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Why does a worm's skin need to be wet for oxygen to diffuse across it?
Pages I've read about worms' respiratory systems says that the skin needs to be wet (covered in mucus) or oxygen won't diffuse across the skin. Why? If there is more oxygen outside the worm's skin than inside, what prevents it from diffusing across the skin, even if the skin is dried out?

The quick answer: When the skin dries, the lipids in the cell membranes of the skin tissue undergo a phase transition which makes the membranes less permeable for oxygen.
Explanation: The lipids of the cell membrane can exist in different phase states. In the liquid disordered phase the lipids are relatively flexible and mobile, making this phase more oxygen permeable compared to the liquid ordered phase, in which the lipids are more rigidly packed.
The phase transition temperature of lipids increases upon dehydration (another reference), meaning that at the same ambient temperature, a dry lipid membrane is in the liquid ordered state and a wet lipid membrane is in the liquid disordered state.
Therefore, a dry cell membrane is less oxygen permeable than a wet one.

Because you are talking about diffusion, thus there needs to be a continuous pathway of gas or liquid for the molecule to move through. Membranes stop behaving like liquid when you dehydrate them.  Oxygen cannot diffuse through extracellular solids (not at a meaningful rate anyway), which is all that is left why the skin dries out, so there needs to be a liquid path for it to follow. The water around a cell membrane helps weaken the binding energy allowing materal to pass between the lipid molecules, without the water is becomes a functional solid.
Skin does not replace water with air when it dries out, it collapses in on itself losing volume so all you have is solids (or things close enough to solid to act as a barrier), those no path for the oxygen. It is the same reason CO2 cannot diffuse through a coke can, it can't diffuse through a solid.
Edit, there is some gas exchange but it is very minor especially compared to what happens normally, and occurs because there is an occasional gas path. Cell membranes can be diffused across, but they slow it down, layer upon layer of them packed tightly as you have in dehydrated skin produce much the same effect as a solid, reducing the diffusion rate the point it can barely be measured and is nowhere near what the organism needs.
Animals that do not need ot gas exchange across the skin add layers of waxes to the skin making it an even better barrier and thus making it even more water tight.

Isn't the worm's skin still solid underneath the mucus?

@MarkEichenlaub  No, like most other biological tissue it is a gel, a liquid held together by a matrix of solids. That is why the mucus evolved, to prevent the skin from dehydrating. There are air tight skins in other organisms, (by creating waxy barriers), generally they experience minimal gas exchange.

Respiration in aquatic organisms involves diffusion of dissolved gases present in the aquatic medium across their permeable cell membrane . In worms which lives in moist environment the skin functions as a respiratory surface and requires the surface to be moist to enable exchange of gases.

Thank you, but I don't see this an answer to the question. "to permit exchange of gasses across moist skin" why does the skin have to be moist? "which is stable when moist." What does it mean to be "stable"? Why is moisture important to that?

Hi Mala. When directly quoting a source, it's required that the words be in blockquotes with the source listed (just listing the source isn't enough), or the material is considered to be plagiarized. It's kind to answer the question, but this is not the correct way to do it.

Dear  Mark Eicheniiaub  Thanks . Stable relates to the functional status . To enable exchange of dissolved gases present in their. ( for worms which inhabit moist places) aquatic  environment requires wet surface .

Yes, but why does the surface have to be wet?

The dissolved oxygen in water needs moist surface to get diffused in to the cutaneous blood vessels located in the skin of worms . - basically to ensure that oxygen can be dissolved and absorbed by the circulatory system to fulfill the requirements of the organisms  to reach to the deeper parts of the body. Required amount of oxygen  can not be delivered directly in its gaseous form.

But why does it need moisture to diffuse?

Dear Mark Eichenlaub -Thanks .The rate of diffusion  varies with the area of diffusion, Concentration gradient and the thickness of the surface area as per Fick's law . A molecule of water which is at higher concentration inside the body than outside - diffuses out and makes the diffusion surface moist.  Gas exchanging surface in land animals are internal  to prevent  much loss of water from the body.


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Speed of passive transport of ions in the dendrite
I tried hard to get them, but I didn't get any numbers. My (subjectively) best Google search was for "speed propagation post-synaptic potential".
My question is:

How fast are ions transported passively inside the dendritic tree (and soma),
  probably depending on their atomic mass, charge, and of the local geometry?

Especially I want to know when a post-synaptic potential generated x μm away from the axon hillock "arrives" there, i.e. can be detected/summed up with other PSPs. Disregarding all of the eventualities (see above):

What is the order of magnitude of the speed of passively transported
  ions in the dendritic tree?

"I assume that ..." - why do you assume this?

Your edits do improve the question, but you are still asking two very different questions.
We don't really need to answer these questions:

How fast are ions transported passively inside the dendritic tree (and soma), probably depending on their atomic mass, charge, and of the local geometry?
What is the order of magnitude of the speed of passively transported ions in the dendritic tree?

to answer this part:

Especially I want to know when a post-synaptic potential generated x μm away from the axon hillock "arrives" there, i.e. can be detected/summed up with other PSPs

The speed of propagation of electrical signals in neurons don't depend on particular masses of particular ions or diffusion per se. Instead, passive electrical conduction is best understood using the cable equations which treats conductance within neurons as electrical RC circuit. The electric field propagates at the speed of light.
Therefore, EPSPs actually propagate almost instantaneously (given how short the distances involved are relative to speed of light) in that they produce an electric field. However, the peak decays with distance, and the rise time of an EPSP depends on the compartment because of capacitive filtering along the length of the dendrite. The decay peak is described by the length constant:
$$\lambda = \sqrt{\frac{r_m}{r_i+r_o}}$$
In this equation, rm is the resistance of the membrane, ri is the resistance of the intracellular space, and ro is the resistance of the extracellular space and is effectively negligible.
The length constant is the distance at which the peak amplitude will have decayed 63% from the peak at the signal origin.
The temporal filtering comes from the capacitive properties of the membrane along the length of the dendrite. The authoritative works describing these properties are several papers in the 1960s from Rall, Rall, W. (1962). Theory of physiological properties of dendrites. Annals of the New York Academy of Sciences, 96(1), 1071-1092. and Rall, W. (1969). Time constants and electrotonic length of membrane cylinders and neurons. Biophysical Journal, 9(12), 1483-1508. are good references.
The effective time constant for signals originating closer to the soma is much faster because there is less membrane to charge along the way. Exactly "how far" you have to travel to make a certain amount of difference depends on the properties of the membrane, which vary across neurons, vary in different parts of the dendritic tree, and vary dynamically within a neuron due to synaptic transmission.
Magee, J. C. (2000). Dendritic integration of excitatory synaptic input. Nature reviews. Neuroscience, 1(3), 181. is a fairly accessible review that covers a lot of these issues and more. It's important to recognize that although passive propagation of signals is important in dendrites, it's never purely passive and active conductances have important roles as well; in many cells, these active conductances plus differences in the initial shape of EPSPs throughout the dendritic tree act to mitigate the effects of distance.
See also Koch, C., Rapp, M., & Segev, I. (1996). A brief history of time (constants). Cerebral cortex, 6(2), 93-101. for more on the time constant and some evolution of the ideas about neuronal time constants since Rall.

Thanks. But alas, you destroyed my hope that the propagation of potentials (PSPs and action potentials) might be understandable by the flow of charged ions.

Oh but the mathematics of electricity are much more tractable than Monte Carlo simulations of ion flow in a complex environment, so it isn't a hope at all but a dread. :)

I'm having a horrid back spasm at the moment or I'd finish my answer but I'll just add in a comment that the things you actually care about for temporal integration are the durations of EPSPs, rather than their rise times.

Will I find the number I was asking for (the order of magnitude of the speed by which EPSP signals are transported) in one of the papers you mention? Or do I have to calculate it solving complicated equations with some typical parameters?
Alternatively, the effective speed can simply be defined as "(measured) distance of synapse and axon hillock" divided by "(measured) time until EPSP becomes effective at the axon hillock". Finally, this is what I am looking for.

(The question arises, how this time can be measured. Maybe by stimulating simultaneously some synapses that have the same distance to the axon hillock and which are sufficient to evoke an action potential?

What you are really looking for (I think) is the rise time of EPSPs and how that varies with distance from the soma; you will definitely find at least an order of magnitude approximation for that in the papers I linked. I'd suggest starting from Magee. If you had a particular cellular morphology you wanted to test (even a toy one), then probably the best way to do these measurements is in a simulation environment like NEURON from Yale. "time until EPSP becomes effective": again, the parameters you should be interested are 1) time to peak, 2) width. These will describe an 'effective window.'

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Homogeneous and complex nuclei
In the Wikipedia article on nuclei one reads:

"The neurons in one nucleus usually have roughly similar connections
  and functions."

I read this as "a nucleus usually is roughly homogenous", i.e. contains a small number of neuron types, distributed roughly equally and with a roughly homogenous connectivity pattern.
But it is also stated:

"A nucleus may itself have a complex internal structure, with multiple
  types of neurons arranged in clumps (subnuclei) or layers."

What I would like to know:

Is my reading correct?
Are there really more nuclei of the more simple (homogeneous) type than of the more complex type?
Which are prototypical examples of both of the types (more simple and more complex)?
Which are the greatest nuclei of "the" simple type (with respect to volume or number of neurons, taking "simple" with a grain of salt)?

I think you are reading too much into that statement. The proper reading of that statement is to add on the implied "..compared to other nuclei." That is, what defines a nucleus, in most cases, is some shared similarity in connectivity. That does not mean homogeneity.

I also think your reading of the second statement is incorrect; it does not suggest that there are "simple and complex" nuclei as two distinct categories, rather it is indicating that "complexity" varies, and gives a couple examples; essentially, it is exactly saying that you should not assume homogeneity.

I don't think it makes much sense to think in terms of "number" of nuclei, and anyways, nuclei can be somewhat arbitrary. For example, take the auditory thalamus: the medial geniculate nucleus (MGN). The MGN is typically divided into three parts: the dorsal, ventral, and medial divisions. Someone chose to call them all the medial geniculate nucleus, based on gross appearance, but with more functional understanding we can classify each part separately. Should this be one nucleus or three? It really doesn't matter, it's just semantics and terminology to get people talking about the same structure. In one context, it makes sense to talk about the whole MGN, in other cases it makes sense to differentiate between MGv, MGm, and MGd. You could call them subnuclei, or nuclei, or whatever you want. Most people choose to just be consistent with the terminology used in their field for historical reasons because it doesn't matter.
I don't really think it makes sense to think of in terms of prototypes; nuclei are different from each other.
Again, you'd have to first define simple and complex. I don't think there is meaningful dichotomous distinction.

I am aware that there is no strict dichotomy between "simple" and "complex" but a continuum. Maybe I should have pointed this out.

Okay - your questions #2 and #4 don't work if that is true. #3 maybe but I think it's still a problematic; the simple/complex continuum is also not one-dimensional (i.e., there are different potential types/definitions for complexity).

You are right! But why do you say "the simple/complex continuum is also not one-dimensional"? Isn't this at the very heart of the problem? Given this "problem": How could one ever approach it?

Exactly - in my opinion it's an ill-posed problem. So, the issue isn't trying to approach the problem, but deciding not to. I think it's more helpful to appreciate and embrace the diversity of nuclei; the same approach is important in biology in general. It's much harder to reduce biological concepts to strict rules the way other fields sometimes strive for. If you pick any two nuclei, and claim one is simpler than the other, I can almost guarantee someone can make an argument for the inverse based on a different definition of complexity.

Nevertheless, there is possibly some truth in the dichotomy (as in most dichotomies). And why throw the baby out with the bathwater?

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Development of the commissural fibers
Having a look at the corpus callosum one sees that the axons passing the corpus callosum (the  commissural fibers) connect mirror-symmetric counter regions of the cortex (roughly).

Is there a model that explains how the growing axons find their way to their far-away targets in this highly structured way?
(One possibility would be that the counter regions originally were close to each other but separated during brain development.)


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Do skin mites reproduce on human face during night?
I've seen this circulating on social networks:

I was wondering to what extent is it true. Do skin mites really get on the skin surface to reproduce? Why is it so?

Yes, it is true that these mites exist on healthy human skin, on >98% of people, no matter the country or hygiene.
However, I'm sorry to say that this photograph is not the follicle mite Demodex folliculorum. This image has been widely circulated around the internet as Demodex, but it is actually the head of a silkworm, Bombyx mori. The above version has been modified slightly from the original, but you can see the original here: https://www.sciencephoto.com/media/720736/view/silkworm-head-sem
And here is a zoomed out version of a silkworm: https://macrocritters.wordpress.com/2012/11/26/photographing-down-the-food-web-silkworms-bombyx-mori/
You can find a real close-up of Demodex here: https://www.sciencesource.com/archive/Demodex-folliculorum-(SEM)-SS2367855.html

Is there a reference on the Demodex population spread? Also the last link is behind paywall.

Doesn't answer the main question about mite reproduction, but it does address the "is it true?" portion of the OP's post. Good on you for catching it. +1

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What are these bulbous-ended filaments?
Yesterday I noticed an array of filament type structures, each with a bulbous feature at the end, hanging off my car door. As can be seen in the first image, these structures are quite small (comparing to door handle/key hole). I live in Kentucky, USA. What are they?

They look like lacewing eggs, though related insects can have similar-looking eggs. Lacewings are beneficial insects; their eggs are laid on stalks, like this:

Edit to point to other questions and answers here:

Is this some sort of fungus?
What are these (eggs?) ? ( Location - India )


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Glycolytic non-oxidative pathway
I am currently digging in some books to understand the three major metabolic pathways involved in physical training. The most difficult one for me is the glycolytic non-oxidative pathway (also more commonly known as the anaerobic lactic pathway) and I would like some help from people versed in this field.
In this pathway, as far as I understand, glycolysis produces pyruvate. In this process, NADH and H+ ions are produced along the way.
Then, if there is still a high energy demand (i.e. glycolysis is still necessary); NADH binds with pyruvate to form lactate and free up NAD+ which is necessary to sustain the glycolysis (otherwhise, pyruvate would be consumed via an oxidative pathway i.e. oxidative glycosis or slow glycolysis). This can theoretically continue until glycogen is depleted or severely diminished as far as I understand.
The problem comes then from the H+ ions produced during the glycolysis. These ions cause acidosis of the muscles if not removed. However, they can be removed if sufficient oxygen is present to form water. And here is my main question :
Why, during high intensity exercise, would oxygen be insufficient to take care of the H+ ions produced by the glycolysis ? Is it because muscles used during high intensity are not the best ones for using/transporting oxygen? Is it also because these H+ ions cannot be transported towards neighbouring muscles able to oxidise H+ ions ?
I understand this is a difficult question and maybe there is no precise answer at the moment. If you could point me toward a good ressource that deals with this question, I would be glad. I currently base myself on McArdle book on exercise physiology.

This is a great question, but not really on topic for fitness. I am migrating it to biology, where it may get a higher level of attention.

I am going to try to walk through this problem, in a step-by-step manner in relation to exercise, starting from at rest, and ending at the point in which the body is no longer able to maintain its energy-charge.
At Rest
The body mainly utilises oxidative phosphorylation to maintain its energy-demands. In cells where great amounts of energy need to be produced very quickly, eg. cells that are actively replicating, glycolysis is the preferred mode of energy production because this pathway is able to very quickly produce large amounts of ATP, and lactate is able to quickly diffuse in to the bloodstream. Lactate will travel in the bloodstream, to the liver, to be recycled back to glucose through an anabolic process called gluconeogenesis. This recycling pathway is known as the Cori-cycle. Essentially, what is happening is, parts of the body that are in need of high amounts of energy, will "dump" their wastes to the bloodstream, to be dealt with by other organs.
Science and Skiing VI, 2015, pp 17-30. George Brooks of the University of California summarises lactate recycling quite nicely here.
Beginning Exercise
Muscle cells will begin to quickly utilise ATP-stores, and release glucose from the glycogen-stores, and release oxygen-stores from myoglobin.
As these stores begin to become depleted, the body will begin to go in to overdrive, in an attempt to restore itself to a resting-state. Thus, your heart-rate will increase, breathing will become faster, and glycolytic pathways will be activated through feed-forward mechanisms.
During Exercise
I have touched on this before, in another post that you may find interesting. I believe that if you read through this though, that you will understand why there is low levels of oxygen, and what the body does to attempt to circumvent this.
There will be very low levels of oxygen throughout the active tissues. The body will do everything it can to try to restore this, but it will ultimately fail to do so. Thus, the only real option it has is to rely on glycolysis in the tissues that are causing "problems". The rate of ATP-production is most dependent on the rate at which a cell can take glucose in to the cell.
The electron-transport-chain is only able to synthesise ATP at its maximum velocity - this maximum velocity is proportional to the concentration of oxygen. The rate of glycolysis is, however, essentially, only affected by the rate at which lactate can be removed from the cell and the rate at which glucose can be absorbed by the cell.
Of course, the muscles that are being used will only be concerned with producing energy. Therefore, all of the lactate that they produce will be dumped in to the bloodstream, where it will travel to the liver, in the previously mentioned cori cycle.

Overall, the issue is not in the muscle-cell's ability to regenerate NAD+. This is the easy part, seeing as there is no net-change in the concentration of NAD+ when glucose is converted to lactic acid. And also, things such as malate-aspartate shuttles, citrate-pyruvate shuttles, and glycerol 3-Phosphate shuttles can be used to maintain redox-balance. These are only but a few examples of how to maintain redox-balance.
You must also remember that carbohydrates are not the only class of molecules involved in these cycles; degraded proteins and fats can also be used to supply the TCA-cycle with alternative means of energy-production. Pyruvate probably would not even be able to be converted in to acetyl-CoA anyway, since pyruvate dehydrogenase requires the presence of oxygen to function.
Problems however do arise once the body is unable to deal with all of the waste that it is producing. There will reach a point, where the liver cells will be physically incapable of accepting any new lactate-molecules. And so, lactate will accumulate in the bloodstream. With an accumulation of lactate in the bloodstream, lactate will be unable to diffuse to the outside of the cell. Thus, cells will be unable to convert pyruvate in to lactate.
The reason why ATP-regeneration eventually fails to keep up with the rate of ATP-usage, is because the rate of conversion to lactate decreases. The rate of conversion to lactate decreases, because the concentration of lactate increases
I tried to make a little illustration of what I mean above, below. Hope this helps to conceptualize it.

In this second picture, there is too much lactate for diffusion to occur.

Supporting information
Taken from Quantifying intracellular rates of glycolytic and oxidative ATP production and consumption using extracellular flux measurements; Mookerjee et al. 2017
"These maximum values of JATPglyc and JATPox define the bioenergetic capacity of the cells. As shown in Fig. 5D, the maximum individual capacities of JATPglyc and JATPox in the bioenergetic space plot intersect at (62.5, 46.5) for a theoretical maximum bioenergetic capacity of 62.5 + 46.5 = 109.0 pmol of ATP/min/μg of protein. At this maximum point, the glycolytic index (GImax capacity) would be 62.5/109 = 57.3%, making C2C12 myoblasts primarily glycolytic when running at their maximum ATP production rate. Compared with the actual value of JATP production in the presence of glucose (55.2), the bioenergetic capacity was 109/55.2 = 197% of the rate with glucose (Fig. 5D). This bioenergetic capacity of 197% of the rate with glucose (alternatively, a reserve capacity of 109.0 − 55.2 = 53.8 pmol of ATP/min/μg of protein) reveals that the C2C12 cells under our experimental assay conditions with added glucose were operating comfortably within their capacity to generate ATP and were well set up to respond to any acute increases in ATP demand by increasing either glycolytic or oxidative ATP production, or both."
In these experiments, the researchers were trying to figure out what proportion of ATP would be created by glycolytic and oxidative pathways in muscle cells (and other cell-types). Their findings, were that, indeed, the majority of ATP production in muscle cells comes from glycolysis.
During exercise, this difference in amounts of ATP production between glycolysis and oxidative phosphorylation would probably be even greater.

I noticed that someone does not like this answer. If you could provide feedback on how to improve this or tell me why I am wrong, it would be greatly appreciated. Thanks.

Bob - I did not downvote you.  However this is incorrect (not completely so please don't take offense -- just missing some key factors). @xusr is on the right track. Will add on in a sec

True. However, it is not really about the amount of ATP that can be produced. It is about how quickly that ATP can be produced. By using glycolysis, the cell will be able to produce a greater amount of ATP than it would be able to if it were trying to cycle through the entire TCA-cycle & ETC. Also, the TCA/ETC does not shut down.. Not at all; it will however utilize alternative substrates, such as amino acids or fatty acids. The amino acids and fatty acids will be present in sufficient amounts to fuel the TCA relative to the amounts of oxygen that is present. And, as I said, when a cell is

using glycolysis to produce lactic acid. This lactic acid will be dumped in to the bloodstream to be processed by different organs - mainly the liver. Cancer cells use a similar mechanism - for those of you who have studied cancer, you know this.. Cancer cells do not use oxidative phosphorylation, because they can grow much more quickly by relying on glycolysis, and allowing the rest of the body to deal with the lactic acid.

@Mike-DHSc , Yes please do add on. I'm interested to see what you think.

@Bob Yes exactly where I was going -- I'm not a chemistry guy - I'm a PT so you'll run laps around me in that area.  You actually hit most areas (and some I didn't even pick up on the first time around) - was trying to find an excerpt from a book that explains it well but no luck.

I'm posting 2 images now -- maybe you can make better sense of them then me.

@Mike-DHSc Great! I'll take a look. But, which part was the part that you thought was incorrect? I'd like to look in to that a bit more also.

One sec I'll add them shortly

From What I understand (I am an engineer, not a chemist), I'll tag along with Bob. What I understand is, during intense exercise, your body is doing whatever it can to maintain its balance. So oxidative processes (using fat mainly I guess) are running at 100% (VO2max) but are not sufficient to produce ATP quickly enough (the ATP production rate is not enough to compensate ATP use rate). So non-oxidative processes such as ATP-PC (quickly depleted) and non-oxidative glycolysis enter the game. Oxidative glycolysis is not able to proceed because

non-oxidative is more efficient in terms of ATP production rate (not in terms of ATP yield per glucose molecule) and the body favours this one in view of the energy demand

@FenryrMKIII No, it would mainly use glucose, not as much fat. And, "efficiency" is relative to whichever state the body is currently in. While at rest, oxidative phosphorylation is more than enough to maintain appropriate ATP-levels, and you get ~36ATP per glucose molecule, so in resting cells this is much more efficient because it also allows preservation of resources. I don't really think you can say any one pathway is "more efficient".. Cells will always try to react in such a way that is optimal to a given situation - and if burning through the bodies glucose-stores to produce lactate

happens to be the optimal option during exercise, that is what the cell will do. To think of certain processes as being the "most efficient" leads people to believe things like "the paradox to anaerobic energy production during exercise". So yes, you are right on the money with: "your body doing whatever it can to maintain its balance".

Let's forget the word efficient. Rather, non-oxidative glycolysis is the pathway that is able to provide ATP at a sufficient rate so that ATP stores are replenished sufficiently fast compared to their use. Now one thing I don't understand from your answer is how can the body use glucose with oxidative processes while under intense activity ? Since in such situation, according to my understanding, glucose is needed for the non-oxidative glycolysis and oxidative glycolysis being the only other pathway to use glucose,

it is not possible for the body to perform oxidative glycolysis while non-oxidative is underway

@FenryrMKIII "Non-oxidative glycolysis ... provides ATP at a sufficient rate", correct! And, I do not think that the body would use very much glucose for oxidative phosphorylation - since the enzyme (PDH) that converts glucose in to AcCoa will not be active due to the low levels of oxygen. Instead, I think the TCA cycle would more so be powered by amino acids and fat (although minimal amounts of glucose might still get theough).

To my understanding, conversion of glucose to AcCoa is not active because the body knows (I don't know how exactly) that he needs to sustain non-oxidative glycolysis (not because oxygen levels are low, oxygen is in fact very present to my understanding given the intense activity). If he goes the AcCoa way, then pyruvate is used and no lactate is formed. Therefore, NAD+ is not replenished to fuel glycolysis and it stops and there is an ATP production hole. In the end I think we agree: during intense activity, non-oxidative glycolysis and oxidation of fat and amino acids provide the ATP.

Well, oxygen is "busy" being the terminal electron acceptor of the electron transport chain (ETC) - which is fueled by NADH/FADH2 produced by the TCA cycle.. But yeah, close enough!  As you can see, it's a very complicated question you have asked.

That is why I asked it :) Because in the books I have, the way they explain it is not clear enough and they contradict themselves sometimes.

No! The oxygen levels have decreased, IIRC the pO2 (in the blood tissue, at least) can drop down by something like 50torr - which is enough of a pressure drop to inactivate PDH - that's what causes the preference of glucose towards glycolysis. But, yeah, oxygen is definitely still there - just not as much of it, so the TCA/ETC will still work, just not as well as it was working prior to exercise.. Everything else that you said after "If he goes the AcCoa way, then pyruvate..." I agree with.

Can you please stop excessive commenting and discuss over in the chat?

pyruvate dehydrogenase requires oxygen as a cofactor to function No, it does not. In biochemistry a cofactor is a non-protein component of an enzyme's active site. The linked paper explores the way in which hypoxia influences the regulation of PDH through phosphorylation.

@AlanBoyd Good catch, thanks. Better?

Thanks @xusr, but I'm going to have to ask you to kindly start reading more carefully, ie. stop skimming through. Because, no where did I ever say that O2 is consumed/produced in the TCA. And also, you don't need to become Alan's echo - we already noted the whole phosphorylation thing at least three hours before your comment.

Fantastic question!  Hopefully this somewhat helps.  It's very difficult to simply this process as it's quite complex.
During high intensity exercise, energy demands exceed either:

The O2 supply
The rate of use exceeds the at which it becomes available.

So the respiratory chain cannot process all of the H+ joined to NADH.
Continued release of anaerobic energy during glycolysis depends on NAD+'s availability to oxidize 3-phosphoglyceraldehyde -- otherwise glycolysis grinds to a halt.

During anaerobic glycolysis -- NAD+ "frees up" when excess hydrogen's combine temporarily with pyruvate to form lactate.  Lactate formation requires one additional step catalyzed by lactate dehydrogenase.

The storage of H+ with pyruvate represents a temporary "collector" of the end product of anaerobic glycolysis.  Once lactate is formed it diffuses away into the interstitial space and blood for buffering and removal.
However, this avenue for energy is temporary.  Blood lactate and muscle lactate levels increase and ATP regeneration fails to keep pace with the rate of use.  Fatigue sets in and performance diminishes.

EDIT

H+ = a free electron
Increasing the concentration of free H+ ions = lowers the pH (so a pH
of 1 is very acidic and has a very high concentration of free H+
ions, a PH of say 9 has a lower concentration of H+ ions and is less
acidic).
Oxidation is losing electrons – reduction is gaining electrons.
During glycolysis NADH is oxidized.  The regeneration of NAD+ (this
is the reduced form of NADH)  during the reduction of pyruvate to
lactate is required for glycolysis to continue under anaerobic
conditions.
Several key steps in the oxidation of glucose to pyruvate involve the
reduction of the electron/energy shuttle NAD+ to NADH. It's required
to reoxidize the NADH to NAD+ in order to avoid consuming the
available pools of NAD+ and to thus avoid stopping glycolysis.
Put differently, during glycolysis, cells can generate large amounts
of NADH and slowly exhaust their supplies of NAD+. If glycolysis is
to continue, the cell must find a way to regenerate NAD+, either by
synthesis or by some form of recycling.
Let me know if that helps!

UPDATE
So these slides will have to do for now (best I have available to post).  Put very simply in anaerobic conditions - there comes a point where there is not enough NAD+ available to convert pyruvate to lactate.
Would H+ ions just accumulate and increase local acidosis?

Thanks for your answer. So lactate production allows capturing h+. Then why is there acidosis during non-oxidative glycolysis? Not all h+ are captured? Also you say there is either lack of oxygen use (I can understand that if muscles are  not well trained to process oxygen or if they are fast twitch which possess less mitochondria for oxidative processes) or lack of supply. How can there be lack of supply during high intensity? Is this because the oxidative pathways are already at 100% and use all the available oxygen? Thanks for the clarification

I edited my post.  Hopefully that helps

Two errors in the edit: H+ is not an electron; NAD+ is the oxidised form; there is only one step in glycolysis where NADH is generated.

@Bob Well, obviously, but that isn't what the sentence Several key steps in the oxidation of glucose to pyruvate involve the reduction of the electron/energy shuttle NAD+ to NADH. conveys, at least to me.

Okay. So, have you heard of alternative splicing? Basically, different organs/tissues can have proteins that perform the same function, but the efficiency at which the proteins function will vary. So, in your first picture there, it is showing that the LDH-protein in the heart is less likely to use glycolysis to produce lactate - since, because the heart is quiet vital to life, damage to this organ needs to be minimised. In your second picture there, it is showing that pyruvate will not be converted to acetyl-coenzyme A in the absence of oxygen - which is required by pyruvate dehydrogenase.

I disagree though with: "there comes a point where there is not enough NAD+ available to convert pyruvate to lactate." this should not be a problem - because of the reasons I listed in my answer. The problem arises when there is a build up of lactate - because the equilibrium will not allow any further shift from pyruvate. So, basically, yeah - "H+ ions just accumulate and increase local acidosis", although it isn't actually the problem.. the problem is the presence of lactate. "H+" does not actually exist as a free ion.

"This avenue for energy is temporary because blood lactate and muscle lactate levels increase and ATP regeneration fails to keep pace with the rate of use. Fatigue sets in and performance diminishes.
Anaerobic Conditions mediate fatigue by inactivating various enzymes in energy transfer and impairing the muscles contractile properties."  I'm reading otherwise...

@Mike-DHSc Yes, but this has nothing to do with the concentration of NAD+. Remember, each time you convert glucose to lactic acid, there is no net-change in the concentration of NAD+. The reason why ATP-regeneration eventually fails to keep up with the rate of ATP-usage, is because the rate of conversion to lactate decreases. The rate of conversion to lactate decreases, because the concentration of lactate increases.

@Bob ah I see -- you seem to have a very strong understanding exactly what's going on.  What you've outlined matches what I'm reading.  I put too much stock in NAD+ Regeneration being some type of rate limiting step.  You're correct - thanks!

I am also looking for more references to add to my answer. I probably should have done this in the beginning, because I do realise that this particular topic seems to contradict a lot of the things that classic biologists take to be gospel. If you find anything interesting, I would like to read it also. One of the references that I am reading right now claims that glucose - uptake is one of the main limiting step in the initial stages of switching to mostly glycolysis. I'll post it once I think I've found a sufficient amount of supporting information.

A cited detailed explanation would definitely be helpful.  I primarily read rehab / health / fitness studies articles etc.-- for work and fun.  If something in that realm comes up I'll let you know.
Wish they had a member reviewed medical based forum on this site to answer questions and add that type of information.


text:
Example of impossibility in the nested hierarchy?
I have conversations with evolution deniers, and I've read that the best single piece of evidence for evolution is the congruence of the genetic and morphological nested hierarchies, and the fact that they are predicted on evolution, but not on intelligent design.
I think I have an example of what would falsify the nested hierarchy; please check me on this, I want to get this right.
Because evolution is a historical process, an organism can only share characteristics, or have varied characteristics, of one of its ancestors.  If an organism had characteristics that came laterally (?) across the nested hierarchy, as opposed to up or down through its ancestry, that would falsify the hierarchy.  An example of this would be a primate with two post-orbital fenestrae (see pic)..
And, we don't find such organisms.
This is not predicted on design because if you design from scratch, without the necessity of varying ancestors' characteristics, you are not limited by not designing a primate with two post-orbital fenestrae.
Do I have this right?

Your view of evolution is wrong

If an organism had characteristics that came laterally (?) across the nested hierarchy, as opposed to up or down through its ancestry, that would falsify the hierarchy

The expression "falsfying the hierarchy" does not mean much, so I won't comment on it.
Note two things
1) Convergent evolution
 - It is not so uncommon that different lineages evolve similar traits when facing similar selection pressures. This is called convergent evolution.
2) Horizontal transfer
 - It is not so uncommon that pieces of DNA find itself (via a number of different mechanism) in a different lineage. A gene can therefore jump from one lineage to another one. This causes the gene tree of a given gene to not match the species tree. Other processes can cause such mismatch though. This is called horizontal gene transfer.
So, in short, no your view of what you call "impossibility in the nested hierarchy" is wrong.
Intelligent design
Intelligent design is not a scientific hypothesis. It means that it does not make logical sense and it does not make clear predictions that can be tested. By contrast, the theory of evolution is a set of hypothesis all of which that have been formally tested have shown to be confirmed by evidence (that's why the theory of evolution is called a theory;
see here for the semantic).
It is therefore impossible to say whether intelligent design is correct or wrong because it does not say anything. One cannot compare the predictions of the theory of evolution with the ones of intelligent design as intelligent design does not make clear predictions. One can only argue why the theory of evolution
is a set of (confirmed) hypotheses while intelligent design is not a hypothesis (or set of hypotheses).

While evolution generally predicts a nested hierarchy for shared traits of organisms, it's not generally that simple - there are some cases that can lead to exceptions of strictly nested hierarchy.
The first (obvious) one is convergent evolution: if there is an easy biological 'solution' to a certain problem (caused by the environment), then evolution will often find that solution independent where it started from. A good example for this are back fins in fish and marine mammals, which are very similar but not actually related. Of course this is no argument against evolution, it's just a bit more complicated to explain, why different evolutionary starting points can lead to (seemingly) the same outcome.
A second possible exception is caused by the fact that organisms do not just gain new traits during evolution, they can also loose them (if they don't serve any purpose any more).
A very good example for this are teeth: sharks have them, some fish have them, mammals have them, as do many reptiles, but birds generally don't have teeth. Still this is no argument against evolution - first because birds don't need teeth so why should they keep them? Secondly, the genetic program to make teeth is not absent or missing in birds - its just disabled: when researchers tinkered around with this, they managed to make chicken with alligator (or dinosaur) like teeth

Nicolai, thanks very much.  Aside from those exceptions like the ones you mentioned, would you say that my example is a good illustration of the basic idea of why the nested hierarchy is predicted by evolution?

@Slothrop yeah your example is definitely right. Generally you expect a new trait formed at a junction in the taxonomic tree to be present in most species that are descendent from this point.

As an add-on, genetic evidence is often an excellent tool in cases of convergent evolution that are not as clear-cut. In most cases, convergent phenotypic solutions come with dissimilar genetic ones.


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What is the difference between prefrontal cortex and frontal lobe?
They are both in the front. Looks like they're the exact same thing.
Is one part of the other?
What?
Why is it called prefrontral cortex? What does pre before frontal mean? Before front?

Please don't spam the same question, especially when you already got an answer and when your question was criticized for its simplicity and lack of effort. Prefrontal and frontal lobe are not the same thing, though prefrontal cortex is located in frontal lobe.

It's not the same question. Okay where else should I ask this sort of questions?

The answer says that prefrontal cortex is called such because it is behind the prefrontal bone that doesn't even exist in modern mamal. I seriously doubt the only answer. I think understanding etymology of certain anatomical term would help many people tremendously in remembering those terms.

Yes it is the same question. If you doubt an answer, address those doubts on the original answer, don't make a new identical question. Prefrontal cortex was named well before modern neuroscience by an anatomist who was familiar with animals of all sorts and apparently chose to make an analogy in naming, which is quite common in anatomy.


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Is autoclaving sucrose solution necessary?
I use 10% sucrose solution to feed lab mosquitoes. Until now, I mix sucrose in autoclaved water and use it directly for feeding mosquitoes. Is it necessary to autoclave the sucrose solution itself before use?

aren't there are standard protocols for feeding these lab animals? or some sort of International Mosquito Research Association

I tried my best, but couldn't find any standard protocol. They have just mentioned what percentage of sucrose solution must be used. There is no information about autoclaving or filtering sucrose before use.

Sugars usually get charred when autoclaved or at very high temperatures. Autoclaving sugars is unadvisable.

instead what you can do is add the sugar after autoclaving the remaining components, in a hood.

Or filter the solution through a 0.2µm filter.

If the sucrose is to be used as a food source for mosquitoes do either of the possible problems – charring or fungal contamination – actually matter? Also see my contribution to the charring debate in my comment on the answer from Karthik.

I found a standard protocol for the same here : http://vosshall.rockefeller.edu/assets/file/Vosshall%20Lab%20Mosquito%20Rearing%20SOP%20DEC%2012-2014.pdf
Take a look at page no.8. They suggest to autoclave the sucrose solution.

The protocol refers to a preprogrammed cycle and doesn't specify psi. I vaguely recall using a lower psi setting for sugar solutions – 6 psi/110°C? – as compared to standard 15psi/121°C so maybe that is what this refers to.

I wouldn't autoclave this solution - sucrose will partly break down into glucose and fructose. A portion of the sugars will also caramellize and color the solution yellow to brown.
If you need the solution to be sterile, I would filter sterilize it, although this can be hard because of the higher viscosity of the sugar solution. If you haven't seen any negative effects of preparing the solution fresh with autoclaved water, I don't think there is any need to change your protocol.

I routinely autoclave 20% sucrose and don't see any evidence of caramellization. Also, 10% sucrose would not be difficult to filter.

@canadianer I stopped it, after we got brown solutions back. Seems to depend on the autoclave. Our solution was to make really high concentrated solutions (and these are hard to filter), to have the osmotic pressure on our side against contaminations. Works pretty well.


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Is this a nest and which wasp species?
A friend found this stuck to his insect screen today.
He said it felt like dust.
This wasp/bee was alive.
Location is Germany.
Is this a nest?
First look:

After peeling it open:

Looks like this is a European wool carder bee (Anthidium manicatum)
More precisely a female, judging by the round end of the abdomen.

Information regarding the nest it was found in:

These bees construct their nests in preexisting cavities, using the trichomes of wooly plants.
Females use their mandibles, which are sharply toothed, to remove trichomes from the stems and leaves of various plants. They then roll up the trichomes into a ball and bring them to a preexisting cavity. Inside the cavity, the bees fashion the trichome ball into cells, where they deposit an egg as well as a provisioning mass consisting of nectar and pollen. Once finished, she seals the entrance to the cavity with a terminal plug, which consists of inorganic and organic materials that she brings to the nest. Source


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Recommendation for book about soil and their food webs
Are there any de facto books for studying soil biology; specifically with details in the context of food webs? I am trying to teach myself about the subject and would like a good introductory book, although I will take any recommendations. Thanks

A very good resource can be found here:
http://esdac.jrc.ec.europa.eu/content/global-soil-biodiversity-atlas
If you focus on soil analysis this resource could be helpful:
http://www.geokniga.org/bookfiles/geokniga-handbook-soil-analysis.pdf
I could also recommend the book
http://www.springer.com/gp/book/9783642309410
with which I worked extensively. It covers the soil chemistry very well.

I really enjoyed reading "Essential Soil Science" by M.R Ashman and G.Puri.
https://g.co/kgs/SCjpSi
Seems to be easy to get online as a pdf as well.


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Online resource for downloading gene variant data?
I have a long list of gene variations. For example, Here are 4 of them:
CBL Q249E
TERT H412Y
SF3B1 R625H
EGFR L747_T751delinsP
The first term identifies the gene, the second identifies the variation.
I am a data scientist with no background in biology or medicine. I am looking for an online resource where I could download synonyms, descriptive data, and other relevant info for all the gene variants.
I have seen two sites where data is offered for some gene variants, but not for others. For example, the EGFR L747_T751delinsP variant is well documented at this and this site.
While CBL Q249E is documented at the ckb.jax site but not the reactome site. Other variants are documented at reactome but not ckb.jax, etc.
Plus, there appears to be no easily downloadable file containing this data. Before I go scraping what I need off of a hodgepodge of websites, I wanted to check with you smart people to see if there is a user-freindly resource out there that has this data in a downloadable format.

Tried this one? http://dgv.tcag.ca/dgv/app/home

Seems your variants are all possibly harmful mutations to human genes, in that case ClinVar can be quite useful, it returns hits to all your variants except L747_T751delinsP. I have never used the ClinVar API so I'm afraid I can't vouch for how easy to use that is.
When ClinVar doesn't have the variant (or info about it) you need you could search EBI to see if other sites have information for this variant, when queried with L747_T751delinsP EBI actually shows us that it has been entered into Reactome twice. (welcome to the mess that is sequence annotation!).
This might be outside of your scope but if you have an interesting variant that you cannot find information on you could try to find the most similar (known) variant using BLAST.

Yes, these are all potentially harmful mutations. Although passenger genes with mutations could ultimately be beneficial (harmful to the cancer), if I understand correctly. Thanks for these great resources. Could it be that L747_T751delinsP has 2 entries at Reactome because it is a type of variation that can occur in different genes?

@ben seems like the only difference between the two entries is that the protein of "p-6Y-EGFR" entry has a bunch of phosphorylated tyrosine residues. Basically it seems the two entries cover the same gene, same variant in this gene and same protein sequence but the p-6Y entry has extra modifications to this protein. This probably does indicate difference in function but this should give you an idea of how confusing, and difficult to automate, this can get.

You can use the Table Browser.
For the variants, in the group field select variation, in the track field, select any database you are interested in, finally insert the genome position of your gene of interest and you will be able to download the relative data.
For the synonyms, descriptive data, and other relevant info for all the gene variants, in the group field select Phenotype and Literature and from the track field, select any database you are interested in. You may need to download data from multiple databases to get all the info you want, but the whole procedure is quite fast and you can do it directly from the browser.

Thanks. I do have location info for each of the genes in my data (which I got from a website--can't remember which off the top of my head right now), so I can fill in the important fields at Table Browser. Problem now is that the names of the variations given at this site do not match any in my list of variations. They all start with "rs" followed by a number, whereas you can see in the original question above the variations in my data follow a different nomenclature. Any idea how to translate between the two?

@ben It's not trivial to find the correct ID, different databases use a different one. The rs suffix is from the dbSNP database. The mutation you are looking for EGFR L747_T751>P is an indel, you can find it on the Cosmic database

I think the correct nomenclature is EGFR L747_T751delinsP, based on http://varnomen.hgvs.org/recommendations/protein/variant/delins/
You can also use a translator tool like TransVar
@smock2020 and @JAX_CKB


text:
What species is this turtle in Houston?
This turtle was displaced by hurricane Harvey in Houston, Texas, USA (Buffalo  Bayou and Dunlavy). It appears to be a snapper. Can someone identify the exact species?

That's an Alligator snapping turtle, Macrochelys temminckii.
Here is another picture of it (from the same Wikipedia page linked above):

It should not be mistaken for the Common snapping turtle, which belongs to a different Genus.
There is a problem, though: in 2014 Thomas et al. divided the Genus Macrochelys (which originally contained only one species, Macrochelys temminckii) in three species: Macrochelys temminckii itself, Macrochelys suwanniensis and Macrochelys apalachicolae.
Therefore, narrowing this down to the exact species (according to the current taxonomy of the Genus) may be way more complicated.

Source:

Thomas, T, Granatosky, M, Bourque, J, Krysko, K, Moler, P, Gamble, T, Suarez, Leone, E, Enge, K, & Roman, J, 2014. Taxonomic assessment of Alligator Snapping Turtles (Chelydridae: Macrochelys), with the description of two new species from the southeastern United States. Zootaxa 3786 (2): 141–165

Above answer is correct but the other two recently differentiated species are both East of Texas, so this is for sure temminckii.


text:
Can cancers caused due to viruses be contagious?
Generally, viruses are infectious in nature and there are several cancer-causing viruses that are known (i.e. oncovirus)
My question is:
Are these oncoviruses infectious in nature? If so, what is the way in which they can be transmitted?
(edit:just a background to connect the title and the question (as mentioned by user iayork):While reading my text(which led me to the doubt) I was considering the virus as a causal organism and the disease as cancer(malignant tumour cells).The cancer cells are non-contagious however I wanted to understand if the disease  was.Thus I was interested on the routes of the transmission of the viruses.Also note (which I had already asked user Chris in the comment) "most cancer disease are non contagious but if cancer disease was due to virus if it was contagious or not"

You may want to reword the title so that it matches the question. It should be something like "Can viruses that cause cancer be contagious?". Otherwise it sounds like you're asking if the cancer itself is contagious, which is a totally different question. I see your edit, but the ambiguity still remains.

Just to be clear, not sure whether you understand this part or not, but viruses that "cause" cancer do not guarantee cancer, they increase the risk of cancer in affected individuals.

The question title and the question itself ask two slightly (but critically) different questions.

Can cancers caused due to viruses be contagious? NO
Are these oncoviruses infectious in nature? YES

The tumors caused by the viruses are not contagious.  You can't take the tumor and transfer it to a new host and see a new cancer.  The viruses that cause the tumor are contagious, but in many cases by the time the tumor has arisen the viruses are no longer in a contagious form.  A tumor that's caused by HPV doesn't have contagious virus in it (see explanation below), and you can't transplant the tumor into a new host.  There still may be contagious virus present in the patient, but the tumor itself is not contagious.
Explanation HPV causes cancer by having a part (and only a part) of its genome integrated into the host genome, so cancers associated with it inevitably have a defective virus genome. There could theoretically be infectious virus in the neighboring tissues, but the cancer is driven by non-contagious virus. See for example The role of integration in oncogenic progression of HPV-associated cancers for a fairly basic explanation

I think your answer is pointing us to a language problem. You as a biologist may think that "a cancer" is a synonym for "a tumor" and so you wrote an answer geared towards this interpretation. For a member of the general public, "a cancer" can well be "the disease a person with tumors has" which is contagious at some stages. Maybe this should be made more explicit before people without enough background are totally confused.

@rumtscho That is not the general public definition of cancer, and it is not contagious at any stage in humans.

Generally tumors are not contagious, but we know of at least one case where that is not true. A communicable facial tumor has decimated tasmanian devil populations, though it is spread through an allograft, not a virus. https://en.wikipedia.org/wiki/Devil_facial_tumour_disease

there is also evidence of contagious cancers in clams http://www.sciencemag.org/news/2016/06/contagious-cancer-found-clams-and-mussels

Since the question is about viral tumors, it's probably actively confusing to start talking about non-viral contagious tumors like the bivalve and Devil versions.

@iayork "A tumor that's caused by HPV doesn't have contagious virus in it" a reference would be helpful.thanks.

Yes, Oncoviruses are infectious in nature. A good example is the Human Papilloma Virus, which does not immediately cause cancer, but can cause precancerous lesions in infected regions including cervix, vulva, vagina, penis, anus, mouth, or throat (see references 1 and 2). HPV is transmitted during sexual activities (hence the broad range of infected tissues due to different practices).
There is now a vaccine available since a few years which allows prevention against infections with the HPV types 16 and 18, which cause most of these infections. If it is administered before the first sexual activity, it provides a good protection against infection with these HPV types.
Other tumor viruses like Hepatitis C or Kaposi's sarcoma-associated herpesvirus, to name just two, are also infectious. If they weren't, they wouldn't be able to spread.
As @iawork says, it is important to say that the cancers which are caused by these viruses are not contagious, only the viruses are.
References:

Human papillomavirus (HPV) and cervical cancer
HPV-associated diseases.

thank u for the answer.jst to be precise,then can it be said that when we say that cancers are non-contagious it actually excludes a virus caused cancer which is actually infectious?

@CATHARANTHUS Normal cancers are not contagious. The either arise due to a genetical predisposition or acquired mutation. The virus is the agent that causes these mutations (which could also be a chemical). It happens to be that viruses are infectious.

@iayork : Huh...  Apparently reading comprehension is not my thing this morning.  Meh.  Removed.

@BryanKrause I removed this part of the comment.

Oncoviruses are most commonly transmitted sexually however in the cases of EBV (Epstein-Barr Virus) and MCV (Merkel cell polyomavirus) can be transmitted in other ways such as through an oral or respiratory route.
These viruses are contagious however as mentioned by others the cancers caused my these viruses are not contagious. In the case of HPV for instance the cancer tends to be caused through the virus integrating with the host cell and expressing two oncoproteins (E6/E7) which interact with tumor-suppressing proteins resulting in uncontrolled cell growth. The virus itself cannot bind to live tissue it instead is limited to the basal cells of stratified epithelium such tissue can be found in the cervix which is why HPV is responsible for upwards of 90% of cervical cancer cases. Because viral integration usually needs to occur for cancer to occur the virus itself needs to be contracted for integration to occur.
Also as mentioned above two genotypes of HPV (16 and 18) are responsible for most cases of cancer but there are over 200 genotypes of HPV of which there is a large number which are considered oncoviruses such as 31, 33, 39, 45, 52, 58, and 59. And another of others which are still subject to debate - many of which are not covered by the current vaccine.


text:
Spatial distribution of axons connecting distant groups of neurons
It would help me to shape my picture of the brain, if I knew the following:
Consider two specified groups of neurons A and B in the brain that are well-located but quite distant from each other (e.g. two roughly spherical nuclei, or two Brodman areas corresponding across hemispheres), and which are (more or less) directly connected synaptically, i.e. axons of the first group build synapses with dendrites of the second, the distance being mainly bridged by the axons. I assume there are lots of examples on different scales.
My question is: Is there a preferred way how the axons are organized, i.e. spatially distributed in the brain? Do they run  mostly parallel to each other in bundles, or are there (maybe exceptional) cases, where the axons (or small subsets of axons) take individual routes, possibly quite far from each other?

I am aware that with intermediate groups of neurons, there are different and non-parallel pathways of one group of neurons to the other. So my question is explicitly about directly connected groups.
(Are there too many simplifying assumptions in my question that make it vacuous?)


text:
How to interpret McDonald-Kreitman test results?
It is easy to get the numbers right and calculate neutrality index. It is easy to memorize "equals", "greater", "lesser", etc. At least on the exams, when certain level of simplicity is assumed. But instead of memorizing I'd prefer to understand. So far I struggle to get past the numbers. Could anyone, please, explain reasoning behind the them? Why certain values means the trait is advantageous or not? An easy to understand example would be helpful as well. Thank you.

This video by Mohammed Noor will be of interest to you!

@Remi.b I'm coming from his lecture exactly. In general the lecture is great and I can understand everything, but not the M-K test part. I even passed the exam - that's why I said above it's easy to pass, not so easy to understand.

A helpful way to phrase it for me is that "If there's a disproportionate fraction of non-synonymous mutations between species relative to what exists within species, it is because non-synonymous mutations are being selected for in the one species but not in the other, thus there's positive selection."
By the way I'm not an expert in this so take the explanation with a grain of salt.

Welcome to the site!  It would be great if you could dig up some sources to back up this answer.  Thanks!

(intraspecies non-synonymous polymorphisms)/(intraspecies synonymous polymorphisms) should equal the (mutation rate of non-synonymous mutations × number of non-synonymous sites)/(mutation rate of synonymous mutations × number of synonymous sites). Note that the mutation rate of synonymous mutations is just µ. Let F be the proportion of the synonymous mutations that are not deleterious so that the mutation rate of non-synonymous sites is Fµ. Let k be the ratio of synonymous sites over non-synonymous sites. Then the above fraction is equal to F/k. The same logic can be applied to find that the fraction of (interspecies non-syn polymorphisms)/(interspecies syn polymorphisms)=F/k, assuming the probability of fixation is roughly the same for synonymous and non-synonymous sites (neutral theory's assumption).

Welcome. Could you add your sources to allow other users to background read on your answer?


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Red blood cells
How can we classify red blood cells while they lack nucleus?
From my point of view i find it difficult to be classified as we have all cells with nucleus, even prokaryotic cells which have no nucleus membrane but they have a nucleus material which is DNA.
Maybe if we classify it as a type of cell which lacks nucleus and others are cells with nucleus

What do you mean by classify? Red blood cells have a highly distinctive shape, which you can use to discriminate them against other blood cells.

Human RBC develop from a nucleated cell which, clearly, is eukaryotic. They lose their nucleus at the end of their developmental pathway. It wouldn't make any sense to reclassify them. If you need an adjective to describe them it is: anucleate.

As with many types of blood cells, subsetting cell types in a heterogeneous population can be done by flow cytometry. This is really quite a nice paper because it explores the differences between erythroid lineage cells and other cell types. Based on their immunophenotyping at different stages of erythroid differentiation, you can see that the cells begin to lose discerning markers as they get closer to losing the nucleus.
Also for your reference, a chart on blood cell differentiation.
Take home point: I would classify them as erythroid cells, erythrocytes on the basis of CD235+, CD71-, CD45-, CD117- by flow cytometry. CD235 may not be present in non-primate blood (ref).
CD numbers are referred to as clusters of differentiation, or as you've described it, how do we know what a cell is if it's indistinguishable from a mixed bag? These markers are used routinely in immunology for cell classification, though as commented red blood cells are easy to spot. My only thought is you may mistake a reticulocyte for a RBC by conventional light microscopy without the appropriate stain, so it's worth being careful if you're new to viewing these cells in a microscope.
We don't need to create an entirely new classification of cell, however. Think of RBC as terminally differentiated blood cells.


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Reason for conversion of glucose to fructose in glycolysis
In glycolysis, glucose is converted to glucose 6-phosphate so it can not diffuse out of the membrane. Then it is converted to fructose 6-phosphate.
Why is this? Perhaps it makes it less stable so it is easier to break down into pyruvate?
That is just a guess, is anyone able to provide more information about this?

Don't guess. Please do some research before posting basic questions that can be answered by reading a text book of biochemistry. For example Chapter 16 of Berg et al. online.

However as I do not think either of the answers (including the one you accepted) are adequate, the point is less obvious than I imagined.  I have therefore provided my own answer.

Clarifying the question
The pathway of glycolysis starts a hexose (glucose), but at a certain point — the aldolase reaction — two molecules of a triose are generated, then interconverted to the same triose, after which the pathway continues to pyruvate, generating net ATP. These triose molecules each carry a phosphate, which, as the poster mentions, prevents them diffusing through the cell membrane, so the hexose precursor needs to carry two phosphates. Thus the question “why is fructose formed?” can be restated as:

“Why is the hexose precursor of the two triose phosphates fructose 1,6-bis phosphate, and not simply glucose 1,6-bis phosphate?”

Short Answer
The chemical structure of glucose is not suitable to form a bis-phosphate compound that can yield interconvertable triose phosphates in the biochemical reactions the cell employs.
Fuller Answer with Chemical Details
First consider the linear and cyclized structures of relevant phosphate derivatives of glucose and fructose:

Glucose 1,6-bis phosphate may be unfamiliar: it is found in cells in low amounts and may have some regulatory function. Inspection shows that, because the aldehydic group is at the 1-position of glucose, a phosphate can only be added at that position after cyclization generates an alcohol there. Once glucose 1,6-bis phosphate has been formed it cannot convert to a straight-chain structure, unlike fructose 1,6-bis phosphate where the ketonic group is in the 2-position. (Hence none is shown.) This is the key point.
Now let us turn to the triose–hexose interconversion, which is necessary for both glycolysis and gluconeogenesis, which ever originated first. This has two requirements:

That the triose phosphate molecules can react with one another to
form the hexose carbon backbone (easier to consider the reaction in
this direction).
That if different triose molecules are required they can easily
interconvert from (or to) a single triose.

Requirement 1 is satisfied most easily in biological systems by an aldol condensation such as the aldolase reaction (also found in the Calvin cycle) in which the nucleophilic carbon of an enolate attacks the carbon of an aldehyde.
Requirement 2 can be satisfied by the isomerization of an aldehyde (like glyceraldehyde 3-phosphate) to a ketone (like dihydroxyacetone phosphate).

The fact that a ketone like dihydroxyacetone phosphate has the potential to form an enolate (shown above) explains the particular suitability of these trioses in relation to the aldose reaction:

[Taken from Chemistry Libre Texts.]
The initial product of this reaction is, of necessity, a linear hexose 1,6 bis-phosphate — with the fructose as the hexose as its carbonyl is at C2. After the fructose 1,6-bis phosphate has lost the phosphate at the C1 position it can isomerize to glucose 6-phosphate (with the C1 position free to form an aldehyde) in a similar manner to the triose phosphate isomerization.
So it is not just the symmetry of fructose (noted by the poster in a comment) that is important — but the structure of glucose itself. Glucose 1,6-bis phosphate is not, of course, the only sugar that can become ‘locked’ in its cyclic form. For example, the deoxy-ribose rings in the backbone of DNA cannot linearize because the bases are attached to the C1ʹ where the aldehydic group was originally.

Avoiding diffusion is one reason to phosphorylate glucose, the other is that it is removed from the osmotic balance between inside and outside of the membrane, so it can be transported at a high rate.
The Glucose-6-phosphate can then be used as a substrate for different pathways, namely glycolysis and the pentose phosphate way, and (depending on the organism) also be converted into glycogen and starch for further storage.
The reason for the phosphorylation lies further downstream in glycolysis: The isomerization by the glucose phosphate isomerase and the subsequent second phosphorylation into Fructose-1,6-biphosphate make the conversion and dedication of the molecule into the glycolysis irreversible.
Fructose-1,6-biphosphate is then cleaved by the aldolase into two C3-units: Dihydroxyacetone phosphate (DHAP) and Glyceraldehyde 3-phosphate (GA-3-P). GA-3-P is converted into DHAP, so that downstream only one metabolite needs to be processed.

Very good response thank you, in addition I finded out that fructose 1,6 biphosphate is somewhat more "simetrical" than glucose-6-phosphate, if it wasn't isomerized it would only form 1 usable substrate, the other would be slightly off shape and wouldn't fit in enzymes further in the chain, I not sure if this is accurate, but it sounds logical.

@RafaelFranco - please don't thank people - upvote the answer if it's useful and accept it when it answers your question. That way other users can immediately assess the impact of the answer.

So what part of your answer is to the question of “why fructose?”. I quote: “Then it [glucose 6-phosphate] is converted into fructose-6-phosphate, why is this?”

If there is no glucose there is no need for glycolysis: I deduce from this truism that – at some early stage in the evolution of metabolism – a pathway resembling gluconeogenesis must have arisen before glycolysis. This is just another way of stating the obvious fact that autotrophy must have preceded heterotrophy.
If the aldolase reaction for triose → hexose evolved around glyceraldehyde 3-phosphate/dihydroxyacetone phosphate then perhaps the involvement of fructose 1,6-bisphosphate was dictated by the underlying chemistry of the aldolase condensation, and the steps to glucose followed from there. Note that the main carbon fixation pathway in photoautotrophs does indeed use this process: carbon fixation by RuBisCO generates 3-phosphoglycerate and the subsequent action of triosephosphate isomerase and aldolase generates fructose 1,6-bisphosphate.
So, my main point is that seeking the underlying design principles in the glycolytic pathway may be futile: glycolysis represents the catabolic use of a sequence of reactions that originally evolved for the purpose of anabolism.

Disclaimer: I have probably read this idea somewhere but I have no recollection of where. If anyone can point to an authoritative version of this please do so.

The anonymous downvoter strikes again.

Alan, regardless of whether gluconeogenesis or glycolysis came first (interesting — you should post this as a separate question) the question is remains — “why is there a fructose hexose stage between the triose and the glucose hexose?” That is the essence of what the poster is asking, even if he is coming at it from glycolysis.


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What would EEG recordings reveal if their resolution was better?
1. Temporal resolution
Of course, we would see higher frequencies. But would these be informative? Aren't the frequencies measured today near the border to noise?
2. Spatial resolution
I guess LFP measurement goes in this direction (closer to the sources of the signals being measured). But what would we learn by that? Finding small-scale regions (below Brodman area size) which behave phase-locked/synchronously?
3. fMRI
The same questions could be asked with respect to fMRI. But I guess, as long as temporal resolution is as poor as it is today (and which cannot be much better), we don't have to ask for spatial resolution, or do we?

Short answer: No. The limiting factor is not the resolution (it cannot get much better), is the fact that is a signal coming from billions of cells doing different things so by definition noisy and messy. Only when there is very high synchronicity we can get something out of it (e.g. sleep phases).

I assume you answer to question 3.
Billions of cells?

No, for fMRT the problem at the moment is "poor" temporal and spatial resolution. If we had faster imaging we could have better spatial resolution. However remember that fMRT it's only a proxy for neurons activity...hence it measure slightly different things than electrophysiology and will never have its resolution.

I've read that MRT measures process that take up to a few seconds to occur (neurovascular). What benefits could a higher temporal resolution have?

The temporal resolution of EEG is already considered to be very good. The problem is spatial resolution. Even the loss of very high frequency activity, like individual spikes, is really a problem of spatial rather than temporal resolution: the spiking cells are too far away, so it is only possible to detect them if they are very synchronized (in which case they still show up as lower frequency signals).
Because EEG recordings are so far from the sources they are recording from, and because even structures deep in the brain can contribute to surface potentials,the signals end up as complex averages over a large space. There is an entire field called EEG source modeling that tries to use signal processing methods to improve this spatial resolution.
However, you don't really have to ask this as a hypothetical question, since we already have methods that have better resolution than EEG. Electrocorticograms (ECoG) are the most similar, and most applicable to human studies. ECoG arrays are very similar to EEG, but they are placed directly on the dura, under the skull. They increase spatial resolution because they cut down distances dramatically by not having to record through the skull.
As you mention in your question, local field potentials (LFP) get even closer to where the measured currents are occurring, by recording from within the brain itself. The spatial resolution of LFPs themselves can also be improved by recording from multiple electrodes and computing a current source density. This also helps mitigate the effects of volume conduction.
fMRI is a completely separate issue. Often, EEG and fMRI results can act in conjunction, using EEG to determine time and fMRI to determine space (note that although there are limits to the spatial resolution of fMRI, for a human subject it is dramatically more spatially precise than EEG, especially for any structures not at the very surface of the brain, including any of the sulci of neocortex). fMRI spatial resolution can be improved by using stronger magnets, but eventually there are technological (and expense) limitations, but as you say the temporal resolution is fixed, and even the spatial resolution has some practical limitations.
To generally answer your title question: if the spatial resolution of EEG is improved (practically, this means either source modeling or using ECoG or LFP), one is better able to identify the brain structures that are producing the signals observed in the EEG, and able to be more confident that the signals observed are "real" rather than an artifact of filtering over space. For example, a higher-frequency traveling wave could appear as a lower-frequency signal on an EEG, or a localized, high-intensity event could appear like a generalized, low-intensity event; higher spatial resolution would allow you to distinguish between the two in both cases.

May I contact you directly by email? If so, please confirm, when you grabbed my mail address: stricker@syspedia.de - so I can delete this comment as soon as possible.

@HansStricker You can invite me to chat here if you'd like.


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Forest Fires and Horsetails
In our school textbook, it is written that sometime forest fires can occur due to rubbing of two horsetails. In the image that I searched online, the plant itself looks thin and rod like with leaflike structures arising from nodes. But many other plants have similar structure. So it might not be its morphology.
What special thing about horsetail starts the fire? Why don't other plants show same thing?

I didn't believe this was a real thing, and I'm still very skeptical, but it is something that's claimed to happen!

Their stems & leaves have a siliceous epidermis, so if rubbing b/n 2 horsetails occurs, a forest fire may be produced

--The Bottled Ocean of Biology, by Nisarg Desai, 2017
Why don't other plants show same thing? Another plant, bamboo, is supposed to do the same thing:

How these fires originate is uncertain ... it has been suggested that a probable cause is the rubbing together of the silica-coated bamboo stems as they sway in the breeze.

--Burma, by R. Talbot Kelly (2004)
The same claim about bamboo is made in an Indian Government document on forest fire management.
What special thing about horsetail starts the fire? Apparently the claim is that it's the silica in the stems of the plant that is the important factor, and that horsetail and bamboo are both unusual in that regard. This does seem to be true:

... in general, ferns, gymnosperms and angiosperms accumulated less Si in their shoots than non-vascular plant species and horsetails.

--Phylogenetic Variation in the Silicon Composition of Plants
Bamboo isn't mentioned in that article, but the presence of silicon in bamboo is supported elsewhere:

One of the advantages of bamboo over wood is that bamboo contains some silicon in both inner surface (pith-ring) and outer surface (rind) of the bamboo culm.

--Calcium phosphate formation induced on silica in bamboo
As I say I remain very skeptical. There's no evidence shown that this has actually happened. Is it telling that all these claims come from the same general region (India and Burma)? My guess is that this is an old wives' tale that's been written down and uncritically accepted, but if someone has actually seen this happen I'd be happy to be proven wrong, because the idea of plants sparking out flames in the wind is a pretty cool one.
Edit to add a link claiming that bamboo-on-bamboo generates sparks due to the silicates:

The method consists of striking sparks out of  the culm of Schizostachyum bamboo with flint, broken pottery, china or even another piece of bamboo. The sparks that occur by striking the Schizostachyum bamboo are presumably generated by the high silica content in this genus of bamboo.

--Bamboo Strike-A-Light, by Tom Lourens, Ash Kivilaakso and Ed Read (My emphasis)
Edit to add that the overall concept of plants starting their own fires has been seriously looked at; the author is skeptical:

Individual plant traits (such as leaf moisture content, retention of dead branches and foliage, oil rich foliage) are known to affect the flammability of plants but there is no evidence these characters evolved specifically to self-immolate, although some of these traits may have been secondarily modified to increase the propensity to burn. ... It is more parsimonious to conclude plants have evolved mechanisms to tolerate, but not promote, landscape fire.

--Have plants evolved to self-immolate?
Notably, in his list of factors potentially allowing self-immolation, he does not list silica, and horsetail isn't mentioned at all.

What would the underlying chemistry/physics of this be – can silica generate sparks through friction?

Apparently it does! See edit

Could be that horsetails, as primitive plants, in certain soils, accumulate and concentrate atoms (hyperaccumulators) and just like certain minerals that spark or certain compounds that flare when dry, are source of ignition ie Flash Powder

this would be better suited as a comment

Is this purely speculation, or is there any evidence for this?

...accumulate atoms?

hyperaccumulation genes (HA genes) are found in over 450 plant species, including Arabidopsis and Brassicaceae.

It's a cool idea and it's visibly a myth. No, Apparently it's never been seriously attempted or proven.
No wood friction ignition techniques that I know of use the sides of stems to obtain the 233 degrees combustion temperature of paper, they use the cross section and atm pressure. Equisetum couldn't achieve that because it's not heavy enough to get that kind of pressure on the stems, and it's not tinder plant. It sounds like they were having 300 kph winds!
There is an Equisetum species known as the scouring rush:
The rough stems have been used to scour or clean pots, and used as sandpaper.
Boiled and dried Equisetum hyemale is used as traditional polishing material, similar to a fine grit sandpaper, in Japan.
The stems are used to make fires:
 The silicated stems were used by Native Americans (and still used by some people today) to start hand-drilled fires.
It's probably the basis of a myth that they can start fires. Many horsetails are marsh plants with very deep roots and water storing rhyzomes. They are well studied for growth after forest fires, but there are no clear references to friction of the plants causing spontaneous combustion of the plant, a dubious theory.
... Ignition temp of various woods  190°-260°


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What is this viny plant in the UK?
I am in Northumberland, UK. This is growing in my veggie plot and cannot find out what plant it is....looks like a triffid!! It is one stem growing out of the ground and has many stems growing on the side of the main one which lie along the soil with no roots appearing.
I placed a couple of pea pods beside the brick to show the size. Hope someone can help. Thank you.

The closest that I can get is some sort of chicory, but I'm not confident enough to make this an actual answer.

Neither, it's a very silly title, probably composed to attract attention. I am voting to close this question until you give your question a more descriptive title.

Thank you,  Alan, I am inclined to agree that it is a Cichorium mainly because I cannot find any thing else.

Terribly sorry, David, for upsetting you and possibly it was to attract attention but it was a valid question as nobody seems to know exactly what this plant is. I am guessing you got out of the wrong side of the bed yesterday.

Alan is right to call this a Cichorium. It is  Cichorium endivia, Endive. It is a tropical plant that is widely cultivated for its edible leaves. However, when it flowers the leaves die, so you don't recognize the plant as Endive. The dying leaves can be seen on the picture below, from the Dutch wikipedia page.

https://nl.m.wikipedia.org/wiki/Andijvie

+1 Thanks for clarifying this, I couldn't find an image that convinced me like this one does.

Thank you, both, the photo does indeed look exactly like what is in my plot. I have always thought of endive as been the dense curly head of salad greens. I found this very interesting having got a google translation of The Netherlands Wikipedia. Funnily enough, I have not sown nor planted Cichoriums of any kind so probably blown in on the wind.


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Plant Identification Help

Can someone help me identify this plant? Flowers bloom in summer, then red seeds form afterwards.  Leaf length is about 10 inches max.  I live in Southern California and it is grown in a container under my patio.
Thanks for your help.

This seems to be Scadoxus Puniceus, also known as the Paintbrush Lily (not to be confused with other species with the same common name). The dutch originally cultivated scadoxus puniceus, and your specimen could be one of several hybrids of the original.
Dave's Garden has plenty of pictures of the species. He didn't have any fruit at the same stage of ripeness as yours, but the likeness is still rather compelling.

For a slightly more reliable source (if a little older), the South African Medical Journal also identifies Scadoxus Puniceus in a study of accidental poisonings by herbal medicine. The flower might be a touch wider than yours, but you almost certainly still have a Scadoxus, and within-species variations can easily account for such a small difference.

Copyright Disclaimer: All included photos would typically fall under fair use due to their limited scope compared to the original work and due to their non-commercial use as a benefit to the public. If any of the copyright holders disagree, feel free to contact me so we can resolve the problem.

Welcome to the biology SE and congrats on your first answer, that I believe to be correct. However, on BiologySE it is required that you substantiate your claim with evidence, for example a picture or a description why it is this species.

@RHA Thank you. Is this more like what you had in mind?


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Number of hair cycles in humans
I've seen several websites claim the amount of hair cycles a follicle will go through is predetermined at around 25-30 complete cycles. Is there any genetic evidence to validate this claim? How can this even be determined apart from observationally seeing people lose hair as they age?
Here's a link referring to what I'm talking about:

The number of hair growth cycles is limited: our hair will experience about 25 to 30 cycles like this during our lifetime.

note that is an individual follicle, we do grow new ones.

The link in this question is dead. :(


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How do migrating geese handle hurricanes?
I live on the East coast of the United States, where we are in hurricane season. This week during my morning bike rides in Charlotte, North Carolina, I have seen migrating Canadian geese.
I'm curious if migrating geese have any adaptations for sensing and dealing with hurricanes? Do they treat it like any other rain and wait it out or are there observations of them avoiding a storm?
Here is the range of the Canada Goose.

Do geese migrate far enough south during hurricane season, so that they'd be likely to encounter hurricanes?

yes. I see them overhead now and there is a hurricane coming my way.

Are they actually migrating, or just flying around?  It seems way too early for migration.  And would they have specific adaptations for hurricanes, as opposed to storms in general?

Strongly related question


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Can anyone expolain this? Cell culture vials have strange hair-like condensation patterns
What is the hair-like polymer that condenses on the caps of the plastic cell vial? Inside vial are cells in a mixture of FBS and DMSO. The vials were frozen slowly in a special isopropanol-filled container (isopropanol does not touch the vials) to -80 degrees celsius, then put on dry-ice to move to a liquid nitrogen cryogenic freezer. The hair-like crystals appear to be water, but bend toward my finger when nearby, similar to the static attraction.
I suspect the has something to do with DMSO/isopropanol leaking out, and the very low temperatures cause this strange condensation pattern, but I'm not sure.

This question might be better suited for the Chemistry or Physics SE


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What type of guatemala beetle is this?

it was in Guatemala
it was really big like 4 inches
sorry I don't have a better photo

Search on Buprestidae family.

This click beetle belongs to the species Chalcolepidius rugatus.

According to the original description, this species is clothed, dorsally with white pubescence, with the sides of pronotum and elytra marginated by yellow, and ventrally, with brown pubescence. source

source

source

Distribution

source


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What is meant by genomic imprinting being reversible?
I'm not trying to understand the underlying molecular processes, rather understand it conceptually.
This is what it says in my coursebook:

"The imprint, obtained during gametogenesis, is reversible: an allele
with paternal imprint will, after transmission through the female
germline, be changed into an allele with maternal imprint.
In other
words:
Paternal imprinting means that some gene obtained from your
father is 'silenced'. These 'silenced tags' remain during your whole
life, but are reset during the formation of egg-cells or sperm-cells.
Some genes are always silenced in egg-cells, others in sperm-cells.
There is a continuous activation and deactivation in function of the
parent who transmits the gene"

I don't understand how the first paragraph and the last paragraph can both be correct.
If the paternal imprint changes into a maternal imprint after passing through the germline, this implies that the gene is just deactivated in the chromosome that is passed on and we call is paternal or maternal depending on who passes it on.
On the other hand, the last paragraph (and the middle one) imply that, if you receive a gene with maternal imprint from your mother as a man, your body resets the 'silencing' during gametogenesis, realizes a sperm cell is being made and decides not to silence it since it will now be passed on from a father. Only this can explain why it would lead to continuous activation/deactivation or reversibility.
Which of the two is correct?

Only during the formation of egg-cells or sperm-cells one can leave the maternal or paternal imprint, respectively. So for example a man, will leave its paternal imprint on an allele (during spermatogenesis) that was given by his mother (while the allele was maternally imprinted in the rest of his body).

I understand that, but the first line implies constant switching between paternal and maternal imprinting, which implies that the allele is constantly deactivated, since it's always imprinted and that's the definition of imprinting.
The last line says there's constant activation/deactivation of the allele, how can this be true if there is a constantly switching imprint as opposed to imprint/no imprint?

Sorry but I don't understand the confusion. The first sentence is the same as I try to explain. The imprinting changes only during gametogenesis, in other words during sperm or egg formation. Only then the imprint is changed (to paternal or maternal respectively). This is what they mean with reversible. I don't see that it implies constant switching. What word does imply this??

"There is a continuous activation and deactivation in function of the parent who transmits the gene"

Yeah in either father's or mother's gametogenesis, respectively, the allele will be activated or inactivated. Maybe a real life example will help you understand how it works, Prader-Willi and Angelman syndrome...

Okay, so, you say the allele will be activated. The allele is now active in the gamete. Since it is active, there is no more imprint (The definition of imprinting implies INactivity). In your comment you said "The imprinting changes only during gametogenesis (...). Only then the imprint is changed (to paternal or maternal respectively)." If, as you say, it changes to a maternal or paternal imprint, it implies INactivity (again referring to the definition of imprinting).

Did you read the links in my comment?, I can't explain it better than this.

I think I understand it now, the gene that's being deactivated isn't the same for paternal imprinting and maternal imprinting. This wasn't explicitly mentioned in the course so I didn't think to make a distinction. Now it makes sense that the imprint of 1 gene disappears so it becomes active, while the imprint of the other appears and it becomes inactive. Which also explains activation/deactivation together with a switching of imprint. Thank you!


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What is the 'job' of the byproduct water in the Electron Transport Chain?
I understand what happens in the Electron Transport Cycle, but I fail to understand that after Oxygen has accepted an electron, it forms water, but why? what happens to the water? I can take an educated guess but again its a guess.
Does it then react with ADP?
Thanks in advance! I'm doing an animal welfare course and as part of it I need to study basic biology.

The formation of water in the matrix at the end of the electron transport chain helps to maintain the hydrogen gradient between the intermembrane space and the matrix.

Thanks for your question.
One reason is, if this chemical reaction does not happen so there will be a lot of electrons in mitochondria in a short time consequently the environment inside the mitochondria will be charged in negative and as we know the environment inside the all parts of cells should not change during the time
and on the other hand, these extra electrons may carry out some chemical reactions which result in producing some materials which are not good for cell, for ex H2O2, as we know it is a poisonous material for cell.
But maybe you ask why H2O and not another product? because H2O exists in cell, in a large amount, it is solvent for many materials, it is not poisonous for cell, and many other reasons.

As we know, many other reasons all these things make you look ignorant to the answer. Maybe you ask why $\ce{H_2O}$ and not other product No, as much as I can see, the OP is not asking this in any way.


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Why minimum infective dose of a virus is not just 1 particle?
I've stumbled upon a term "minimum infective dose" (for example, of HIV), but don't exactly understand what is it? Why it is not always equal to 1 virus particle? I expect 1 lucky virus to be able to start infection just like 1 lucky spark can start a fire.
The following options comes to mind:

Multiple particles of the same virus need to act in cooperation to trigger their reproduction;
There is some 100% working, but limited use immunity that knocks down first N viruses;
Infection probability lower than some theshold % is not considered by statistics.

In general, how infection probability and severity correlates with the number of particles? Is it linear (double the number of viruses => double probability or infection) or something trickier?

You just answered your own question. "I expect 1 lucky virus to be able to start infection just like 1 lucky spark can start a fire." How often does a spark - a single spark - start a fire? How many times will the flint be struck to get enough sparks that one will land on the exact spot needed to start a fire? The rest of your answer depends on the virus and the host.

Then it should be said not "minimum infective dose", but a "minimum dose that cause infection with N% certainity" or "probability of infection from a single virus".

The meaning is implied in the term. Remember that scientific inference is based on repeated observations. Observations closer to the mean are more likely to be given more importance than rare outliers.

From Merriam Webster:

the smallest quantity of infective material that regularly produces infection

(emphasis mine)
The word "minimum" here is not meant as a strict minimum it is meant as a statistical bound, the absolute probability for which depends on the types of tests done and their inherent accuracy/inaccuracy.
Reasons that this "minimum" is greater than 1 could include:

Probability that a given particle actually finds a suitable host cell, enters the cell, and replicates; failures can occur at many stages along that chain
Rate of immune system reaction/response. At low exposure levels, the immune system may detect and clear the infection at a rate faster than it can spread, such that the infection stays asymptomatic. Some vaccines use weakened or low doses of pathogens specifically to evoke an immune response. The intent is that the weakened pathogen will not spread fast enough to overcome the immune response and will not produce a full disease.
Clearance of the infectious agent before it reaches symptomatic levels. This probably applies more to bacteria but I don't see why it couldn't also apply to viruses. I think the best example is exposure to bacteria that cause gastrointestinal infections like E.coli or Salmonella. Small numbers may grow and multiply in the gut, but they grow slowly if they aren't present in a high enough concentration and they may pass through the gut before causing any noticeable symptoms.

The minimum infective dose can also vary from individual to individual or due to environmental factors (for example, see this paper).

Some additional references:
Leggett, H. C., Cornwallis, C. K., & West, S. A. (2012). Mechanisms of pathogenesis, infective dose and virulence in human parasites. PLoS pathogens, 8(2), e1002512.
Ward, R. L., Akin, E. W., & D'Alessio, D. J. (1984). Minimum infective dose of animal viruses. Critical Reviews in Environmental Control, 14(4), 297-310.
Yezli, S., & Otter, J. A. (2011). Minimum infective dose of the major human respiratory and enteric viruses transmitted through food and the environment. Food and Environmental Virology, 3(1), 1-30.

So unless there is exact probability threshold for the word "regularly" it is not a strict definition. Is it like 0.2% or 2% or 20% or 99.7%?

@Vi. Exactly, it is not a strict definition. Individual works that present a minimum infective dose explain their methodology.