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Will being very muscular (to the point that one is characterised as obese by BMI) increase blood pressure?
It is widely accepted that obesity/overweight (which I believe refers to people with a high amount of fat cells instead of bodybuilders who weigh a lot due to lots of muscle cells) have higher blood pressure due to various reasons e.g."larger body mass increase resistance to flow", "increase insulin resistance that increases cholesterol and risk of blocked arteries", "more blood (i.e. plasma) is required to supply the larger body mass thus puts pressure on vascular system", "increased weight takes more pressure to move blood around the body" and etc.
Therefore, based on the arguments above, is it fair to also say that muscular bodybuilders who are obese by BMI metric, have higher blood pressure?

May I ask why is this question downvoted? Is there something wrong with this question?

Perhaps it was downvoted because it's better suited to health or physical fitness sites.  Or because it can be answered with a simple Google search.  (The consensus from skimming a few articles suggests that while it's not a good idea to do serious weight training if you already have serious HBP, it doesn't cause it.)

Thanks for taking ur time. I've done some research on this topic but the answers come in the form of how "exercise or people with lots of fat cells thus are obese affect BP" rather as how "muscular people who are obese by bmi standard affect BP". Even then, the theories given as to why people with lots of fat cell have higher BP are somewhat skeptical, and the theories (e.g. more body mass thus require more blood plasma to deliver more O2) should translate to very muscular people who are obese by bmi metric.

Interesting question! I’ve been studying the effects of BMI on blood pressure over the last four weeks. In my study, those with higher BMI’s did in fact have raised blood pressure in comparison to those in a healthy weight range. However, this was a controlled study where participants were selected and so this solely focused on individuals who were classed as overweight or obese due to excessive fat. Often, BMI isn’t an accurate way to measure body weight, for reasons such as muscular persons being classified as overweight or obese. HOWEVER! This is where it gets interesting, being fat puts strain on your heart, your heart must work harder to support your body. BUT, animal fats play a large part in raised blood pressure. The lipids from animal fats form deposits within your arteries causing a blockage. So would it be safe to say that those of a muscular build consume more animal fats to promote muscle growth? Maybe! Hope this helps :)

Hello Emma. Can you please add some references to support your answer? Good references include peer-reviewed articles, books and websites of scientific organizations.


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Why is a solution of cesium chloride used in Meselson & Stahl's DNA replication experiment?
Centrifugation involves separating particles of different sizes, masses, density and etc.
In the experiment, the DNA macromolecules are suspended in a solution of cesium chloride gradient and then centrifuged.
Why is cesium chloride needed? Considering the possible DNA produced in the experiment will be the same size but of different mass resulting in different density, DNA will be separated based on their density by virtue (without the need for cesium chloride) under the influence of a centrifugal force.
I noticed someone asked the same question on Khanacademy but there was no answer for it. Other websites I found doesn't seem to offer a valid answer e.g. here which says " the DNA comes to equilibrium in the gradient where its density equals the density of the surrounding CsCl" which I think doesn't really matter when considering the argument I proposed above in the third paragraph.
Here is a diagram of the experiment for reference. Thanks in advance.

In saline solution all the DNA ends up at the very bottom.
Under centrifugation, the Caesium Chloride solution forms a density gradient, each DNA rises or sinks to the equivalent density.
The same procedure is used with Sucrose solutions for other separations.

Thanks for the input. May I ask why is it that in saline solution all the DNA ends up at the very bottom? Assuming the saline premise is true, then can distilled water be used instead?

With distilled water the DNA will sink even faster.

The differences in sedimentation speed between the differently marked DNA molecules are not lare enough to allow separation in a low-density medium such as saline, or distilled water. As mentioned by @Polypipe Wrangler DNA will always completely sediment to the bottom of the tube.
To improve separation a so called isopycnic centrifugation is performed. Basically, CsCl is used to form a gradient of increasing density from top to bottom during centrifugation. The DNA molecules will float to the density zones that match their own density. This allows separating similar molecules with small differences in density.

source: Stack Exchange

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

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Are phylogenetic trees from sequence data assuming neutral evolution?
phylogenetic trees built from DNA/protein sequences use sequence differences between these biological sequences as proxies for relatedness.
More specifically, maximum-likelihood phylogenetic trees (which are arguably the most commonly used/most accurate way to build phylogenetic trees) assume an evolutionary model (i.e. a way in which sequences diverge) and try to learn parameters that best explain the sequence divergence we see in our DNA/protein sequences.
In my mind, everything is clear and straight forward if you assume neutral evolution and constant mutation rates. Under this model, sequences will simply randomly mutate at a constant rate, and the more different two sequences are, the more distantly related they will be (on average, at least).
Now, what happens if we assume non-neutral, i.e. positive or negative selection? Can maximum-likelihood trees detect this? How do they handle this? Can they? Should we even build phylogenetic trees on sequences that evolve non-neutrally? I cannot wrap my head around

Before neutral or non-neutral evolution you should care of site specific evolutionnary rate disccussed in the paper linked by Roger Vadim.

Constructing a phylogeny requires a distance/similarity metrics for comparing sequences (in fact, constructing phylogeny can be viewed as hierarchical clustering). One however is not obliged to use evolutionary matrix for this - one can construct a phylogenetic tree using, e.g., Hamming distance and simple neighbor-joining algorithm - and this tree will be already valuable. See, e.g., Bilogical sequence analysis for introduction to the basic techniques.
Using sequence substitution matrices to define inter-sequence distances to construct phylogenies is groudned in the molecular clock hypothesis, according to which the substitution rate remains constant over time. The classical text here is Inferring phylogenies. The difference with other methods of constructing phylogenices is that the length of the tree branches can be interpreted as time, e.g., since the two sequences diverged. This is a strong assumption, but in many acses justified and producing useful results - e.g., this is how one could trace the early HIV evolution. There have been also attempts to improve the branch lengths using actual metadata for the sequence collection, as e.g., in this paper.
Substitution matrices are however rather flexible, in terms of the number of parameters they contain, particularly chen dealing with proteins (see Substitution model and PAM. Moreover, the substitution matrices can be site-specific, although this may result in overparametrization, known as infinitely many parameters problem, when teh results become unreliable. It is however fully reasonable to assume different substitution matrices for, e.g., synonimous and non-synonimous mutations. Here is a recent paper exploring this problem - I suppose the references in it could be a reasonable departing point for further study.

Thanks for your detailed answer Roger. Could I ask you to tell me your thoughts on the following:
Assume you have an initial genetically uniform population of bacteria. You then separate them into two populations A and B. Population A you let evolve without constrains (all genes will accrue genetic variation over time), Population B you put under extreme positive selection, such that over time population B acquires less genetic variation (only some sites are allowed to diverge).
How do you think the tree will look like? Won't the branch to A be too short?

@PejoPhylo under strong selection the tme may flow "with different speed", taht is the substitution rates will be different. There is a so-called $d_N/d_S$ approach actually uses this to detect selection - the synonimous sites are assumed to undergo neutral evolution, while non-synonimous sites  may be under a selection pressure - in this case the number of non-synonimous substitutions will be disproportionally big, which is taken as the evidence of selection.

Hi Roger, thanks for your further answers, so doesn't that mean that indeed the branch leading to A will be (mistakenly) shorter then the branch leading to B?

@PejoPhylo A short comment: with only two sequences, one can only measure the distance between them. One needs more sequences to speak of "shorter" branches (usually one uses an outgroup to root and calibrate the tree). In your bacteria example the selection will likely act only on a few sites (e.g., those responsible for the response to antibiotics), the rest will evolve neutrally. But yes, you either need that the majority of the sites evolve neutrally or you only use neutral sites (certain genes or synonimous sites) to reconstruct the phylogeny. Otherwise the estimates may be quite off.

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How different is breathing in wildfire smoke in urban areas compared to sitting by a campfire for a night?
The air quality in the Bay Area is currently the worst in the world, due to the devastating Butte County wildfires. I understand smoke inhalation can cause inflammation and respiratory issues, especially with chronic exposure, but I'm wondering in actuality, how different is the exposure to wildfire smoke in urban areas (AQI 100-300) over the course of a few days, compared to sitting by a campfire for a night?

I'm voting to close this question as off-topic because it is not about biology in terms of SE Biology, but about air polution.

The effects of air pollution on the human body seems like biology to me. Plus, it is topical and relevant to every person who has ever been camping. I think it is an interesting question that I would like to know the answer to.

Generally one sits upwind of a campfire, so as not to breathe the smoke.  And if the wind shifts, everyone moves :-)


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Killing microorganisms on agar plates?
If I grow microorganisms on agar plates and I expose them to UV light. How exactly will I know that the microorganisms have been killed? I was watching a video that showed spots in the petri dish where the microorganisms were killed when viewed under microscope but will this be visible to the naked eye? If not, is there any way that I can show without the use of a microscope the fact that the organisms have been killed?

It would help if you speficied the microorganisms in question. Some fungi grows when exposed to certain wavelengths of UV light

Looks like this is a follow up to this question on this forum.
The short answer to your question is you will not be able to indicate that a cell or colony on an agar plate is dead even with a microscope unless you are using fluorescent dyes (i.e., some form of live/dead staining). There are quite a few ways to do this, but they will all require that you have access to a microbiology laboratory.
Now, if your objective is to simply show that UV light kills microorganisms, this is easily done as an experiment with one target microorganism (i.e., one species). I'm going to obfuscate details aplenty here, but I'll offer you a description anyway.
You'll need replicate plates of agar colonies inoculated with the same quantity of the microorganism--this is typically achieved by propagating the microorganism in liquid medium and depositing equal quantities of the medium onto multiple agar plates. Once your plates have been incubated to obtain some colonies, retain one plate as control (this will not be exposed), and expose the remaining plates to your UV source. [Ensure that you've counted the number of colonies in every plate--including the control--before you subjected them to UV irradiation.]
Now comes the hard part. You will need to re-suspend the colonies from your plates in liquid media and re-plate them on agar. You can either choose a single colony from each plate (ideally, colonies that are similar in size across plates) for re-suspension, or you can re-suspend all colonies visible to the naked eye. Either way, re-suspend your colonies in liquid media, and deposit them on agar thereafter, and incubate the agar plates.
If everything went right, the number of colonies you would observe in the re-plated control plate should be higher than the number of colonies in the UV-exposed "re-plates." What that indicates is that at least some of the colonies that were exposed to UV irradiation died, and thus did not show up as colonies upon re-plating. This would loosely "prove" that exposure to UV irradiation kills microorganisms (with many, many caveats).
All that being said, I would not attempt this at home. To the best of my knowledge, this shouldn't even be doable at home without spending a significant amount of money to obtain some of the necessary equipment (which I have not described here). Further, doing this experiment in the format I described would likely yield very noisy results--the way I've described it is more back of the envelope experimentation than something proper.
If you are keenly interested in this topic, find the nearest microbiology department, and talk to a subject expert. They might even let you try this experiment out for yourself in their lab.
Edit - the core methodology I've described here is CFU counting (CFU - colony forming units).

Why bother inoculating liquid media when you can just replica plate onto fresh plates?

You could of course, but picking colonies is already messy enough, and I just wanted to offer a solution where the user didn't inadvertently end up streak-plating and end up with even more noisier data.

There is no picking colonies with replica plating though nor streaking? And you can easily calculate proportion of viable cells by looking at the original plate and the replica.

Sorry, I misread (and also misunderstood) your comment. I read that as "replicate", and didn't catch on (and I thought you were referring to colony picking). Would this actually work though? Per my understanding irradiation would not uniformly inactivate entire colonies, and it looks to me that replica plating an irradiated plate would yield an erroneous CFU count.

I'm not sure, that's why I asked you the question. If the UV radiation does not kill off all the cells then how would culturing colonies work? Wouldn't you just be growing up the survivors?

Per my understanding, if you have x number of CFUs prior (already present as y number of colonies), and if the stress has either killed some portion of the x CFUs (or put them in VBNC state), then you would only obtain < y number of colonies, since there would only be < x number of CFUs available for colony formation. I think the important thing that re-suspension in liquid media achieves is randomization of all cells (dead or alive) prior to plating, which you would not get from replica plating, and this is perhaps more "accurate" (notwithstanding CFU counting's own issues).


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difference between population genetics and genomics
I don't have a biological question therefore, this might be be quite basic. But I want to know does genomics entail population genetics or these are completely different fields?

Did you read the wikipedia entries for these two terms? Can you add them to your post and comment on what is unclear?

They are different. Genomics is the general science of sequencing whole genomes (or sometimes, the majority of the genome, or all the protein-coding genes, as in transcriptomes). Population genetics uses molecular data (usually DNA sequences, but not always) to make deductions about the characteristics of a population, or the relationships among biological populations. Genomic data could be used to draw conclusions about population genetics, but genomics can be used in many other sciences, and population genetics can be performed with other kinds of data besides genomes.


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What is the composition of a standard diluent buffer in a leptin ELISA kit?
I am trying to find the composition of the diluent buffer used for the dilution of a human leptin stock to be used in an ELISA assay. The manufacturer of the kit (https://www.thermofisher.com/elisa/product/Leptin-Human-ELISA-Kit/KAC2281) only indicates that the buffer contains 8mM of sodium azide, but I cannot find the precise composition of the buffer anywhere on the internet.

Simple reason: They want you to buy their buffer and not make it on your own.

Totally get that, but is there anybody who has found what those buffers usually contain?


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In what ways does the number of legs affect an animal's functioning?
After much research, I've only been able to find specific examples of leg-number's impact on locomotion and dexterity (and/or object manipulation). I feel as though there must be other ways it has a role in an animal's anatomy and function.
Examples I imagined but couldn't evidence include;

Respiration rate (relating to S.A. for tracheoles in Arthropods).
Similar to no. 1 but not quite the same - the structure of the circulatory system.
Insects'/tetrapods' stabilty (especially regarding an ant's capacity for load-bearing).
The brain's capacity for higher order thought processes (does conscious control of more limbs limit this?).
Efficiency of thermoregulation (also related to differences in S.A.).

I would most appreciate an explanation for how a given animal's number of legs gives it an aptitude for a type of locomotion (such as sprinting, climbing or burrowing). I would also like simple yes/no answers to the ideas listed above - as to whether they are implicated in the number of legs.


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Cell image database for citotoxicity test
Is there any cell image database for citotoxicity tests? I know that there are several image databases available (like this, this and this one), but none of them have the images for citotoxicity tests.
Thanks in advance,


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Why is pyruvate not used in IV drip instead of glucose?
Pyruvate is used in Krebs cycle and oxidative phosphorylation to generate most of the ATP required.
Isn't it more direct to use pyruvate in IV drip compared to glucose? Also, we will only lose 2 ATP and 2 NADP if we use pyruvate instead of glucose through glycolysis?
Is it due to the production and storage cost of pyruvate? Does pyruvate "degrade" faster than glucose?

Does pyruvate occur naturally? If there isn't any benefit to using pyruvate as opposed to glucose (it only gives more energy for the same mass, and glycolysis doesn't take much time compared to the Krebs cycle and the ETC), and if it takes effort to make pyruvate (I don't think it occurs naturally), why not just use glucose which occurs naturally in quite abundant amounts? In asking why pyruvate isn't used in IV drips, maybe you should consider why pyruvate should be used. That will help us see if there is any potential benefit to using pyruvate instead of glucose.

I would not advise you to make suggestions for medical procedures based on the knowledge of biochemistry your question reveals, but if you are determined to do so, SE Medical Sciences would be a more appropriate place. However before posting I would clarify your vague concept of "direct" and research the purpose of a IV drip. The Wikipedia article suggests the importance for hydration and salt balance as well as substitution for normal blood nutrient, glucose. How is pyruvate intended to substitute for the latter in brain and red cells?

@David - There may well be a role for pyruvate (NaPyruvate) in IV drips for patients with sepsis, or in resuscitation scenarios. It might even be a good fluid for rehydration. This question isn't as far fetched as it seems to you. The IV fluids we have are far from ideal for every situation and are used mainly because of familiarity.

@Zo-Bro-23 - Where does glucose occur "naturally in quite abundant amounts?"

@anongoodnurse this webpage lists some sources. Starch would be an obvious answer, and sugar contains glucose too. Honey contains glucose monosaccharides in some amount. While it glucose may not occur naturally in a usable form, it is relatively easy to extract glucose from these various sources, and commercial glucose production is quite viable (an obvious example is the glucose used for IV drips). Pyruvate seems much more difficult to isolate and produce, and its natural abundance is low compared to glucose (please correct me if I'm wrong!).

@Zo-Bro-23 - Glucose (alone) is not "quite abundant". Sucrose is, starch is, etc. but glucose has to be derived. Just because it's used in IV's (as dextrose) doesn't mean it's "quite abundant (naturally)". Lots of things that aren't abundant are used in IVs, like inotropes, etc. My point is that you were fairly aggressively challenging the OP when you didn't seem to know all that much yourself.

@anongoodnurse got it! While that wasn't my intention (I was asking the OP a genuine question), I'll be more careful about my tone in the future.

@Zo-Bro-23 - Thank you for the gracious response. It's hard to get the intended tone from the written word, so it's easy to misinterpret genuine concern for criticism, especially to the OP, so I find it better to err on the side of a softer approach, but that's just me. I'll delete my comments to you once you've read this (let me know.) Again, thanks.

@anongoodnurse I agree! It's especially easy to misunderstand someone's tone or intention on a text-based forum like this. I should be more careful about how I phrase my responses in the future.
You needn't delete your comments; it might be useful for someone else in the future. Thanks for your courteous response. Cheers!

A really nice question! Many organisms are capable of taking up glycolysis or Kreb's cycle intermediates and feeding them into their respective pathways. Therefore it feels natural to ask why humans can't do the same with pyruvate. While I cannot find a precise answer, I will do my best to argue why it isn't the wisest to swap in pyruvate in place of glucose.

Transport: Molecules like pyruvate and glucose do not diffuse very well across lipid bilayers and need specific transporters. All cells have abundant glucose transporters on their surfaces that enable glucose uptake. Pyruvate can be transported into cells via monocarboxylate transporters [1]. In general, I would assume that most cells are better adapted to take up glucose from their environments than pyruvate, although I cannot find evidence to substantiate this.
Glycolysis is important! Glycolysis does more for the cell than just breaking down glucose to pyruvate. Many intermediates feed into other pathways, and many pathways can feed into glycolysis through them. It is an important metabolic junction. Skipping glycolysis would deprive the cell of that metabolic branching. Take a look at [2] to see how glycolysis connects with some other metabolic pathways.
Energy loss: 2 ATP and 2 NADH add up to about 8 ATP lost. May seem like a small amount, but it adds up.

Biochemistry aside, some points raised by the comments here as well are valid: glucose is easy to manufacture or isolate, while pyruvate isn't. If the wheel isn't broken, don't fix it!
[1]https://en.wikipedia.org/wiki/Monocarboxylate_transporter
[2]https://www.researchgate.net/figure/Landscape-of-glycolysis-and-its-associated-metabolic-pathways-Schematic-representation_fig1_319159257

"If the wheel isn't broken, don't fix it."I would have upvoted this but for that last statement. It might be round, but how do you know it's the proper wheel? If we didn't search for better alternatives, we will never find something even better. There are so many examples in medicine of accepted/"best" practice being turned upside down by one person questioning the status quo, my favorite example being Dr. Barry Marshall. How many millions of people whose lives he made much better we'll never know. (Had he made his discovery 10 years earlier, my mother might still be alive.)


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Antibody detection - infection-induced vs vaccine-induced - is it common (or not) for a test to be positive for both?
Given a pathogen and a corresponding vaccine, and given an immune response to either one that results in antibody creation, would it be expected that a clinical test or assay for said antibodies would find it difficult (or SHOULD find it difficult) to distinguish between antibodies generated from exposure to the live pathogen vs a well-designed vaccine?
Or asked another way, would it be the goal of a well-designed vaccine to elicit an immune response that would generate antibodies that are indistinguishable from those generated by exposure to the actual pathogen?  Such that an antibody test would test positive in either case?
Or perhaps more to the point - are there examples of vaccines (prior to 2019) that lead to the creation of antibodies that are not detected by clinical tests for naturally-induced antibodies (where such tests exist) ?

Short answer: no.
Because all vaccines (that I know of) rely on protein or polysaccharide production in some form, whether "natural" (e.g. inactivated virion, subunit vaccines) or "artificial" (purified protein from expressed genes) forms, and the aim is to elicit an immune response that targets the natural pathogen form, so you need to generate an antibody response that covers that form. Vaccines do indeed induce antibodies
Conversely, naturally acquired infections produce antibodies that may not be seen in a vaccine induced response - this is particularly so for vaccines against a single target. For instance, many of the antibodies against SARS-CoV-2 are against the spike protein only, but the natural infection has all the other proteins in the mix, so you get antibodies against things like the Envelope protein and other expressed proteins. If you can detect these antibodies, then you can distinguish between vaccine and naturally acquired immune responses, but not the other way around.
I have however, thought of a mechanism by which a vaccine might induce different immune responses - if the vaccine itself is in a vector that generates an immune response. This is the case for the ChAdOx1 (Astrazeneca) vaccine, where the spike protein is presented on the surface of a non-infectious chimpanzee adenovirus virion. In this case, the adenovirus component could (and presumably does) induce an immune response. However, this is not against the component you are being vaccinated for, rather against the thing carrying the vaccine component.

I was always under the impression that once you get vaccinated against a virus then testing to see if you have antibodies for that virus (to see if you actually have been exposed or infected by it) is meaningless because the test will just pick up on the antibodies to the vaccine so you will test positive from that point going forward.

Is there an example of a human vaccine that will not induce a false-positive test to antibodies produced from exposure to the live / actual virus?

@PeggySchafer - re: your 1st comment - correct that's because the antibodies generated are against the same target. The aim of vaccination is to mimic infection, but in a safe manner.

@PeggySchafer re: 2nd comment - as I said in the post - no, not that I am aware of, because they target things that are the same as the natural infection.

Then I wonder why the FDA says that currently available blood serum covid antibody tests will not detect antibodies produced in response to the vaccines.

Can you link where they say this? Check the "help" link to the right of the comment box to format links properly.

Many vaccines for SARS-CoV-2 use just the S(pike) protein as an antigen; as bob1 notes, those vaccines would not generate a false positive result for serology tests targeted at e.g. nucleocapsid. There's an FDA list of tests with details at https://www.fda.gov/medical-devices/coronavirus-disease-2019-covid-19-emergency-use-authorizations-medical-devices/eua-authorized-serology-test-performance


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Why isn't the human zygote considered a human life how is a living anatomically modern human defined biologically?
It has 46 chromosomes by default when healthy(Differences almost always are pathological) and has almost every biological functions, processes a Newborn or and Adult person has.
It even invades fertile ground(womb) to survive.

As a new user to this site you are expected to take the Tour and also take the trouble to write a coherent question that is not a continuation from the title. And then you choose this list, frequented by people whose expertise you don’t know anything about to ask a question about a subject which has been discussed extensively by people whose qualifications etc. are known. Furthermore your question is asked in an aggressive manner — not “Is the human zygote considered…” but “Why isn’t the human zygote…”. This suggests that you are abusing this community. Please rephrase or go away.

@David Certainly there is no unanimus consent from the Biology community or at least a good majority of Biologists-Natural Anthropologists (circa 60-70%) that a human zygote is a living anatomically modern human. Otherwise there would be no pro-life/pro-choice argument. Hence the title why isn't it. Since it indeed is not. I am asking people from both sides. Biologists who consider it and biologists who do not. Write a coherent question that is not a continuation from the title? The title is the question itself. The body gives my reasoning why was such a doubt instilled.

Titles have different functions to Questions and should be separate. A title indicates what a question is about. (And here you have two sentences without a stop between them.) A better title would be something like. "Is a human zygote living?". The reader of a question, especially on a phone, expects to read something coherent. If you must have such a long title, copy it and paste it into the question. Nobody wants to read something that starts with "It" where they have to try to discover what "it" is. And this is a question and answer site, not, as "consider" implies, a discussion site. "

@David Would "What is a living anatomically modern human?" or "What is a living human" or "What is a human" do? I am certainly not asking if a zygote is living. I am asking if it is a living anatomically modern human. What is essential is the definition of a living anatomically modern human. If you have that i.e the sufficient criteria for a human, a zygote either meets them or does not. I am not wanting to discuss rather I want a scientific explanation. Does "consider" necessarily imply an intention to discuss? I want an answer not an exchange of opinions. My replies ask for clarifications.

Any of those are suitable titles, assuming they indicate your topic. However I have no idea what a “living anatomical modern human” is (I am a molecular scientist) but suspect that it is a subjective concept relating to the abortion question and not appropriate for this list. Don’t get me wrong, this is a valid topic for discussion but as a social and moral question. You won’t get a quick fix by asking for an opinion from the frequenters of this list.

@David https://books.google.gr/books?id=tzb5BwAAQBAJ&redir_esc=y I just thought Homo sapiens would look old fashioned or I would be "abusing" scientific lingo. How else could I distinguish "modern" humans from varieties of extinct archaic humans. Homo sapiens sapiens? I am interested in humans as defined by taxonomy as a distinct species.

Your blood cells could be considered a human life because they can be used to extact DNA to make a clone or a zygote these days. so when you bleed you could be like "oh no, i have killed a million little humans?!" Does a human have no organs, no nerve cells, no blood cells, no skin, no legs, no voice, no ears, no eyes, lives in water, is smaller than a human hair?

@com.prehensible Blood cells are fully differentiated and senescent. They do not reproduce or grow.

Sorry, that's wrong, blood cells are anucleate... they contin no DNA.. stem cells ca become zygotes, and they can implant your stem cells into an egg and probably do without the zygote altogether. Stem cells come from around the body, so your liver, marron, skin, and other cells are humans in the same way as zygotes.

@com.prehensible They can clone you but that would be another person. Ever heard of Dolly the Sheep? The Zygote had its telomeres re-lenghted by telomerase. Ter is a proto-oncogene. Each person has 70-100 divisions the so called Hayflick Limit. When you clone a person or a cell they do not live as long because some divisions have been spent. Your cells do not grow by themselves they do not strive to live. A Zygote actually infiltrates the Womb. Try to get your liver cells to do the same. Liver cells have differentiated even if just a bit. They can only give rise to liver cells.

Good point. I have to read about clonotes. Is a cloned humsn not human? Even if he is aged prematurely? Are liver stem cells aged?

@com.prehensible Ask your own questions. A cloned human is a human. Liver stem cells are aged.

IanC's answer is great, but is missing one and possibly the most important point. There is a distinction between being alive or having life, and "life" in the sense that we associate with words like individual, personhood, being. In the first sense; the biological sense, a zygote is most definitely alive; a living thing; a lifeform etc. But in the second sense, the more colloquial sense, it's not "a life" because it's an organism more akin to a bacteria or yeast etc. than a conscious human being. A zygote is not a person or an individual simply because at that stage the human does not possess those qualities that are sometimes considered to be qualifying for personhood or "a life". Think about it this way, would you consider a body that was just pronounced "dead" to be a life? Most people wouldn't, they would considered it a life that passed away. Yet a recently deceased body contains all the living cells and chromosomes the person had before dying. So "life" cannot be strictly applied to cells and number chromosomes based on common usage of the term.

A corpse doesn't grow nor it strives to survive. The Zygote - Morula invades the womb to survive. The Zygote even grows on its own before implanting itself. Anything fertile will suffice. I am certain that apparently the corpse resembles a human more than a zygote but I am inquiring about biological processes in themselves. With biological processes in mind I think a Zygote is more "human" than a corpse!

Don’t feed the trolls.

The discussion of when a life starts is a little more complicated than that. Many views and disagreements between them fuel the discussions of pro-life/abortion groups.
Some of the views and what they consider the beginning of life:
Metabolic view: Considers that there's no singular developmental moment that marks the beginning of life. Any single or multicellular organism should be considered a unit of life, and the development of those organisms is continuous. In that view, the spem and egg are already considered alive.
Genetic view: Supports that life begins when an genetically unique individual is created. That would mean that life begins when fertilization occurs. There are some arguments against this view. For example, fertilization doesn't occur in a single moment, but in a period of time. Another argument against this view is the "twinning argument". Even after the fertilization, it's possible the zygote will divide itself in two or more zygotes (twins). Thus, fertilization itself wasn't the point where the individual was clearly defined. Also, genetic uniqueness can't be used to define an individual because two different individuals can share the same genetic code (identical twins).
Embryological view: Defends that life begins at gastrulation, the point where the zygote is not able to divide itself anymore. This view ends up giving support to birth-control methods such as the "morning after" pill and contragestational agents as long as they are used during the first 2 weeks of pregnancy.
Neurological view: It makes sense to support that the same measurement used to define when life ends could/should be used to define when life begins. Contemporary American and Japanese societies (amongst others) define death as the moment where no recognizable pattern is produced by the brain in an EEG. Consequently, the beginning of life would occur when there's a recognizable EEG pattern being produced by the fetus. This happens around 24-27 weeks after conception.
Ecological/Technological view: Defends that life begins when the developing individual can survive without the support of its developing environment (i.e.: a mother's womb). The limiting factor for that to happen is usually the development of the lungs.
Reference:
Scott F. Gilbert’s, "When does human life begin?" - http://science.jburroughs.org/mbahe/BioEthics/Articles/Whendoeshumanlifebegin.pdf

Please be carefull. I did not ask or discuss when life starts. The first step for me is to define what precisely is a living anatomically modern human, a living homo sapiens sapiens. I do not care about individuality and uniqueness. Human life in itself to the exclusion of all other issues.

That's exactly the point of the answer. There are many different views of what constitutes a living human, and none of them is universally accepted, though some of them are more/less backed up by science. It's more of an ongoing discussion (a very delicate one to be honest, because people's emotions and beliefs are involved).

Don’t feed the trolls.


text:
Photosynthesis immature fruits
Do immature fruits perform photosynthesis? Yes they have chlorophyll bodies. But do they have stomata through which they can absorb carbondioxide like the green leaves? Sincerely Ulrik

Yes.  Both fruits and seeds often possess stomata as well as chloroplasts, which have been shown to be quite important in many cases for seed and fruit development.  It makes sense when you think about it.  If these vital components of the plant can make some of their own energy, rather than relying entirely on sugar reserves produced elsewhere (especially given how much sugar your average fruit has to produce), this would be a vastly more efficient system.  If you are interested in a more detailed look at fruit and seed stomata, the following paper should make for a good starting point:
https://www.jstor.org/stable/2442508?seq=1#page_scan_tab_contents
The authors of this paper conducted an in depth investigation of the structure and functions of the fruit and seed stomata present in a number of species within the Eschscholzia genus.  It's an interesting read.

Yes. I grow grapes. Next year I shall seek out two clusters of grapes. One I shall leave exposed to sunlight, the other I shall cover with alu-foil. I shall let you know the result.


text:
Water sample preservation
I am taking my students to collect water samples from different bodies of water. These bodies of water include the local river, a park pond, and water accumulation from recent rain. Once we gather the samples students will be analyzing the samples under standard light microscopes. I was wondering what is the best way to preserve any life that may be found in the samples in case there is no immediate opportunity to analyze the samples under the microscopes? Is there a specific time frame to analyze the samples before they have to be replaced? Also if they are kept in a bottle/jar does the container have to be unsealed or with perforations to allow air flow? Thank you.

What sort of timeframe? Collect in the morning & analyze in the afternoon would be good. Next day? Next week? Next month?

The samples will be analyzed within a week. Collection will take place Monday and the analysis of samples no later than the Friday of the same week they were collected.

Things start changing in minutes in sea water: I picked this up from some book on salt water aquariums when I had them.. I can tell you delicate inverts start dying in one day when power failure shuts down the circulation pumps although battery powered air pumps are running.  The main reason I gave up on salt after about 15 years.

Depending on what you are trying to look at, for zooplankton you can take water samples and filter them through a 100-200um mesh and store them in glass or plastic bottles. For my research we used mason jars that were cleaned thoroughly. After filtering just submerge the biomass in 70-90% ethanol and they can be stored in a fridge for quite some time.
If you want to look at phytoplankton, you can look into using Lugols Solution for preserving your samples. The nice thing about using lugols is that it will stain the phytoplankton as well. Your best bet for these is to store in amber bottles and keep in cool dark place. Here is a decent guide on how to collect the samples and prep the solution.


text:
Parasite? or a possible home infestation?

I found this bug on my bed tonight.  It's smaller than a sesame seed. 6 legs and 2 antenna.
Is this causing my dog and I to itch? Should I be concerned?

It is a minute pirate bug, in the family Anthocoridae. https://en.wikipedia.org/wiki/Anthocoridae They are generally thought to be beneficial insects, in that they are predators of pests. Do you have some house plants that may be infested with something else they are feeding on (like aphids)? Unfortunately, minute pirate bugs do bite, and the bite is painful. https://hortnews.extension.iastate.edu/2017/10/minute-pirate-bugs-are-biting-argh
But these are not human parasites, and I would not be concerned. Just find what they are feeding on, and take care of that.


text:
Will modern-day insects grow to massive size in a high-oxygen environment?
It's a reasonably well-known fact that insects grew to massive sizes due to the excessive concentration of oxygen in the prehistoric-Earth's atmosphere.
If one were to try to recreate this high-oxygen environment in a lab setting, would insects reared within grow to massive size?

Yep! In the group I work in we have a little pet project doing things like that. Different environmental conditions totally change insect’s body sizes. Getting up to truly massive sizes is a bit more tricky, but it works pretty well.

@CalendarJ it would be excellent if you draft this up as an answer with a bit more detail. Thanks!

While @CalendarJ comments "Yep!" above, a quick search suggests that experimental hyperoxia typically only increases insect body sizes slightly. Everything below is from VandenBrooks et al. 2012 (of course there could be other sources that contradict this!)

A few beetles have been reported to reach larger sizes when reared in hyperoxia, but most of the species examined reach similar body sizes in 40% oxygen as in normoxia (Harrison et al. 2009).

and:

Here we investigated the impacts of Paleozoic oxygen levels (12–31%) on the development of Blatella germanica cockroaches. Body size decreased strongly in hypoxia, but was only mildly affected by hyperoxia.

and this figure:

These results show that male cockroaches grow much larger under present-day (normoxic; 21% oxygen, highlighted box) and elevated (hyperoxic; >= 24% oxygen) levels than under low (anoxic; 12%) conditions, but the hyperoxia-grown roaches are only a bit larger than normoxia-grown ones. (Similar results for females not shown.)

VandenBrooks, John M., Elyse E. Munoz, Michael D. Weed, Colleen F. Ford, Michael A. Harrison, and Jon F. Harrison. “Impacts of Paleo-Oxygen Levels on the Size, Development, Reproduction, and Tracheal Systems of Blatella Germanica.” Evolutionary Biology 39, no. 1 (March 1, 2012): 83–93. https://doi.org/10.1007/s11692-011-9138-3.

I think you perhaps have a misconception.  Body size is mainly controlled by genetics, thus we have species of "bugs" that are very small, others from closely-related lineages that are much larger.  Take for instance flies, which come in sizes from fruit flies through house flies up to horseflies.  They're all pretty similar (under magnification) to a non-specialist, yet it seems unlikely that raising a fruit fly in an oxygen-rich environment would make it grow to the size of a house fly, let alone a horse fly.
It doesn't take much thought to come up with many similar examples, such as beetles and butterflies, with species that come in a range of sizes.  It seems obvious that they've evolved a size which fits their evolutionary niche, and if they grew too large, they would be unlikely to survive.
Oxygen concentration is one of the factors that puts limits on the size of insects, but to get real size increases, you need to evolve new species that take advantage of increased oxygen, not just grow your 1st generation offspring.

Yes, this basically summarizes the answer I was seeking in this question; whether or not the difference in size of Paleozoic insects was caused by a genetic difference.

The latest documentary I watched about the Meganeura (a giant Dragonfly from Pre-Cambrian) seems to confirm your intuition.
Based on experiments by John VandenBrooks at Midwestern University, with bugs in conditions A with less oxygen than current Earth atmosphere, and a 31% oxygen atmosphere in conditions B:
The bugs from group B were roughly twice as big. It was a bit frightening. (I don't know if there's a paper that shows the size difference statistics for several individuals.)
Here's the documentary for French TV "Science Grand Format":

there is a lightweight interview of the scientist at 06:15
experiments on cockroaches at 06:50
they show the bugs different sizes at 7:45.

Do you have a citation/link to the documentary that you could provide?

@CalendarJ have added sources. Althought the scientist is interviewed and explain his results, I have not checked his research papers.


text:
Explain why bones cannot undergo interstitial growth as cartilage does
I got a question from a textbook <<Seeley's Anatomy & Physiology Twelfth Edition>> that does not have an answer at the back of the book (only odd numbered questions do have an answer and this question is even):

Explain why bones cannot undergo interstitial growth as cartilage does.

i can only think of two reasons:

In bones, calcification causes the chondrocytes to die, so cartilage cannot form in the bone, leading to no interstitial growth in the bone.

Cartilages are usually only found at the tip of the bones, so its growth can cause the bone to lengthen, which is interstitial growth.

I got a nagging feeling that there is got to be more. Did i miss any other reason? (Also are my reasons correct?)

While mature cartilage is solid, the extracellular matrix secreted by chondroblasts during cartilage formation is soft enough to allow for both cell division and tissue expansion. This is interstitial growth.
As the matrix hardens, secretion and proliferation slow down and then stop altogether. Isogenous groups are a testimony of the last cell divisions before the surrounding matrix turns solid. From this point on, further growth can only take place by apposition, i.e. new cartilage matrix is secreted by chondroblasts found in the perichondrium.
Bone matrix becomes mineralized (and therefore very hard) soon after its organic components are secreted by osteoblasts. Osteoblasts that get trapped in the matrix shrink and become quiescent. Thus, there can be no expansion from within, i.e. no interstitial growth.
Bone grows exclusively by apposition, where further osteoblasts differentiate from precursors and deposit new matrix on top of the existing bone.
While this is the answer to the original question, your tentative responses suggest that you need to do some further reading. You seem to refer to the interaction between the two tissues during endochondral ossification, which is a separate, more complex topic.


text:
Why does miRNA not get translated?
If miRNA and mRNA are made of the same nucleotides, then why are miRNA not translated like mRNA?
Is it due to miRNA lack of start codon? Or lack of promoters?
Has it got anything to do with RISC?

As you've noted, different RNA molecules are treated differently in (eukaryotic) cells (other common RNAs are tRNAs and rRNAs).  Factors influencing this include the RNA sequence involving both sequence motifs and non-canonical secondary structures, chemical modifications such as caps and poly-A tails on mRNAs, interactions with protein complexes (such as transcription complexes or ribosomal complexes), and localization within the cell.
Regarding translation of RNAs, a useful review is "Principles of Translational Control: An Overview" Hershey et al 2012
Germane to your question, initiation of translation is complex and specific. The authors note

"A conspicuous feature of eukaryotic protein synthesis is the fact
that mRNAs are translated in the cytoplasm, making translation
uncoupled from transcription. Mature eukaryotic mRNAs possess a
m7G-cap at their 5′-terminus and, in most cases, a poly (A) tail at
their 3′-terminus. ... the pathway and mechanism for the formation of
40S and 80S initiation complexes differ substantially from those in
bacteria. For example, a large number of initiation factors (at least
12) promote the binding of the mRNA and initiator methionyl-tRNAi
(Met-tRNAi)—which is not formylated—to the 40S ribosomal subunit. "

Regarding miRNAs, a useful review is "Overview of MicroRNA Biogenesis, Mechanisms of Actions, and Circulation" O'Brien et al 2018
In particular, Fig. 1 is a useful cartoon diagram of the different known pathways producing and processing miRNAs and the subcellular locations of these events.
Later on, they also discuss RISC as one of the mechanisms of miRNA-based gene regulation.
As detailed knowledge of subcellular processes has exploded in the last two decades, it's always good to try to use the most up-to-date textbooks or reviews you can find.


text:
Identity By Descent vs Identity By State
Background
The concepts of Identity By Descent (IBD) vs Identity By State (IBS) are central in population genetics, yet I fail to fully wrap my head around the definitions.
You can find examples where my understanding of IBD vs IBS is quite poor in @DermotHarnett's answer here or in the comments with @PaulStaab here. @PaulStaab suggests that different authors have used different definitions of IBD and IBS.
What is unclear to me
From what I remember from Hartl and Clark (I don't have the book with me to quote), IBD depends on an arbitrary time threshold in the past beyond which if coalescent events occurred, then we still call the two alleles IBS (Identical by state) and not IBD. The idea that the concept of IBD depends on an arbitrary threshold bothers me though!
I suppose that two alleles can be IBD without being IBS in the case where a mutation or recombination event in the middle of the sequence of interest prior (looking backward in time; more recent) to their coalescence. I suppose two alleles can be IBS can not be IBD only if we use an arbitrary threshold that is older than their coalescent time or if convergent/parallel evolution happened.
Questions

Does IBD depends on an arbitrary threshold?
Are there several definitions of IBD and IBS in use?
Does IBD implies IBS?
Does IBS implies IBD?
Can you please make a short review of these definitions to clear things up?

The issue of IBD and IBS can indeed be confusing.
The identity by state definition refers to the fact that at some point two individuals, even if they are not related to each other, present the same allele at a specific locus. Because of their un-relatedness this similarity probably arose from a similar mutational event.
On the other side, with IBD two individuals happen to share the same allele because of their coancestry.
Alleles that are identical by descent are also identical by state. But the opposite is not true. (see also https://www.biostars.org/p/174048/#174049 and Powell et al 2010, Nature Reviews Genetics 11, 800–805 (1 November 2010) | doi:10.1038/nrg2865).
Now, about the threshold that you were mentioning in your question, I am not entirely sure what you mean. Eventually, all individuals are traceable to a MRCA (most recent common ancestor). So, I think the threshold you talk about refers to the size of the population in analysis. Depending on the size of your population you will have different proportions of alleles that are IBD and IBS.
Hope this help.

The "arbitrary threshold" is part of the definition usually given of IBD in textbooks. The problem is that, if you go back far enough, all alleles are descended from a common ancestor allele. So to define it, according to the textbook explanation that both me and the asker feel uneasy about, what you do is: choose a number of generations back, say, five: decide to consider all the alleles at that generation, unrelated to each other (not IBD); and then define IBD as "having a common ancestor allele more recent than that number of generations back".

This won't be a complete explanation: I'm bothered by these questions myself. But I'll say what I do know.
First:
Yes, Identity By Descent (IBD) is defined relative to a chosen threshold number of generations, at least in the sense that I understand it (in case there is more than one sense - I think there are ones allowing for mutation?). At the chosen number of generations back, we assume that all of those ancestors were unrelated. This seems troublesome! But two things might help it seem less so. First: when we ask if two individuals are related or not, we're really asking whether they're more closely related than the average relatedness of the background population. Second: the pedigree method of estimating kinship and inbreeding coefficients, is just that, a way of estimating, which may fail if its assumptions fail (e.g. if the ancestors at the threshold were not randomly chosen from a randomly mating population).
To illustrate, consider a question about a fictional individual with a fictional family tree (spoilers for Game of Thrones, season 1): How inbred is Joffrey Baratheon?
We know that Joffrey Baratheon is not, in fact, the son of King Robert Baratheon, but rather the product of secret incest between his mother Queen Cersei Lannister and her twin brother Jaime Lannister. If that were all we knew about the situation, we would draw the following pedigree:

By using this pedigree, we are implicitly assuming that Cersei and Jaime's parents are unrelated, i.e. randomly chosen from a large randomly mating background population (and assuming that if Cersei and Jaime are more likely than random individuals to share an allele, that this is due solely to IBD from one or the other of those randomly chosen parents, i.e. due to their being close relatives). Based on this assumption, applying the usual method to this pedigree, we estimate Joffrey's coefficient of inbreeding as $0.25$.
However, if we look deeper into the Lannister family tree, we realize that Cersei and Jaime are actually more closely related than a typical brother-sister pair: their parents were not randomly chosen, but were themselves related (though not closely enough to be scandalous for Westerosi society); their father Tywin Lannister, and their mother Joanna Lannister, were cousins. Using this information we draw a more complete pedigree:

Using the usual pedigree method again, we are now making a different assumption. We are no longer assuming that Joffrey's grandparents Tywin and Joanna were randomly chosen from the background population. We are instead assuming Joffrey's great-great-grandparents, Gerold Lannister and the Lady Rohanne Webber, were randomly chosen from the population. This assumption seems more reasonable. Since this new pedigree implies more inbreeding in Joffrey's ancestry, we guess that the method should give a higher estimate for his inbreeding coefficient: indeed it does, giving us an estimate of $0.28125$.
Here's how this illustrates the subjectivity of defining IBD. When we used the first pedigree, we were asking: What's the probability that both alleles at a locus in Joffrey's genome, are descended from the same allele in the grandparent generation? When we used the second pedigree, we were asking: What's the probability that both alleles at a locus in Joffrey's genome, are descended from the same allele in the great-great-grandparent generation? These are two different questions, and of course gave two different answers. The trouble, of course, is that the question of how inbred Joffrey is relative to the background population, only has one answer (which the pedigree answers may estimate more or less well)!
Second:
Although important coeffients like the "inbreeding coefficient" or "coefficient of relationship" are often presented in textbooks as being defined in terms of the probability of some pair of alleles being IBD, this cannot be the actual definition. This is because probabilities can't be negative, but relatedness can be (if two individuals are less related than average), as can the inbreeding coefficient (if the animal is outbred, i.e. its parents had negative relatedness). The possibility of negative relatedness even has interesting evolutionary implications. As a sort of flipside of Hamilton's rule for altruistic kin selection - where it can be evolutionarily beneficial for a gene to cause a bearer to harm oneself, in order to help a relative, i.e. an individual more likely than average to also carry a copy of that gene - negative relatedness makes it possible to have spiteful anti-kin selection - where it pays a gene to cause its bearer to harm itself, for no benefit at all, but solely to harm an individual less likely than average to carry a copy of itself (and more likely to carry its competitors)!
Indeed, in his original formulation of these and related coefficients, Sewall Wright did not invoke probabilities or identity by descent at all. For relatedness he talked about the correlation between individuals' allelic states (this requires assigning numbers to alleles, e.g. $A=1$ and $a=0$). Note that correlation coefficients can be negative. The "probability of IBD" interpretation was introduced by Malécot; it's made it into population genetics textbooks mostly just because it's easier to teach (despite the seemingly paradoxical subjectivity of reference number of generations, and the inconsistency with the possibility of negative relatedness).
Wright's explanation of the inbreeding coefficient is more intuitive: he points out that the most important effect of inbreeding is reduction in heterozygosity. Consider a randomly mating population: an individual randomly chosen from it, will have a certain fraction of its loci heterozygous. But an inbred individual will have fewer loci heterozygous (more loci homozygous). Malécot interpreted that excess homozygosity as being "due to coancestry [since a subjectively chosen reference generation]", but we can ignore that conceptual baggage, and just talk about the excess homozygosity (deficiency in heterozygosity) itself. Thus a better definition of the inbreeding coefficient is
$F = \frac{H_e - H}{H_e}$
where $H_e$ is the heterozygosity you would expect of the offspring of a random mating given the population's allele frequencies, and $H$ is the inbred individual's actual heterozygosity. A good presentation of this interpretation appears in Hartl's Primer of Population Genetics.
Note that this definition, unlike the probability definition (but like the correlation definition of relatedness) can be negative: outbred individuals have less homozygosity (more heterozygosity) than expected under random mating.

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text:
How are neurons / synapses "biased"?
I'm trying to see if I understand this correctly. I've read the question Can the human brain be reduced to a binary system? and one of the answers explains:

While action potentials are usually binary, you should note that
  synaptic communication between neurons is generally not binary. Most
  synapses work by neurotransmittors, and this is a chemically mediated
  graded response that, for example, act on voltage-gated ion channels.

Looking into the graded response article on Wikipedia:

Postsynaptic potentials are changes in the membrane potential of the
  postsynaptic terminal of a chemical synapse. Postsynaptic potentials
  are graded potentials, and should not be confused with action
  potentials although their function is to initiate or inhibit action
  potentials

Ok, so from what I understand, involving what I learned in this video about action potential, and those two quotes, there can be a "bias" in the synapse process of neurons that make them more or less likely to reach the threshold for action potential when they receive neurotransmitters as the result of the activity from axons connected to their dendrites. Basically, I have the idea that somehow, the synapse area between neural connections becomes trained based on past interactions on whether or not to fire "easily" or be "reluctant" to fire or else fires more powerfully or weakly contributing more or less toward action potential of neurons on the receiving end.
Edit: On second thought, I also recall learning about a mechanism enforcing recharge time between firing, so the neurons are throttled if they fire too rapidly, a mechanism which, (iirc) if defected can cause epilepsy. Really not sure about that, but it would sort of be the opposite of "training" it seems to me.
So I have a few questions surrounding this subject:

Are some "actions" or "transmissions" (for lack of the correct terminology, when the neuron fires) more powerful than others, contributing more dramatically to action potentials of neurons receiving neurotransmitters when it fires?
Or if I'm on the wrong track with that question, how does the bias occur / form over time? Is a bias based on short term or long term series of interactions? How many past interactions are significant in the current state of the bias at any given time?
Is there bias at all?

The term that most scientists use to describe a synapse's "bias" is synaptic strength. The strengths of synapses depend on their "history".  The change of synaptic strength is called synaptic plasticity. This topic is closely related to memory formation and is a very broad question to answer (groups of wikipedia/scholarpedia pages and tons of reviews, not single publications).
Generally, the strength of a synapse, i.e. the size of the effect of a presynaptic stimulus on the postsynaptic neuron depends on presynaptic and postsynaptic factors. To name just a few:

the number of vesicles released from the terminal,
the expression levels of the neurotransmitter reuptake and/or breakdown enzymes,
the expression level, location and posttranslational modifications of postsynaptic receptors and
uncountable other factors.

Although there have been decades research and a nobel prize (to Eric Kandel) on the topic, there is still a lot to find out.
For a start, you might want to look up
Synaptic plasticity and/or
Spike-timing dependent plasticity (long term potentiation and long term depression).
LTP is also a good example to answer all three of your questions (if I understood them correctly).

third question: yes.
second question: LTP (and other mechanisms).
first question: Different frequencies of spike trains are more or less effective at triggering LTP, making them more or less powerful to the change in synaptic strength, affecting the response of future input to the same synapse.

Nice answer, +1! I have added some more details to your answer as my own answer. Feel free to improve/criticize :)

@a tiger has given a nice answer, but to me it seems too summarized. So I just want to elaborate it by giving some more details. Also, let me tell you at first that it is a very broad topic, so covering up everything in anything less than a book is pretty much impossible. I'll only add points enough for an introductory answer. I will answer your questions one by one.

Are some "actions" or "transmissions" more powerful than others, contributing more dramatically to action potentials of neurons receiving neurotransmitters when it fires?
Yes, that is why they are called graded potentials. Graded potentials are actually different from normal action potentials in that action potentials follow the all or none law whereas the strength of a graded potential can vary depending on how many ion channels it stimulates. You might better understand this by the equations they follow.
Normal action potentials follow Nernst Equation i.e.
$E_{eq,K^+} = \underline{RT}\times \ln \underline{[K^+]_{out}}$
$\hspace{20mm}nF\hspace{12.5mm}[K^+]_{in}$
On the other hand, graded potentials follow the Goldman Equation i.e.
$E_{m} = \underline{RT}\times \ln \underline{P_K[K^+]_{out} + P_{Na}[Na^+]_{out} + P_{Cl}[Cl^-]_{in}}$
$\hspace{14mm}F\hspace{14.5mm}{P_K[K^+]_{in} + P_{Na}[Na^+]_{in} + P_{Cl}[Cl^-]_{out}}$
which is significantly different from Nernst equation. The biggest difference is that as per Goldman equation, the net potential depends on the concentration of more than one ion, meaning that it can attain a range of values, unlike that from Nernst equation. This directly answers your question that Yes, some graded potentials can be different from others in strength and time, thus giving different contributions to action potential on the following neuron. Yes, time too. It is so because different ion channels remain in different states (open, close, inactivated) for different times and take different times for transitions. You might understand this by this diagram:

How does the bias occur/form over time? Is a bias based on short term or long term series of interactions?
Generally, bias is formed by continuous strengthening of a synapse based on its activity over recent time, a process known as LTP or Long Term Potentiation. LTP can lead to a long-lasting strengthening of a synapse and is hence considered to play a major role in formation of memories in brain. When a synapse is repeatedly stimulated over time, the following neuron creates more dendritic receptors so that more effective potential can be generated. Over time, the first neuron starts releasing more and more neurotransmitters whenever it is excited. These two factors, when combined, lead to stronger synaptic connection i.e. formation of bias. You can see the following images for better understanding:

In fact, a bias results from both short term and long term potentiation. The former i.e. STP is a transient increase in synaptic strength of two neurons usually due to increase in synaptic vesicle release probability. It can also be caused by diseases such as tetanus. So, if you look at the big picture, then yes, a bias is the result of both short term and long term interactions between two or more neurons.

How many past interactions are significant in the current state of the bias at any given time?
Bias formation is a long process which requires many steps, including gene expression and protein synthesis. That is why, LTP has been divided into two (and sometimes three) different phases: E-LTP (early phase or LTP1) and L-LTP (late phase, further divided into LTP2 and LTP3). A schematic diagram of LTP is below:

Thus, in short, we don't know exactly how long it takes for LTP formation, and there probably is no exact time required for its formation.
Is there bias at all?
I should have answered this question at first, but since I do so at last, I will add some more points. Biasing, or synaptic plasticity, is the ability of synapses to strengthen (by LTP) or weaken (by LTD) over time due to change in their activity patterns. Its mechanism has been theorized to be dependent on:

change in probability of glutamate release.
insertion or removal of post-synaptic AMPA receptors.
phosphorylation and  dephosphorylation inducing a change in AMPA receptor conductance.

The third one is a more complex part of the process, while the first two processes have been examined by a mathematical formula for calcium-based model of plasticity as:
$\underline{dW_i(t)} = \underline{\{\Omega([Ca^{2+}]_i) - W_i\}}$
$\hspace{3mm}dt\hspace{22mm}\tau([Ca^{2+}]_i)$
where:

$W_i$ is the synaptic weight of the $i^{th}$ input axon
$\tau$ is a time constant, dependent on the insertion and removal rates of neurotransmitter receptors, which is dependent on $[Ca^{2+}]$
$\Omega$ (the concentration of calcium) is also a function of the concentration of calcium ($\Omega = \beta A^{fp}_m$) that depends linearly on the number of receptors on the membrane of the neuron at some fixed point.

So in short, Yes, biasing does exist in neurons and plays an important part in many important phenomena such as memories.

P.S. I also want to add about relation of synaptic plasticity with epilepsy as you talked about in your question. Though we don't know everything about epilepsy, we know that synaptic plasticity indeed does play a role in epileptic seizures. During epilepsy, seizure threshold i.e. amount of stimulus required for action potential, is lowered. Also, because of factors such as long term potentiation, even a small potential gets enhanced into a larger potential. All these factors, along with some other unknown ones, when combined, lead to a seizure or attack.
Also, epilepsy is also caused due to decreased resistance of neurons towards a stimulus and a decrease in the refractory period of ion channels (what you call recharge time). Due to decrease in this recharge time, neurons are able to generate kind of unnecessary action potentials which ultimately leads to a seizure. As said, refractory period is the time immediately after depolarization of ion channels during which it is unable to transmit another signal. A simple graph shows refractory period like this:

I might be a bit biased here myself (pun intended ;-) ), but IMHO you gave a  specific answer to a broad question. My impression is that you gave details, but not all details that would be necessary to give a full answer (which is almost impossible in this case), underselling the complexity at hand. E.g. you are only talking about AMPA receptors, but there is more to it than AMPA. In answer 4, you mention a few LTP mechanisms, but this is far from a complete list. I think it is very nice of you to have put so much effort into an answer, but I think it gives a wrong impression of completeness.

@atiger I just wanted to give more details for your answer. If you see, our answers are very similar, mine just being a bit longer and detailed. It is obvious that we don't know everything about anything, so giving a complete answer would be just utopia ;) anyways, I'll slowly add more and more details until the answer starts becoming too long.

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text:
How far up a limb can a severed artery retract?
This is about the application of tourniquets. I was taught a hand width above wound, but recently I read severd arteries can in some cases retract higher than that which would then bleed into the arm.
Doesn't matter if cut or tear, and if the limb is torn off or just the artery cut through, but on arms and legs, how far up can it retract?

Welcome to SE Biology! You may consider posting this question to SE Medical Sciences instead (https://medicalsciences.stackexchange.com/), where it would be more appropriate and you will likely get better answers.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. I’m voting to close this question because it seems more appropriate for [MedicalSciences.SE] (please don't repost — instead request migration). Thanks!


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Tools I can use to find similar genes
What tools are available to estimate the function and purpose of a gene ? I think the right approach is to find similar sequences of genes that we know the function of.
All the information I have on a gene is (for example):
KXN84633.1

and
>lcl|Query_208731:23119-24312
CTACAGACATATCCCATCCAGAAGAAATCTTTATCTATCGAATACCTTCGCGATAACGCGTATCTACGCG
CTCGAACAGGCCAAATAGCTGCAATGTTAAGGCTGAGGGATAGTATTTCCAAAAACCTATCCCGGCATTT
TGAGGTACATTTACTTTCTTCCGTATCTGGCCTGACTAAAAATCCTGCGTAGTCTCAAGGGTTTACATAT
ACTCATACGCCTATAATAACAGCTAGCGATTGCGAAGGCGCAGGCGAAGCATTTCGCATATCACCTATCC
AACCTACCACCCCCTCTCTCTCAAAAACTGACGCAAGTTCAGACGCAAATACCCCTATAGAGTTCTTTTC
ACGTCCTGCATATCTCACAGTCTCGCATCAACTTCATCTAGAATCCTTCACCACGGCTCTCTCTCGCGTG
TATACCCTTTCACCATGTTTTCGTGCGGAACGATCTATGACTGGACGACATCTGGCCGAGTTCTGGATGC
TTGAGGCCGAGTGGAACCTTGCAACGCGTTGCGATAGCTTAGAAGAAATTTGTGCCTTTGTGGAAGGCTT
AATTCGGACGTCGGTAGATCATGAGTCGCAGGATGTCAAGGCTCTGTGGGCGGAGAAAGGAGCGGAAGTA
GAGGAATTCAAGATGTTTCGTGCCGCATTTGACAACGCTCAGCCTTGGAGGCGATTAACATACTCGGATG
CAGTCGAGGCGTTGAGCACGGCTTATGTCAACGGACATCCTTTCGAATTCAAACCTGTCTGGGGCGAATC
ACTCTCGAGCGAACATGAACGTTGGCTGGCAGAGGTGTACGTTGGTGGACCAGTGTTCGTGACAGACTAC
CCTATCAAACTTAAACCGTTTTATATGCGGGTCAACGAAGATGGGAAAACCGTTGCGTGTTTCGATTTGA
TTGTACCTCATGCTGGTGAACTTGTGGGTGGAAGTGTGAGGGAGGAGAGATGGGATGTCCTCTCAAAACG
GATGGCAGAGCATGGATTGTTGCCTCACCCTGACCAGAATGAGGGTGCCCCAACTGATTCGACATATGAA
TGGTATCTGGATTTACGCAAGTATGGTGGAGCGCCGCATGCAGGGTTTGGTCTTGGGTTTGAAAGGCTGG
TGAGCTGGGTTGGAGGGATTGACAATGTGCGAGAATGCATCGGCATGCCTCGGTGGACTGGGAGAATGAT
TATG
>lcl|Query_208731:22646-23071
ATGCTCCTTCGCAGGTTATACTCGACTGCTGCACATCCTGCCAGGTTCAAACTACCGCCGACAATCAAAC
AGGTGCTTTCAGCTAATGGCAGCGAAAGTTCAGCGACATCAGTGACTGGCTGGATTAAATCTATCCGTAA
ACAGAAAAACATAACCTTCGCTGTAGTCAGTGATGGTACAACACCAGAGGGCCTGCAAGCAGTTGTGTCA
AAAGAACAGGGTACTTCCCCAGAAATGTTGAAAAGGTCAGTTCATCTCTCACAGCTCGAAACCGGAACAC
TCACCAATTGAAGACTTACGAACGGTACAGCAGTGCGGCTCACAGGAAATCTAATTCAGTCTCCTGGCCG
AGGTCAAGAATGGGAGCTTGTCATTCAAGAAGGTGACAAGAACGCTATCGAAATCCTCGGCGACTGTGAT
ATTGAC
>lcl|Query_208731:c22559-22323
ATATCACATTCAACATCCAGGGTAATGACATCGCCATGTCGCTAGACAGCGTCGACAATGACTTCCAAGA
AACACTCGTTCCCATCTCCACTGGAATCTCTCTGGAACTCGATCTTATCAAACCCCGTCAACCGCAAGAG
CAAGAGTCCAAACTAGCAATCTGTCTTCACCCCTGGTCTCGACTCGGAGGACGCAAAAGCGACCCGTGCG
GTGTCTTATTCCACGAGCTCAGGTCGA
>lcl|Query_208731:c23949-23902
CACGAACACTGGTCCACCAACGTACACCTCTGCCAGCCAACGTTCATG

obviously I am new to this :)

This sounds like a homework question, although your previous posts perhaps suggest otherwise. In any case, you should give us a bit of background. Where did you get what looks like an accession number (that I can't find on the internet) and these sequences (which I can) — why the Query annotation? Have you searched the internet for methods to compare an unknown sequence with known ones. We can tell you, but our homework policy would have you try yourself first.

I'm just a software developer having a little dabble to see what I can get to. It is indeed a button mushroom gene.

I personally do not find the second part with the queries helpful without greater context.
The first part appears to be an accession number (more information on these can be found here: https://www.ncbi.nlm.nih.gov/Sequin/acc.html). By going to NCBI (https://www.ncbi.nlm.nih.gov/) and searching that accession number, you can get a lot of information quickly and easily.  Searching this particular number shows it to be a Asparagine-tRNA ligase from the fungal genus Leucoagaricus (https://www.ncbi.nlm.nih.gov/protein/KXN84633.1/).
If you simply have a DNA or protein sequence and no accession number, you can perform a BLAST (https://blast.ncbi.nlm.nih.gov/Blast.cgi).  This will search your sequence against a massive database of annotated DNA or protein sequences. The specific type of BLAST to run and the ideal parameters will take some reading on your part to determine.  However, if you're just starting out, nucleotide BLAST for DNA sequences, protein BLAST for protein sequences, and default parameters will often suffice. This search will provide you with the best "hits" to the database which you can then follow up on to get an idea of the function of your original sequence.

thank you, that may do the trick.


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marine animal tracking databases
Which databases you know that store data on tracking of marine animals?
I am interested particularly on mammals (for which I know meop storing data on sea lions) but also on fish schools (not sure they exist though).

could you explain what sort of information you need in more detail

I am interested in spatial tracking. Track animals' movements and vertical movements

One major tagging effort/database is the TOPP program-- "Tagging of Pelagic Predators". They track Pacific Blue Marlin, Mako Sharks, Whale Sharks, Salmon Sharks, Pacific Bluefin Tuna, White Sharks, Atlantic Bluefin Tuna, Northern Elephant Seals, and Leatherback Sea Turtles. I'm not sure if their data are publically available.
Info here: http://gtopp.org/ and here: http://oceanview.pfeg.noaa.gov/TOPP/

WhaleNet is less pretty, but has older marine mammal tracking data: Gray Seal, Harbor Seals, Harp Seals, Harbor Porpoise; dolphins (archived) and whales (archived): http://whale.wheelock.edu/whalenet-stuff/stop_cover.html

Sea turtle tracks can be found at http://www.seaturtle.org/tracking/

Check out MoveBank.org. It provides access to online animal tracking data (whales, turtles, seabirds, etc.). Some come with ancillary data like depth. Best of luck!

The Animal Telemetry Network (ATM) was "established to provide unity, stability and continuity to the national infrastructure that facilitates the collection, management and availability of this marine animal telemetry data. To accomplish its mission, the ATN is being implemented in three Phases and on these three foundational pillars: 1) Building Alliances and Collaborations, 2) Providing Telemetry Data Aggregation, Management, Display and Delivery, and 3) Funding High Priority Regional Baseline Animal Telemetry Observations." The network provides access to maps with data, will sometimes provide links to publicly available data, and provides point of contact for each dataset.


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Enzymes and Reversibility of Reactions
Richard Feynman mentions in the third chapter of The Feynman Lectures:

So the real system is in the GDP-GTP transformation; in the dark the GTP which has been stored up during the day is used to run the whole cycle around the other way. An enzyme you see, does not care in which direction the reaction goes, for if it did it would violate one of the laws of physics. 1

Which law of physics is Feynman referring to and how would it "caring" violate it?
Chapter 3 Vol. I of The Feynman Lectures, just search for "violate"

I think Feynman is referring to the second law of thermodynamics.
The entire statement is this:

The most important feature of the cycle of Fig. 3–1 is the transformation from GDP to GTP (guanosine-di-phosphate to guanosine-tri-phosphate) because the one substance has much more energy in it than the other. Just as there is a “box” in certain enzymes for carrying hydrogen atoms around, there are special energy-carrying “boxes” which involve the triphosphate group. So, GTP has more energy than GDP and if the cycle is going one way, we are producing molecules which have extra energy and which can go drive some other cycle which requires energy, for example the contraction of muscle. The muscle will not contract unless there is GTP. We can take muscle fiber, put it in water, and add GTP, and the fibers contract, changing GTP to GDP if the right enzymes are present. So the real system is in the GDP-GTP transformation; in the dark the GTP which has been stored up during the day is used to run the whole cycle around the other way. An enzyme, you see, does not care in which direction the reaction goes, for if it did it would violate one of the laws of physics.

Now, there are some mistakes here. For instance, GTP is not used in the muscle contraction but ATP. Perhaps this was not quite known during Feynman's times. Coming to the point, I think what Feynman means is that external work has to be done by the enzyme (that catalyses the GTP-GTP exchange) if it is actually moving the chemical equilibrium towards one side (against what would happen in an uncatalyzed condition). Some enzymes can actually do that (shift equilibria and catalyse one sided reactions), by using energy from ATP hydrolysis or other energetic transformations but since they are performing work by using energy from an external source, they are also not violating the second law.
That's the essence of the second law of thermodynamics: you cannot move heat from a cold reservoir to a hot reservoir unless external work is done. We don't have "heat" here but there concept is the same for chemical energy and reaction rates.

Whilst I think this is a good answer, I don't think Feynman has in mind the second law precisely. See my answer. The reason I say this is that the issues discussed in my answer are a fairly big, well known theme in physics and were being heavily debated in Feynman's time too.

Actually I don't think Feynman is referring to the second law. Although he is wandering some way off topic in this piece, I believe he's referring to the fact that for all fundamental building-block physical theories, such as electromagnetism, quantum mechanics and Newtonian mechanics, any solution to the relevant equations can be reversed in time to find another solution. That is, fundamental physical laws don't know the difference between past to future and future to past time progression: they work in exactly the same way in both cases. The same holds for general relativity although it is less relevant there because people most often tend to think of the spacetime manifold rather than time evolution. So if the enzyme "cared" or "knew" which way the reaction were going, its behavior would tell against at least one of these fundamental theories of physics which are all reversible.
Imagine a glass falling from a table, hitting the floor and shivvering into thousands of shards. That process conforms with all the fundamental physical theories that govern it: the mechanics of motion and the solid state physics that governs how objects stay together as a whole. Now imagine that we could freeze the time evolution, and change the motion state of every glass shard flying off the impact so that its velocity vector were pointed exactly in the opposite direction, before letting the physical process keep going. You would also have to reverse the direction of the wavefronts of all the acoustic waves travelling off into the floor and air as well as the wavefronts of the electromagnetic radiation produced by the impact. We would see all the shards coming together at the impact site, the glass reassembling itself (the edges would line up so that the chemical bonds would all reform) and jumping back onto the table unblemished! This, believe it or not, is a valid solution to all the relevant equations of physics here, just as valid as the one where the glass falls and shatters.
Feynman here is alluding to something in thermodynamics known as Loschmidt's Paradox: the problem of explaining why physical processes seem to have a preferred direction when the underlying laws are time-reversible. The answer is the second law of thermodynamics whose modern accepted explanation seems to be that the universe, somehow, began in an exquisitely low entropy state such that any "random walk" in phase space undergone by a physical system will increase the system's entropy with overwhelming probability. The same would not be true if the universe began in or near a maximum entropy state. This leaves the mystery as to why the universe began in that state; a highly readable account of these ideas is to be found in:
Roger Penrose, "The Road to Reality: A Complete Guide to the Laws of the Universe", Chapter 27 "The Big Bang and its Thermodynamic Legacy"


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A New Antiviral Drug Strategy?
I am studying viruses and I have a question about antiviral drug strategies. Why haven't researchers tried finding small molecule drugs that will bind to receptors on the host cell, thereby preventing viral attachment to the host cell? I feel as though with this strategy, virus resistance and mutation wouldn't be an issue. Thoughts?

According to wikipedia, there have been drugs targeting CCR5 coreceptor approved for treating HIV. These drugs work by binding to CCR5, thereby prevent binding of HIV and CCR5.
However, drug resistance can still develop. Some HIV can bypass it by shifting tropism to CXCR4. While others can increase its affinity to CCR5.
And some receptors are vital for the functions of cells. If we design drugs to these targets, we should make sure that the drugs only prevent binding of viruses specifically without disrupting their normal functions.

Maraviroc was approved for use by the FDA in August 2007.It is the
  only one thus far approved by the FDA for clinical use, thus becoming
  the first CCR5 inhibitor. A problem of this approach is that, while
  CCR5 is the major co-receptor by which HIV infects cells, it is not
  the only such co-receptor. It is possible that under selective
  pressure HIV will evolve to use another co-receptor. However,
  examination of viral resistance to AD101, molecular antagonist of
  CCR5, indicated that resistant viruses did not switch to another
  coreceptor (CXCR4) but persisted in using CCR5, either through binding
  to alternative domains of CCR5, or by binding to the receptor at a
  higher affinity.
  https://en.m.wikipedia.org/wiki/CCR5

http://www.ncbi.nlm.nih.gov/pubmed/11782552
http://www.sciencedirect.com/science/article/pii/S0042682206008245

Please add relevant citations to your answer.

I learnt it from wikipedia, it didn't show any external links about drug resistance. If you want more credible sources, I'll try to find them.

I posted two additional paper. I haven't finished reading them. I hope these can help.


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Some kind of better oxygen-transport protein or something... Can you help me find it?
I remember reading about artificial or man-made, oxygen-transport protein that is somehow an improvement on hemoglobin, and that it is possibly immune to sickle-cell anemia, or something... But I forgot where I found it and what exactly it is...
Can you guys help me find it?

Is the protein HP7?

Seems like it is HP7. It would be immune to sickle cell anaemia because the disease happens because of a mutation in haemoglobin; any substitute for the diseased haemoglobin would work, including normal haemoglobin. For curing sickle cell anaemia you would need to anyway express it in RBCs. But the group who reported this protein never claimed that it is better than haemoglobin [1 and 2].

So, is there any oxygen transport protein that is better than hemoglobin? ... I remember reading about this where it said that it is an example where nature doesn't do the best it can, but just adequately... ... Looking that up now...

@Malandy Nothing other than HP7 turns up when I google "synthetic/artificial oxygen carrying protein". I have not heard of any protein being better than Hb. Fetal haemoglobin binds oxygen with slightly higher affinity and activation of fetal Hb in sickle cell patients is an ongoing therapeutic research.


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Crossing over and exon shuffling?
Campbell Biology 10e, in discussing the functions of introns, writes:

The presence of introns in a gene may facilitate the evolution of new and potentially beneficial proteins as a result of a process known as exon shuffling. Introns increase the probability of crossing over between the exons of alleles of a gene—simply by providing more terrain for crossovers without interrupting coding sequences. This might result in new combinations of exons and proteins with altered structure and function. We can also imagine the occasional mixing and matching of exons between completely different (nonallelic) genes. Exon shuffling of either sort could lead to new proteins with novel combinations of functions. While most of the shuffling would result in nonbeneficial changes, occasionally a beneficial variant might arise.

Hitherto, I had perceived crossing over as the shuffling of alleles between two homologous chromosomes, not of parts of alleles. That is, breaks in the DNA during synapsis would occur in between loci, not within them. Am I wrong to think that? My books tell me that, with regards to evolution, sources of genetic variation include mutations and genetic recombination. Genetic recombination includes random fertilization, independent assortment of homologs, and crossing over, yet it is only mutations that can produce new genetic material. If exons were crossed over, then new alleles would be formed, would they not? Is this a type of mutation? (I do not recall studying such a specific case of mutations.)

Crossing over primarily happens because of homologous recombination (HR). From the molecular point of view, it can happen between any homologous regions and it is not necessary that an entire allele has to be crossed over. During the process of HR, a DNA double strand break occurs. This is followed by resection (exonucleolytic degradation of one of the strands — 5'→3', from the break-point) by the MRX complex which leads to formation of ssDNA ends. The length of these ssDNA ends dictate the total length of crossover region.

 Taken from: Branzei, Dana, and Marco Foiani. "Regulation of DNA repair throughout the cell cycle." Nature reviews Molecular cell biology 9.4 (2008): 297-308.

This length can be from around 1.5kb to over 10kb depending on the repair kinetics with possibly an average of 3kb (more than half the cases) [1, 2]. Therefore, the author speculates that the probability of intra-gene crossover would increase with increase in intron length. However, in my knowledge, there are no recent reports to validate this hypothesis.
Edit:
Going back to the original question. It is not necessary that entire alleles are crossed over. Generally the genome has some recombination "hotspots" flanked by what are known as LD (linkage disequilibrium) blocks. An LD block need not cover an entire gene, as observed by Twells et al. (2003)[3] :

LD breaks down in the region LRP5 g.5257T → G–LRP5 g.28149C → T, in
  intron 1 of theLRP5 gene. A second block of very strong LD
  (‖D'‖ > 0.9) is observed, LRP5 g.28149C → T–LRP5 g.45704G → A,
  spanning 17.6 kb of intron 1 to intron 3 of the LRP5 gene.

References:

Chung, Woo-Hyun, et al. "Defective resection at DNA double-strand breaks leads to de novo telomere formation and enhances gene targeting." PLoS Genet 6.5 (2010): e1000948.
Zhou, Yi, et al. "Quantitation of DNA double-strand break resection intermediates in human cells." Nucleic Acids Research (2013): gkt1309.
Twells, Rebecca CJ, et al. "Haplotype structure, LD blocks, and uneven recombination within the LRP5 gene." Genome Research 13.5 (2003): 845-855.

1) Does crossing over occur between gene loci, or can it occur within them?
The cross-over events can happen within genes in introns and/or exons and still lead to viable gametes.  The text is stating that it's the increased length from introns that increases the probability of a cross-over event there, which is basically true.  This is simplified, and there are hotspots for crossing over and low probability areas.  The exon shuffling between completely different genes would not occur by crossing over; there are other mechanisms that would lead to these kinds of structural rearrangements in gametes.
2) Would a new allele be formed by a cross-over between exons, and is this a type of mutation?
A new allele could be formed if one arrangement of exons is allele1, another is allele2, and the cross-over involving 1 and 2 is uniquely allele3. If this happens by a cross-over event, it is not a mutation.  Also, there is no "new" genetic material in allele3 even though it could be considered a new allele; it is only a new combination of sequence that existed in 1 and 2.


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Which is the best model organism to implement an evolutionary study for P.falciparum?
I have to study and implement some evolutionary statistics for P.falciparum. In your opinion and by your experience, which organism should I consider in order to take the orthologs to implement this study?In general, If I wanted to extend this study to P.knowlesi, P.vivax and in general to all the parasites evolutionary related to the asian monkey plasmodia, which organism you suggest me to consider as a template? I thought about P.berghei but, since I have to consider also the Vinckeia parasites (mouse plasmodia) is there a good organism, out of the plasmodium genus, that could come in handy serving as a reference point for all these species?
Obliged

Is there a reason to not do all of them, if you are only doing computational analysis ("evolutionary statistics")? The meaningfulness of the work will increase significantly with each additional organism included.

Yes the analysis is set to take in consideration the whole set of the organisms. I have only to find a good protozoan to take the orthologs. In human M. musculus is good enough, but for plasmodia?I though about some haemosporidia. What can you suggest  me?

i would suggest taking orthologs from as many species as possible (ideally 10+ minimum) and using their phylogeny to combine information. estimates will only get better with more information.

Thank you for your precious suggestion


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Could be misleading using some terms to describe certain phenomena?
I am implementing a series of comparative analyses related to Low Complexity Regions in some organisms. Given that these regions show a wide range of length (measured in amino acids) and different characteristics, writing my report I would like to use "mosaicism" to describe this interspersion. Given that the term mosaicism is used to describe when someone have two or more genetically different cells inside his or her organism, I am in doubt if using this word could be misleading or, given that the term per-se indicates a set of gussets that compose a picture, to consider it somewhat elegant given that is clear enough what I am talking about.
Obliged

Please [edit] your question and give some more background (or provide helpful links) regarding what "Low Complexity Regions" are and explain their characteristics. Based on what you did say, I'm not sure "mosaic" is the best way of describing the phenomenon.

Regardless of what term you choose, define at the beginning how you'll be using it for the purposes of your analyses.  Clarity is probably more important the precise word you settle on

Do you know what a mosaic is? Do you really understand why the term mosaicism is employed. I am not clear what the phenomenon is you are describing. You use the word interspersion. What is wrong with that? Can you draw a diagram in which this phenomenon is compared to a non-interspersed reference so we can see whether the word fits or another may be better, or indeed whether an additional adjective will remove any ambiguity.


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TMB vs ECL for ELISA: which detection method is more sensitive?
I failed to find a comparison, does anyone know which ELISA detection method is more sensitive of these two: ECL, TMB?
Many thanks!

In general, ECL is more sensitive than TMB for ELISA detection. The minimum detection limit of TMB is 60pg/mL and 20pg/mL for ultra TMB [1], whereas the detection limit of ECL can be as low as about 1.7pg/mL  [2].
Resources:

https://info.gbiosciences.com/blog/elisa-substrates-a-selection-guide

https://www.thermofisher.cn/cn/zh/home/life-science/antibodies/immunoassays/elisa-kits/elisa-enzyme-substrates.html


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rapidly growing mold on flat surface
For an experiment I'm conducting, I need to grow mold on a 2 foot square piece of white fiberglass. I'm in Florida, with high heat and humility, so mold already grows easily. I've seen elsewhere that mold needs organic matter to feed on, to grow rapidly. Ironically, I've seen mold grow on the side of fiberglass motor-homes and showers with no present organic matter. Any suggestions on how to grow mold rapidly on my piece of fiberglass? I thought of locating fiberglass outside, in sun. I could mist it every hour or 2 to create more moisture. Maybe there is something I could rub/spray on the fiberglass sheet to encourage rapid growth? Any other suggestions about applying moisture, light, etc?

Hi Andrew, (great name) what type of mold is it?

I'm not sure of type of mold. I'm trying to replicate the mold growth which naturally occurs here in Florida, USA.  Could be a few species of fungi. Just trying to figure out how to grow dense mold quickly.

Mold is a general name for many species of Fungi, which are heterotroph so they need organic material to feed on. You can see them grow on fiberglass because many organic material can accumulate near or on fiberglass (skin cells, plants root hairs, microbes, oils) and become substrate for the mold.
If you want to grow a specific mold you should first identify it to find the best substrate for that species and not for other. If you simply want mold you can use some kind of starch on the fiberglass and keep it moist (not wet, wetness will give you also oomycetes and bacteria). No need to spray it every 2hrs. You can close the fiberglass with a box, dark box is better (bacteria grow best with light).
You can take (with mask and gloves) some mold and put it on your fiberglass to promote the growing of that mold.
Describing your mold or posting a picture can help to identify. If you see two different colors report both of them and location (center, periphery)

Thank you. What are some general examples of starches I can use to accelerate growth of mold, densely and quickly?

I use potato but any should work. Depending on the Fungi paper of cardobard can be more selective towards it