanderthal and modern human lineages diverged. I'm not sure what exactly their most common recent ancestor was (I see some sources suggesting homo heidelbergensis), but in any case I'm interested in the innovative/apomorphic features of neanderthals relative to that MRCA. What new features did they have, and what existing features changed most?
In particular I am not asking how neanderthals differ from modern humans.
This question is partially inspired by popular science pieces (e.g., Human Hands More Primitive than Chimp Hands) discussing human hands, which are essentially basal, vs. chimpanzee hands which are less similar to the common ancestor.

Two issues here: 1) What features are you talking about? Morphological trait or Ecological niche? 2) You are asking for a species comparison but you don't want the comparison to be done with modern humans. You who should the neanderthals be compared to? To the MRCA? If this the case you are just asking how the neanderthals evolved since they split with modern humans, right?

@Remi.b: 1) Morphological traits and 2) comparison with the MRCA, and yes -- just asking how they changed since they split. I suppose for #1 the traits will relate to their ecological niche and so that information might also be useful.


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How did the first life form on Earth reproduce without DNA?
How did the earliest life forms exist without DNA? The most likely scenario I can think of for life happening from nothing is that, over billions of years, with trillions of water molecules and dust particles and chemicals moving around, eventually a small clump of this murky stuff formed a pattern. Or maybe, under some lucky conditions, a whole mud pit of such a inorganic system started forming into structures which had a pattern of motion, and one of those structures became the first sub-cell, like a primitive ribosome or something. I remember learning some parts of cells were once separate entities, but there are massive gaps in that idea.
The primary gap being: How did reproduction occur in that incredibly lucky, freak incident of a tiny dust clump or whatever? How did reproduction occur without DNA? Do scientists have a theory on how the first reproduction occurred?

I find it surprising that people usually think of incredibly lucky events. I mean, 3-4 billion years is an incredible amount of time. 100 years is already a lot of time. Adding a zero makes it 1000. What happend 1000 years ago... hum. Another 0 will bring us beyond the origin of cultural development I guess. Oh hey, there are another 5 zeros to add :)

Jack Szostak's lab works on this kind of stuff. It really seems impossible the know how life first originated, but he and his colleagues have some hypotheses that can at least be shown to be plausible. Check out this video: https://m.youtube.com/watch?v=PqPGOhXoprU

Before DNA must have come RNA, as DNA is only a way of storing information. And primeval soup experiments suggest that amino acids should have played a significant role in the early stages of reproductive life, because they are one of the first molecules that form.

There are a lot of organic molecules formed naturally in the universe, I'd guess that those are a part of the pussle.

@canadianer I think Jack's claims (specially about lipid membranes) are controversial.

@cel Revisiting this question, I think luck is balanced by complexity in this case. Yes, billions of years are a long time for extraordinary things to not be so "lucky" but also the complexity of the system can have an equally massive exponential unlikeliness. And in evolution we say that millions of years will eventually produce a change that works, but what happens if the thing that works cant reproduce? Because reproduction is the main factor. So Im just curious to know exactly how we can explain this. We've made hypotheses for pretty ancient feats in biology.

@Viziionary Take into account that complexity increases over time. You don't start from a very complex system from the beginning, rather simple systems accumulate complexity over time. At the beginning, given a rich "primordial soup" you can imagine billions of molecules interacting and forming very different systems (pathways, micelles, etc..) if one of that systems is complex enough to accomplish reproduction the game is on.

So earth is estimated to be around 4.5 billion years old, and life has existed for about 3.4-3.9 billion years of that, around >75% the time. For a little perspective, Homo sapiens have been around for up to ~250,000 years, just 0.00005% of the time earth has existed. In that time the earth has changed massively, early earth was pretty hostile, but that could have made it a good place to develop early life.
What was the pre-cursors to self-replicating DNA like?
Well one popular theory is the RNA world hypothesis, which suggests that precursors to life as we know it were RNA molecules that could self replicate (reproduce). These RNA molecules supposedly evolved in to life in the DNA/RNA/Protein world via an intermediate stage of ribonucleoproteins. The reason why RNA could have preceeded DNA based life is because it has the potential to carry information and to be the catalyst of its own synthesis.

"The unique potential of RNA molecules to act both as information carrier and as catalyst forms the basis of the RNA world hypothesis.
"RNA therefore has all the properties required of a molecule that could catalyze its own synthesis (Figure 6-92). Although self-replicating systems of RNA molecules have not been found in nature, scientists are hopeful that they can be constructed in the laboratory." in Molecular Biology of the Cell

However, the RNA world probably wasn't the first step on the road to self-replicating life, but other polymers with characteristics similar to RNA that could have acted as the template and catalyst required for RNA synthesis.

"Although RNA seems well suited to form the basis for a self-replicating set of biochemical catalysts, it is unlikely that RNA was the first kind of molecule to do so. From a purely chemical standpoint, it is difficult to imagine how long RNA molecules could be formed initially by purely nonenzymatic means. For one thing, the precursors of RNA, the ribonucleotides, are difficult to form nonenzymatically." in Molecular Biology of the Cell

-

"Shapiro doesn't think it's necessary to invoke multiple universes or life-laden comets crashing into ancient Earth. Instead, he thinks life started with molecules that were smaller and less complex than RNA, which performed simple chemical reactions that eventually led to a self-sustaining system involving the formation of more complex molecules." on LiveScience.com

This means that the first self-replicating RNA molecules were preceded by other molecules that were important in the progression from simple atoms, through non-biotic molecules, to large self replicating polymers which can be considered life. Copley et al suggest a progression in detail, with monomers being an early step in the progression (see figure 4 in the paper, and section 4 for extensive detail) where monomers precede multimers, which precede micro-RNA.

"Our model describes a continuous path for emergence of this sophisticated system
  from a simpler reaction network fueled by geochemical processes. The processes involved in metabolism and replication were intertwined from the very beginning, a concept that neatly eliminates the chicken/egg problem. Further, this model suggests that many features of the RNA World, and indeed modern life, arose long before the RNA World and were retained as pre-biotic systems became more sophisticated." - Copley et al

An alternative and slightly different theory suggests that viruses were the precursors to modern life, a so called Virus world. Similarly it supposes that early replicators were RNA based, but that viruses evolved in to the earliest forms of self replicating DNA carriers.

"The Virus World Theory is closely related to the RNA World Theory, which says life first evolved as small pieces of RNA that slowly developed into complex DNA-carrying organisms. The Virus World Theory agrees that life's genetic material began as RNA. But it differs by arguing that the ancestors of viruses evolved before cells." from NationalGeographic.com.

Further good reading here, here, and here. I also recommend the book The Story of Life as an interesting related read.

I just want to add a link to this answer. This video https://youtu.be/w2lqZL153JE illustrates how simple molecules can replicate without the need of any enzymatic reaction.

Short answer
Before the RNA world, mineral surfaces may have facilitated the prebiotic containment and organization of biomolecules. Minerals are believed to have promoted the transition from a dilute chaotic prebiotic “soup” to highly ordered local domains rich in key biomolecules.
Background
As pointed out by others, the transition from a hereditary DNA world as we now know it, is believed to have evolved through an RNA dominated world. Life in this RNA world is believed to have deployed self-replicating ribonucleic acid (RNA) molecules and it is hypothesized it was the precursor to all current life on Earth. Because RNA can store hereditary information and can have enzymatic properties, it can potentially be self-replicating and catalyze critical biochemical processes. In contrast, DNA can only store information. Hence, RNAs could be used as information storage and catalysis (Alberts et al., 2002). One of the strong motivators for this hypothesis is that ribosomes contain catalytic RNA that is critically involved in protein synthesis (Orgel, 2004).
However, I think the question here is, what happened before the emergence of RNA, i.e., what led to the formation of RNA in a prebiotic world? The question of life’s origin is in essence a problem of the information storage and transfer from a prebiotic, geochemical environment to the first life forms, as aptly stated in the question. Crystalline surfaces of common rock-forming minerals are likely to have played an important roles in life’s prebiotic origins.

Metal sulfides (such as pyrite) and oxides promote a variety of organic reactions, including nitrogen reduction, hydroformylation and amination.
Fine-grained clay minerals and hydroxides facilitate lipid self-organization which could have mediated the formation of lipid membranes necessary for cell membrane formation. The cell is the building block of all life and critical to its existence is its integrity. A closed membrane allows to build up a membrane potential necessary to sequester biomolecules inside and keep toxins and waste products out.
Inorganic minerals have been shown to be able to mediate the polymerization of RNA monomers. Hence, minerals may have been the prebiotic template for RNA.
Surfaces of common rock-forming oxides, silicates, and carbonates selectively concentrate amino acids, sugars, and other molecular species essential to present-day life. These minerals are also capable of stabilizing these monomers. Cells are much like little containers with essential biomolecules. The capabilities of minerals to sequester them, accompanied by the intrinsic capability to form lipid structures could potentially make minerals hot spots for life formation.
Chiral mineral surfaces are actually able to separate left- and right-handed molecules. Chirality is central to current life. For example, in humans the major form of amino acids is the levo form, or left-hand variation. (Hazen & Sverjensky, 2010)

References
- Alberts et al., Molecular Biology of the Cell. 4th ed. New York: Garland Science (2002)
- Hazen & Sverjensky, Cold Spring Harb Perspect Biol (2010); 2(5): a002162
- Orgel, Crit Rev Biochem Mol Biol (2004);39(2):99-123

You can do without DNA, you need RNA to make proteins. Living organisms create and maintain a bubble that is very far removed from thermal equilibrium. So, you can speculate that at the origin of life, conditions existed where processes that are far from thermal equilibrium could still occur naturally without the support structures one finds inside living cells. This suggests conditions involving very low temperatures e.g. in comets.
If you consider complex molecules forming in comets then some unstable intermediary molecule can be metastable at the low temperatures there. Chemical compounds will only react with their immediate neighbor, not with molecules that are a bit farther away. This allows for intermediary unstable compounds to be created and to survive for long enough until it gets a chance to undergo further reactions making it more stable. Of course many more unstable molecules will be formed in such a process.
Imagine this happening in a comet kicked out from the Oort cloud that is periodically coming close to the Sun for a short while. When it is far away from the Sun, chemical reactions induced by cosmic rays happen in the interior which creates all sorts of strange chemical compounds. When it comes close to the Sun part of the comet melts and then some of the chemicals formed can disperse. The molecules that are more stable will have a better survival probability.
Darwinian selection of molecules may thus happen inside comets and that may have led to RNA molecules and many of the proteins and enzymes that we today find inside cells. All these enzymes and RNA together could then replicate by interacting indirectly with each other, but they are then not organized inside cells. You can speculate that cells could have evolved much later on Earth after  the organic materials from comets arrived on Earth.
Alternatively, you can consider scenarios where during the Late Heavy Bombardment processes leading to life where going on both on Earth, Mars and Venus. It is known from studies that the impacts that happened during that time were powerful enough to eject materials from one planet and dump them on other planets and that molecules essential for life could survive the entire transfer process. This means that it's possible that one part of what is necessary for life was developed on, say, Mars, another part developed on Venus (which at that time had oceans) and yet another part developed here on Earth and that it all came together during the Late Heavy Bombardment.
The results of a recent experiment on the formation of organic compounds in the interstellar environment has appeared in this article.

The molecules that are more stable will have a better survival probability. Darwinian selection of molecules may thus happen [...] and [...] may have led to RNA molecules and many of the proteins [...]* - Of all the compounds I can think of, RNA and especially proteins are ranking amongst the least stable. I like your approach, but I don't get your reasoning. Further, references would be appropriate too.

@Christiaan I'll try to dig up some refs, the basic scenario was mentioned in an old NGC documentary, they showed experiments being done involving freezing materials similar to what you find in comets and then bombarding that with radiation, partially thawing it, refreezing and then repeat this cycle.

Well another (and less popular) theory called Panspermia says that life, actually, came from space, it was not originated here in earth. So this completely change everything, because the conditions where life would have been formed could be very different from our's planet, so we can't make any predictions with this considerations in mind. But thinking in the DNA and our planet, the possibility that the DNA replicates with the help of other molecules could be possible. I don't think that it's necessary the steps of DNA to RNA and proteins or even DNA to proteins, to explain his reproduction, maybe some proteins with catalytic activity already exists and DNA with some good information in itself, it reproduce and continue evolving till have enough information to create other molecules with beneficial properties. We all know that proteins can actually be created by pure chemical reactions, i think that's the real secret of the life. We dont need a creator molecule to manufacture the entities entrusted with the job of create other molecules. The rest of the story is just the azar.


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Crude oil contamination hazard
I'm not sure if this is physics, biology or chemistry related so I will start here.
I'm from a city (Baku, Azerbaijan) where crude oil is known to be extracted since ancient times. Oil is no longer being produced within city limits however soil is still heavily contaminated in some parts of the city.
Recently a major project has started to turn one of the most contaminated parts of the century old oilfield (see http://en.wikipedia.org/wiki/Black_City_(Baku) for more) into urban territory.
Developer promises that all contaminated soil is being removed and recultivated but I still have some doubts about it. I also don't trust official reports so would like to conduct my own investigation.
What is the health hazard of soil contamination? Are hydrocarbon vapors direct health hazard? Or may be it's radon that surfaces with oil? What and how to check? Would I be ok if I just check radioactive contamination with dosimeter/radiometer?
Edit:
You can ignore water contamination and direct contact with chemicals. I'm talking only about vapors during hot season.

Soil contamination or soil pollution is caused by the presence of xenobiotic (human-made) chemicals or other alteration in the natural soil environment. It is typically caused by industrial activity, agricultural chemicals, or improper disposal of waste. The most common chemicals involved are petroleum hydrocarbons, polynuclear aromatic hydrocarbons (such as naphthalene and benzo(a)pyrene), solvents, pesticides, lead, and other heavy metals. Contamination is correlated with the degree of industrialization and intensity of chemical usage.

http://en.wikipedia.org/wiki/Soil_contamination

The acute health effects of hydrocarbon mixtures are generally associated with exposure concentrations at thousands of ppm. However, the exposure concentration and exposure duration leading to the onset of acute health effects varies between individual hydrocarbons, and this may influence the effects of exposure to mixtures.Health effects associated with a single exposure to hydrocarbons are asphyxiation, narcosis (ie depression of the central nervous system; anaesthesia), cardiac arrest and aspiration. Of these, the first two are probably the most significant in the offshore context.

http://www.hse.gov.uk/offshore/notices/sn_04_04.htm

In relation to the assessment of vapour risk,petroleum hydrocarbons and chlorinated hydrocarbons differ in their potential forvapour intrusion (VI) risks, primarily because petroleum hydrocarbons (PHCs) readily
  biodegrade in the subsurface when sufficient oxygen is available(USEPA 2011,2012a). Hence while a number of aspects of this guidance are general and can beapplied to a range of volatile compounds, the guidance is intended to specificallyaddress PVI and should not be applied to sites contaminated with other compounds
  including chlorinated hydrocarbons and landfill gas.

http://clu-in.org/download/issues/vi/CRCCARETechreport23-PetroleumhydrocarbonvapourintrusionassessmentAustralianguidance2.pdf

Organic compounds can be a major pollution problem in groundwater. Their presence in water can create a hazard to public health and the environment. This page will focus on the BTEX's which makes up one of the main groups of soluble organic compounds that find their way into our soil and groundwater. One of the most common sources for BTEX-contamination of soil and groundwater are spills involving the release of petroleum products such as gasoline, diesel fuel and lubricating and heating oil from leaking oil tanks. Because of their polarity and very soluble characteristics, the organic chemicals (BTEX's) of petroleum products will be able to enter the soil and groundwater systems and cause serious pollution problems.

http://www.webapps.cee.vt.edu/ewr/environmental/teach/gwprimer/btex/btex.html

Petroleum vapours at percentage concentrations are flammable, potentially explosive
  and acutely toxic; lower explosive limits (LEL) for many volatile hydrocarbons are in the
  low percentage range. Petroleum vapours are denser than air. Some components of
  petroleum vapour are also chronically toxic at trace concentrations and as such are also
  considered under the heading VOCs [volatile organic compounds ].

http://www.epa.nsw.gov.au/resources/clm/120932GroundGas.pdf
This document contains site investigation details which describes how to find traces of compounds in soil and water.
.

I appreciate the collection of information from many different sites. I think this would be most helpful to the author if you synthesized the information a little more, presented some main takeaway points? Also, I noticed you have copy-pasted a number of paragraphs directly from the different links. While it's good you show your sources, you might want to look at the guidelines on referencing and see if you can make these quotes conform better to standards: http://biology.stackexchange.com/help/referencing. In particular, I think you could make it clear which parts are direct quotes.

@A.Kennard  As the author asked multiple questions I thought it will be nice if I give him direct copies from those links and those sentences seems fine to me, and mostly I thought when he visit those pages he can identify those sentences there and continue reading. It is so much appreciable that you spend some time to guide me through SE. Thanks for your valuable advice, I'll try to improve.

Thanks Jvrek! It seems like it shouldn't be a cause to cancer or similar nasty stuff unless really high concentrations. I've been living in close proximity to the area and haven't noticed any immediate and obvious health problems. I'm just total noob on the subject therefore hesitate a lot.


text:
In molecular docking, what is the difference between ligand and cofactor?
In molecular docking aspect, what is the difference between the Ligand and Cofactor? Can a Cofactor be used like a ligand for docking with the target?

Ligand is an umbrella term for non-covalently bound anything. A cofactor, substrate, or allosteric regulator could be a ligand. This is a biochemical definition ligand, don't confuse it with a formal chemistry definition of ligand.
What's generally important about cofactors is they're not protein, but they're essential to the protein's biological activity. They could be a metal ion, organic complex, a vitamin, etc. Organic complexes that act as cofactors are also known as coenzymes. Cofactors that bind tightly or become covalently bound are called prosthetic groups. The protein without the required cofactors is called an apoenzyme, and with it's cofactors is called the holoenzyme.
Keep in mind to be on-topic for this site you need to do some research ahead of time and produce a focused, studied question. Wikipedia regularly provides the same answer verbatim!

@Kendall  I read this article before, but I expect answer in 'Molecular Docking' aspect. I mean, whether the cofactor can also be considered as ligand for docking? Does removing the cofactor affects nature of the docking?

Apoenzymes largely don't attain their catalytic effect due to conformational changes or active site changes that cofactors induce upon binding in forming a holoenzyme. This means that sometimes there will be two docking states: one for the cofactor/coenyme, and if there is a conformational change another docking state for the substrate. In short though, it depends.

Kendall So, In molecular docking of ligands... Should the cofactors must also be included?

You need to know what you're modeling. If you're modeling the docking of a cofactor to an apoenzyme, that's a different study than the binding of a substrate to a holoenzyme. Since apoenzymes lack catalytic activity, you wouldn't want to model binding of a substrate to an apoenzyme, however, so you would probably be modeling the interactions with a holoenzyme (which has cofactors bound). The design of your study and what your goals are will dramatically affect that question.


text:
Why should a tumor look like a crab?

Origin of the word "cancer"
The disease was first called cancer by Greek physician Hippocrates (460-370 BC). He is considered the “Father of Medicine”. Hippocrates used the terms carcinos and carcinoma to describe non-ulcer forming and ulcer-forming tumors. In Greek this means a crab. The description was names after the crab because the finger-like spreading projections from a cancer called to mind the shape of a crab. – source

So the cancer cells spread in a way that tumor looks like a crab. Why? Why doesn't it, for example, have a potato-like spread in which cancer cells form a sphere?

I'd guess that the projections are supportive vasculature. Also keep in mind that tumours don't actually really look anything like crabs. The Greeks seem to have been quite imaginative (see constellations).

Potatoes aren't very invasive - that is, they can't crawl where they don't belong, they can't spread between tissues, etc. I'm very sure this is why they weren't described as potato-like. Also, the picture you have is a scanning electron microscopic image. This is not what the Greeks saw. They probably were describing an invasive tissue with projections and vascularization.

Oh, the pic is only a simulation of what Greeks saw, I just wanted it to be there to stop some "users" from asking: What do you mean by crab? :-)

+1 for vasculature. I don't know this definitively but it makes a lot of sense

It's also worth pointing out that potatoes are from South America and were not introduced to the old world until the 16th century (source). Even if the tumor did look like a potato, Hippocrates simply wouldn't have had the vocabulary to describe it as such.

The term is mostly symbolic and tumours were compared to crabs perhaps because they are tenacious like crabs. This was what I read somewhere long time back. This site has some discussion on the etymology of cancer (disease).

Such projections are more formally known as spiculations. Most commonly, we talk about spiculations with respect to the radiographic appearance of malignant breast and lung lesions. This paper* describes the correlation between the mammorgraphic appearance of spiculated breast lesions and their pathology (microscopic appearance), which is a reasonable start at addressing the "why" question you pose. The authors define spiculations as follows:

A spiculated breast lesion is defined as a mass or an architectural distortion characterized by thin lines radiating from its margins.

Here is a picture taken from that paper which shows the mammographic appearance on the left and the microscopic appearance on the right, with the arrows pointing to the spiculations.

The linked paper gives many other examples of the microscopic and radiographic analysis of such tumors. It also explains that the two primary reasons for the spiculated shape are:

desmoplastic response
tumor infiltration (which occurs along anatomic ductal structures)

According to this report, the first explanation is more common. To understand the why behind the shape, we need to know the mechanism of this desmoplastic response. As described in the linked Wikipedia article, desmoplasia is not actually the tumor itself but dense fibrous tissue that is induced with malignant tumors invade healthy tissue. The mechanism of this is not entirely clear, but the Wikipedia article sets forth two theories:

The reactive stroma hypothesis postulates that tumor cells cause the proliferation of fibroblasts and subsequent secretion of collagen that acts as a scaffold. This scaffold apparently forms the outline of the "crablegs".
The tumor-induced stromal change hypothesis states that tumor cells themselves differentiate into fibroblasts and secrete the collagen that forms the spiculated scaffold.

*Franquet T, De Miguel C, Cozcolluela R, Donoso L. Radiographics. Spiculated lesions of the breast: mammographic-pathologic correlation. 1993 Jul;13(4):841-52.

"Cancer" is so named because the cancers Hippocrates first observed looked like crabs to him. If he had first observed cancers that most resembled potatoes, cancer probably would have been named differently today.

Cancerous growths reminded Hippocrates of a moving crab, which led to
  the terms carcinoma (malignant tumor) and cancer (ulcerated malignant
  tumor).

Reference http://onlinelibrary.wiley.com/doi/10.1002/cncr.25553/full
My point is, there is no "need" for a tumor to look like a crab or any other particular shape. Most tumors are probably irregular in shape. Most often they just look like lumps. I think breast cancer turns out to look like a crab fairly often (not sure why) and it was precisely breast cancer that Hippocrates was studying, probably because it's fairly close to the surface of the body, and, hence, fairly accessible and easy to observe. That's not irrelevant when there are no proper surgical techniques and anaesthetics.

Why is this downvoted?

I didn't downvote, but this answer doesn't seem to significantly answer the question.

Yeah, looks like I wasn't paying much attention and misunderstood the question. :)


text:
At what point during an action potential are the sodium potassium pumps working?
I'm trying to understand how all of the potentials during an action potential are created. My question specifically is about the sodium potassium pumps, however I would also be grateful if someone could verify if I have grasped the concepts correctly.
From what I understand, the resting membrane potential is at around $-60\rm\,mV$, close to the equilibrium potential for potassium (from the Nernst equation) because the permeability of potassium is much greater than that of sodium, even though the permeability is low.
However, the resting potential is not as negative as the equilibrium potential for potassium because of some permeability of sodium and the permeability of potassium is very low so the tiny permeability of sodium has some impact in preventing the potential reaching the equilibrium potential of potassium.
When the threshold potential of $-50\rm\,mV$ is reached, the voltage gated $\ce{Na+}$ ion channels open, and sodium ions enter the cell, causing depolarisation. The potential rises to about $+40\rm\,mV$, which is close to the equilibrium potential for sodium (because the permeability for sodium is much greater than for potassium). However, it doesn't quite reach the equilibrium potential for sodium because of some potassium ions leaving the cell.
When the $+40\rm\,mV$ threshold is reached, sodium channels close and potassium channels open. Because of the now much higher permeability of potassium ions compared with when the membrane is at its resting potential, the potential becomes much closer to the equilibrium potential for potassium, which I think is about $-90\rm\,mV$, and therefore the cell hyperpolarises. Then the potassium channels close.
Now I'm unsure as to how the resting membrane potential is reached from the hyper polarised state, and I also do not see where the action of the sodium potassium pumps comes into this.

The Sodium-Potassium Pumps are always at work. One can think of them as a continuous process that maintains the equilibrium potential for the individual ions. They always are grabbing internal sodium and exchanging it with external potassium at the cost of ATP.
However a neuron's rest state (in your example -60 mV) is a combination of the equilibrium of the Sodium, Potassium, Chlorine, and other ions. Thus when the membrane hyperpolarizes beyond the rest potential, it is actually the leak potential that brings the membrane potential back up, not the Sodium-Potassium pump.
Leak potentials arise from ions (usually chorine) that pass through the membrane via channels that are always open. Furthermore, sodium channels reactivate and a small amount open to  sodium to enter. (Recall as a population there is usually a small amount of sodium channels open at rest. Another contributing factor is as the potassium channels close the other to factors dominate and slowly bring the membrane back to rest state. Remember that rest is defined as the balance of currents, there will always be small amounts of currents flowing. So even though the neuron is rest small amounts of sodium leak in and less potassium out. The sodium potassium pump maintains the equilbrium potential that allows these currents to flow.
The Sodium-Potassium pump is a slower process, so it usually can be ignored over a single spike. But If there is a high frequency spike train then the small amount of sodium that enters the cell and potassium that exits the cell can add up and effect the equilibrium potentials of the individual Ions. This of course changes the firing properties of the neuron.

I am having trouble finding non academic sources for my last claim, I shall come back and add more sources later once I find them.

thank you for your reply! I'm just slightly confused as you said that it is the membranes leakiness  that restores the equilibrium potential, however from what I understand there is only significant movement of potassium ions when the ion channels are 'closed', in which case the positive potassium ions would be leaving the cell and it would become more hyper polarised? Please correct me where I have misunderstood!

@21joanna12 The wrong idea that you have that is blocking you is that at rest there are only potassium channels open. That isn't the case. There are a small amount of sodium channels and a decent number of chloride channels, too, and putting them all together gives rise to a resting membrane potential of around -65mV. It would be great if there were some kind of equation that took all this into account. Hey, there is! http://paynesnotebook.net/Research/Neurotools/GHKEquation/

"Thus when the membrane hyperpolarizes beyond the rest potential, it is actually the leak potential that brings the membrane potential back up, not the Sodium-Potassium pump." - hey xelo747 do you have a reference to this statement?

@bonCodigo Here is a link that describe everything in great detail. https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/a/the-membrane-potential

Very good question. Most of your arguments, to the best of my knowledge are accurate. As to answer your questions, I'll provide a basic model of understanding. (Disclaimer:- I'm sorry if the explanation seems overly-messed up and confusing)
At any moment, the potential difference across the cell membrane has to be such that it makes all fluxes balanced. Let us assume there is a cell with nothing but potassium and non-diffusible negative porteins. Since potassium is the only ion that can have a flux, the only balanced position will be the one with zero flux, because any net ionic movement will cause a change of potential and hence will not be the balanced state. Zero flux will be reached when the concentration ratio of potassium outside and inside is such that the potential difference is equal to potassium's Nernst potential.
To complicate it, let's add sodium. Now the balanced state should have zero net flux. But this does not mean that the fluxes of both the ions is zero. They can be equal and opposite. Let us assume that the permeability of the membrane is equal for both. Then, the balanced potential would be equidistant from the Nernst potential of both the ions. This is because, permeability, in an abstract way, is a measure of the resistance. Flux is the potential difference (between the Nernst potential, where the flux would be zero, and the membrane potential) divided by the resistance (like a simple current), which would be equal only if this difference is same, which is, for a membrane potential midway between their Nernst potentials. Hence, the ion which has a higher permeability, will have a lesser resistance, and would hence require the potential difference to be low, so that the ratio of $PD$ and $R$ be equal to the other ion with a large $PD$ and a high $R$ (low permeability). This $PD$, is not the membrane potential but the difference between this potential and the Nernst potential.
Now, for your first question

...resting membrane potential is reached from the hyper polarised state....

This is simple to understand because the opening of the potassium channels which caused the potential drop to $-90$ has now been reset and the permeabilities have been reset to the original resting values. Since the balanced state depends on the permebilities only, the balanced state of this is the RMP ($-60$), which the cell will achieve. Since $-90$ is unbalanced, the slightly unbalanced flux will cause a drift of the potential towards $-60$ and when it reaches it, the fluxes will match and hence won't deviate any further. The drift is because more of one ion is moving than the other, causing a net movement of charges across the membrane.

.... action of the sodium potassium pumps comes into this....

This is easy to understand but tough to compute. Since the sodium potassium pump is unbalanced, (it puts out 3 sodiums and takes in 2 potassiums), it contributes a net flux always. Hence, the remaining channels, instead of having exactly equal sodium potassium fluxes, will have to have a slight potassium excess to offset the minor flux contributed by the pump. As a result, the effect can be computed in two ways.

We find the net flux contribution of the pump. Now we know by what amount should the potassium flux be greater than the sodium in the remainign channels which follow the PD/R formula and hence we can caluclate the PD such that the fluxes have a certain difference (equal to the flux contributed by the pump)
We perform experiments and directly find a net amount of potential "correction" which has to be added to the potential calculated by matching fluxes because of the pump, which will remarkably stay constant. This method is easier and the value of the correction can be obtained from literature online.

Hope this helped. Feel free to ask for clarifications. If you want net links or references, ask. :)


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Biochemical coupling between two enzymatic reactions - Enzymes physically associated?
I am wondering what the exact definition of biochemical coupling between two enzymatic reactions is. I know that these two enzymatic reactions have to

share the same intermediate(s)
one is thermodynamically favorable and the other is not.

So  the thermodynamically unfavorable reaction can happen when it coupled with the  thermodynamically favorable reaction. I just want to confirm that : Do these two enzymes have to be physically associated with each other? Since I do not have any evidence to support the physically interactions between these two enzymes, can I still use the term "biochemical coupling"?
Many thanks.

The enzymes don't need physical interactions to couple reactions. Some enzymes do share subunits which are physically associated, but this is a special case. The following review gives a sort of general example during glycolysis,

For example, in the biochemical pathway that breaks down glucose for energy, two enzymes work one after the other to create a high-energy ATP molecule:

We can also look at the peptidyltransferase reaction during the elongation step in translation. Earlier, an aminoacyl tRNA synthetase catalyzed the covalent addition of an amino acid to it's associated tRNA. The energy from breaking this bond in the ribosome provides energy for the peptidyltransferase to link the two amino acids together. This isn't assuming the ATP/GTP needed by elongation factors, etc.

In any coupled system the activity of one component is dependent on the other. For example translation and transcription are coupled; here translation is dependent on transcription but not vice versa. Coupling need not be bidirectional.
There is no question of unfavourable thermodynamics.
For coupled biochemical reactions:

One of the reactions should be dependent on the other. In multicomponent systems there should be at least a pairwise unidirectional dependency (A→B, B→C, C→D). In other words there should be a pathway that connects all the components.
There need not be any physical interaction


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Can dolphins actually communicate linguistically?
Humans use "language." By language, I mean the thing I am using right now to talk to you.
I know dolphins and orcas have very complex communication systems and also seem to process linguistic and gestural commands.
But do they have their own languages? Where is the evidence for or against? If we take two group of dolphins Group A and Group B, would Group A speak one language and Group B speak another?

We don't know. They are certainly very good at learning our languages, but we don't know if they have their own in the wild. This isn't really an answer (I don't have enough reputation to post this as a comment) , but this article may help.

I heard that they have different languages/dialects, problem is rather if one could consider them complicated enough

As a matter of fact, orcas too are dolphins!

Dolphins and orcas do have dialects. Of course there are species specific dialects and it has been shown that orcas reared with bottlenose dolphins tend to learn the latter's dialect. Dolphins of the same species also seem to have regional dialects, as mentioned in this BBC post (I personally do not trust in non-research articles much, but nonetheless in this case the article indicates a certain possibility of a phenomenon). However, this page also reports the same finding and this source seems to be much more reliable. There are citations too that are at present inaccessible to me. Both the sources say that bottlenose dolphins from Shannon estuary in Ireland, "speak" different dialect compared to those from Cardigan Bay in Wales.
The actual research work is this:

Hickey, R. (2005) Comparison of whistle repertoire and characteristics between Cardigan Bay and the Shannon estuary
  populations of Bottlenose dolphins (Tursiops truncatus) with
  implications for passive and active survey techniques. School of
  Biological Sciences, University of Wales, Bangor

Apart from having regional dialects, the cetacean communication also seems to have other features of a "language". I am pasting excerpts from this article which basically reports a study on the acoustic communication or codas in sperm whales. This may apply to dolphins as well.

Individuals within social units have preferred associates among
  members (Gero et al. 2008), indicating differences in the way an
  individual interacts with other members of its unit. These preferred
  associations among unit members suggest the possibility of an
  individual discrimination system.

.... most adult animals within a social unit shared the most common coda
  types, with the exception of the mother-calf pair whose repertoires
  were different from those of other unit members and each other. Apart
  from the mother-calf differences, the repertoire similarities of other
  members did not support the hypothesis of individually distinctive
  coda type repertoires. This sharing of coda repertoires suggests that
  they allow group membership recognition, at either the unit or clan
  levels. This hypothesis is further supported by the fact that social
  units seem to form groups preferentially with other units of their own
  clan (Rendell & Whitehead 2003b).

To be able to learn human sign language (remember Flipper?), their brains are certainly hard-wired for complex communication.
I once read a paper that showed a whale repeating the same song almost exactly. The song was one and a half hour long. Couldn't find it now, but I found some nice articles showing the complexity, consistency and evolution of whale songs. They also show that different populations have different songs (languages or dialects, if you prefer), and that these songs evolve through the years.
Orcas and dolphins are members of the Odontoceti, while whales are Mysticeti. I don't know if the verbal communication of the first group is as elaborated as that of the second, but I don't discard this hypothesis.
Whale Song Explained - great work of art using colored symbols to illustrate the different patterns of sound that make up whale songs.
Songs of Humpback Whales
Large Scale Changes over 19 Years in Songs of Humpback Whales in Bermuda
Dynamic Horizontal Cultural Transmission of Humpback Whale Song at the Ocean Basin Scale


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Formation of Life
Originally, life evolved from non-living matter. Why is life only generated from other life nowadays, and why doesn't it evolve from inanimate matter, like it did originally billions of years ago, when life evolved on Earth?
Maybe I should reword this further. Living organisms reproduce other living organisms but the first living organism came from non living material or chemicals. So could life be created in a laboratory as it originally was ? Originally the process leading to a life form took one billion years, so would this be the answer to my question that it takes too long and that is why it is not being repeated again ?

Welcome to Biology SE and thanks for your interesting question! I edited your question slightly to improve readability. Please feel free to roll back.

Thanks Chris for finding my question interesting and for rewording it to improve it's readability. I am looking forward to reading answers to this question .

Szostack from Harvard in this video The Origin Of Life on Earth discusses various fundamentals to prebiotic biophysics that might provide insights although no definitive.

Abiogenesis, the development of living things from non living matter, is not something we know much about, since it happened about 4 billion of years before we were around and haven't reproduced it in the lab. My guess is that it's not easy. However, the Miller-Urey experiment and others have told us something about abiogenic production of organic compounds.
The first living organism on Earth ( Let's imaging some self-replicating RNA ) was probably very inefficient, copied itself slowly and made a lot of errors. At the time it could survive because there wasn't any competition. However, as time went on some of these copies were more efficient and copied themselves more quickly, outnumbering the original sequences and driving them into extinction. Wait another 3.5 - 4 billion years and you have modern life.
If abiogenesis were to occur on Earth today, the resulting organism would likely be inefficient like the first organism. However, now it would face immense competition from very efficient modern organisms and would probably be eaten.
This is speculation, but I assume that any new type of life on Earth would be carbon based, since organic carbon based building blocks are abundant. If anything, abiogenesis might be easier on modern earth than early earth because the starting materials (nucleotides, amino acids) are readily available, but competition from modern life and reactive oxygen in the atmosphere would hinder any new abiogenesis.

Interesting note about reactive oxygen there at the end — indeed, the Great Oxygenation Event, when oxygen began to be present in the atmosphere, was one of the most significant extinction events in the history of life on Earth.

@augurar I never thought oxygen would be that reactive until I started doing LC-MS and kept finding stuff 16 or 32 mass units too heavy, even after keeping them at -20 in the dark.

There are two questions here:

Why does life only generate life?
Why doesn't life continue to be generated on Earth?

The first one is easy. We don't only generate life. If that were true, it might be illegal to flush toilets. Life forms of some kind would occupy all the space in our atmosphere. Babies - or some living things - would rise up from our graves. Conceivably none of the millions/billions of people who have died from the beginning of history (and well before that) would be dead. Add to that animals, and everything in the other Kingdoms included in Life, and there would be nothing left perhaps except for life. To be honest, life generates heat, death and simple substances much more commonly than it generates life.
If you mean, why does like produce like (in your case, a life generates a similar life form*, that's because of genetic material. New life is based on the genetic material of the preceding life form. People don't give birth to zebras, zebras do. When the genetic material is damaged enough, we give birth to a non-viable or diseased child. If a mutation is favorable, it is (under the right circumstances) spread through an advantage. An example of this is the appearance of lactase, an enzyme which allows adults to derive continued nutrition from animal milk.
As to your second question: why doesn't life continue to be generated on Earth? Are you 100% sure that it isn't happening? How would you recognize a life form foreign to our own? How many different kinds of life can evolve under the same planetary conditions, the same planetary element ratios, etc.? If a very rudimentary silicon-based life form evolved in, say, the last 2,000,000 years, would you know how to look for it? In other words, are you defining life only as we now know it - a carbon based, DNA-propigated form?
Furthermore, if a non-carbon based life form could only evolve on this planet to a very basic, simple level, would you give credence to it as a newly evolved "life" form? Intelligent life is rare. I would guess that very simple life forms are far less rare in the Universe.
How would you classify (or explain) the chemosynthetic bacteria that oxidize sulfur instead of oxygen?
I realize that there are a lot of questions here and not many answers. But part of finding an answer is asking the right questions.
The Origins of Lactase Persistence in Europe

By question (1) I think the PO means why life is only generated by living organisms. In other words, there is only a single question I guess.

@ChrisStronks - I do tend to take people at their word...

Asking good questions is an art.

formulating good answers too - +1

I think this is mostly answering another question than what is being asked (especially looking at the original formulation by the original poster), and the second part of the answer, which is more relevant, is mostly speculation. LUCA is also an accepted and well-supported concept, and if you are challenging that all life on earth has a common ancestor you need to back this up by references (I'm not sure that you are though?).

You might also want to mention the theory that life didn't actually originate on Earth, but was seeded here by comets/meteors/whatever.

Chemosynthetic bacteria are a poor example.  All known life shares certain characteristics, in particular the same system of mapping DNA codons to amino acids (the genetic code).  In fact, almost all species use the exact same mapping from codons to amino acids, with minor exceptions.  If a life form were discovered that did not have DNA or transcribed it differently, that would be a good reason to suspect an independent origin.

Abiogenisis, where imperfect micelles (spheres) of hydrophobic carbon chain formatiions leads to potentials for capturing and mixing elements and molecules forming peptides, polypeptides and protiens that can then catalyze enzymes to patterns to the micelle to a cell of sorts.
Was it inside a terrestrial micelle that life formed or Did amazing spiraling symetry of life get help or even need it from galactic wave patterns, crystal energy of minerals or was it just a mixing up microscopic pieces of Pythogerian parts and geometry.
Either and anyway, given low energy potentials needed for effeciency of a new life form, unless it was non carbon based, it would have practically zero chance of survival where energetic mass of life that already exists just chews it up and mutates spin offs. Only a dynamic shift in genetics as we know it would allow us to detect divergent life.
That said, got to love the ugly waterbear.

It would be great of you added some references to support your response!

Check out iBiology playlist on Youtube to get you started Bez.


text:
Is high metabolism linked to high evolutionary turnover?
I recently read The Dinosaur Heresies by Robert T. Bakker, a 1986 popular science book presenting arguments for an active lifestyle and high metabolic rate in dinosaurs.
One of the arguments that Bakker presents relates to the pattern of species and genera in the fossil record over time.  He states that "warm-blooded" animals (i.e. animals with high metabolic rates) are expected to have higher turnover of taxa and faster rates of diversification.  Dinosaurs have high species and genus turnover and rapid diversification, which Bakker interprets as evidence for a high metabolism.
This argument rests on the claim that high metabolism is correlated with high evolutionary turnover.  Setting dinosaur physiology aside, I wonder how reliable the underlying assumption really is.
Is there good evidence that metabolism and evolutionary rates are causally linked, perhaps due to the ecological strategies that warm-blooded animals tend to adopt?

The question is very interesting. I don't think you express any argument though but only a hypothesis. From your post, the hypothesis that "animals with high metabolism have higher rate of speciation" seem to come from nowhere. Can you try to express Bakker's  logic behind this hypothesis?

@Remi.b Bakker argues that dinosaurs had a high metabolism, based on the rates of divergence and extinction in the fossil record.  However, this argument relies on the claim that high metabolism is in fact correlated with high evolutionary turnover.  My question is whether this underlying claim is indeed well-supported by evidence.

Oh ok. It is not an argument then. It is a claim that such evidence exist. An argument should follow a logical thinking, an argument is not a non-referenced claim. So, you are asking if the claim is supported by evidence or not.

Metabolism and evolutionary rates are linked, but not in the way you describe.
First consider that metabolism is intrinsically linked to body size. The larger an animal is, the smaller amount of energy per unit mass it takes to maintain that body. This can then be extended to many things about an organism, such as life span, gestation time, population growth, etc. (see Brown et al. 2004 for more detail).
Next consider that metabolism changes with temperature. Take an ectotherm (an organism who's internal temperature is the same as the ambient environment, traditionally called cold-blooded creatures) like a lizard, which will go thru temperature fluctuations throughout the day. It will have higher metabolism when the temperature is higher. A lizard living in a warm environment like the tropics will have an overall higher metabolism than a lizard of the same size living in a temperate climate. With that higher metabolism comes a different life span, gestation time, population growth, etc. even though their body sizes are the same.
When temperature is considered and corrected for, all organisms have attributes that scale directly with body size. A plant literally has the same metabolic rate as a lizard if they are a similar mass and live at the same temperatures. (Seriously, see the Brown paper).
Now onto evolution. Rates of evolution depend on many things, but primarily two. Generation time (the time for 1 generation of a population to reproduce) and mutation rates of DNA.
A longer generation time decreases the rate of evolution. For example a single celled organism reproducing every month will evolve faster than an elephant reproducing every decade.
Larger rates of mutation in DNA increase the rate of evolution. If DNA does not change then evolution cannot happen. So the faster DNA changes (thru mutation rates) the faster the potential evolution can be.
Generation time increases with increased body size/metabolism (Brown et al. 2004). Mutation rates decrease with increased size/metabolism (Gillooly et al. 2005).
With those two general patterns, one can say that the rate of evolution decreases with increased metabolism.
Now onto dinosaur evolution. You said that R. Bakker observed that dinosaurs had a higher rate of evolution than expected. With the hypothesis that a higher metabolism caused this. I'll assume they had the same physiological constraints as animals of today, which is reasonable considering they are ancestors of birds. Which everything I just laid out I would propose R. Bakker hypothesis is false, since a higher metabolism means a higher generation time and lower mutation rates, which would lead to decreased rate of evolution.
The latest science says that dinosaurs were endothermic (regulate their own temperature) up to a point (Witze 2014), so their internal temperatures were not as warm as mammals, but probably warmer than most fish and reptiles.
So when accounting for size they likely had lower evolutionary rates than mammals, and higher rates than fish, reptiles, insects, or other ectotherms.
Why then does R. Bakker observe higher evolutionary rates in the fossil record then? I can think of just a general reason why. The timescale of dinosaurs is on the order of 10's of millions of years. Much longer than the tiny amounts of evolution that we have observed in the past 100 years of science. There could easily be processes happening at those long time scales that we aren't considering.
References
Brown, J. H., Gillooly, J. F., Allen, A. P., Savage, V. M., & West, G. B. (2004). Toward a metabolic theory of ecology. Ecology, 85(7), 1771-1789.Link
Gillooly, J. F., Allen, A. P., West, G. B., & Brown, J. H. (2005). The rate of DNA evolution: effects of body size and temperature on the molecular clock. Proceedings of the National Academy of Sciences of the United States of America, 102(1), 140-145. Link
Witze, Alexandra  (2014). Dinosaurs neither warm-blooded nor cold-blooded. Nature. 2014 Link

Interesting, and thanks for the "metabolic theory" links.  However, what you say in the third-to-last paragraph is actually the opposite of what you said in the preceding paragraphs.  Higher metabolism means lower generation time and higher mutation rates, and hence a faster rate of evolution.  This is in agreement with Bakker's arguments.

Regarding dinosaur mesothermy, the debate is far from settled.  While some researchers favor a "mesothermic" model, one can find other papers arguing for complete endothermy like that of modern birds and mammals (e.g. Seymour 2013).

Regarding the last paragraph — much of what we know about evolution comes from the fossil record, so I'm not sure what you mean by "processes happening at those long time scales that we aren't considering".  When Bakker says that evolutionary rates for dinosaurs in the fossil record are high, he's comparing them to other groups in the fossil record, not just to recent observations over the last hundred years.

Pretty sure my comments are consistent throughout. As metabolism increases generation time increases and mutation rates decrease. That's what observations from today tell us. Assuming dinosaurs followed the same patterns then you can't say that their higher than expected evolution rates are due to high metabolism.

Process at long time scales could be many things. For example, how should we interpret the evolution of a small bodied creature to a large bodied one over several million years? I have no idea, but something like that could affect how we compare evolution in the fossil record with evolution we see in laboratories.


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