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How can dehydrogenation steps in some biochemical pathways produce ATP?
Dehydrogenation reaction of alkanes is inherently endothermic as one removes two thermodynamically more stable C-H bonds and replaces it with one less stable C=C. Although the product is conjugated with the carbonyl group, this stabilization should be negligible, shouldn't it?
How comes then according to the scheme below, the result of this reaction are two high-potential electrons capable of forming ATP from ADP? Is the reaction concerted with some other not shown here? Or is the enzyme regenerated afterwards with some input of energy?

cross-post https://chemistry.stackexchange.com/questions/86929/how-can-dehydrogenation-steps-in-some-biochemical-pathways-produce-atp

You have to consider the full redox reaction to determine if the reaction is favourable or not. It's not correct to think of enoyl-CoA alone as "higher energy" than acyl-CoA, because of the free energy difference $\Delta G$ of the half-reaction:
acyl-CoA  $\leftrightarrow$  enoyl-CoA + 2 $e^-$
cannot be determined without knowing what the electron acceptor is. You might be thinking of the enoyl group as "higher energy" because it is reactive towards H$_2$ (as in hydrogenation reactions), but that's not the relevant redox couple here.
In this case, we should consider the energetics of the entire process of electron transport, as shown in your diagram. Since the intermediates (FAD, ETF, quinones) all cancel out, the overall reaction without ATP synthesis is:
acyl-CoA + 1/2 O$_2$ $\leftrightarrow$  enoyl-CoA + H$_2$O
This reaction is highly favourable, with a $\Delta G$ of about -150 kJ/mol, because O$_2$ is a very good electron acceptor. (See this site for free energy calculations.) This is more than enough to drive ATP synthesis (about 45 kJ/mol).

The reason is that the reaction is not solely a dehydrogenation, but more properly, oxidation of the two central atoms.
In the C-H bond, the C is more electronegative, which means the electrons they share will be more on their side - the carbon is in a reduced state. In the reaction you pointed, it's not only the H+ that leaves, but also one electron per H+ (so that makes one H atom leaving, but since electron was more of the C than the H, it's actually the C that is losing an electron - being oxidated). Those electrons are then stored on an electron carrier (FAD --> FADH2), which goes on to provide those electrons to the electron transport chain in the mitochondria, enabling the production of ATP. (know more about this process: https://en.wikipedia.org/wiki/Oxidative_phosphorylation)

But where do you take the energy to remove those hydrogen atoms (protons with electron)? From what you wrote it seems that you 'magically' remove electrons from more electronegative element producing intermediate higher in energy (Enoyl-CoA), and then you use those same electrons to produce even more energy stored in bond energy of ATP?! From this it seems, that it must be there some kind of concerted exergonic reaction that drives the reaction.


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Strongest bone in body
AS internet  tells is it is thigh bone which is strongest, but why, it carry only upper part of body, does not heel or any foot bones should be strongest in body as they carry full body weight ?

No, foot bones don't carry full body weight, the weight is distributed half between two lower limbs, then again half at foot between calcaneus and big toe , small toe heads. So, foot bones may not be carrying as much weight as femur.

@JM97 as a student of physics I must say all weight on  standing at least must fall on Talus bone of heel, as F=mg works toward center of earth

Again, I would say neck of femur is stronger since it's not breaking eventhough it's not in line with the direction of weight. Neck of femur is withstanding more force( due to the torque).

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Why have a placebo control group when testing a new drug if existing drugs can be used?
It is general practice to compare a new treatment against a sham treatment (placebo), and then use those results to compare efficacy of the new treatment (call it B) to an existing treatment (call it A), at least when existing treatments are available.
However, it seems reasonable and more ethical to use A and B together in a study, rather than giving one group a sham treatment. In other words, instead of a placebo group and a treatment group, why aren't there two treatment groups, one with A and one with B? Statistical noise such as regression to the mean, natural progression of the disease, etc would all show up in both groups, so if B gave better results than A, we should be able to say directly from that result that B works better than A, and we would be doing so in a more direct way than comparing the effect sizes of B vs placebo to the effect sizes of A vs placebo.

While more ethical and reasonable, and often / usually legally required, comparing a drug to another drug can also has one potential draw-back: assume that drug A) improves survival from 1% to 10%, and drug B), which would be tested after A), would improve from 10% to 11%. In this case it might be practically impossible without a large group of patients to statistically show an improvement over A) - as the potentially less sophisticated, drug A) would have already been released

I fail to see the point.

@DonBranson I see nothing wrong with them knowing they may be given the 'placebo', as long as they don't know which one they are ('placebo'/other drug vs the drug being tested)

Ben Goldacre talks about this is in his book "Bad Science" for a fair while. He makes the point that good science now-a-days compares against the current market leader, while bad science compares against a placebo. It's relatively easy to do better than placebo. It's also worth noting that just because a drug doesn't do outright better than the market leader doesn't mean it isn't useful. For example, it may be applicable to people with certain allergies or have a less intense dosing regime. It may be able to be used in a combination therapy while the market leader can't.

When you want to check if your light bulb is broken or not, do you flick the light switch and see if the room gets illuminated; or do you measure the difference in light intensity between one room and another? The two tests are completely different. The first tries to confirm that the drug works; the second compares the drug's working to another drug. You're essentially suggesting that a driving exam (testing aptitude) can be done by having students race (testing who's best) and giving a driving license to whoever wins the race (as they are clearly better at driving than the others).

(To finish my thought) Relative results are potentially meaningless. That student who wins the race may be better than the other students, but that doesn't give you an objective confirmation that the student actually meets the required skill level for driving a car in traffic.

@Flater Relatively studies are meaningless with no base idea. Obviously, to get to large scale human studies, you have to prove that the drug is non-harmful (to the extent that harm can be expected for the treatment). When Doctors are comparing medication, they're not concerned about whether the drug has passed FDA approval, they're concerned about who "won the race", as per your example. The driving test is FDA approval, the race is the treatment comparison.

@Don Branson: You would just ask all patients for allergies against anything in A, anything in B, and additional other random allergies that might generally influence results (as some allergies might interfere with how they feel in general, which is something you might be asking about regularly)

@SGR: This may be going out of scope for my on-topic knowledge, but isn't there more than one measure for the effectiveness of a drug? Assuming that drugs are rated by "winning the race", why would we still commonly have many different types of pain killers etc. available, instead of just the "winner"? Aren't there other considerations too, e.g. having lower efficacy but avoiding otherwise undesirable side effects? Who would win in a race between ibuprofen and paracetamol, and why are both still available if one wins over the other?

@Flater Yes, there are, which I highlighted in my first post. I was reducing my argument down to your analogy. To expand on it, a Doctor isn't concerned about whether the light turns on or off, but whether the light bulb they're considering using is brighter, or more energy efficient, or the hue is better for reducing eye strain, etc. They assume the light bulb works and only having a placebo trial just tells them the bulb is functioning.

@SGR: Sure, but comparing drugs is a second step, after you've first tested that the drug works. OP's assertion is that we can skip the first step because the second step invariably proves the first; which may be true in regards to efficacy, but not necessarily to note side effects, especially those that may be opposite. Imagine if drug A makes your skin go lighter, and drug B makes your skin go darker (but they both cure the disease). Without a placebo trial; you'd only see the relative difference, but can't tell which drug is causing the most discoloration.

@SFR: The example of discoloration is a bit simple, given that you can take pictures of the people in advance. But not every side effect is objectively measurable by an outside observer (hence why we do trials in the first place), I picked a simple side effect for the sake of example.

Flater, we're assuming that the standard of care has already been tested against something else, or a placebo. If it has been established that the standard of care works, then your argument falls flat.

You are correct. For serious diseases, it would be unethical to withhold the existing treatment (Treatment A) for a placebo. Treatment A is called "standard of care", and new treatments are compared to this.

I can't ask this as a main question, but I guess in comments it's fine. How frequently is an A vs B as opposed to placebo vs B method used, or can you at least provide an example clinical trial?

@DanielGoldman This review seems to be an extensive discussion and provides examples.

Could you perhaps expand on your answer a bit, and maybe include something from what tsttst said? I could just take your answer and the comments and write my own answer, but I think if you expanded on yours, I could tag yours as accepted.

@canadianer Doesn't seem to provide figures for rates of A vs B vs Placebo vs B, just a comprehensive answer for the question here.

It's worth pointing out that the purpose of the placebo isn't really to test against no treatment, it's to test against the belief of receiving an effective treatment, for both the subject and the researcher.  Loooong answer incoming...
Firstly, it's a lovely issue with medical trials that if you get a statistically valid comparison between a group who don't believe they're taking an effective drug and a control group that know they aren't taking anything, you'll find the placebo group has a better result.  Part of it will be psychosomatic, part of it will be biased reporting of symptoms, part of it might be slight changes to routine during the trial.  The end result, though, is that a placebo treatment does tend to have a slight effect in the direction intended.
IIRC, there were some less ethical studies at one point that demonstrated that if you tell a subject that their placebo drug has negative side effects, they may actually experience those effects even though the drug has no ability to cause them.  Certainly there are studies in of the negative effects during studies not intended to cause them, documenting such things as withdrawal effects from being on a placebo course.  In the case of negative results the term "nocebo" tends to be more appropriate.
Secondly, a placebo is important for the researchers as well.  The core requirement of a double blind test is that neither the subject nor the researcher knows which treatment the subject is on.  You might be able to pull off a single blind test for a comparative test but I would personally say it would be ethically problematic for a researcher to be administering an active treatment without knowing which it was.  You can dodge the problem with a placebo by making the inactive treatment identical in administration to the active one.
If your test isn't double blind, there's a real risk of researchers having expectation bias skewing the data collecting and results.  Unchecked this can result in tests seeming to show a treatment as being far more effective than it actually is, or as having far less serious side effects than it actually causes.
Thirdly, building on those two points and more directly answering the question, you tend to need a placebo group because that can be considered a standard reference.
So, in the first case, even assuming a blind trial, there is going to be some placebo effect going on, but having only two active groups means you can't filter out that effect.  How much of the new treatment's effect was due to placebo?  Would the old treatment's group have gotten better or worse results if they knew they were on a "proven" treatment?  Would the new treatment's group have gotten better or worse results if they didn't think there was a chance of them being on the old treatment?  You can't easily and reliably answer these questions without control groups, or if you can the results still won't be accepted as readily.
In the second case the issue is that of comparability.  Even with decent correction for researcher bias you can't really get rid of the issue that the results are a comparison between two treatments.  To compare to a third you'd have to try and infer it against the existing treatment's results against placebo.  It'd go something like "Treatment A resulted in 10 more successful cases than Treatment B; Treatment B resulted in 20 more successful cases than placebo; Treatment C resulted in 40 more successful cases than placebo, so we thin Treatment C would be more effective than Treatment A when compared with no treatment at all".  How much trust would you place in that sort of reasoning?  And that's assuming you have comparisons against placebo for the other treatments... if every treatment has been measured against one or more other active treatments in studies you'll instead have some horrible network of relative efficacy to work though.  Common reference points are your friend.
That's for the simple case... now imagine the more complex case.  Your two groups are being tracked for a dozen or more data points, the new treatment does better than the old in some but worse in others.  You have lists of side effects from both groups and there's only partial overlap there.  Of course you have no control to help you remove biases and placebo effects.  The resulting paper is going to end up as a straight comparison between the two treatments and a pretty high standard of objectivity and clean structuring is going to be needed to avoid a reviewer concluding that the results are subjective and unreliable.  Trying to go from that paper to compare with other treatments is similarly harder.
It's easier to convince someone that your treatment is safer and more effective if you have clean studies to back it up.  That's not to say comparison trials aren't useful in some cases, particularly where there's a strong ethical reason for not withholding a known treatment, but I personally would prefer to have an experiment against an inactive control group before trying to compare two active processes.
I'm also reasonably sure that tests against placebo are done with the subject's expectations being managed appropriately.  Ethically the subject has to be informed that there is a chance they will be in the control group and a chance the treatment won't have the expected results.  To give informed consent to the trial the subject has to understand that the treatment might not be as good as the older treatments.  Thus while there is the ethical issue of effectively withholding treatment, it's being done with the consent and co-operation of the patient, hopefully with the intention of improving medicine as a whole.  Having a test protocol that doesn't feature informed consent is risking some serious consequences down the line due to the much bigger ethical no-no that is forced human experimentation.
Even finding a universal cancer cure won't save a researcher from a major breach of ethics in the process of finding it.

Also, be aware of the existence of counterintuitive non-transitivity in cases where you are trying to say A>B & B>C => A>C in a statistical context. Look up Nontransitive dice and Simpson's Paradox for examples.

@user6697063 yeah, Simpson's is really vicious if not accounted for.  Non-trans dice is an interesting one, the fallacy is obvious only once you're looking for one. An obvious degenerative for Wiki's example is "1/3 A > B > C; 1/3 B > C > A; 1/3 C > A > B;" to give a 2/3 chance for each of A>B, B>C and C>A

Drug companies often do exactly what you describe. That's why there are active control drug trials where there is no placebo - one group receives the experimental drug, and the other receives the "standard" treatment.
I worked on the technology side of drug trial administration for a Contract Research Organization (CRO) for awhile, and many of our clients (which included large, recognizable pharmaceutical companies) were doing this.

Approval pathways for investigational treatments for a particular indication involve a development program in which multiple studies at different phases are conducted in order to establish statistical evidence of efficacy and safety.  A well-designed program proceeds from animal studies of the mechanism of action and toxicology, to large-scale pivotal (adequate and well-controlled) studies that furnish the bulk of evidence to support regulatory filing and approval; and if approved, are followed by post-marketing studies that continue to collect safety information and how the treatment is utilized in less structured clinical settings and patient populations.
As such, early-phase clinical studies expose a limited number of subjects and may not be controlled (whether with placebo or an active comparator or standard of care).  The study population may not even have the condition being treated.  The goal here is to show the treatment is safe, or safe enough to expose a larger population to it.
Mid-phase studies are intended to begin gathering preliminary evidence of efficacy as well as to explore avenues by which efficacy can be established (e.g., endpoint selection, population selection, dose selection) in order to support the design of a pivotal trial.  These studies have medium-sized sample sizes and should employ a type of treatment control, whether with placebo, placebo on top of standard of care, or with active comparator, depending on numerous factors, such as whether there exists approved therapy for the indication or if it is an orphan indication; if it is ethical to use placebo alone; and so forth.  This is the essence of your question and to address it fully is beyond the scope of this reply.  It is the responsibility of IRBs to ensure that the trial is designed ethically and the rights of participants protected.  However, because in a mid-phase trial the goal is not to formally conclude efficacy but merely establish preliminary evidence of such, less importance is placed on comparing the experimental therapy to existing available treatments.  In these studies, it is generally acceptable to use placebo control (unless doing so is clearly unethical) and implement a protocol-defined rescue therapy option.
For a late-stage or pivotal trial intended to support NDA, there are clear statistical requirements for ensuring that the evidence for a treatment effect is in fact valid and genuine.  If a previously approved therapy is available, such a trial will generally be required to compare the experimental treatment(s) against it, in order to answer the question of whether the experimental therapy offers a superior benefit/risk profile.
The takeaway is that there are many considerations that delineate how trials may be designed:  what is the indication; who will be exposed; are there other available therapies; does the route of administration permit placebo; and so forth.  As a result, scientists and statisticians have developed numerous and often clever approaches to designing controlled clinical trials in such a way that participants are not unduly harmed, even when placebo controls are used.

"such a trial will generally be required to compare the experimental treatment(s) against it" <--- that's an interesting piece of information... who actually has that requirement?  Are we talking legal, FDA approval or medical association setting that requirement?

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Question about phylogenies and DNA sequencing
I'm reading this web page which talks about phylogenies and DNA sequencing:
https://bioinf.comav.upv.es/courses/biotech3/theory/phylogeny.html
A certain sentence says, "If we consider dolphins and sharks to be closely related because they share a similar shape we would be mistaken."
If we were to take the DNA sequence of the dolphins and sharks and compare the genes encoding for shape, wouldn't they be very similar? Wouldn't we then be able to conclude that dolphins and sharks are similar?
Or is the workaround that we would examine the entire genome, i.e. the entire DNA sequence, to see if that's the only similarity they have?

Genes reflect a phylogeny of their own. So no, the genes for "shape" (if they existed) would be very different between dolphins and sharks. Every single gene in a dolphin is more similar to its homologous counterpart in a cow than to any gene in a shark. Gene by gene, or with the entire genome, it would not matter. The similarities between sharks and dolphins are due to convergence. Convergence make sense in that there is selective pressure to have streamlines bodies to swim through the water. It is possible for genes to converge as well, but the nucleotides would differ, just as the fins on sharks and dolphins differ.

There really aren't "genes encoding for shape".  If you looked at genes encoding important metabolic pathways, it would be clear that dolphins are mammals, and sharks are not.

Ok, I see. But for example if we took really related organisms, let's say marsupial wolves and placental wolves, which are two completely different species that are unrelated. Couldn't we mistakenly conclude that they're extremely closely related even if we were to sequence their genomes? For example, we'd see that they have perhaps similar teeth, or fur, etc.

If you looked at all the coding genes, and the patterns of synteny, you would see that marsupial wolves and placental wolves looked like they belongs to different subclasses.  External similarities mask differences present at the DNA level.

There are no unrelated organisms. Wolves are related to ferns, which are related to bacteria, because life is monophyletic. Marsupial wolves and placental wolves look alike because of convergence on an efficient phenotype. However every single gene in a marsupial wolf is closer to those of Koalas than it is to a placental wolf.


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What is the symbiotic relationship between truffle fungi and their host trees?
I understand that truffles share a symbiotic relationship as they reside among the root systems of host trees, but I cannot find any material that specifies the details of such a relationship. In other words, what exactly do truffles get from their host trees, and what do they provide in turn?

Some mushrooms can fix nitrogen from the air like oyster mushrooms and Frankia, and Truffles may do, I don't know, and truffles are symbiotic with huge microorganism colonies which can breathe nitrogen, so it's a 3 way resource exchange, Trees, Mushrooms and Bacteira, making sugar from sun, decomposing organic matter into smaller molecules, and breathing nitrogen via microorganisms.   this video taught me about truffles a few months ago: https://www.youtube.com/watch?v=XMNM7AYcSLU

A truffle is the fruiting body of a subterranean Ascomycete fungus, predominantly one of the many species of the genus Tuber. Truffles are ectomycorrhizal fungi and form symbiotic relationships with the roots of several tree species including beech, birch, hazel, hornbeam, oak, pine, and poplar.
Mycorrhizal symbiosis is a mutualistic association between a fungus and the roots of a plant (usually a tree) in which (typically) the fungus obtains energy in the form of carbohydrates from the plant, and the plant gains the benefits of the mycelium's higher absorptive capacity for water and mineral nutrients, partly because of the large surface area of fungal hyphae, which are much longer and finer than plant root hairs, and partly because some such fungi can mobilize soil minerals unavailable to the plants' roots. The effect is thus to improve the plant's mineral absorption capabilities.
Based on the quote below from the website of a truffle nursery in Australia (http://trufficulture.com.au/what_are_truffles.html), it sounds like truffle symbiosis is a completely standard mycorrhizal symbiotic relationship.

The truffle coats the tips of the tree roots to form mycorrhiza which
  act as an extension of the tree's root system. The tree provides the
  truffle with a source of photosynthesised carbohydrates, and in return
  the fine, thread-like filaments (mycelia) of the truffle, extract and
  trade soil minerals and nutrients which would normally be unavailable
  to the tree. Thus the mycorrhiza is able to increase the effectiveness
  of the trees roots, enabling the tree to grow in soils which would
  normally be too nutrient deficient to support them.


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How can myoglobin be responsible for the red color of meat if it is located in the cytoplasm?
How can myoglobin be responsible for the red color of meat if it is located in the cytoplasm, as the visible part of muscle cells is the membrane (at least as I believe)?
Sources:
https://en.wikipedia.org/wiki/Myoglobin
http://jeb.biologists.org/content/207/20/3441

Presumably for the same reason that red cells are, well, red.

— I am not a moderator. As a retired educator I believe that students learn better if they are asked to think about their questions. The additional examples I provided should suggest to you that cell membranes are effectively transparent — think about any other pigmented cell. So your question becomes one of the optical physics of biological membranes. I suggest you phrase it in those terms and submit it to a more appropriate list.

+David I don't see any example you've provided, maybe due to a server error. Secondly, I didn't know that cell membranes were transparent; in any case it would have been better if you had answered normally and not only by letting a comment. Thanks!

I am not a physicist, which is why I phrased the comment the way I did. I presume cell membranes must be transparent from examples such as haemoglobin but I cannot answer the question why, which presumably lies in the realm of biophysical optics.


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Functional role of the myelin sheath
One usually reads that the functional role of the myelin sheath is being a good insulator, accelerating the speed of action potential propagation along the myelinated axon.
I tried to understand this and came up with these possibilities:

The immediate reason why action potential propagation along myelinated axons is "faster than normal" is a relative lack of leak channels in the membrane. I.e. it is the membrane of the neuron (not the myelin sheath itself) that is a "better insulator than normal". Why there are no leak channels underneath the myelin sheath would be another question. But the myelin sheath would probably be one of the reasons. Thus, it would be an insulator only "indirectly".
Or there are leak channels, but there's no place to go for the ions out of the neuron (no extracellular fluid to diffuse to)?In this case, it would be the myelin sheath that is the "immediate" insulator. But the leak channels would be useless. (So why to maintain them?)

So my question is:

Are there significantly less leak channels underneath the myelin sheath than normal,
  or not?

The myelin itself is an insulator. It wouldn't matter if there are leak channels under the myelin sheath or not: they are covered by a thick, fatty, non-conductive layer of folded membranes. Your title "Functional role of the myelin sheath" is not really related to the question you ask "Are there significantly less leak channels underneath the myelin sheath than normal, or not?" The answer to the second question has nothing to do with the function of the myelin sheath, the question would be whether cells have trafficking mechanisms to keep leak channels out of places where they are useless.

I disagree with your last sentence, starting with "the answer to the second question": The myelin sheath itself might be a cause and part of a trafficking mechanism to keep leak channels out of place... and so has possibly to do with it.

@BryanKrause:  You say "it wouldn't matter if there are leak channels under the myelin sheath or not". I claim: it does, because it is expensive. (It would be cheaper not to have them, without loss of functionality.)

"I claim: it does, because it is expensive" - exactly, but then we aren't talking about the function of the myelin sheath anymore, which was the title of your question. Do you want to ask about function of myelin? If so, the presence of leak channels under the myelin is irrelevant. Do you want to talk about efficiency? If so, then the function of myelin is irrelevant.

This is already answered here

@BryanKrause: Why not just accept that these two questions are tightly and obviously related?


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Treatment validation on mouse models
I am struggling to set up a project proposal for validation of a known treatment for metastatic colorectal cancer in mouse models.
I want to see how SNPs in patients contribute to their drug resistance and/or toxicity. For the validation of these SNPs as predictive biomarkers, I will use cell lines and mouse models. But, how am I supposed to "induce" these specific SNPs in the mice? CRISPR/Cas9 can be used for the alteration of bigger parts.
Any idea is a useful idea!


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How would homologous recombination and mutations affect speciation?
I'm wondering how homologous recombination and mutations can affect how speciation can occur from one species (so that 2 will be created).
I'm doing research and I found that different mutations and genetic combinations occur in two geographically separated populations which can lead to speciation.
I know recombination can result in different genetic combinations, but how does that factor into a phylogenetic tree? Wouldn't recombination technically play no role in leading to evolution?
My (sort of) guess is that say recombination creates a population with a lot of AA genes and the other population, say by chance (genetic drift), has a population with a lot of aa genes.
We know A and a differ by perhaps a few SNPs, so on average, the two populations would become slightly different from one another due to genetic drift and geographic separation.
Do I have the right idea here? I'm not 100% sure how recombination during prophase I would affect recombination. Hoping someone can clarify this for me or provide some new insights.
Thank you!

Recombination occurs when homologous DNA sequences pair with each other and cross over, essentially swapping genetic material. Now, say that this crossover junction is in the middle of a gene, and we have some genetic differences in the top half and some in the bottom that distinguish the two alleles. If recombination occurs in the middle of the gene, then a new combination of alleles is created that didn't exist before. This new version of the chromosome can now be passed on as a single unit via sexual reproduction.
I left out a lot of details obviously, but this is the basic idea. The reason why recombination adds to genetic diversity and can lead to speciation is because it is essentially mixing and matching existing combinations to create new alleles.


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Veins collapse when empty
Veins collapse when empty. That's because they have thin and almost inelastic walls. What has inelasticity and thinness of the walls to do with the collapsing of the veins?

Your body exists at a certain pressure, determined by your surroundings; usually, this is about 1 atmosphere of pressure, but it can go up or down (e.g. when you fly on an airplane, or when you go diving). The pressure that your surroundings put on your skin is transmitted throughout your body, and your body "pushed back" against it.
However, this means that all your blood vessels have that pressure weighing down on them along their length. Normally, when they're full of blood, the pressure of that blood will press the blood vessel outwards to counter-act this. Without the blood, however, that pressure within the blood vessel is no longer sufficient to withstand the pressure being exerted on it from the outside.
Since the walls of the blood vessels aren't thick enough to have enough structural integrity to withstand that pressure differential, they then proceed to collapse.


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Rabies virus mortality
Why rabies virus has nearly 100% fatality rate in human (see this virology blog; thanks to @iayork for the link) if not vaccinated early, even some people have survived Ebola, then why does rabies doe not get extinct as its most virulent form will kill host and virus also?

Would be good to have a reference for the claim rabies virus has 100% kill rate in human if not vaccinated early

@Remi.b http://www.who.int/mediacentre/factsheets/fs099/en/

@murmansk Maybe I looked poorly but I failed to find the claim you are making. Sorry to be a pain but could you highlight where the claim is being made?

Speaking as a virologist and veterinarian it's absolutely true that the mortality for human rabies approaches 100%. How lethal is rabies virus?, List of human disease case fatality rates, Rabies - Prognosis

@Charles http://www.who.int/rabies/resources/SEA_CD_278_FAQs_Rabies.pdf question no 11

@Charles there are a half-dozen known survivors, but considering that the virus kills over 50,000 people every year, bloviating about the difference between 100% and 99.9999999% seems pretty silly.

@iayork This is quantitative science. Please do not try to argue that it's "silly" to distinguish the difference between 99.999% of the time, and 100% of the time. Depending on the system/behavior in consideration, this can have absolutely profound implications.

@Remi.b if you want to mark this as a duplicate for the question you answered, I'd suggest significantly improving your answer there; it completely ignores a very large literature on pathogen selection.

@Charles I've now edited OP's post.

@Remi.b I noticed :) I've removed previous comments, and have reversed my vote.

@iayork If the current answer at the other is not fully satisfactory, then a new post should address the reason why it is not fully satisfactory, not just ask the same question over again. I would not mind if the OP wants to argue that his post is specific to rabies and it is interesting because... but it should be clarified then IMHO

@Remi.b There are already better answers in Why have parasites not evolved to be harmless?

It's a common misconception that pathogens "don't want to kill their hosts". In reality, pathogens don't "care" at all about killing their hosts. All pathogens "want" to do is transmit from one host to the next. (Taking out the teleogenic language: There's no natural selection on a pathogen to reduce virulence as such. The selection on a pathogen is for transmission.)
In some cases, transmission is optimized when the virus is less virulent. In other cases, transmission works just fine when the virus is highly virulent. Rabies is one of the latter cases.
If a pathogen is spread by, say, respiratory contact, then having a host that is ambulatory and seemingly healthy may allow the first host to contact many others, so reducing virulence may enhance transmission in that specific case.
If the pathogen is spread by sand fleas (as in myxoma in Australian rabbits), then rapidly killing the host is counterproductive, because fleas leave a dead body. But keeping the host healthy is also counterproductive because a healthy rabbit scratches away its fleas. Optimal transmission turned out to work with a virus that kills 50-75% of its victims, because that makes the host very sick for a long time, allowing the fleas to bite it unimpeded.
Rabies spreads by damaging the brain, making the host aggressive, and spreading through bites in saliva (among other ways, but that's an important one). Serious brain damage to the point of wildly abnormal behavior is really not compatible with a host living a long time, so optimal rabies transmission means very high host mortality.
Finally, humans are not natural hosts for rabies and rarely transmit the virus, so in any case there's minimal natural selection for any virulence changes in humans. But it likely wouldn't matter, for the reasons above.


text:
Difference between spiking and firing
In the article "A Topological Paradigm for Hippocampal Spatial Map
Formation Using Persistent Homology" by Y. Dabaghian, F. Mémoli, L. Frank, G. Carlsson I read some sentences with huge confusion concerning the use of the termss firing and spiking. Do they mean the same thing? It seems to me that when they say a place cell is firing or a place cell is spiking they refer to exactly the same thing. The confusion comes from using both words in the same sentence as in the following sample sentences from the article (emphasis mine):

Indeed, a rat’s path through a small space can later be re-traced with a high degree of accuracy by recording hippocampal spiking activity during its explorations and then
  analyzing the location, size, and firing rates of a mere 40–50
  place fields [...]
To understand what algorithms the brain might use to decode
  hippocampal place cell firing, then, we should rely solely on the
  information provided by place cell spiking activity [...]
It is, in fact, generally assumed that neurons downstream of the hippocampus interpret place cell spiking patterns based on co-firing [...]
It should thus be possible to trace the emergence of topological information as more and more spikes are fired [...]
There are biophysical variables (firing rates, spike amplitude, etc.) [...]

In your quotes, the terms spiking and firing are used as synonyms. Indeed, both terms refer to the same phenomenon of action potential generation and in this context there is no physiological functional difference between spiking and firing.
However, note that in some contexts there may be a difference, namely some authors distinguish between a neuron spiking and bursting; the former referring to a tonic firing mode, the latter to a bursting firing mode (e.g. Ramcharan et al. (2000)).
Reference
- Ramcharan et al., Vis Neurosci (2000); 17(1):55-62

If they are the same how can we explain the second quote:"To understand what algorithms the brain might use to decode hippocampal place cell firing, then, we should rely solely on the information provided by place cell spiking activity." It seems to me that if we replace spiking by firing the sentence has no meaning at all !!

@palio the authors use it as synonyms.

@palio, AliceD is correct. In that particular sentence they mean 'spiking as opposed to external information' such as the "geometry of [...] the environment". The authors could be more clear overall. I haven't read the paper but I spotted at least a couple of logical fallacies.

I agree except for the bit about spiking and bursting; I don't know of anyone who would say a cell that is bursting is not also "spiking."

@BryanKrause agreed, that's why I say explicitly some authors and adding a reference besides.

@AliceD That's partly why I brought it up, though, because that reference does not refer to tonic patterns as "spiking" and burst patterns as "burst firing" - it uses "spike" and "firing" to refer to both in various places. They also talk about "low threshold calcium spikes" but that's a separate phenomenon that can underlie bursting but is not really part of the action potential itself (and is always delineated by specifically referring to calcium spikes/LTS/low threshold calcium spike).


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Biology Intuition and Origin of the "facts"
I am a graduate physics student but also taking biology classes. I am new to the field of bio. Most of what we do in class seem like memorizations and stating-facts. I am wondering:

How can I develop intuition for biology? (Aside from memorizing and practicing.) I am not even sure what intuition would be like in the case of biology?
Where are all the known facts in biology (and chemistry) come from? Have to be from EXPERIMENTS though, I hope to understand the origins of the I-was-being-told-this-way facts such as the composition of DNA and the types of bonding. By understanding, I don't necessarily mean the exact experimental procedure, but the general idea of how everything came about. (I am mainly interested in molecular and cell bio).
Much appreciation for any input!

It feels different to learn biology than learning learning physics, just like it feels different to learn statistics than learning computer science. Every field is just a bit different! There's not much you can about it! That being said, of course, knowledge comes from experimentation. If your professor does not offer you explaination of how we discovered the things he present to you, then I am sorry but in the general term we cannot do much for you. Just learn for yourself. For example, on the structure of DNA, you might want to read about the experiments by Watson and Cricks.

Maybe you are asking "why are things the way they are". Again, I am sorry if your professor does not offer you such knowledge but I am afraid we cannot answer that question in such general terms here. Maybe the study of evolutionary biology will give you a bit more of a feeling of answering the "why" question. There is a famous phrasing saying nothing makes sense in biology except in the light of evolution. You might want to have a look at an intro course to evolutionary biology.

I'm voting to close this question as off-topic for the reasons explained above.

As someone who was trained in physics but is working in bioinformatics. I can only echo @Remi.b 's comments. Physicists tend to want big abstractions and simple rules, but biology is a maze of exceptions and edge cases, not to mention emergent phenomena. "In Surely You're Joking Mr. Feynman", Richard Feynman describes a summer he spent working in a biology lab. He was amazed at how easy it was to ask questions that no one knew the answer to, and how hard it was to frame and conduct the experiments that tackled the question.

Most biology textbooks I saw in my days as a student used at least partially an experimental approach to describing the facts presented, since the purpose of learning about biology in a general sense is often to understand "how biology is done" (which seems to be your desire as well) rather than just the facts. If your courses/books aren't doing that, I'd suggest simply picking up a different textbook.

Another possibility is that you are in a higher-level class that's trying to setup a backbone for teaching something new. It would be far too time-consuming to go into the background behind all of those facts, they're just reviewing them so that you can proceed in the course. A lower level course could go into more depth.

Thanks very much for the input. I do lack the experience in the field.

It's just that for instance in physics, I can boil, say Einstein's Equation in general relativity, down to the basic F=ma. But right now I just don't see how I can do the similar with biology. For instance, explaining DNA down to the atoms (?) or boiling down a certain disease into the make up of polymers (?) Again, I seem to not have much intuition in the field of biology at all. Sorry if I came across as too ignorant.

Experiments: Incubators, test-tubes, fridges, spectrometers, centrifuges, forceps, test tubes, petri dishes, microscopes, scales and balances, chemistry tests, electron microscopes, calipers, stains, statistics, population sample collections. You can't boil a disease. you can observe it by microscope and measure it. The most important equation that you need to know is that Biology = Chaos and measurements. ex. you can boil your body = 99 percent CHON organic chemistry by mass.

Googling "landmark experiments in biology" came up with a lot of hits, what was wrong with the experiments cited in any of those works?  Mendel's pea experiments should be easy enough to understand.
Honestly I don't see how it will benefit you to know the organic chemistry work that went into determining the chemical structure of adenine.

don't close it  yet, i'll explain to him that biology has 80,million species, 800 million proteins that are invisible and unkown, and organisms with 100ds of different tissues that vie in between all the physical forces of speed, heat, etc, and that he should at first study BioPhysics if that's what he's comfortable with.

Not to be snarky, but I'm not sure what you are asking for. All of biophysics on an index card?
There are over 200 billion atoms in a single copy of the human genome and there are highly non-linear interactions between many of those atoms. Now extend that to the interactions between the 10 trillion copies of the genome in a typical human. Note that many of those copies are chemically interacting after some fashion. In your physics education have you every solved, even numerically, a system of 10^24 particles all with highly non-linear interactions? Simple rules like F=MA are not going to help at all because the emergent properties end up dominating everything.
The crazy thing in biology is that the emergent behavior of complex systems sometimes does offer incredible simplifications. I spend my days pretending that the human genome consists of strings of symbols that obey simple statistical properties. The incredible thing is that such an absurdly simplifying model sometimes does provide useful results and insights.
Biology is generally the study of these emergent properties, which are not generally derivable from simple rules of basic physics. That is why there is so much memorization. Intuition is not magic. Intuition is simply the inarticulate expression of our training and experience. That means there is no way to develop intuition without memorization or practice. You may have some intuition for some areas of physics, but that has presumably came after years of studying physics in secondary school, undergraduate, and graduate school. Intuition in some field of biology will have the same price tag.
I can offer some help with the experimental background for molecular biology. Read The Eighth Day of Creation. It's a well written, semi-popular history of molecular genetics and includes details on many of the key experiments.

Famous experiments roughly chronological:
1400's they gave elephants wine in the tower of london and belived in 4 elements and blood letting.
Human and animal dissections
Observation of oxygen generated by plants in light
Observation of red blood cells and micro-organisms
First notions of the Cells, cell theory
First microscopes at the same time as first telescopes
Major experimental biology for inheritance of flower colors by Mendel
Advanced medecine and use of electricity on corpses
Theory of evolution using many specimens and case studies
Methodical ecology treaties and reports for many animals by Fabre
Methodical reports of ocean fossils and sea life, fossil biology
First scientific reports of antisceptics
Measures of plant O2 production as a function of light color and temperature
Discovery of vaccines
Discovery of penicillin and antibiotics
Synthesis and measure of soil chemistry
First precise measurements of pH
Discovery of cell nucleus
Discovery of virii
Discovery of DNA
First electron microscopes
Beginning of centrifuge, spectroscopy,
Consider the diversity of animal species and cosmic bodies.
In cosmology you have 10-15 Clades of cosmic bodies, 50 of fundamental particles, 4 forces. There are only 100 common elements.
In biology, 80,000,000 species, 1,000,000 Clades of animals/plants/funghi, 100,000,000 different Enzymes and Proteins which are all invisible, and that beat supercomputers since 2003, 1000,000,000 different organic chemicals.
Microbiology flourished in tandem with Astronomy with the development of dutch lenses used for navigation. Cell theory is a biological equivalent to cosmology.
Biology has 3.9 billion years of cumulative encoding and additive development, as in that every being is like an SHA64 algorythm, that cumulative complexity is arranged into a tree.
Physics doesn't have friends and foes, cumulative memory, encryption, computation ability, 1 billion chemicals, cell walls and cells, number of legs, appendages, reproduduction, division, child rearing, it's a completely different recipe.
Physics is simpler. It's the same as being stuck inside one single protein, where the edge of the protein is the cosmological boundary, and being able to gather masses of data about the contents of that boundary and the nature of the physical universe. The maths formula to represent every protein is probably as big as the universe, there's no size and time boundary in either, except that we are seeing inwards that complexity.
biology is reined by chaos, so the maths of it has many billion degrees, you are talking about an equation with a,b,c,d,e,f,g,h,i,j,k, etc with billions of variables, and the maths formulas are billions of lines long. how are biologists supposed to deal with that?
Physicists are stunned by schrodinger's cat, probability issue.
What is the probablity of predicting where an animal will be on the same time on 2 different days? If you can write equations for that, then physics and biology will be the same. Biologists are not even going to try to write an equation for that kind of thing! they just have to use statistics all the time.
The maths of Biology are the biggest chaos system that man has ever peered into.
They are so incredibly confusing and unfathomable.
Try to write some equations in biology to predict movements of elements. you can't equate a bird like a photon, they are more chaotic and complex.
Biology has trees. Where do trees exist in physics? The biology tree has 80 million known branches.


text:
Why aren't white blood cells called pus cells?
So, pus is just a concentration of dead white blood cells that results from your body detecting an infection or a foreign body that needs to be removed and sending a whole bunch of white blood cells to fight it, right?
Why aren't they called pus cells, then, if pus is the form they take when they're concentrated enough to be visible to the naked eye?

Blood clots, among other things. Why don't we just call red blood cells "clot cells"? Because that's not all they do. Just like WBCs.

Because they're the cells that make up your blood, and they're why it's red when you cut yourself and you can see it flowing? Same reason why muscle cells are called muscle cells and nerve cells are called muscle cells. But you can't see the white blood cells, so why aren't they named after the tissue that they form?
Also, aren't the platelets the ones that cause the clots, anyway?

They are called white blood cells, because they look white when purified. So in fact, their naming is following your expectations. https://en.wikipedia.org/wiki/White_blood_cell#Etymology

Pus is comprised of two types of cells - neutrophils and macrophages.
These are cells sent by the body to combat pathogens.
There are a variety of other leukocytes(WBCs)(like lymphocytes, which is another broad term among many others) in the body that aren't part of pus which is why they aren't called pus cells.


text:
Ascending loop of Henle
When ions diffuse out passively or are actively transported out of the ascending loop of Henle, do those ions just hang around or do they go into the circulatory system and leave the kidney.
I ask because I know the medulla must stay salty but I always assumed that those ions were then entering blood vessels for another purpose.

Do ions in the medullary interstitium just hang out, or go into the circulatory system and leave the kidney?

Both!
You've grasped one of the fundamental principles of the renal physiology -- the medulla must stay salty. Lets start there and see if we can't work out what happens.
As the filtrate flows through the tubule, solutes are removed from the lumen at the thick ascending limb and added to the medullary ECF. This concentrates solutes in the medulla, producing the corticomedullary gradient (the medulla must stay salty). This is called countercurrent multiplication, and explains how such a large osmolar gradient occurs between the cortex and the medulla.
At steady state, with an established corticomedullary gradient, what happens? Solutes continue to be reabsorbed by the tubular cells in the thick ascending limb. In order for it to be steady state, each ion reabsorbed into the ECF needs to go somewhere. One of three things could happen to these ions:

Secretion or diffusion into the collecting duct (and excretion as urine)
Diffusion into the cortex (dissipating the corticomedullary gradient)
Diffusion into the capillaries in the medulla, the vasa recta (exiting the kidney through the renal vein)

In fact, all of these things happen to a certain extent.
Secretion and diffusion into the collecting duct (1) are regulated by changes in the expression of pumps and channels. Diffusion into the cortex (2) is kept to a minimum by diffusion into the vasa recta (3), what we call countercurrent exchange.

I always assumed that those ions were then entering blood vessels for another purpose.

So this does happen, but remember, the main reason for concentrating solutes in the medulla is so that the kidney can, if it needs to, excrete a very concentrated urine. Ions enter the blood vessels for the same purpose, in order to prevent them from diffusing back to the cortex, dissipating the corticomedullary gradient.
The concepts of countercurrent multiplication and countercurrent exchange were proposed in the 1940s and supported by a series of experiments in the 1950s. The landmark 1959 paper by Gottschalk and Mylle in The American Journal of Physiology was reprinted in 1997 by JASN and available for download without a paywall. It's an excellent read! As they predicted, we've learned a lot more, but this model still holds up, and is what we teach in renal physiology to this day.
This is their figure:

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


text:
Confusion about the construction of the rat's mental map
I'm reading the article "A Topological Paradigm for Hippocampal Spatial Map Formation Using Persistent Homology" by Y. Dabaghian, F. Mémoli, L. Frank, G. Carlsson
I try to understand the following graph:

In part a) of the graph, we are seeing a bunch of colored points. These points are in the hippocampus of the rat as opposed to the idea that these points are in the plane on which the rat is moving, and so each point is a place cell of the hippocampus that has fired at some moment in some place of the plane on which the rat is moving. Normally there is a huge number of points in this picture but we chose to put only those who fired, those who did not fire are deleted from the picture of part a). Also, each point (which means each place cell) has one color, and two place cells having the same color designate that the two place cells are considered identical and will be treated as a single place cell in the part b) of the figure.
In part b), we record the time at which each point has fired, with each point being represented by a bar on the time axis and all the bars are identical (same height, and same thickness).
In part c) the picture is in the plane on which the rat is moving as opposed to the idea that the picture of part c) is in the hippocampus of the rat. In part c) we are trying to derive the place fields from part b). Deriving the place fields means here that we are deriving the path that the rat has taken. In particular, place fields are in the plane on which the rat is moving and not in the hippocampus, and each place field in the plane is determined by seeing which place cells in the hippocampus has fired at that area of the plane.
Is my understanding correct? I'm not a specialist but I need to understand each detail of this graph because my work depends on it. My confusion comes from the fact that there are two regions here: the hippocampus of the rat and the plane on which the rat is moving and I need to be sure in which region the picture is.

You have a couple small misunderstandings that I think are making it hard to understand the figure. There is no map of the hippocampus pictured here!
1) Note: this is a schematic figure. These aren't real data, although there are real data that show this pattern. This is meant to be an easy to understand diagram that explains how place cells work.
2) Panel (a) is EXTERNAL SPACE. Essentially it's a "top down" view of a floor that the rat is running around on.
3) Panel (b) shows spike trains for three different cells: theses cells have been arbitrarily color-coded. The hash shows the times that cells 1, 2, or 3 fired spikes. There are just three cells shown in this figure: there aren't any combinations of cells considered one color or multiple cells in one color, just three cells and three colors.
4) Panel (a) is showing how researchers have connected spiking data, like in (b), to the animal's location. The procedure is this:

Start with a blank map of space.
Record from Cell 1. Every time cell 1 fires, mark a blue dot in panel (a) indicating where the animal was when Cell 1 fired.
Record from Cell 2. Every time cell 2 fires, mark a green dot in panel (a).
Record from Cell 3. Every time cell 3 fires, mark a red dot in panel (a).
(the previous steps could be done for many more than 3 cells simultaneously or in sequence; in this example they are just using 3 cells)

5) Panel (c) is in world space, just like in panel (a), and it shows a hypothesized way that the animal could be using the activity of cells 1, 2, and 3 to determine where it is in space. A researcher recording from cells 1, 2, and 3 could also use those recordings to make a guess of where the animal is. If only cell 3 fires within some window of time (an appropriate window is indicated by the outlined ovals in (b) ), and cells 1 and 2 do not, then the best guess is that the animal is in the upper left area that's shaded only red. If all three cells fire, then the best guess is that the animal is in the very center overlapped region of space.
The dashed line shows a hypothetical path the animal might take through it's environment. If the animal took this path, we'd expect to see place cells firing just like they did in panel (b): first only the blue cell, then blue+green, then all three, then red+green, and finally red only.
6) Very importantly: the animal has way way more cells encoding place than just these three. It would be really confusing to plot them all out in discriminable colors like these, but it is this more complex map with thousands of dimensions that gives the animal a good internal representation of its current location.
Hope this helps!

Thank you very much, the only thing that remains ambiguous is panel a). Indeed, cofiring corresponds to two or the three place cells to fire at the same place in the floor, and when this happens we will see three points with three different colors one over the other as if they make the same point but we don't see any occurrence of this in panel a), could it be that   they did that on purpose for simplicity of the picture since a point with three different colors would not be representable in the picture or did they supposed that there is no cofiring in this picture to make drawing simpler?

also why in panel b) the authors replaced the dots by bars, does this have a meaning or just a mere visualization choice ?

Spikes are point processes in time, whereas space is continuous. a) is a representation of spikes in space; b) is a representation of spikes in time. There's no time dimension in (a), except for how time is represented non-continuously as changes in space. If you notice in (b), even at periods of cofiring, the spikes may not be perfectly synchronous. If the animal moves, the points are in different space. Again, these are also schematic data plotted to give you an idea of what's going on; in real data, you could have thousands more points and might make the figure hard to read.


text:
Why are there no fresh water osmoconformers?
I'm just having trouble understanding this. I know that often marine fish are osmoconformers, and freshwater (like bony fish) are often osmoregulators, but why?

There are virtually no freshwater osmoconformers but there are some exceptions like being both an osmoconformer and an osmoregulator based on the salinity of the environment.
Osmoconformers keep their internal fluids isotonic to their environment and they maintain an internal salinity similar to the surrounding water. The concentration of solutes in freshwater is very low and if any organism were to have that low concentration of solutes in its body, it would not have enough proteins, ions, etc. to effectively conduct the biochemistry of living.
Here is a rare example of a freshwater species Daphnia which can be both an osmoconformer and an osmoregulator:

For freshwater osmoconformer species, most of the time there is a gradient between their internal
  osmotic concentration and that of the external environment; consequently, osmoconformers will
  vary in their cellular osmotic volume contents and as a result, some FW species (e.g. Daphnia),
  osmoregulate at low salinity levels but are osmoconformers at raised salinities. Some physiological
  processes, including reproduction and metabolic rate however, can be affected negatively by these
  changes (this group regulate their osmotic pressure actively) (Chen and Stillman, 2012).
https://eprints.qut.edu.au/107457/1/Azam_Moshtaghi_Thesis.pdf

Additionally, there is the term euryhaline used for the aquatic organisms who are able to tolerate a wide range of salinity. There are fish species that can live in salt water, fresh water and brackish water. You can see a list in the Wikipedia/Euryhaline Article.


text:
Did insects and arachnids diverge before or after moving to land?

Question: Are arachnids and insects so distantly related that they were already diverging before their (independent) emergence(s) on land?

I am curious to know what the fossil record and molecular evidence has had to say so far about such questions.
To the extent that arachnids and insects might not be any more closely related to one another than they are to crustaceans, and crustaceans are mostly aquatic, it does not seem impossible/implausible to me that the terrestrial transitions of insects and arachnids could have been independent of one another. In fact, considering that wood lice are crustaceans, one can conclude that there have already been at least two independent terrestrial transitions for arthropods, so postulating a third seems less of a stretch to me.
I suppose the thought process behind this is related to this question. Specifically, to the best of my knowledge, flight emerged several times among distinct insect lineages after appearing on land, in cases of convergent evolution. The fact that no lineage of arachnids ever evolved winged flight while many lineages of insect evolved flight independently of one another suggests that the "fundamental recipe" for insects and arachnids is substantially different, i.e. that they are not as closely related as one might have otherwise thought.

Arachnids and Insects are exceedingly distantly related. Although both are arthropods, there are other Chelicerates, Myriapods, and all of Crustacea separating them on the tree. Both diversified on land, independently

Those are two very separate questions. Arachnids include terrestrial groups such as spiders, scorpions, and other arthropods. Arachnids are members of Chelicerata, which includes horseshoe crabs, Sea scorpions (extinct), and probably Trilobites (extinct). Chelicerates evolved in the marine environment, and invaded land afterwards. Arachnids and Insects evolved on land. Hexapods are nested within Crustacea, in a group called Pancrustacea. The likely sister taxon of Hexapoda (Insects, including Protura, Collembola and Diplura) are Remipedia, which are aquatic. See Misof et al. 2014 for the most complete molecular phylogeny, with dates. http://science.sciencemag.org/content/346/6210/763

Wikipedia appears to contain at least some part of the answers to this question, specifically here and here. Specifically, it mentions that arachnids are chelicerates, which diverged from other arthropods during the Cambrian (according to molecular evidence?) or at latest during the late Ordovician (according to the fossil record). Spiders and other tetrapulmonates (not including scorpions) apparently evolved from trigonotarbids, whose (terrestrial?) fossil record dates back to the late Silurian. So apparently not only arthropods, but even arachnids in particular, have had multiple terrestrial transitions. Chelicerates are also part of the larger clade Arachnomorpha, which is perhaps more speculative because it includes several extinct classes of arthropods for which there is only a fossil record and no molecular evidence.
Regardless of the validity of the Arachnomorpha grouping, however, their appears to be a consensu that the chelicerates are a "sister group" (i.e. separate branch) from the Mandibulata, containing crustaceans and insects. (I.e. regardless of which group trilobites and other types of extinct arthropod are more closely related to.) In fact, since insects apparently evolved from crustaceans, crustaceans are most likely paraphyletic (like monkeys or reptiles), such that Mandibulata is essentially the "monophyletic version" of crustaceans. Also apparently my belief that flight evolved multiple times independently among insects appears to be false, inasmuch as the group of all winged (or formerly winged) insects is believed to be monophyletic. The fossil record for insects apparently also consists of terrestrial specimens (well, this is also true for arachnids, since they evolved from the terrestrial trigonotarbids), and dates back to the Ordovician.
But anyway, to the extent that arachnids are chelicerates and insects are crustaceans, and that the chelicerates and crustaceans diverged from each other either during or before the Cambrian period, indeed arachnids and insects are de facto very distantly related and must have emerged on land independently of one another (in fact, both the chelicerates and crustaceans must have both had multiple terrestrial transitions, it seems, which seems quite an accomplishment). In particular, this appears to be another case where major evolutionary divergences were occurring long before the non-expert layperson would be able to identify them based on the fossil record.

Don't forget Myriapoda, which are also part of Mandibulata. But yes, Chelicerates are the likely sister group of Mandibulata. Insects evolved flight only once.


text:
What is this thing found in my saliva?
Found in my saliva
(Optical microscope 40x)

Just to make sure, since you have a lot of external objects in the field of view: are you sure that it's part of the sample and not some dirt on the microscope?

I don't think so, we cleaned everything before, and it seems to have a nucleus


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Evolution of leukemia pluripotent short-term cells
I have a problem in understanding the introduction of this paper entitled  "Stability and bifurcation in a model for the dynamics of stem-like cells in leukemia under treatment". As I have no background in biology, it's difficult for me to get the meaning of some terms like:

Short-term cells
Multipotent progenitor cells
Goldie-Coldman Law

On the other hand, the second paragraph is completely confusing to me:

Let $Q$ denote the density of stem-cells population. A percentage $\eta_1$ of these ones are supposed to undergo asymmetric division with one daughter cell identical to the mother cell and the other one committed to differentiation. A percentage $\eta_2$ of the stem-like population differentiate symmetrically and go to the line of mature cells. The rest of them, a percentage $(1- \eta_1 - \eta_2)$ is supposed to self-renew: both cells that result from mitosis are identical to the cell that entred to the cell cycle. The same duration $\tau$ of the cell cycle is supposed for all types of division.

Is there a charitable soul to indicate some web page or youtube video on the subject?

Some background: leukemia is an immune cancer so it comes from the hematopoietic system. Thus, it would be useful to look into Hematopoietic stem cells (HSCs). Note that, in general, the (semantic) hierarchy of stem cells goes: totipotent, pluripotent, and multipotent, in order of less generality (i.e. more differentiated, or more mature as a cell in other words). Maybe reading about stem cells in general would be useful too.

HSCs have two subtypes: one which can indefinitely renew itself, and one which has a timed lifespan (i.e. it stops being capable of generating new cells of different types after awhile).  It is interesting to note that leukemias have  an analog of these, which is what is being referenced, presumably, in the paper.
See Normal and leukemic hematopoiesis: Are leukemias a stem cell disorder or a reacquisition of stem cell characteristics? for a bit more on this.
Multipotent progenitor cells (MPCs) are also capable of generating new cells, but are capable of less variety than plutipotent stem cells.
They can "choose" to become a more differentiated cell (i.e. choose a lineage).
They also cannot self-replicate (i.e. to divide and create new multipotent progenitors) indefinitely, though they can do it for some number of steps usually.
In other words, an MPC will generate a finite number of cells, whereas a true stem cell can divide indefinitely, given the resources.
The Goldie-Coldman Law (also called hypothesis) can be summarized via:

This hypothesis predicts that the tumor cells develop resistant phenotypic variations towards chemotherapeutic agents. This resistance is independent of the chemotherapeutic agent and dependent on the number of cell divisions that occur after treatment begins. The larger the tumor size or the longer delay in initiating chemotherapy, the more resistant cells. The implication is that a regimen of alternating cycles of two different non–cross-resistant chemotherapy medicines yields a better chance of tumor eradication.
    (From here).

       In other words, it is a model for how cancers become resistant to drugs. See also Improving       Cancer Treatment via Mathematical Modeling: Surmounting the Challenges is Worth the Effort.

Ok, onto the second paragraph. I will be very informal here :)

Let $Q$ denote the density of stem-cells population.

Within a cell population (cancer or otherwise), often there is a small subpopulation of stem cells (the rest of the cells are differentiated cells). So if there are $N$ cells in total, roughly $S=QN$ will be the number of stem cells present.

A percentage $\eta_1$ of these ones are supposed to undergo asymmetric division with one daughter cell identical to the mother cell and the other one committed to differentiation.

Within the population of stem cells (which are a subpopulation of cells), there will be further subcategories with different reproductive behaviours.
Notice there are really only 3 options: a stem cell becomes (a) two stem cells, (b) two differentiated cells, and (c) one stem and one differentiated cell.
This sentence means that roughly $s_1 = \eta_1 S$ cells will divide in the asymmetric pattern given above.

A percentage $\eta_2$ of the stem-like population differentiate symmetrically and go to the line of mature cells.

This means the number of symmetric divider cells is roughly $s_2 = \eta_2 S$ (both outputs will be differentiated.

The rest of them, a percentage $p = 1−\eta_1−\eta_2$ is supposed to self-renew: both cells that result from mitosis are identical to the cell that entered to the cell cycle.

Finally, around $s_3=pS$ cells become stem cells again, i.e. division type (a).

The same duration $\tau$ of the cell cycle is supposed for all types of division.

In order to divide, every cell has to undergo a complex process called the cell cycle. This takes time; in other words, it upper-bounds/limits the rate at which cells can divide. Presumably, different cells take different lengths of times to divide. This assumption above ignores this issue.

Edit (062018): let's take a look at the equation
$$
\tilde{r}(P) = r_1(P)\frac{x_0 - R_0}{x_0^{-p+1}} \;\text{  with  }\;
r_1(P) = \frac{P^m}{P^m + P^m_0}
$$
where $Q$ is the density of the stem cell population, $P$ is the amount of plasmatic drug, $P_0$ is the half-maximum activity concentration, $m$ is the Hill coefficient, $x_0$ is the number of infected cells, $R_0$ is the number of resistant cells, $p$ is the probability of mutation, and $q=-p\in (-1,0]$.
From a high level perspective, we need to account for three effects of treatment:
(1) the building of the cancer's resistance to that treatment,
(2) the increase in drug effect as it gets absorbed and decrease as it is excreted, and
(3) the effect of the drug on the target cells.
First, notice in the differential equations:
\begin{align}
\dot{Q} = f(Q,t) - \tilde{r}(P)Q^{q+1} \\
\dot{D} = -\lambda_0 D + K \\
\dot{P} = -vP + \lambda_0 D
\end{align}
that (2) is being handled in the equations for $D$ and $P$.
Drugs start in some compartment (like the intestines when you swallow a pill) where they are not so useful against leukemia. Here they start with some concentration $K$, and the amount of drug decreases with first-order kinetics, i.e. the first order linear differential equation that shows $D$ decreasing. See an article on pharmacokinetics for more info on this.
Once the drug is absorbed (i.e. contributes to $P$ instead of $D$), it enters the plasma and starts to have an effect on the leukemia cells. (Notice that (2) is being handled here as well, in the $-vP$ term of the differential formula for $P$, which measures how fast your body is destroying the drug.)
Naturally, only the drug concentration $P$ in the blood plasma can affect the cancer cells; hence, the term for $\tilde{r}$ only depends on $P$!
Next, we can see how the model accounts for (3) in the differential equation for $Q$. Again, we have first-order kinetics of $Q$ (by the first-order linear differential relation), modulated by $r$ and $q$. Since $q + 1 > 0$ and $\tilde{r} \geq 0$, we know that as $\tilde{r}$ increases, we are causing $Q$ to decrease faster, i.e. we are hurting the cancer more (good!). Thus we expect that as $P$ (the drug concentration) increases, $\tilde{r}$ should also increase.
Ok, so now for (1). Notice that the equation for $\tilde{r}$ breaks into 2 terms. The second term is $R_T=(x_0- R_0)/x_0^{-p+1}$. This captures the effect of resistance, as the cancer evolves via mutation to gain resistance to the drug. Notice there is no dependence on the drug itself (just as described in the Goldie-Coldman hypothesis). (Note that this may not be realistic, since the drug will induce an (un)natural selection pressure on the cells and encourage the ones that resist the drug to proliferate more easily; however it does simplify the model).
Notice that $R_T$ decreases as $R_0$ increases, meaning that as the number of resistant cells increases, the efficacy of the treatment decreases.
The first term, i.e. $r_1(P)$, describes the effectiveness of the drug as a function of its concentration via the classical Hill equation.
Simplistically speaking, drugs often act via receptor molecules on the surfaces of cells; once all these receptors are saturated, the drug cannot affect the cell anymore! Hence, the effect of a drug "levels off": as its concentration increases, it will bind more and more receptors (and thus have more and more effect, albeit at a diminishing rate), until saturation occurs and adding more drug (i.e. increasing $P$ no longer does anything). You can see this in the equation for $r_1$ since $\lim_{P\rightarrow\infty} r_1(P) = 1$ (though of course $\partial_P r_1 > 0$ still). The $m$ and the $P_0$ simply control this relationship: the Hill coefficient $m$ describes the "cooperative binding" properties of the drug (see the link above for details), i.e. whether binding accelerates further binding or not, while $P_0$ (usually denoted $K_A$, or called the dissociation constant) describes the ligand concentration at which half the target sites are occupied.
Higher $P_0$ means that occupying half the receptor sites requires a higher concentration, which means you need more drug for the same effect, i.e. the efficacy of the drug is poorer; this is why $P_0$ appears on the denominator: as it increases, the effect of the drug on the cells (given by $\tilde{r}$) will decrease.
Essentially, $m$ controls how fast the drug reaches peak efficacy (how steep the curve is), while $P_0$ controls the physical properties of molecular binding (the translation component of the curve).

Thank you for your answer. How do I biologically interpret the formula
$\bar{r}(P)=r_1(P)\frac{x_0-R_0}{x_0^{-p +1}}$ with $r_1(P)=\frac{P^m}{P^m +P_0^m}$.

Dear @Sanaa, I have added to my answer. Hopefully it helps! Incidentally, if you have more questions, I'd prefer if you asked a new question. (It is already tedious for me to scroll up and down to add to this one because it is so long).


text:
Mammalian scales
Many small mammals have scaly skin on their tails and sometimes limbs. The examples can be found among rodents (rats, degu, scaly-tailed squirrels), insectivores (shrews, desmans), oppossums, musky rat kangaroo. There are much more prominent examples like pangolin scales but I would like to concentrate on as simple things as possible.
I would like to know the answers or at least what is known on the following quiestions.

Are scales of these different mammals actually something similar or
is it just an illusion?
Does the scaly pattern at least in some cases represent some primitive characteristic of a common mammalian ancestor?
In case of positive answer on the previous question is there any connection to the scales of the diapsid reptiles? As I understand the latter are built from $\beta$-keratin absent in mammals but perhaps there are still similarities or even a common origin.

For now my search on this topic resulted in some contradictory claims without any solid references. I would update in case I find anything that seems relevant.

https://biology.stackexchange.com/questions/1138/what-did-pangolin-scales-evolve-from ......... http://thomas-hopp.com/blog/2013/01/26/even-more-dinosaur-skin/

@com.prehensible Well, there's a reference on pangoline scale evolution (which I sadly can't read right now) but from reading the abstract I'm not sure that would answer my question. And surely the answers on that question don't answer mine. I probably shouldn't have mention the pangoline at all...

The most primitive mammals from the list are probably Opossums and Beavers, which have the most reptile like tails of all. http://dolly.jorgensenweb.net/nordicnature/wp-content/uploads/2014/04/beaver_tail_Jamtli.jpg ......
http://media.gettyimages.com/photos/closeup-of-beaver-tail-northern-ontario-canada-picture-id128069910

@com.prehensible ...or their ancestors had furry tails and this is actually a derived trait. Contrary to cartoons platypus has furry tail!

@com.prehensible For me (not possessing any considerable knowledge on this topic) this is main weakness of the idea that protomammals had scaly tails and limbs - as far as I know monotremes don't have any scales. Though that may prove nothing as they are not very diverse and experienced considerable evolution themselves

It interesting to note though that some mammaliaformes (not even mammals) like castorocauda seem to have scaly tail though that could be again a convergent evolution.

The fossil of castorocauda from 140million years ago is simply incredible, it is conserved with hairs and scales, totally awesome mammaliaform, they must have been warm blooded and perhaps even bore live young. very amazing. https://news.uchicago.edu/sites/default/files/images/image/20150216/uxomsdakjb1905320150216.jpg

from general reading, I saw today that placentals and marsupials split 160mn years ago, and that the oldest human relative fossil is 2 rat teeth from 145mn years ago. rhino's can be a bit similar to lizards: https://www.google.fr/search?biw=895&bih=530&tbm=isch&sa=1&ei=jQQzWrqgLszyUp6wvXg&q=rhinoceros+skin&oq=rhinoceros+skin&gs_l=psy-ab.3..0l3j0i8i30k1j0i24k1l5.10814.13050.0.13273.12.9.0.3.3.0.81.618.9.9.0....0...1c.1.64.psy-ab..0.12.623...0i67k1j0i5i30k1.0.CjBRmWxVvxE#imgrc=ZqL7FEToFozO0M:


text:
How do tear glands secrete tears?
Keep in mind I'm not asking what the function of tears are or what causes tearing,(there's a lot of good answers on it already). My question is: how exactly is the tear gland able to actively push out fluids when it receives a stimuli? What exactly is the tear gland doing and how does it produce tears? How does it start and stop?


text:
What is the difference between Leloir and Non-Leloir glucosyl transferases?
The following questions were on the slides for my biotech course and I haven't been able to find any information on what the answer is.
What is the difference between Leloir and Non-Leloir glucosyl transferases?

LeLoir glucosyltransferases use uridine-diphosphate (UDP) 'activated' sugars as substrate, for example UDP-glucose, where 'LeLoir' refers to the LeLoir pathway, the metabolic pathway that inter-converts glucose and galactose (or, more strictly, the inter-conversion of UDP-glucose and UDP-galactose)
Non-LeLoir glucosyltranserases use sucrose as substrate and do not require the sugar to be be conjugated to UDP (or to be 'activated' in any way), and as such are very useful in the biotechnology industry.
See
A new pathway for the synthesis of oligosaccharides by the use of non-Leloir glycosyltransferases)

LeLoir was an eminent Argentinian biochemist.
For the enzymes of the LeLoir pathway,
The Leloir pathway: a mechanistic imperative for three enzymes to change the stereochemical configuration of a single carbon in galactose
by Perry A Frey is IMO definitive (and the pdf is freely available).
(Glucose and galactose are epimers: they differ only by the configuratation at C4. A key enzyme of the LeLoir pathway is UDP-glucose 4-epimerase, which contains a tightly bound NAD(+) and epimerization proceeds by oxidation/reduction (strictly, hydride abstraction/addition) at C-4, where the tightly bound NAD(+) is transiently reduced during catalysis: ie, NAD acts a (transient) hydride 'repository'! To the best of my knowledge, no enzyme has ever been found that directly catalyses the epimerization of glucose to galactose (although there appears to be no thermodynamic reason why this is not possible): the sugar must be conjugated to UDP in order to be a substrate for UDP-glucose 4-epimerase)


text:
If a hand was suddenly chopped off while holding something, would the severed hand still hold a grip?
This question was inspired by Star Wars Episode V: The Empire Strikes Back. In it, Luke Skywalker is battling Darth Vader in a lightsaber duel. Vader manages to win out and chops off Luke's hand, which is holding the lightsaber.

My question is: would his severed hand still hold a grip on the lightsaber? Or would it fall slack and lose grip, likely separating as it falls into the pit?
While this question is from a sci-fi series with a fantasy means of dismemberment, it might apply to other real-world situations (for instance, an industrial worker holding a tool while a piece of machinery accidentally severs his hand).

It seems unlikely, since most of the muscles that provide the gripping force are in the forearm.  Try gripping something forcefully* and notice which muscles tense up.  (*Of course anyone who's done much fencing knows that you don't grip with too much force.)

@jamesqf I'm not real fond of this type of question, but it seems like you could make a simple answer out of that comment.

(Disclaimer: I have no personal or medical experience of cutting off hands, or any other body parts, so this is purely theoretical.)
It seems unlikely, since most of the muscles that provide the gripping force are in the forearm and are transmitted via tendons in the wrists. Try gripping something forcefully* and notice which muscles tense up, and how the tendons on the inside of the wrist transmit the force.  Cutting the tendons would eliminate the force.
Of course anyone who's done much fencing knows that you don't grip with too much force, because that interferes with the fine control provided by the fingers.


text:
Ipsilateral vs contralateral side of body
I know that the dorsal columns carry ipsilateral information. Is this fact relative to the dorsal column in question?
If I want to talk about the right dorsal column, then the right side of the body would be considered ispilateral. But, if i then go on to talk about the left dorsal column, does this mean that the left side of the body is now considered ipsilateral?

Yes. Ipsilateral and contralateral always have to be relative to something; ipsilateral means "same side" and contralateral means "other side" - you can't really be the same or other side of something unless you have a reference point.


text:
Solubility of thromboxane A2 agonist U-46619 in H2O
First of all, I'm not sure I can dissolve U-46619 in water so that's also part of the question.
If it is soluble in water, how much can I dissolve before saturation?
If not, what's the right solvent to dissolve this agonist?


text:
How do our sensory organs work automatically without our conscious effort?
I wonder how our different sensory organs (e.g., eyes, nose, ears, etc.) work automatically without our conscious efforts or without our command. We don't have to tell our eyes how to see, our ears how to hear, etc. How does this work?

Read: Autonomic Nervous system

I think this is really two questions, 1: how do our senses work. And 2: why don't/can't we control them consciously.

Because consciousness evolved much much later than sense organs, and consciously seeing does not make much sense evolutionarily speaking.
We can consciously direct some sense organs, like the eyes, but signals sent sense organs by their very nature have to activated by outside stimuli otherwise they don't work as sense organs. If I could command my taste buds to taste cheese pizza while eating hay or poison it kinda defeats the purpose of having taste buds in the first place.
You really don't tell most of your body to do anything it happens automatically, becasue there is no benefit to doing it consciously, humans have more ability for fine motor control of some muscles becasue they help with things like speech or tool making, but having to learn to consciously control pupil dilation would take much longer and likely result in quite a bit of damage to the eye.
Now our eyes do have to learn how to see (or at least how to focus) and our brain has to learn how to interpret the impulses from our sense organs, but this is not really conscious learning. there is a cool experiment you can to to reteach your brain wrong see the inverted vision experiment but all the learning is without you being aware of it.

The Autonomic Nervous System (ANS) controls the actions that are performed without our conscious efforts.
It controls the automatic activities in the body. For instance, we cannot voluntarily increase or decrease our heart rate or slow down our digestive tract, these are the work performed by Autonomic Nervous system. I would suggest you to read about autonomic nervous system, you will understand.

Welcome to Biology! Whilst this may theoretically answer the question, it would be preferable to include the essential parts of the answer here, and provide the link for reference. You have basically re-stated the premise of the question and provided a link, but no physiological mechanism of why that is.

The autonomic nervous system does not include the senses.

The special sense organs are really extensions of the brain and activation of the organs via stimuli such as light or sound directly fire neurons that message the cortex. This is not learned but just straight neural activation. Interpretation of those senses is called perception and that is learned as you grow, and achieve self perception.
http://www.medicalook.com/human_anatomy/systems/Sensory_organs.html


text:
What is the role of triton in buffer for western blot assay?
What is the role of triton in buffer for western blot assay?
I understand it has to do with preventing non-specific binding of the antibody.

That's exactly it. Triton is a detergent and incorporating it just makes it a little more difficult for everything to bind. Here's how I imagine blocking buffer working:
PBS/TBS: buffering pH
milk/BSA: uniformly interacting with the entirety of the blot. The idea is that these will a) adsorb to the parts of the blot that don't already have much sample in them (since "empty" areas of the blot would otherwise adsorb the detection antibody/ies (this is a source of nonspecific binding).
Triton (or, more commonly, Tween-20): OK, now think about what's on your blot. Your antibody will have weak interactions with just about anything there. A detergent interacts with everything it touches (antibody and adsorbed proteins on the blot) to reduce binding affinity in lots of these interactions (although, some interesting counterexamples can be found here), thereby making the less-favorable binding even less favorable, decreasing the chances of your detection antibody retaining these weaker (off-target) interactions. The preceding article also suggests that the use of nonionic detergents lowers the signal intensity of the Western (and to a different degree across proteins).

Low concentrations of nonionic detergents can help to solubilize a complex mixture of proteins.  In other words, some of the antibodies in the serum might precipitate, which would effectively lower their concentration in solution.  If some of the primary antibody precipitates and binds to the filter then it could lead to a higher background signal when it is recognized by the secondary antibody, prior to the detection step.


text:
How fast the brain recover itself at sleep? What can be done to accelerate this process?
In Computer Science we have "Big O Notation" to describe how efficient is an algorithm at processing some task. Those can be linear, time constant, exponential among others.
Using that analogy, How much time the brain needs at sleep to recover itself from an intensive day at work/over stimulation/training/learning/etc?
After it reach it's "specific time", I know that we dream, and that can take very few minutes. Last night I've dreamt of hardest college exams, even done my last one in 2011. So, dreaming time is a period where the brain clean itself from toxins? I've waked up early, so I should have "dreamed a litle bit more" to recover, or the dream it's just the output imaging of the brain recovery process?
What can I do to recover faster? Things like dimmer and silent ambient help better than the total time slept? How they affect and interrelate? If you can provide technical and scientific papers, it will help a lot!
Thanks a lot for your time and patience!
Edit: "Typed Bio O instead of Big O".

You should see some talks from TED about deep sleep.
One researcher summarized that adults generally need 8 hours every night to be at optimum strength. What is most important though is the Delta-wave sleep that occurs during very deep sleep.  To accelerate the process: It's pretty fringe research, what he said is early days... Alledgedly, playing a certain kind of noise triggered near the delta wave phase promotes Delta wave activity in the brain as measured with electrodes. it's essentially slow delta-synchronised seashore kinds of of grey noise played in sleep at the right moment. He said they were working on a device for it.

here's the talk.
https://www.ted.com/talks/dan_gartenberg_the_brain_benefits_of_deep_sleep_and_how_to_get_more_of_it
My own method to have amazing sleep is lots of nights at my girlfriends and to change mattress every few days mat my house, because my unconscious breathing is forced to exercise different muscles of the chest based on whether I am on a swimming pool matress, a futon, a cozy matress, covers similar to sleeping on a lawn. Physiology and muscles benefit from varied exercise, including the 8 hours of chest muscles during sleep. another matress for example I feel all the breathing in the lower belly. I just got out a pool matress for the last 2 nights on boards and rugs, and I dreamed that I was flying around the mountains and cities for about 3 hours and that other people were flying too, which is always nice. I swear I was sleeping a bit rough 3 days earlier on a normal mattres. other factor for me optimum warmth and lots of water for me:) i'm weird though because I had liver damage from a pesticide and following doctor care when I was 18 and I need drink more and sleep hot in order to sleep well.


text:
Do cells communicate only in binary levels?
In modern communication we generally have various schemes to communicate the given signal, one of them is to convey information with different levels. does cell signaling too have levels apart from binary 'Yes' and 'No'.
For instance if a cell 'A' wants to communicate with another cell 'B'. I know it can do that by varying the concentration of molecules in the given media and 'B' will decide in favor of 'Yes' or 'No' based on the concentration sensed. But my question is does this sensing always happens in binary levels or is there some thing like:

If nothing sensed do operation 'a'
If moderate concentration sensed do operation 'b'
If high concentration sensed do operation 'c'

I mean communication not done in binary levels but may be quaternary levels. If yes can any reference be provided?

Binary responses are associated with switches, which in turn are associated with bifurcations in the steady states of the biological system in question. Varying some system's parameter (such as a cell's signalling strength) cells can switch from 'on' to 'off' (or viceversa) states. As an example, check out Gardner's toggle switch
(https://www.nature.com/articles/35002131), in which this property is exploited in a synthetic system.
However, cell-cell interactions can be much more complicated, allowing behaviours other than binary responses, such as multistability or oscillations. Thus, upon varying a parameter, a cell's state can, for example, go from a particular 'off' state, chango to an oscillating state and then change again to an 'on' state. Thus not only binary responses operate in cell communications, but many intermediate responses are also possible. For a review in multistability in biological systems, check out: http://m.pnas.org/content/101/7/1822.long
Hope it helps!

To add further possibilities: There are also cases which mix digital and analog; eg. Tay et al. Nature, 2010, Single-cell NF-κB dynamics reveal digital activation and analogue information processing ( http://www.mcb5068.wustl.edu/MCB/DiscussionSection/PDF_Files/SingleCellNFkB.pdf )


text:
How is mRNA directed out of the nucleus to its ultimate cytoplasmic location?
In the process of translation, I learnt that following formation the mRNA must exit the nucleus through a nuclear pore and attach to a ribosome.
My question is how does mRNA navigate itself out of this pore, and find itself a ribosome to bind to?
Is this a process of diffusion or is there any other mechanism involved?

Maybe this thread helps? https://biology.stackexchange.com/questions/1736/rna-or-ribosome-which-one-moves-during-translation

Hello Dwarz! That was helpful but I think the motion being discussed there is that as the mRNA moves through the ribosome, while I am puzzled by how it arrives there. Thanks though, it was interesting to know

There is a complex progress involving many proteins that directs RNAs to the nuclear pore complex and ensures that they are moved into the cytoplasm. Below is part of a diagram (edited) from a Nature review article on this topic, showing the transport of mRNA. It is available from the authors online.

Another general review with an illustrative poster is by SR Carmody and SR Wente, and can be found in the Journal of Cell Science.
As far as I am aware, interaction of mRNA with cytoplasmic ribosomes occurs by diffusion. Direction of the ribosomes to specific locations, such as the endoplasmic reticulum, can occur, but is generally through recognition of features of the nascent peptide after tranlation has started. The Wikipedia article on protein targeting provides an introduction to this area.


text:
What prevents neurones from touching at chemical synapses?
The synaptic clefts are really small, but the neurones which they are between do not touch even against forces like gravity.
What really prevents them from coming into direct contact at the synapse, and also what would happen if they did come into contact?

In which type of synapse? In electrical synapses they are in direct contact, in chemical synapses the basal lamina anchors them.

Thanks! I was referring to chemical synapses. I will try to find out more about the basal lamina.

I think there is nothing preventing neurons from touching each other but there is nothing also binding them together. Usually, cells have tight junctions that bind them tight to each other, the lack of which would assume a synapse-like cleft. Beware, the rest of the neuron is scaffolded by glia and the like. No references, just intuition and discussion - hence just a comment