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DNA Replication
I just wanted to understand the basic steps behind the replication of the lagging strand of DNA:

Have helicase unwind it first
DNA Primase lays down RNA primers in fragments, called Okazaki fragments
DNA polymerase III goes through and corrects all the mistakes (essentially replace the Uracil with Thymine)
DNA polymerase I goes through and removes RNA primer
DNA ligase hooks up each of the 5' to 3' end fragments

Is this the correct order of steps? If so, does the leading strand need any RNA primer or does the DNA polymerase just start and go to the end without any help?
Thanks

I think that you have a couple of points wrong. Since your question is asked using bacterial terminology, I'll stick to that.
The leading strand, the one that is initiated at the origin of replication, is synthesised by pol III which is a highly processive polymerase, i.e. it keeps on going for long periods, making very long products. In principle a single pol III molecule could produce the entire leading strand copy of the template.
The lagging strand is, as you say, initiated at multiple RNA primers. The enzyme that extends these primers is pol I. As polI  extends a primer it creates an Okazaki fragment (i.e. this is not an alternative name for the primer itself). Eventually the pol I will encounter the 5' end of another RNA primer. At this point the 5'>3' exonuclease activity of the pol I comes into play and removes the primer, replacing it with DNA. The pol I will probably also degrade some of the DNA that has been added to that primer by another pol I, resynthesising it as it goes. This is so-called "nick tranlation" since as the pol I moves along the template it moves a nick in the new strand as it goes. pol I is not a very processive enzyme however and will fall off, leaving the nick to be sealed by DNA  ligase.
The leading strand does require a primer, and in most cases this is an RNA laid down by the initiation complex at the origin of replication. In some cases, a protein provides an -OH  group for DNA polymerase to initiate at.


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How do we memorize something?
When we see something, how and where in the brain do we remember it and are able to recognize it later?
What happens in the brain that makes this possible?

I tried googling but didn't found the answer. There must be someone that knows this.

A few terms that may help your googling: engrams, synaptic plasticity, hippocampus :)

The current working theory (note this is still an open question, but there are many leads being followed):
Sensory systems receive a combination of signals from an event, which are initially bound to the hippocampus (this is called episodic memory).  Then, typically during sleep, the memories are consolidated.
A simplified view is that consolidation basically consists of communication between the neocortex and the hippocampus, and the memories are thought to be "saved" in the neocortex.  Thus, amnesia patients with hippocampal damage still have all their long-term memories, they just can't create new memories (because their old memories were already consolidated to neocortex).
Your neocortex has many subregions with many functions.  One is the temporal lobe, where semantic memory seems to be stored.  So your episodic memory may record several interactions apples and, over time, your semantic memory will be updated (as memory consolidation occurs) to "consolidate" your concept of "apple".
The temporal lobe is highly connected with the occipital lobe (where visual information is processed) and the two likely work together to identify objects using the consolidated information.
On the molecular level, how the memories are actually stored.  The most well known concept is connectionism: different connection strengths between neurons carry different information.  But there's also genetic expression going on, and there was recently some research on prion-like proteins contributing to memory as well as astrocytes.
Realize, of course, that a lot of this is cutting edge research... and therefore could be wrong or contain numerous oversights and simplifications.

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Are brain cells replaced over time?
You know how your cells die all the time and new ones are made to replace them, so you practically have a new body every maybe 5 years?
Many people say you become a completely different person every several years, but what about neural cells, do they get replaced?
I believe it would cause a lot of information to get lost if this happened.

I just would like to comment that while others have, correctly, emphasized the existence of neurogenesis, it is more the exception than the rule. Outside the hippocampus and confined cortical regions, typically neurons do not regenerate.

By brain cells, I'll assume you mean neurons (the other type are called glial cells). Yes, new neurons arise in a least certain parts of the brain, and yes, they do cause memories to weaken or disappear. This has been shown in mice, guinea pigs and degus.
It would be wrong to assume that neurogenesis occurs with the frequency of, say, gastric cell or skin turnover. Up until recently, it was not thought to occur at all.
Learning and remembering use various cortical structures, including the hippocampus.Throughout life, new neurons (neurogenesis) are continuously added to the dentate gyrus. These additions remodel hippocampal circuits, and when this occurs after memory formation, this neurogenesis leads to degradation or forgetting of established memories. This was shown in adult mice. Conversely, decreasing neurogenesis after memory formation decreased forgetting.[1]
It is not only plasticity that makes the brain adaptable to continuous changes in environmental demands. Adult-born neurons integrate into preexisting neuronal networks and participate in information processing. Adult neurogenesis itself is a type of circuit plasticity required for hippocampus-dependent learning and memory recall. Adult hippocampal neurogenesis may also promote forgetting.[2]
The more neurogenesis there is, the more memories are broken down. Since we retain many memories over our lifetime, it's pretty safe to say out brains don't "turn over" every five years (or even over longer periods); some parts of our brain don't seem to undergo neurogenesis at all.[3]
[1] Hippocampal Neurogenesis Regulates Forgetting During Adulthood and Infancy Science 9 May 2014
[2] A Price to Pay for Adult Neurogenesis Science 9 May 2014
[3] Neurogenesis in the Adult Brain The Journal of Neuroscience February 1, 2002

I liked that article [1]. Forgetfulness of babies explained.

Very interesting! Is there any data on increase in brain size due to neurogenesis (in micro or perhaps millimeters?)

What about other neurons, which are not involved in adult neurogenesis? How frequently are they replaced?

Addition to anongoodnurse's answer.
Different organisms have different numbers of neurogenic niches (regions where neurons form). For example zebrafish[1] has six niches compared to two in mammals and it is known to have active neurogenesis throughout life. In mammals, apart from the dentate gyrus (subgranular zone) of hippocampus, the other prominent neurogenic niche is the subventricular zone (SVZ) - the region adjoining the ventricles. Immature neurons born at the SVZ migrate to olfactory bulb via the rostral migratory stream[2, 3].
You can also refer to this detailed review [4] on Adult Neurogenesis.

References:
[1] Lindsey, Benjamin W., Audrey Darabie, and Vincent Tropepe. "The cellular composition of neurogenic periventricular zones in the adult zebrafish forebrain." Journal of Comparative Neurology 520.10 (2012): 2275-2316.
[2] Pencea, Viorica, et al. "Neurogenesis in the subventricular zone and rostral migratory stream of the neonatal and adult primate forebrain." Experimental neurology 172.1 (2001): 1-16.
[3] Bath KG, Lee FS. "Neurotrophic Factor Control of Adult SVZ Neurogenesis". Developmental neurobiology. 2010;70(5):339-349
[4] Ming, Guo-li, and Hongjun Song. "Adult neurogenesis in the mammalian brain: significant answers and significant questions." Neuron 70.4 (2011): 687-702.

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why water is a proof of a life?
I read that NASA looks for water on Mars or other planets as a sign of a life.
I wonder why scientists look for water as proof of a life? isn't there any animal that drinks another liquid like alcohol or something?

duplicate: "An identical copy; a facsimile." please see the definition of the duplicate on http://www.thefreedictionary.com/duplicate it is not a duplicate...

A "duplicate" means the same or a very similar question has already been asked and has one or more sufficient answers. If there is something that has not been addressed to your satisfaction, feel free to edit your question to explain what further information you're looking for.

sorry, I shouldn't have fed the troll...

Water is not a proof of life. It is just indicating that life might be possible there.


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Creating expression template from PCR: What annealing temperature to use?
I am creating a transcription template for expression in PURExpress and was confused about the annealing temperature to use.
I have two primers with the T7 promoter and an RBS on the forward primer and a termination sequence on the reverse primer.  The melting temperature of these primers are 84.4 and 83.8 degrees C.  The melting temperature of the regions that are complementary to the gene of interest I want to amplify by PCR are both about 65 degrees C.
What annealing temperature should I use a h?  Since at the beginning of the PCR reaction I will have mostly template that will have the complementary sequences of the primers binding to the GOI and not the 5' and 3' extensions.

It seems the answer, which may be context specific, is to use an annealing temperature about 5 degrees below the entire oligo melting temperature.  I did not get any bands at lower temperatures.

I have to add a comment that I asked PI who focus is synthetic biology, and that PI told me to use an annealing temperature 5 degrees below the melting temperature of the area of the primer that bind directly to the starting template.  I think the answer is somewhere in the middle.


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How prevalent is Taq polymerase in adding 3' A overhangs to the PCR product?
I am conducting a mutagenesis on a gene in vivo of which I need to ligate into an expression vector.  The primers I have designed overlap restriction sites of which I plan to use to ligate into the expression vector.  The parts between the primers I will try to create mutants with error prone PCR.
My concern is the 3' A overhangs that are created from Taq polymerase.  How prevalent is this?  If it is highly common, what is the best way to account for these additions when trying to ligate my PCR product into the vector?

I am not sure of a case where Taq doesn't add 3' A overhangs.
You could use TA cloning to clone your PCR product.  The basic principle is to use a vector with 3' T overhangs.  If you have a vector without these overhangs, you can use a terminal transferase + dTTPs to create them (or even Taq, but this is not as great because it adds a purification step to isolate the vectors with overhangs; terminal transferase is much more efficient).  You can then ligate your PCR product that has a 3' overhang.
Protocols for adding the 3' T overhangs to your vector are given in Zhou and Gomez-Sanchez 2000.

T4 polymerase does not add overhangs (it adds them but then deletes them), but I think this polymerase has too high fidelity for mutagenesis.

From what I understand, the A' overhang does eventually  fall off. However, TA cloning is a much easier route if you have a TA vector.

@Kevin: I have revised my answer to include a description of TA cloning, which does not involve T4 polymerase at all. (I assume you confused the letter A for the number 4.)

In any case if restriction sites flank the PCR product, then you can go ahead and perform a restriction digestion and ligation. If you are too concerned by the A overhang then you can use Pfu polymerase for PCR or alternatively treat the PCR product with Klenow.

Use pGemT to clone your PCR product into. It is exactly designed to take products with 3' overhangs and features blue/white selection so is pretty easy to do! Then you would cut out of pGem with the restriction sites you added during your PCR and ligate it into your expression vector.


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Why are animal births not taken as seriously as human births?
When humans give birth, more than often medical assistance is needed. Others gather around and frantically look for any way to help. But when an animal gives birth, it is usually seen as a moment where you give the female its space and let the birth occur naturally and without any assistance. The animal is of course in serious pain just as a female human but this is more than often not taken into account. Why is it that animal births are not taken as seriously?

When you say "seen", do you mean "seen by humans" or "seen by animals of the same species"? That is, is your question one of human psychology, or of animal behavior?

I don't thing you can generalize this broadly.  There are human societies where the women generally give birth alone.  But more importantly, "animals" is a big group.  Some animals that bear live young labor extensively, but others don't (e.g., kangaroo).  And some others have external fertilization so there is no labor at all.

Our heads are bigger.
There's some debate on the issue, but in essence, human brains, and therefore heads, are very large relative to our body size.  This is handy for all the intelligent things we like to do, but can be rather painful during birth.  Because we walk upright, the size of a newborn's head is actually a non-trivial fact during the birthing process.  There are two major implications.
The first is that human birth hurts.  You can watch the birth of other animals and they seem to brush it off, but for humans, forcing that huge head through a relatively small birth canal is difficult.  Evolution has (supposedly) limited the size of the hips because, while that would allow an easier birthing process, it would negatively impact our ability to walk.  As such, it has to hurt.
Secondly, in order to make the process easier, humans rotate during birth.  The end result is that, unlike even other closely related primates, humans come out backward in a way that is very difficult for a birthing female to attend to.  This almost requires having another person or two on hand to help out.  This would, of course, be a huge reinforcement for social connections.
A few books I know of touch on this.  Up From Dragons deals with the brain size/hip size issue and The Invisible Sex talks about rotation during the birthing process and the social implications.

And, if your question pertains to "seen by animals of the same species", there are at least anecdotal accounts of animal-assisted births, as in this case of a "monkey midwife".
The linked article also mentions another feature of "social" births, which is that it can might help juvenile females learn.


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Does evolution take place universally?
Why does evolution (namely the evolution of primates into humans) take place both uniformly and universally on the earth? Why aren't there any creatures who have not taken the same evolutionary steps as their same species elsewhere on earth? For example, why aren't there any humans on other parts of the world who look the same as our evolutionary descendants?

Could you clarify what you're asking a bit?  As it stands, it's a little unclear; it sounds like you're asking why there are primates if humans evolved from them.  I think you're a little mistaken on evolutionary history.  Humans did not evolve from chimpanzees, for example, but rather both species evolved from a common ancestor.  See the chimpanzee-human last common ancestor article.  So yes, this process is happening, has happened, and will happen again.

@Amory I realize humans evolved from a common ancestor. My question was why does evolution take place at the same rate with the same results to every member of the species all around the world? Why doesn't it vary even dramatically?

The evolution path a population takes depends on many factors. Environment, random genetic drift, random mutations, population size, population structure, ... If you think of a population that has been splited into two, the two descending population might differ in their initial alleles frequency just after the split or differ by their initial population size. Then environment might differ, the mutation they get might differ, etc... It can drives two initially similar population into very different species.

@0x499... Another thing to consider is that in the modern world, there's no longer the same severity of selection pressures required to cause dramatic shifts in evolution of our species.  There are minor evolutionary shifts, like slightly increased rates of sickle cell or g6pd deficiency in malaria-endemic areas of the globe, but not the kind of thing you seem to be referring to.

"Uniformly and universally"? WTF are you talking about? Primates do not, on a daily basis, "evolve" into humans. Monkeys stay monkeys, chimps stay chimps, and humans - well, humans, in general behave like a bunch of bone-headed jackasses, and yet they remain humans. Evolution acts on populations of organisms, typically over long time spans in response to a variety of stressors. Global warming should prove interesting, evolutionarily-speaking... :-)

My question was why does evolution take place at the same rate with the same results to every member of the species all around the world?

It doesn't.  Evolution acts on populations, not individuals.  I will never evolve, you will never evolve, but humans are evolving, and sure, certain pockets evolve at different rates.  Here's a long but straight-forward write up that deals with perhaps the best example, beak size in Darwin's finches.  A select population of birds on an island may be evolving rapidly and differently than that same species elsewhere, perhaps eventually resulting in a divergent species.  There is no need for natural selection to operate equally everywhere; in fact, the pressures must be different otherwise we would never see the diverse set of species we do observe.

Why does evolution (namely the evolution of primates into humans) take place both uniformly and universally on the earth?

Short answer: it doesn't. All human beings descended from the same group of Homo sapiens. There has been some genetic deviation since, but not enough to call it a "species". Evolution happens, but at very long time scales and not at any sort of defined pace.
Read this first.
Long answer: As the link above shows, evolution is dependent on several key factors. Heritable variation and change to selective pressures.

Why aren't there any creatures who have not taken the same evolutionary steps as their same species elsewhere on earth?

Think of humans! Different races, especially ones that have not intermixed, are significantly different. indigenous Africans, indigenous Europeans, and indigenous Japanese, for example. All of these races has genetically diverged into distinct populations with different traits, but the isolation between them hasn't been that long. That's why all humans can still reproduce.

Why aren't there any humans on other parts of the world who look the same as our evolutionary descendants?

Over a very long period of time, Homo sapiens had evolved to become a more advanced, competitively dominant species. although Neanderthals and Homo sapiens did intermix for a while, we're not completely sure how they went extinct. One of the reasons stated is that it's hard for a worse species to exist when a better species comes along.

If I got your question correctly,
you were aware that humans in some way, shape or form have descended from a common ancestor shared with other primates;
You then realized the relative 'distance' of modern Homo Sapiens from these other primates;
You concluded (or know) that there have been various morphological stages in between, none of which has survived until today;
You were basically puzzled by the question why no intermittent evolutionary stages exist of say the human species. Actually, this is not a bad question.
I think it can be explained with population growth. The modern species has just multiplied so dramatically, continuously selecting for certain features, that there was ultimately less and less room for older forms which have not been able to survive into today.
Monkeys also exist today, which means they have 'survived', but their populations are relatively smaller, and in their case, selection has not emphasized too many new features (correct me if I'm totally wrong).
I think especially when selection is fueled by intelligent awareness, its evolutionary momentum increases dramatically. Our older ancestors (early hominid stages) have then simply been outnumbered by the newer ones, dwindled in numbers and simply become extinct whereas the entire monkey-, or for that matter alligator population has selected relatively more traditionally and remained more homogenous (over-simplification!) - so they're still around, too.
On the other hand, today there are in fact many different types of homo sapiens around with somewhat distinct features, but they're all able to reproduce interracially without much of a problem. In the last few hundred thousand years I'd say there was not enough change to reproductively cut off any (isolated?) group from the main gene pool. Just our common, older ancestors were unable to catch up. This could theoretically happen again in the future, maybe not on this interconnected world, but with different human space colonies.

This is another one of those question where the premise is so crazy wrong, it's hard to answer well without writing a thousand words to explain why every sentence is wrong, wrong wrong.

Why does evolution (namely the evolution of primates into humans) take
  place both uniformly and universally on the earth?

That's ridiculous.  Most of the earth doesn't have primates, and 2 million years ago, most of the ones that did exist weren't evolving into humans.  The ancestors of today's New World monkeys didn't evolve into humans.  The ancestors of today's lemurs didn't evolve into humans.

Why aren't there any creatures who have not taken the same
  evolutionary steps as their same species elsewhere on earth?

I don't think this makes any sense as written.  We do observe different species sometimes evolving the same response to pretty similar environments, like cacti on different continents evolving in to similar-looking forms, despite being far apart evolutionary.  But we don't expect every population to evolve the same way, because evolution builds on the random changes that came before in that population.  That's the basic premise of evolution, that's the premise that explains what we see very well, and if you think some other wildly different premise is in effect, and insist on forcing explanations and data to fit something that is just wrong, nothing in biology will make sense to you.

I'd like to remind you of our policy on civility: http://biology.stackexchange.com/help/behavior

authors: Bob Jarvis - Слава Україні


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What determines the strength of a tree
What determines the strength of a tree. A morphologically strong looking tree found broken down at trunk. can we determine the strength/ life of a plant

I think it is fairy obvious what you are asking (what determines the strength of wood to bending/breaking - probably mainly against horizontal forces), but you should really clarify the Q. However, I think that the Q should be left open until the poster has at least had time to see the comments and rephrase the Q.

I was letting my fingers surfed in the internet about this question and found this interesting article : http://www.caves.org/section/vertical/nh/55/TreeAnchors.pdf
Your  question is too broad so I guess the link gives a general answer.
hope this helps


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Why do rodents' teeth continue to grow?
Why do rodents' teeth continue to grow? Enamel formation and/or root formation continue throughout rodents' lives.
What's the mechanism that causes this?

humans may be a tad unusual because their teeth don't continue to grow...

authors: Никита Литовка


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What is the ratio of breathing rate to heart rate?
Breathing rate and heart rate are directly connected. This is because the heart is connected to the lungs via the pulmonary artery.
I first thought that breathing rate would be half of the heart rate since half of the heart cycle occurs in the lungs.
But I know that is not true with a normal 12 BPM(breaths per minute) breathing rate.
So what is the ratio of breathing rate to heart rate?

"This is because the heart is connected to the lungs via the pulmonary artery." It's not like heart rate or breathing rate are regulated by pulmonary arteries. The relation is more sophisticated than that. For example heart rate is controlled by nerves and hormones, and neither comes straight from the lung. But fast breathing leads to changes in blood oxygen and pH, which are picked up by sensors such as the carotid body, which informs the medulla, which then talks to the sinoatrial node. There is also more direct influence, because ample breathing increases pressure in the thorax.
But at each step, there are many other factors interfering, meaning the correlation between the two gets ever looser. There isn't really a "normal" ratio of heart rate to respiration rate. There is a healthy heart rate and a healthy respiratory rate, but they are both wide intervals (60-100 and 12-20, respectively). Dividing one by the other, you get a very wide interval, from 60 beats per minute / 20 breaths per minute = 3, to 100 beats per minute / 12 breaths per minute = 8.
Perhaps in practice the most common values for beats per breath are in a narrower interval. But "normal" values are defined in relationship to abnormal conditions, and there is no disease in which a change in this ratio is a cardinal feature. It makes little sense for clinicians to define a normal range for beats per breath, and therefore it makes little sense for epidemiologists to estimate most common values.

did you mean "breathing rate" in it's not like heart rate or bleeding rate are regulated by pulmonary arteries?

yes, that was a typo

but a disease that changes the HR most likely also changes the BR(breathing rate) and it probably also changes the ratio in lots of people even though the exact ratio varies from individual to individual. One example of something that is beneficial sometimes and changes the HR is ventricular hypertrophy. When caused by excersize it increases stroke volume and thus increases O2 transport which is always a plus. It also lowers the HR in response to the high BP that there is at first so that high BP becomes normal BP so that resting HR is anywhere in the normal range as well as down to 40 BPM.

As I said above, the chances are that when one is high, the other one is high too, and the interval may be narrower than 3-8 beats per breath. But, because it is of limited clinical importance, the ratio was not the focus of high-scale epidemiological studies. To my knowledge, scientists did not look for a "most common", nor for a "healthy" ratio. In the absence of actual data, I was only speculating.

but if breathing rate is clinically important and HR is too than why wouldn't the ratio be important? Cardiovascular disease and Respiratory disease can both change the ratio to where it is out of the normal range of 3-8 beats per breath. And it is important to know whether you have cardiovascular disease, respiratory disease, or both.

like respiratory disease can make it more beats per breath if it is restrictive(In other words problems with getting oxygen into the lungs) and cardiovascular disease can make it less beats per breath if it makes the heart speed up(which it almost always does)

I feel that ideally a healthy adult, under normal static conditions, should breathe 15 times per minute and his pulse rate is should be 60 per minute.

Welcome to SE BIology. I think your answer is plausible but this is a science website so most other uses will like to see data/evidence. Can you update your answer to include some evidence? Thanks.

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why does blood when oxidized over time become bluish green?
Oxygenated blood is bright red and deoxygenated blood is dark red or brown.
If you take oxygenated blood and leave it in the air it will turn dark red, then brown, then finally a bluish green from exposure to atmospheric oxygen.
Why does it oxidize this far to get a copper oxide color to it after it has passed the phase where it is the same color as iron oxide? Why doesn't it stay at the iron oxide color?

green sounds like a copper compound, but I would have thought iron would be present in far higher levels than copper in the blood. Never seen blood turn green, but I don't have that much just laying around. How do you get it to turn green?

often during the last few days of my period it is extremely light bleeding and the blood is brown. After hours of extremely light bleeding it slowly goes from being reddish-brown like iron oxide to bluish-green like copper oxide. Because the 3rd stage of oxidation is so slow I don't see much green blood after 24 hours of extremely light bleeding but I do see more than I did in the few hours that it took to start that stage of oxidation.

Apparently there is a rare condition, sulfhemoglobinemia in which sulphide ions or H2S combine with the haem group in haemoglobin, causing a greenish colour. This can be related to certain drugs being present in the blood.
See here for an example in which surgeons discovered dark green blood in their patient.

well I think in the case of myself that I don't have H2S in the blood and it is a light bluish-green I get after hours of oxidation of reddish brown blood so atmospheric oxygen can slowly oxidize blood from the iron oxide color(that reddish brown) to a copper oxide color(the light bluish green). Thats what I notice during the end of my period where the bleeding is extremely light and sometimes not constant is slow oxidation to a bluish green

But the colour of oxidised blood (ferrihaemoglobin) is established, and there isn't another oxidation stage to go to in the context of the protein. If the Fe(II) is released from the protein it could form Fe(OH)2 which can oxidise to a greenish colour http://en.wikipedia.org/wiki/Iron(II)_hydroxide

so you think that is what it is is Iron hydroxide which gets further oxidised? Well than is it the formation of Iron Hydroxide(given that I have a pad on during that time which absorbs the blood) that is really slow or is it the oxidation of Iron Hydroxide that is really slow?


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Rattlesnakes developing stronger venom
I have heard that rattlesnakes are developing stronger venoms causing more people each year to die from rattlesnake bites.
But why would a snake that is already very venomous need to develop stronger venoms? I mean for the venom resistant ground squirrels couldn't the snake just wait longer or maybe strike more than once before it eats?
And I could see this going to venom overload in the next few centuries. If rattlesnakes keep developing stronger venoms at the pace that they are then rattlesnakes could become as venomous as a cobra or worse. Along with that it might rattle less and less until it just stops using the rattle.
Is is because of the fact that we are developing stronger pit viper antivenoms(mainly by injecting rattlesnake venom, copperhead venom, and cottonmouth venom into an animal with a stronger immune system like a horse and after a while, getting the antibodies needed for the antivenom) that rattlesnakes are developing stronger venoms?

Can you add the source which says that the venom is getting stronger?

https://www.youtube.com/watch?v=CRf4u8qE4Vs This video mentions rattlesnake venom getting stronger and ground squirrels becoming more resistant to rattlesnake venom.

@Caters Youtube is not generally considered a valid source of reference. There must be some kind of report that says so, unless they wouldn't have made the documentary. Even though the documentary is from a credible source, the first exercise should be to verify it. Because the rest of the question is based on the assumption that the initial statement is correct. Also, one cannot watch the entire documentary for a specific fact.

Also have a look at this

I did find an article which mentions the venom strengthening:
http://www.sciencedaily.com/releases/2012/06/120605102638.htm
It may be an evolutionary bonus. Snakes with the most potent venom may leave fewer survivors, particularly with something like humans who would hunt down a snake if they could find it. A snake which leaves fewer survivors may be better able to escape. It may also have more successful hunts which may have been what lead them to become poisonous to begin with.
Unlike the antibiotics arms race against bacteria, it's unlikely that antivenoms are the cause of more dangerous snakes.
As far as "centuries from now" we really can't hypothesize whether more potent venom will continue to be a more helpful evolutionary trait. More potent venom doesn't have an infinitely continuing effectiveness. After a certain point, whatever bitten isn't any more dead with a stronger poison.

Please vote for my answer and marked it as "answer" (the check mark) if you found it at all helpful. Your questions are conjecture and you are not understanding how ecological systems work. The changes in venom are small and not infinite. Other systems tend to balance changes appropriately. The only big changes happening more rapidly than nature is able to cope with are those made by man. It is highly unlikely that a small increase in poison effectiveness will throw the entire system off course.


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What is the role of hippo signalling in oral squamous cells
What role do hippo signalling have on squamous cells in oral health & diseases

This is purely my speculation : If hippo signalling gets defective mouth cancer could result.

Mutations in the Hippo signalling pathway cause unusual organ growth in flies.  After a good deal of intensive research, its been shown that Hippo genes are responsible for suppressing organ growth in development, increasing cell death and slowing proliferation.
Given this role, its not surprising that Hippo genes are also important in cancer.  I'm not an expert in cancer, but a quick search turned up an association of cancer with the Yki (YAP in mammals) transcription activator, an oncogene from the Hippo Pathway.  YAP suppression has been linked to cancerous growth.  And its also been shown that YAP is amplified in oral squamous cell carcinoma cells.  This last is circumstantial but consistent with what we know about YAP.

Hippo Signal may affect the turnover rate of oral mucosa

Could you expand on your answer with additional information and/or citations?


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Bacteria with daily bimodal energy cycle
Many years ago (about 20) I was told the following story by someone who was in field of biology that at some point there was a rift between researchers of some biological organism, that they were divided on if it consumed A and produced B as the by product of the process or reverse or maybe it consumed C and D was the by product.
The divide was so severe that it was a cause of conflicts in the said circles and heated exchanges in conferences.
The issue was resolved when someone noted that holders of A to B were day workers and C to D were night workers, and that the organism is question (bacteria?) behaved one way during day and then the other during night.
I am a programmer and apologies for being so abstract but that is all I remembered/understood from the story.
My question is :
A) If this is a (possibly) true story?
and
B)What might be the organism in the story be and if there might be any links to any related articles?
Please feel free to edit this to make more biology friendly as I have no idea about the proper terms to use to describe the possible story that I heard.

The key term I think you're looking for is bacterial Circadian Rhythms? Most evidence of this comes from studies of photosynthetic Cyanobacteria (which makes a lot of sense) and more recently from host-associated bacteria. This recent ASM article talks about circadian rhythms in different types of bacteria, with links to the primary literature. No mention of anything like the story you shared, but I'm pretty intrigued by it, and would love to find out more.

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


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Are Night Parrots (Pezoporus occidentalis) really extinct?
This incredibly rare animal has been reported to be extinct since 1990, however several cases has been raised that night parrot was spotted in the areas of Australia. What is the cause of their extinction, or in the first place, are they really extinct?

As per Wikipedia it is listed as endangered having been downgraded from critically endangered due to the spread in sightings over the years over a large area. Sightings have been rare with a reported sighting on 12th April 2005 and a dead specimen found in 2006 The first photos and a 17 second video of the bird was taken by a wildlife photographer John Young in 2013. Details can be found in this link.
According to Birdlife.org the reason for its population to decrease significantly include predation by feral cats and foxes, altered fire regimes, competition for food, degradation of habitat near water by stock or rabbits, and reduced availability of water as a result of over-use by feral camels.

At least they are not extinct.. That solves!


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What is meant by 'proteolytic activation' of a virus?
Noob biologist here. I suspect that at the first stage this means 'activating the virus by lysis of a surface/spike protein'? Seems kind of obvious, but I put it here in case 'proteolytic activation' is not in fact merely a subset of 'virus activation', and means something slightly different.
Second, if the above interpretation is correct, what precisely do we mean by virus activation? Is it the release of viral RNA into the host cell cytosol? This would be my guess, as it is necessary (sufficient?) for replication of viral RNA to commence, and viral replication to occur. Another idea is that 'virus entering host cell' is enough to constitute viral activation, though I suspect some viruses can enter cells and remain dormant there. Hardly seems like activation to me.
Would really appreciate clarification of this terminology so I don't have misconceptions when reading literature.

I don’t think “virus activation” means anything more than making a virus that is in an inactive state active. Why would you think otherwise and that it implies anything more specific? (And, unless you’ve performed some experimental procedure to remove organelles, it’s cytoplasm, not cytosol.) “Proteolytic activation” without any further qualification, only adds the mechanism (I assume you know what proteolysis is), so to find out its likely context I had to Google. You can too, but it’s sloppy writing.

@David but what is the defining difference between an active and inactive virus? What is the necessary process that makes an inactive virus now active? Is it the injection of rna into a host cell? Are the released replicated viruses then inactive until they start infecting other cells? Sorry if I'm being pedantic, but I really want to be clear on what is being referred to in the literature.

My point is there is no defining difference other than the English meaning of the word “inactive”. I hadn’t in general considered viruses having in inactive state, and there are so many different viruses that there can be no commonality. If someone writes “proteolytic cleavage of such and such a virus protein so that it is able to initiate membrane fusion” and thereafter abbreviated this as virus activation, that means something. Otherwise, not. As I wrote, sloppy writing — and incomprehensible too. The Emperor is naked.

Viruses all have some mechanism to enter cells' lipid membranes, and these need to be prevented from activating prematurely. Often this means the virus is in an inert state while it is assembled and trafficked out of the host cell, then activated by some chemical signal such as the low pH of inner endosomes. So "activation" is usually going to refer to a chemical change that removes the barriers to cell entry.
For example; in flaviviruses such as Zika or Dengue, the E glycoprotein that handles most of the host entry functions is assembled while bound to prM protein. Once virions are assembled with E in an inert arrangement, prM is proteolytically cleaved. When the new host cell absorbs the virion into an endosome and lowers the pH to digest it, the E glycoproteins rearrange into spikes that can penetrate the endosomal membrane and induce fusion with the viral membrane. If prM isn't cleaved, the virus can't infect cells. Here's a recent paper that discusses this process, with high resolution structures. For these viruses there are two rounds of activation, and only the first one is proteolytic.

For coronaviruses some cell's surface or endosome protease cuts some part of the viral surface protein (mainly S2' site but also pre-priming at S1/S2, the interaction of both is still unclear) which triggers the membrane fusion


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Source for 'EVERY living organism uses ATP as energy carrier', and can we make a synthetic one that doesn't?
I have read it repeatedly that 'all living organisms use ATP as an energy currency etc' and 'some use GTP in addition'. However I am yet to find a reliable resource, rather than just quora/reddit/researchgate posts, that states this.
Also, would it be possible to create a synthetic organism which does not use ATP? Or GTP? What might be the best energy currency to use then?

Well your request for a source is rather like asking who first reported that 2+2=4. Not quite, but that should give the idea to someone who has not studied biochemistry. I doubt that you will find a source, but the following from Jacques Monod — the Nobel laureate — is worth quoting:

“Anything found to be true of E. coli must also be true of elephants.”

In fact, this turns out not to be true for anything, but it is true of the role of ATP.
The better question, I think, is not what the source of such a quotation is, but what is the evidence for such an opinion. The evidence that has accumulated over the last 80 years or so is from examining the metabolic pathways present in different organisms, and, more recently, sequencing their genomes to identify the genes for various enzymes. What has been observed is a core of common pathways, involving a core mechanism of energy metabolism involving ATP. This is consistent with the idea that this arose early in evolution and was fixed in the last common ancestor of living things.
If you want a more recent source to the ideas above, I suggest another SE Biology question, Immortal genes common to all organisms, may provide a starting point.


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The shape of mRNA
I was wondering about the shapes assumed by mRNA. I have read some sources quoting that it is linear (quora, so not very reliable) and also a source that says a hairpin shape is common (nature, so I would rather go with this one).
I was also wondering what additional factors or features ensure the mRNA has this shape. For instance, the first source says that the mRNA 'is linear so that the ribosomes can bind to it'. But, clearly, all that is required for this is that the ribosome binding site is exposed. In that case, the remainder of the mRNA may either spontaneously unravel as it is being translated, or there may be something slightly more specific taking place catalysed by the ribosome, or there may be an additional enzyme that associates and catalyses the unfolding of the mRNA as it is being translated.
The thing is, I just find it difficult to belive that the mRNA would not fold up on itself, but on the other hand if it did, perhaps it would be too stable and would not be degraded sufficiently easily. We would have accmulation of mRNA in the cell, unless there was a protein that specifically degraded it.
My only other hypothesis, if it truly is the case that the mRNA does not fold up, is that it is down to the DNA in the nucleaus being 'too dense' to permit the mRNA folding in the nucleus, and once it exits via a nuclear pore it is immediately being translated and forming a polyribosome complex. So then it can no longer fold.
I do not think that the DNA content in the nucleus is sufficiently dense for steric effects like this. I have seen electron micrograph images in a book (Molecular Biology of the Cell) of mRNA exiting a nuclear pore. It seems quite coiled up. Unfortunately, I have been unable to find a clear representative image online or the associated paper. But perhaps the mRNA can coil up in the nucleus, but is straightened out as it is pulled throught the nuclear pore. Proteins and factors associated with the nuclear pore may catalyse the breaking of the hydrogen bonds.
Any details on this would be much appreciated.

Possible duplicate of What stops messenger RNA from binding to itself?

Unfortunately it is often taught that mRNA is linear, but this is not true at all. Nucleotides within mRNA can form intra-molecular hydrogen bonds with other nucleotides, creating secondary structures, interactions between these secondary structures results in tertiary structures. mRNAs have highly variable secondary structures, primarily due to differences in the sequence of the ORF, so there is not a consensus structure adopted by mRNAs. However, codon degeneracy is important in producing more ordered and stable mRNA secondary structures in ORFs, resulting in increased mRNA half-life. Nucleotides in positions one and two in codons are the most conserved, whereas the third nucleotide position is the least conserved and has elevated GC content, thus making the greatest contribution to the stability of the secondary structure. The 5’ UTR typically contains lots of secondary structures, which may help in modulation of translation initiation, whereas 3’ UTRs contain fewer secondary structure, resulting in structural instability around binding sites for proteins and miRNAs, enhancing miRNA and protein binding. The start and stop codons are less frequently base-paired than the rest of the mRNA, suggesting they exist in local secondary structures which lead to efficient initiation and termination of translation. However, the sequence immediately downstream of the stop codon has a high GC content and an in increase in frequency of base pairing. It has been hypothesised that this strong secondary structure is present to interrupt post-termination ribosomal scanning. Whilst increasing stability of mRNA increases half-life, low secondary structures around binding sites within the mRNA suggests that thermodynamic stability of mRNA is optimised and not-minimised in all scenarios.
With regards to translation initiation there is quite a lot of cool work on dynamic secondary RNA structures for regulating translation initiation, this work primarily revolves around riboregulators and riboswitches. I won't go into detail about them here, but for a great paper on riboregulators see: Green, A. A., Silver, P. A., Collins, J. J. & Yin, P. Toehold switches: de-novo-designed regulators of gene expression. Cell 159, 925–39 (2014)
References:
Comparative analysis of orthologous eukaryotic mRNAs: potential hidden functional signals. Nucleic Acids Res. 32, 1774–82 (2004).Shabalina, S. A., Ogurtsov, A. Y., Rogozin, I. B., Koonin, E. V & Lipman, D. J.
Duan, J. & Antezana, M. A. Mammalian Mutation Pressure, Synonymous Codon Choice, and mRNA Degradation. J. Mol. Evol. 57, 694–701 (2003).
Shabalina, S. A., Ogurtsov, A. Y. & Spiridonov, N. A. A periodic pattern of mRNA secondary structure created by the genetic code. Nucleic Acids Res. 34, 2428–2437 (2006).


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Why aren't viruses considered to be non-cellular life?
I have always thought of viruses as being non-cellular lifeforms. And no, it isn't just because of Wikipedia. I have heard that there are viruses that are so complex, that they are very close to being considered cellular. And some viruses infect other viruses. Wow, I never thought parasitism would scale all the way down to viruses as the host until I found out about viruses that infect other viruses. So, here are the criteria scientists have used for defining living vs non-living for centuries:

Made of at least 1 cell -> Some viruses have membranes and some cells have cell walls. Sure, cell walls are normally made up of complex sugars, but what is to say that there couldn't be lifeforms with proteins as the most prevalent component of a cell wall? And some very large viruses get close to being actual cells.
Metabolism -> This is one thing that even the most complex of viruses fail.
Responding to stimulus -> I think viruses do respond to a stimulus, just not in the way we normally think of responding to a stimulus. I mean, they clearly respond to temperature(cold temperature, won't reproduce or at least will reproduce very slowly, moderate temperature, will definitely reproduce, but not at peak reproduction rate, hot temperature, peak reproduction rate reached) and temperature is a stimulus.
Grow, Develop, Die -> The virus does develop, sort of, when viruses get built in the host cell(which is kind of analogous to an egg cell becoming a baby, only on a much much smaller scale). And viruses do die as well. The only thing they fail at here is growth. The virus doesn't get bigger or more complex than the parent virus unless it mutates and the mutated virus has size and/or complexity promoting genes that the original virus didn't have.
Highly organized -> Small viruses like the flu virus fail at this. Some bigger viruses though don't fail this criterion
Maintain Homeostasis -> All viruses fail at this, even the complex viruses
The ability to reproduce -> Viruses don't reproduce independently from a host but they do reproduce. If viruses were to be considered non-living because of the inability to reproduce independently of a host, than wouldn't your average parasite also be considered non-living for the same reason? Clearly parasites aren't considered non-living just because they can't independently reproduce. Viruses are just parasites of the cell, so I would say that they do meet this criterion, because viruses and their relationship to cells is parasitic. Viruses infecting other viruses also makes me think that viruses meet this criterion
DNA changes and thus the organism evolves -> This is definitely true for viruses. Viruses evolve super fast, even just 1 cell getting infected by 2 viruses simultaneously is enough for completely different viruses to form as the genetic material and capsid proteins are exchanged between viruses as they are built(I have seen this illustrated before with 2 different flu viruses infecting one cell and 4 different viruses coming out of the cell, both the original flu viruses and 2 completely different flu viruses). So the evolution rate of viruses can be as fast as a single generation compared to the thousands of years minimum it takes for the same amount of evolution relatively speaking to occur in a multicellular organism.

Clearly, viruses do meet a lot of the criteria for a living organism. So with this and all the new discoveries of things like viruses getting ever closer to the cell in complexity and viruses that infect other viruses, why aren't viruses considered to be non-cellular lifeforms?

what research have you done to answer this question yourself?

"...all the new discoveries of things like viruses getting ever closer to the cell in complexity..." There are orders of magnitude of difference in complexity between a virus and a basic, replicating cell. There are many other mistakes as well, hence my downvote. Before presenting an idea based on suppositions, you should confirm those suppositions. Don't feel too bad, though. If down votes were given in real life for all the stuff I think I know but really don't, I would be downvoted into ... maybe oblivion. :)

I think part of the negative response you are getting is that you seem to answer your own question — points 2. and 6. seem to rule out viruses as "life". Perhaps you need to clarify what your question really is? ——— You clearly put a lot of work into this question, but I think you might benefit from doing some more background research. In particular, I think you might get a more positive response if you provided references that supported statements about viruses infecting other viruses and "viruses getting ever closer to the cell in complexity".

A virus particle (not virus cell)  DOES not have mitochondria is not irritable(as we've seen in living bacteria  it does not display phototaxis or chemotaxis  pLEASE GO BACK AND RE-STUDY SOME BASICS

Welcome to Biology.SE! Thank you for taking the [tour], but please also consult the help pages for additional advice on [Answer] effectively on this site and the material on expected behavior — see:[help/behavior]. In particular, "yelling" at people to study especially without providing any information appears to violate the "Be nice." guideline. In addition, it is best to avoid answering low-quality questions. Finally, for future answers you are more likely to get a positive response if you provide supporting references. Without that an answer is indistinguishable from opinion. Thank you!


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Genetic disease elimination: Possible?
This is a question having to do with my generation ship story but more specifically, genetics, and even more specifically, genetic disease.
Here are the conditions as far as people with or without genetic disease go:
People with disease: sterilization + alternative ways to have children and absolutely no sex before sterilization
Carriers: warn that their children might need sterilizing
Not carriers: Absolutely nothing
Now I know these types of genetic diseases would be eliminated in 1 generation:

Y linked(Azoospermia for example)
X linked dominant(Such as Vitamin D resistant rickets)
Autosomal dominant(For example Huntington's disease)

A truly codominant genetic disease is impossible because you can't both have and not have the disease simultaneously. Instead it would be better to say it is incomplete dominant.
But with these conditions, is it possible for genetic disease to be totally eliminated after hundreds of generations(say 500 generations)? In other words is it possible for these types of disease to be eliminated:

Incomplete dominant(Alpha-1 antitrypsin deficiency as an example(but I found out this also falls under multiple alleles))
Autosomal recessive(sickle cell anemia for example)
X linked recessive(such as Hemophilia A)
Multiple alleles(Again A1AT deficiency is an example of this)

I found out that human population growth globally averages around 1.1% per year. And a reasonable number to have on a generation ship is 44,000 people. About 9% of them would be 65+, 65% between 15 and 64 with 20% of that being women of reproductive age, 50% being men of reproductive age, 15% post-menopausal women, and a small 5% being those that are still not in puberty, with the other 26% of the population being from 8 to 14, of which 75% are not in puberty yet and 25% are. Sex ratio is 1:1. This would mean a minimum of 815 babies born per year to compensate for 343 deaths per year. Or about 2.3 times as many babies born as deaths.
So given this and the genotype ratios for the possible punnet squares which I already wrote down, how would I figure out the probability that all genetic disease is eliminated after x generations?

It seems you are excluding spontaneous mutations which could lead to genetic diseases. Is that on purpose?

To all the down voters, please leave a comment on how to improve the question. And please don't mix up the biological question "Is it possible?" with the ethical question "Should it be done?". Thank you.

Please rephrase the question (title) to include the detail of being on a starship colony; or generally the fictional setting. The current question suggests you're asking about human genetic engineering. Clicking on that and not reading your question might be the reason for some of the unexplained downvotes.

Or with slightly advanced technology you can simply edit the offsprings genome.

Given your severe selection pressure against disease allele you have implemented, you can have the disease allele eliminated within 1 generation for dominant allele and 2 generations for recessive allele.
You could eliminate all those disease alleles while you were selecting the crew, prior to boarding your generational starship.
Your primary problem is spontaneous mutations. However if you are doing genetic test and this is a starship, you should have access to IVF technology. This will allow you to screen every embryo prior to implantation for genetic defects.

Phenotype-level selection doesn't eradicate recessives
As long as you restrict yourself to purely phenotypic selection, you're extremely unlikely to eradicate recessive genetic diseases at your population size. That's the nature of recessive alleles - they persist in carriers that don't develop the phenotype. To eradicate this, you basically need the luck that in one generation, not a single child gets passed down a mutant allele from a heterozygous parent. The same goes for "incomplete dominant" (the appropriate term to use would be incompletely penetrant). X-linked recessive are more likely to be eradicated because you will never have male parents passing these on (males have only one X which means all recessive X-linked traits manifest in male phenotypes).
Predicted number of generations till eradication
As for the population statistics regarding your recessive eradication, it's not possible to predict after how many generations this will succeed. Depending on the initial prevalence, you will have an exponential decay due to your selection. At some point you will reach a near-zero level at which you won't be able to predict when that lucky moment will happen that no child receives a mutation. A small number of heterozygous individuals could produce a larger number of heterozygotes and infinitely cause low-level recurrence of the disease. At this point it's a computational rather than mathematical problem.
Practical genetics
A simple practical example is my experience with selecting the y allele out of a Drosophila population. y recessively causes yellow rather than brown body colour (basically a form of albinism). I've made a few attempts at selecting it out by discarding yellow-bodied flies, but there were always a few yellow-bodied individuals in the next generation. The only way I've succeeded in eradicating this is by doing crosses with a low parent number (~5 individuals) so that there is a reasonably high chance of picking parents without any mutant y allele.
Possibilities for eradicating alleles
The simplest solution to your problem is genetic screening at the embryonic level, which would allow theoretically to eliminate all pre-existing heritable genetic diseases in one generation. You would need continuous genetic screening to also keep de novo heritable mutations out. As for somatic genetic diseases (e.g. paroxysmal nocturnal haemoglobinuria), you will never eradicate those without targeted genetic engineering to make the problematic hotspots in the genome more damage-resistant.
Side note regarding multiple alleles: Multiple alleles don't require special consideration for your thinking because each allele can either be recessive or dominant to wildtype alleles in its phenotype. Also consider that "healthy" isn't an absolute standard. Genetically speaking, there is no "normal". Most (all?) genes have a range of alleles that persist in nature and cause nothing we would consider a disease or defect phenotype.


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Death from too little salt?
I know that sodium deficiency can be deadly. But why is it deadly? Is it because of your muscles getting so rigid that you can't get something with salt in it? Is it because of your brain not able to send signals? Is it because of excess urination to try to get the sodium levels right? Is it because of anemia leaving red blood cell ghosts(the membranes of rbcs) in your bloodstream? Is it a combination of all these factors?

Can you define "sodium deficiency"? Hyponatremia (not enough sodium in the blood) is usually not caused by insufficient sodium intake. If you eat, you'll get enough sodium.

As @anongoodnurse said hyponatremia causes a lot of very bad things to happen to the human body. Also, as anongoodnurse said, I have never heard of it from lack of consumption. I have only heard of it when people have consumed too much water causing electrolyte imbalance and is basically just a function of osmosis. Remember that cells have aquaporins, so water is exchanged freely. This seems to be an issue during marathons. Now not consuming enough iodine can be a problem, but that is different than hyponatremia.

I mean too little sodium in the whole body when I say sodium deficiency. In other words not only is the blood affected but everything else that needs sodium(muscles, neurons, blood cells(leading to anemia), and kidneys(leading to dehydration) just to name a few. I don't mean too much water intake(mild water toxicity)

What you are suggesting pretty much will not happen. Because of osmoregulation, your kidneys recirculates the sodium to keep levels constant. It is only in cases of extremes such as water poisoning, extreme exertion, or severe gastric distress that fatal electrolyte imbalance results. On average a serving of rice and fish will give you about 410mg of sodium (a typical meal for large portions of the world). The RDA in the US is no greater than 2300mg per day, but that is the upper limit. An average serving of vegetables gives 32mg, so as @anongoodnurse said if you eat, you'll get enough.

But if, for arguments sake, you could have too little salt, then the result would likely be exactly the same as death by hypernatremia or cholera.

But in order to get the sodium concentration right the urine becomes much more dilute and that leads to dehydration. Muscles need sodium and calcium to contract and without that, they get very rigid. Neurons need enough sodium to send a signal. If it is too low it won't send a signal. And with low salt in the blood and high amounts in rbcs the water rushes into the rbcs and potentially bursts them which leads to even more dehydration as well as high blood sodium levels which can lead to high bp. It also leads to anemia which can lead to cyanosis from low oxygen.

Basically with too little sodium, it goes from bad to worse until the heart and lungs are affected and the person dies.

@AMR - drugs, SIADH, and a host of other things cause (chronic) hyponatremia as well. That doesn't mean you're incorrect about what you've stated, though.

Part of this depends on the exact nature of "salt depletion" you're referring to. I have never actually heard of a case of hyponatremia being caused by low consumption of salt. We don't need to consume NaCl. It's present in the foods we eat in adequate amounts. We may want to salt our food, but it's not necessary for life.
Hyponatremia is an electrolyte imbalance, be it due to excess intake of H2O, inappropriate H2O retention, excess Na+ loss, hyperglygemia or other osmotic force, or other cause. For ease of explanation, I'll address acute hyponatremia, as it leads to death more rapidly. Hyponatremia kills because of the difference in the concentration of sodium across cell membranes.
Normal serum Sodium (Na+) is ~140mEq/L. Acute severe hyponatremia occurs when serum Na+ falls rapidly below 120 mEq/l (some authors use 125mEq/L) in less than 48 hours.
Water accounts for 60% of total body weight, with approximately two-thirds being intracellular and one-third extracellular; of that extracellular water, ~75% is in the fluid between/surrounding cells, and 25% is in blood vessels. Distribution of water/Na+ throughout the body is very tightly regulated.
When serum sodium falls too low, free water moves from areas of lower concentration to higher (into the cells). Tissue becomes edematous.  While this isn't a great problem for some tissues, it is for the brain.
The brain is enclosed in a rigid compartment (the skull) with a small amount of fluid (cerebrospinal fluid, or CSF) surrounding it. Inferiorly, there is an small opening called the foramen magmun, where the brainstem leads to the spinal cord.

When water moves from the blood into the cells of the brain attempting to establish osmotic equilibrium, the brain compensates for the increase in volume by forcing CSF out. This buys some time, but not enough; there is headache and nausea. As the brain continues to expand, intercellular fluid is forced out into CSF (which is being displaced by the brain.) This causes hyperexcitability which leads to seizures. In the meantime, astrocytes swell. Blood flow to the brain is reduced because of increased intracranial pressure, which further damages the cells, increases cellular edema and coma ensues.
If this isn't bad enough (it is; it's an almost irreparable  cascade of events), the edema can actually "push" the lower part of the brain down through the foramen magnum resulting in brain stem compression and respiratory arrest. At this point, few people make it back intact with even the best help.
You say,

Basically with too little sodium, it goes from bad to worse until the heart and lungs are affected and the person dies.

Not really. In acute hyponatremia, the brain goes before the rest. Once the brain goes, so follows the body.
in layman's terms
not layman's terms but still easily understandable

It is a big problem for the rbcs as well. Water rushes into the rbcs and they burst leaving behind their cell membranes. This helps balance the sodium levels but it leads to anemia. Anemia then leads to less oxygen transport. Less oxygen transport leads to faster heart rate. This eventually isn't enough to raise oxygen transport because it makes atherosclerosis related heart problems more likely and widespread.

Um... no. I don't think you're prioritizing the effects of hyponatremia. Hemolysis isn't one of the major players in morbidity and mortality from hyponatremia. The red blood cells have leeway. The brain does not. If you already have strong opinions about all this stuff, why are you asking this question?

I am talking about chronic here, not acute. In chronic sodium deficiency it is mainly urination, blood, and the heart and lungs that are affected as well as neurons and muscles

@Caters- I really think you should post your own answer with references. I'm always up for learning new stuff!


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Large coalitions of lions taking over multiple prides?
I have noticed while watching lion documentaries that coalitions with more than 3 males tend to take over multiple prides and have 1 large pride in their territory while coalitions with 3 lions or less tend to take over just 1 pride.
As a very good example the Mapogo brothers(6 lions) take over multiple prides and they even split the territory between a coalition of 4 and a coalition of 2.
On the other side of the spectrum Tau and Banda are just 2 lions in a coalition. They take over just 1 pride with 3 lionesses in heat and no cubs. Tau does it by instinct and Banda is strategic.
Why is there so much of a difference between the small coalitions that take over just 1 pride and the large coalitions that take over multiple prides? Do large coalitions do better when they take over multiple prides from less aggression? Do small coalitions do better when they take over just 1 pride from more and closer defenses against other male lions?

In which documentaries did you learn about this? I want to learn more :)


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Why do I often see male robins with female robins?
Even when it is not breeding season for robins I still often see male robins with female robins. But why?
I know that the male robin often chirps to find female robins within his territory. I also know that the male robin puffs his chest to try to impress a female robin.
But I have seen out in the country that even during the fall and late summer the male robins are still with female robins. I don't know whether it is to raise their fledgling chicks or what because only in videos and pictures have I seen robin chicks and robin eggs.

Male and female robins have the same habitat, so it is not surprising you see them both in the same area. Robins do not mate for life, but do stay together during the full breeding season, which may include 2-3 nestings. Sometimes in the spring a particular male and female will return to the same territory, and may end up staying together for another year, especially if they successfully raised chicks together the previous year.

@MattDMo You can probably expand your comment into an answer if you want.

This has since been asked and answered at http://outdoors.stackexchange.com/q/10290/66 - dunno if you want to close it here?


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Big cat in heat for months?
In this documentary about a lioness and a leopard the leopard is in heat for months.
https://www.youtube.com/watch?v=MGqmylkOuKw
Usually a big cat would be in heat for 5 days and then not in heat for 27 more days. Doesn't matter if it is a lion, tiger, cheetah, jaguar, or leopard, they have a very similar estrus cycle.
Why then is this leopard in heat for months until she finally becomes pregnant? The lioness is only in heat for 2 days because after 48 hours she becomes pregnant. In fact the lioness has 2 litters in the same period of time as the leopard has 1 litter.


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ATP required for cell processes
I haven't been able to find anything that tells me how much ATP is needed for DNA replication, transcription, and translation in humans, just papers that mention ATP used in those processes.
I need to know how much ATP is needed for these processes because once my cell from scratch is alive I feed each cell 50 nanograms of glucose which yields 5 trillion ATP. If I use these numbers plus the numbers for other metabolic processes I get roughly the amount of ATP needed per cell before mitosis. If I know this then I will know if I need to feed my cells more glucose or if 50 nanograms is enough.
So how much ATP is needed for DNA replication, transcription, and translation? I want it in terms of per nucleotide and per amino acid so that I can multiply that by the amount of DNA total, amount of DNA in any given gene, and amount of amino acids in any given protein.

This is difficult to answer. Do you wish to include the ATP required to synthesize nucleobases, nucleoside triphosphates, amino acids, charged tRNA, etc?

I have given a rough answer and you can go into finer details (like accounting for NAD). You have not done any research towards the question and I am inclined to close the question.

The information you provide is not nearly enough to figure out the energy needs of a cell before mitosis. You need to measure at least glucose uptake, lactate release and oxygen consumption, and do growth curves. Every cell line is different, so you need data on your cells. See http://www.ncbi.nlm.nih.gov/pubmed/14697210 and http://www.ncbi.nlm.nih.gov/pubmed/5817088. But you don't need to know this just to culture cells --- as long as they grow and look healthy, and the medium pH is not to low, they have enough glucose.

Culture media for mammalian cells usually contain 1 to 4 gram/l. For example, when 10^6 cells are seeded on a 10 cm dish, you could grow them to about 10^7 for several days using 10 ml culture medium. For some cells you might have to replace medium with fresh one once before they reach 10^7 cells. You could know how much cells need glucose practically. When you have pyruvate in media, it goes TCA cycle so that glucose is not only the source of ATP.

In addition, ATP is required for sugar modification of proteins, protein phosphorylation, and probably amino acid and lipid synthesis as well as mechanical cell movement, vesicle transport, chromosome segregation and ... what else...

I myself have done research by trying to look up how much ATP is needed for DNA replication, transcription, and translation and finding out that ATP is involved in all of these processes.

Well I am growing totipotent stem cells which I am planning to differentiate into all kinds of cells and then build organs cell by cell at newborn size. Totipotent stem cells I assume would take the average amount of energy of all human cells including trophoblasts and embryonic stem cells.

For DNA replication and transcription you need NTPs. In a dsDNA purine content will be same as pyrimidine content. I am considering that all nucleotides are synthesized de novo which would consume more ATP than getting nucleotides from the salvage pathway.

Fig 1: Pyrimidine synthesis. Taken from Wikipedia.

Fig 2: Purine synthesis. Taken from Wikipedia.

CTP synthesis requires one extra ATP:
UTP + Glutamine + ATP + H2O → CTP + ADP + Pi
UTP synthesis requires 2 (Step 1; Fig 1) + 1 (Step 5; Fig 1: PRPP requires 1 ATP to form) +  2 (UMP → UTP) = 5 ATPs
CTP requires 6 ATPs
GTP requires 8 ATPs (Fig 2) (ATP synthesis would also require 8 ATPs but for simplicity let us assume that ATP is already present).
Conversion of dNTP from NTP requires thioredoxin which in turn requires NADP but let us forget that.
Assuming a 50% GC content one base pair of DNA would require in an average 10 ATPs (assume a stretch of 4nt — ACTG, this would require 1+6+5+8 ATPs; i.e. 5 ATPs per nt; 10 ATP per bp)
For RNA the ATP consumption would be 5 ATPs per nt.
For protein synthesis, for every codon, the elongation factor requires one molecule of GTP and aminoacyl-tRNA synthetase requires 1 molecule of ATP. So the net consumption per amino acid would be 9 ATPs.
I am ignoring the initiation reaction that also requires ATP to phosphorylate the initiation factor. Also, I assume that amino acids are obtained from diet and are not synthesized by the organism.


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How to secrete a recombinant protein from E. coli?
What are some secretory pathways that can be used to secrete a recombinant bacterial enzyme from E. coli?
I have a recombinant protein (29kDa) that I will express in E. coli BL21 cells.  For now I have been sonicating E. coli to extract the enzyme, but in the future I would like E. coli to secrete the enzyme.

I think E.coli doesnt have secretory system. You might have to use Bacillus spp. which have a secretory system. Also, you need to add a secretory signal sequence at the N-terminal of the protein.

According to the 2012 iGEM Kyoto team:

The Twin Arginate Translocation pathway(TAT) is [an endogenous] secretion system in E.coli. This system can carry proteins that have torA signal amino acid sequences at N terminal. TatA, TatB, TatC and TatD compose Tat complex on inner membrane. Tat complex recognizes torA signal peptide and then it transports protein (with torA) from cytoplasm to periplasm. In addition, protein that has passed through TAT pathway cut off the torA signal. Proteins which are secreted by this system have no tag that obstruct the activation of the protein.

The team created a cassette with the TAT genes to increase the expression of the pathway and also included the Kil gene, which perforates the outer membrane, possibly aiding the external diffusion of the secreted protein. They noted, rather tongue-in-cheek, that

Needless to say, function of outer membrane as membrane is essential for E.coli to survive. In other words, overexpression of Kil causes cell death. In this reason, we must find suitable amount of expression.

Note: according to their lab notebook, the team never observed extracellular GFP via confocal microscope (search that page for 'confocal'). So. Beware :)
Their project page also includes some references to the following literature:

Tracy Palmer and Ben C. Berks "The twin-arginine translocation (Tat) protein export pathway"
J. H. Choi. S. Y. Lee "Secretory and extracellular production of recombinant proteins using Escherichia coli"
G. Miksch · E. Fiedler · P. Dobrowolski · K. Friehs "The kil gene of the ColE1 plasmid of Escherichia coli controlled by a growth-phase-dependent promoter mediates the secretion of a heterologous periplasmic protein during the stationary phase"
Brad A. Seibel* and Patrick J. Walsh "Trimethylamine oxide accumulation in marine animals: relationship to acylglycerol storage"


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DNA gel extraction: chemical contaminants
I am performing a gel extraction to purify DNA after a double digest with EcoRI and BamHI.  After the gel extraction I need to complete a ligation step before bacterial transformation.  The problem I am having is that the DNA after the gel extraction have some kind of chemical contaminant that won't allow me to quantify the DNA using the Nanodrop spectrophotometer.  I am getting very low 260/230 ratios.
Has anyone had some issues with this?
I am using the Qiagen Qiaquick Gel Extraction Kit.

It could very well be that your digestion isn't proceeding very efficiently and you're just getting low yields. Do you have high A260 and A230 readings both?

Agree, you should check the reading before digestion and see what amount of DNA you're working with.

Have you tried using alternative DNA measurement methods like a Qubit?

That always happens to me but my yields and DNA are always fine. Running it on a gel to check the amount works just as well even if it takes a little longer

I am going to follow the advise I found ( http://seqanswers.com/forums/showthread.php?t=15165 ) and get back if it works.

Here are some possible reasons:

Your yield is very low, which you can infer from a low 260 absorbance. Either make sure your restriction digest is efficient or add more substrate to the digest reaction.
Carbohydrate contamination, which will cause high 230 absorbance. Wash the column one more time with buffer QG (the step is described in the Qiagen gel extraction manual; if you're already doing a wash with buffer QG, do an extra one).
You didn't dry the column enough and some ethanol from the wash remains in the sample. This can also cause high 230 absorbance and your sample with smell of ethanol. Place your column in an empty collection tube and spin it down for a long time (15-20 min). Don't worry, the DNA can withstand it.

I tried your suggestions but still no luck.  I checked the concentrations of the plasmids before digestion and I had about 1000 ng/ul.  I did the additional QG wash step.  I also spun the residual ethanol out for 20 minutes.  I even did an non DNA gel extraction and ran a spec using a Nanodrop with a water blank and its not clean.  I have done many of these before but I am in a new lab now and I don't get quality extracts like usual.  I will give a new kit a try and see what happens.


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How to ligate DNA to an RNA molecule
Is it possible to ligate a small DNA molecule to mRNA?  I was reading a protocol from Current Protocols in Molecular Biology and one of the procedures involve ligating a DNA molecule to mRNA using a DNA splint that overlaps between the 5' of the DNA molecule and the 3' of the mRNA.
Would a reaction like the following work?
5'-phosphorylated DNA linker
mRNA library
DNA splint
T4 DNA ligase + buffer

T4 ssRNA ligase will work for this.. Check this page on NEB site.


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Making sense out of the visual representation of transcription
Most people are familiar with the following diagram. Some genomic DNA with a promoter region, exons and introns. This is transcribed into RNA that is then translated into a polypeptide.

When we look closer at the strand that is being transcribed we can distinguish between the two as the sense and anti-sense strands.

So the transcription factors and RNA polymerase bind and begins transcribing mRNA in the 5' to 3' direction and thus reading the anti-sense strand in the 3' to 5' direction and have the same sequence as the sense DNA strand, substituting U for T in the mRNA.

My question would be, shouldn't the exons be numbered in the reverse order as shown in the first picture I provided. So instead of Promoter -> Exon1 -> Intron -> Exon 2, should it be, Promoter -> Exon N -> Intron -> Exon N-1?
Also, in bioinformatic sites are the gene sequences listed in the sense or anti-sense strand? I have noticed in some bioinformatic tools, to determine what polypeptide will result from a DNA sequence, one must input the sense strand in 5'to 3' orientation and not the anti-sense strand.

All visual representations and nearly all coordinate systems are based on the sense strand. The polymerase machinery has no clue about what is sense and what is antisense, because each is the antisense of the other.
For visual representation this makes much more sense and relays more information as it removes the extra complicated layer of information. And, in most cases the gene structures are declared in the order of the reference genome which is always the positive or sense strand.
Next coming to the bioinformatics part, most of your databases such as UCSC, Ensemble and NCBI maintain gene coordinates on the reference genome, But, there's a catch, when reporting the information through a bed file,
Negative stranded genes are reported as chromosome stop start by NCBI (last I used it was a one a half years ago), UCSC will provide the chromosome start stop and both will report the strandedness, UCSC expects that you the bioinformatician will create the reverse complement when you find the strand information, while NCBI expects that your program will fail a sanity check because stop - start will come as negative, implying that you cannot make a mistake while parsing NCBI bed files. Furthermore, UCSC indexes are maintained as 0 based, while NCBI is maintained as 1 based.
I would urge you to validate this information
But why not just keep a negative strand as well? while keeping the gene coordinates and elements for the antisense in the format you just mentioned.
Because speaking from a Computational point of view it just makes more sense, this system would consume more storage (please remember the entire system was formulated before storage became as cheap as it is today) it would consume more memory during tasks (exactly double of what it is consuming today). So it's just better to have a positive strand reference genome and all genes and elements based on that.
Just an example of how alignment of sequencing reads works,

You align your read to the reference genome
Aligns? If yes it has mapped to the positive strand
No? Reverse complement the read and align back
Aligns? If yes it has mapped to the negative strand
No? Possibly an erroneous read or other artefacts.

GTF/GFF3 has the start stop order along with strand orientation. I think this has become more or less a standard format for annotations for all repositories.

Gene sequences are annotated in the sense strand. So, these diagrams are correct.

In the top diagram, the ATG start is on the left, and the stop codon is on the right.  Exon one is the left most exon.  That's all correctly illustrated.
If you look up a transcript sequence in, say, ensembl, it will be the same way, the start sequence will be in the beginning, the stop codon at the end.  That's the convention.


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How much can be said about behaviour (future) based on bloodgroup?
My bloodgroup for example is A+. How much information is knowing my bloodgroup? How much information can be known from a blood sample? I expect you to be able to clone if known a complete DNA sequence but how much would I recognize myself from a clone you make from my DNA e.g. behaviour?

There are quite a few questions in this post, in future you might want to split them up to receive better responses.

If I know you are A+ I know that you express a certain protein and not another one on your red blood cells. That's it. Note that there are thousands of different proteins in our body. I can probably know much more about your behaviour by Googling your name.

I'm not sure if you talk about personal matters or actual body behviour now. I meant for instance the behaviour of a leg or an arm or my physiology (and not so much online consumer behaviour or profiles)

The neurological basis of behavior is still unclear, and the genetic basis of behavior is even less clear.  What can be said is that genetics may predispose you to certain behaviors, but what the predisposing factors are, and how much they determine your behavior (and how much is due to environmental factors), is unclear.  And this varies for different behaviors -- if you want to read more about a particular behavior, you can try looking up the genetics of addiction.
If we want to examine the genetic basis of behavior, I don't think anyone would be looking at blood group, which is due to some physical characteristic that is not obviously linked with behavior (versus a differently structured neurotransmitter receptor, which is possibly more related). It's like using your height to explain your behavior.
EDIT: On cloning:
I should also mention that human reproductive cloning has not been successfully attempted, and if it were, you wouldn't get an exact copy of the donor of the genetic material (by the current technologies).  The most famous example of reproductive cloning, Dolly the sheep, required more than just nuclear DNA:

Dolly or any other animal created using nuclear transfer technology is
  not truly an identical clone of the donor animal. Only the clone's
  chromosomal or nuclear DNA is the same as the donor. Some of the
  clone's genetic materials come from the mitochondria in the cytoplasm
  of the enucleated egg. Mitochondria, which are organelles that serve
  as power sources to the cell, contain their own short segments of DNA.
  Acquired mutations in mitochondrial DNA are believed to play an
  important role in the aging process.

The source also has more information about cloning: http://www.ornl.gov/sci/techresources/Human_Genome/elsi/cloning.shtml


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How T-Cell recognizes a cell infected by a virus?
According to few articles I read (like BBC about The people with hidden immunity against Covid-19 ):

starting out about four or five days after infection, you begin to see T cells getting activated, and indications they are specifically recognising cells infected with the virus,” says Hayday. These unlucky cells are then dispatched quickly and brutally – either directly by the T cells themselves, or by other parts of the immune system they recruit to do the unpleasant task for them – before the virus has a chance to turn them into factories that churn out more copies of itself.

When virus just entered a cell, but had no chance to churn more copies: Is surface of the cell any different? How T-cell can distinguish infected cell from non-infected?
I am no biologist, but I am fascinated about biology now, and curious to learn more. Sorry if I am not using proper terminology.
I found How do T-cells determine which cells they've already inspected? , but T-cell activation is mentioned only in the context of dendritic cells and lymph nodes. IIUC, T-cells should attack lungs cells to eliminate cells infected by covid-19 there.

Otherwise the coronavirus spike has a signal peptide and a transmembrane domain making it  secreted and anchored onto the cell's surface

All cells chew up internal proteins all the time - it's part of the normal activity of cells to recycle those proteins into amino acids to be rebuilt into other proteins. The first step is chopping up the protein into peptides by the proteasome.
When a virus infects a cell, one key thing it needs to do to replicate is to have the cell start making viral proteins. However, some of these get chewed up, too.
Some of the peptide fragments get bound to major histocompatibility complex class 1 (MHC-1) molecules. These are then transported to the cell surface. This is the cell advertising "hey, this is what I've found in the trash lately."
Sort of like antibodies, T-cells only bind certain antigens, and during development the immune system learns which antigens are self versus foreign by process of elimination: if you detect it during development, it must be yours. Everything else is fair game to attack. When a killer T-cell binds strongly to the MHC-1:peptide complex, it recognizes that this is a foreign peptide and the cell presenting it must be infected or damaged in some way, and this starts a cascade that leads to apoptosis of the infected cell.


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Is it logical for someone to be allergic to the water molecule, but be perfectly fine with drinking milk since it's only 87% water molecules?
Recently this article got into the tabloids. The comments were disabled very quickly. Strange.
The authos says she has Aquagenic Urticaria but it is a skin condition not an allergy, and hence wouldn't cause an internal reaction like she says. She claims that drinking milk does not cause her mouth and throat to blister.
If she is truly allergic to the water molecule as she claims, does it make sense that water with fats and sugars dissolved in it doesn't cause a reaction and she also doesn't have a constant reaction to her internal bodily water?
I've come across at least a dozen cases of women claiming they are allergic to the water molecule and die if they drink water so they drink milk/tea/diet cola instead.
So here we have yet another supposed case of someone having antibodies against the water molecule and being 100% healthy as long as they do not drink water. Does this match up to reality or medical science?

Please don't ask the same question twice.

Short answer
Aquagenic urticaria is though to be caused by dissolved allergens in water and not by water per se.
background
Aquagenic urticaria is a rare condition in which urticaria (hives) develop rapidly after the skin comes in contact with water, regardless of its temperature.
Water allergy in itself is obviously a ridicule, as up to 60% of the human adult body is water. In fact, water is essential to our very existence (Fig. 1). Auto-immune responses to water would be disastrous, as pretty much all of our body would be attacked, likely resulting in anaphylaxis — a potentially life-threatening emergency. Further, small molecules typically are non-allergenic. Examples of allergens are, e.g.., chitine (a large polymer), drugs and even macrostructures such as pollen, all of them a lot bigger molecules than water.
Instead, Aquagenic urticaria is thought to be caused by a substance dissolved in water that enters the skin and triggers an immune response. In this theory, the hives are not caused by water, specifically, but rather an allergen in the water. What also may be the cause is an interaction between water and a substance found in or on the skin generates a toxic material, which leads to the development of hives (Park et al., 2011).
Reference
- Park et al., Ann Dermatol (2011); 23(3): S371–S4.

Fig. 1. Water is essential for a lot of processes. source: USCGS

How does aquagenic urticaria explain these particular cases going into anaphylaxis if they drink just a mouthful or sip of water?

Allergens dissolved in the water - see above :)

Are there also allergens in milk? The first girl claims she only survives on 4 150 ml glasses of whole milk a day, so it's implied she still reacts, but not as bad as rainwater or tap water in her mouth/throat.  She avoids watery foods and lives on cereal without milk and biscuits,  She also reacted to a drip because it was water based.

Yes there are allergens in milk, but other ones. The allergens the girl is responding too are present on her skin.

But she goes into anaphylaxis if she drinks water. So it's something different than just something on her skin because her internal body has a more severe reaction compared to water on the skin

This answer is unlikely to be helpful to the poster, who seems to have some sort of obsession with this question. It's unclear what she's trying to get out of asking it. It is not an answer.

I'd note, this is not the first time a user (possibly the same individual) has repeatedly cross posted this same question.

@DeNovo thanks for pointing this out; I didn't know. It actually looked like a rather well-researched question to me at first glance.

Small molecules can be allergenic if they bind to protein: https://biology.stackexchange.com/questions/7905/what-is-the-smallest-molecule-that-can-present-as-an-antigen-to-the-immune-syste


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Is this "Sympathetic fight response" axis accurate?
Peripheral sensory cell > Preganglionic cell > Dorsal root ganglia cell in the ''Sympathetic chain'' > Ventral root ganglia cell in the ''sympathetic chain'' > Post-ganglionic cell that activates an organ such as the pancreas (or a muscle).

The typical axis of the fight response is depicted in Fig. 1.

Fig. 1. HPA axis. Source: Social Psychology principles
This axis is the hypthalamus-pituitary-adrenal axis, or HPA axis. It mediates not only the fight response and is typically referred to as the fight-flight-fright response. It is the central stress response system that prepares the body in a fraction of a second for survival, basically under the influence of adrenalin and cortisol produced by the adrenal glands.
The circuit you are describing, by the looks of it, is more typical for a reflex arc (Fig. 2.).

Fig. 2. Reflex arc. Source: Sweetibnotes
A typical example of a reflex arcs is the pain-withdrawal reflex. Although the sensory stimulus triggering the reflex arc may also trigger the HPA axis, the basic circuitry of a reflex arc does not include the HPA axis. The pain-withdrawal reflex, for example, is basically designed to jerk a limb away as fast as possible in the presence of acute pain as a protective mechanism.


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Is there a way to know how many sodium channels are active (conducting) at a given time in the brain?
I was doing some reading about anti-epileptic sodium channel blockers, then wondered how many sodium channels are actually conducting (actively passing ions) at any given time, that is, in an "average, awake" brain?

Welcome to Biology. What do you mean with "...but how many are active anyway?" As a side note, Na+ blockage is just one way of suppressing epileptic activity. Lamotrigine, as an example, has a host of other characteristics. In the case of carbamazepine, listed as a Na+ blocker and first-line treatment for generalized epilepsy in adults, it specifically blocks activated channels. So the number of channels blocked depends on brain activity. In a nut shell, I think your question needs specification (e.g., type of drug).

No, it is not on the blocker that I need an advice. I just tried to explain the way my reasoning went. What I mean is in the question : at a given time, in an "average, awake" brain, how many sodium channels are indeed conducting (actively passing ions).

I edited your question and retracted my close vote. Feel free to roll back, but I think it's quite clear now what you're after.

Unfortunately, there is no way to know how many sodium channels are active (or even present) in one person's brain due to the extremely high variability of channel and neuron density in a population and the lack of methodology around quantifying total number of healthy active synapses (1). Diseases like epilepsy can occur due various points of the sodium signaling process going wrong. It could be sodium channels are deformed and not accepting the proper signal, it could a low density of channel proteins, or it could be damage to the neuron themselves (2-4). No one has examined the "normal/healthy range" of sodium channels in the brain. When categorizing sodium channel deficiency scientists will often compare the number of sodium channels in a healthy brain vs. a disease brain using bioluminescence imaging or some other visualization technique. Bioluminescence specially quantifies the number of active sodium channels by binding causing healthy sodium channels light up and then quantifies density by the brightness of the synapse. This is not a direct quantification of the number of proteins, but I can not think of any technique that allows you to count the number of proteins on a cell without damaging the cell. I'm sorry this isn't technically an answer to your question, but hopefully it provides some helpful references to understand molecular brain protein imaging.

Principles of Neuroscience
Low Sodium Channel Density and    Epilepsy
Sodium Channel Mutations and Epilepsy/ Other Nervous    System Disorders
Neuropathy and Sodium Channel Related    Diseases

This is a difficult question because we are talking about properties of channels-molecules which can have stochastic opening and closing rates. The question is made even more difficult by the fact that there are multiple types of sodium channels. One can begin to quantify this by recording from many many cells in the awake animal using in-vivo electrophysiology by washing in sodium channel blockers and looking at sodium currents. Conversely you can start doing antibody staining for sodium channels in a brain area -- then take acute slices from that area and do single-channel recordings so you have some sense of number* probability of opening.