text:
Method of determining base values of traits in isolated populations
Prelude: I came across a discussion about the correct formula for calculating the average IQ of offspring, which goes something like the following
$$ 100 + \frac35 \left( \left(\text{father's IQ} + \frac{\text{mother's IQ}}{2} \right) - 100 \right) $$
but it does not matter for this question, and I do not know or particularly care if this is the correct formula.
As you all know, there is regression to the mean, i.e., if both parents have a freakishly high IQ of, say, 160, but come both from a "base population" with average IQ 100, the formula calculates the average IQ of the offspring to be lower than the arithmetic mean, because the parents are both outliers of their own "base population". Now, the above formula supposedly takes regression to the mean into account (and the mean it takes into account is IQ 100). As some people then pointed out, there is assortative mating, and very smart people descend often from very smart people, so the formula does not work for couples of "good pedigree".
I take it that this regression to the mean happens because these outliers with high IQ still carry some of the genes of the base population with IQ 100 and those are likely to be inherited by their children, thus lowering the IQ of offspring in comparison to their high-IQ parents.
My questions are:

How many generations of ancestors of average IQ, say, 110, do you have to have, in order for the regression of the mean to go towards IQ 110?

More generally and more interestingly, how do you determine what is the average value of a trait of a reasonably isolated subpopulation, that stems from and still lives inside a larger population? I am specifically interested in subpopulations as small as families, families with mean values of traits that deviate significantly from that of the overall population.
Obviously, the first family-generation with a mean IQ of 110 does not make it likely that the mean of the offspring will be 110 as well if the direct ancestors, i.e., the zeroth generations and those before average around 100. At what stage or how many generations in can we reasonably assume that the IQ 110  is the value that the mean regresses to, under the assumption that there is constant assortative mating regarding intelligence and no freakish outliers occur in the family tree?

I guess it boils down to the following. How big do the two family trees of a couple have to be in order to reliably infer the average value of a trait — like intelligence, highly heritable, polygenous — in future offspring?
(No eugenics, no one gets selected other than by their mates, no evil scientists lurking.)

Consider a couple where the male has an IQ of 125 and the female has an IQ of 100.  What average IQ does the formula give?

Update
I put in an answer to this question, with some reservations noted below, as there is a somewhat straightforward genetics answer to at least part of it. I'll leave the answer up for a little while as a sort of placeholder, up to the point that the question hopefully gets taken down.
Original answer
I'll first note the strong "yikes!" aspect of this question, which is closely related to e.g. eugenics.
Question 1
However, I believe that you will be most interested in the "breeder's equation", which is I believe the source of some of your values:
$\Delta Z = h^2S$
$\Delta Z$ = change in mean trait value in a population per unit time (generation usually)
$h^2$ = narrow-sense heritability
$S$ = strength of selection.
I suggest going to that resource for more information.
I will quickly note that this model is strongly dependent on a number of assumptions:

You have accurately estimated the narrow-sense heritability.
You have a large, panmictic population (you have raised this with assortative mating).
a lot of other stuff

(1) in particular is a big deal for IQ or really nearly any human, where there are reported heritability estimates in the 50% range from twin studies, but we honestly don't have a good estimate of this stuff, and there is really strong confounding from environmental variation (contra evo psych). I would not expect ("normal") IQ variation to respond very strongly to selection if environments were held constant. (There are obviously very clear examples of systematic environmental effects on IQ).
When I say "normal" variation, I mean among people who do not have cognitive disabilities related to specific variants of large effect (such as abnormal karyotypes). If you include those, you will get a large initial response to selection due to selecting on that unambiguous variation.
Question 2
Why not just measure the trait of interest?


text:
What are the types of human intersexuality?
Every genetically-male human has a female-like sex organ until about the seventh week of pregnancy1, then, in general, due to male chromosomes' effect → androgens would be produced and cause that organ to change into male sexual organs1.
Such a course may be "biased" (for lack of a better term) towards intersexuality, in each of these contexts:

True hermaphoriditism
Androgen insensitivity, partial or complete
Non androgen insensitivity "feminization" in at least one aspect (for example gender dysphoria in the apparently genetically-male)

What are the types of human intersexuality (are these the only types)?

I suggest adding here clear definitions of what you mean by "sex", "gender", "gender identity", etc. - otehrwise yoru last sentence may be misinterpreted. While the identity and phenotipical features may vary, the genotype is usually unambiguous (unless we account for trisomy).

it is not clear what your question is. SE communities focus on asking and answering questions - you cannot simply have a discussion on the subject here (not that I would be personally against learning more on the subject).

@RogerVadim would you say that the question is clearer now?

Isn't this a bit too general? What do you expect as an answer? - more precisely, can an answer fit into one page?

@RogerVadim I expect a similar list of a few (I would guess 5, probably not more than 10); I am certain that an answer can fit into one page.

in other words, you expect a review from an expert rather than an answer to a specific question. I suggest that you do a bit of research (i.e., googling) on your own and pose a more specific question. It will simply increase yoru chances of getting an answer.

@RogerVadim what you wrote is untrue, I have done a lot of prior research in a that topic and actually asked about what I have found so far which I think is more than enough for asking a question here; I am not looking for a higher chance than there is now.

Besides, there is nothing wrong in asking in expert's review if the question is useful for general audience and the longevity of the post is plausible.

you have nothing to prove to me... let's hope that somebody takes time to write a kind fo review that you ask for.

Hopefully someone here would clear the comment section.

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] effectively on this site and [edit] or delete your question accordingly. In particular, your question is a duplicate and lacks sufficient evidence of prior research — this site has many related posts and wikipedia resources include articles on the Quigley scale and intersex, which includes a relevant list.

Does this answer your question? Is sex a spectrum?

source: Stack Exchange

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

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text:
Are there taxonomic keys for members of the family poeciliidae in America?
I wish to know what are the taxonomic aspects necessary for the identification of certain species of poecilids, specifically what is the role in the counting of rays and spines and also the measurements of the organism. Which documents can I guide myself from? Am looking to know the exact measurements of a specific fish, in this case Poecilia salavatoris.
The fish was found in Honduras, Central America in the state of Francisco Morazán in a fast-moving, shallow, seasonal brook.

The fish in question is 4.5 cm in total length and 3.5 cm in standard length.

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


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After digesting food, where does the energy go before being stored by the body?
I'm trying to piece together a simplified model on how the energy flows in the human body.
From what I understand:

We store enough ATP for around 2 seconds of maximum exertion
We store enough kreatinine for around 8 seconds of heavy exertion
Blood glucose amounts to around 60kcal worth, enough for 30 seconds of intense activity
Our glycogen stores are what we mostly run off in the day to day, the amount seems to be anywhere between 1-3x of the daily resting metabolic requirement, depending on fitness, so 1500 - 4500kcal worth for most people.
Fat is where excess goes but it takes time to build, looking at various studies it seems that the most extreme fat creation/destruction that our bodies are capable of is around 1000kcal worth per day or ~0.29kg/day

Based on this, I'm treating glycogen as our main "battery". Fat is for long term storage and everything else is a chain for increasingly more intense and shorter exertions.
Now to top off our glycogen stores, I see two typical ways - either digest food or burn fat. Leaving fat out for the moment, there seems to be a discrepancy between how quickly we can digest some foods like refined carbs and how fast our bodies can possibly restore our glycogen stores.
It seems that we can absorb some carbs like pure glucose for example almost immediately whereas glycogen stores take at least 20h to restore, even if you're a super fit athlete.
That leaves me with the question - where does this energy go meanwhile?
Of course, I imagine that just eating 1000kcal worth of pure glucose will probably result in a diabetic coma but it doesn't have to be this extreme. Even just eating 1000kcal worth of white bread seems to overwhelm our bodies ability to store it all in glycogen by the time we are done digesting it.
So again, where does this energy go in the meanwhile?

I love that you've presented what looks like research in your question, so +1. :) But where, may I ask, did you get this information?

@anongoodnurse I didn't keep a list of sources but its what I noted down after reading a bunch of related articles and conclusions of studies. The numbers aren't nearly exact but I just need a general idea of how it works to create an approximation for a game. I did continue looking into this meanwhile and found a few errors - for one, blood glucose is never really supposed to be used up and is there just to shuttle the calories around and second, only the glycogen in the liver is available to the whole body (~400kcal worth) but it seems that's enough for a day or so as muscles have their own.

Thanks, that makes sense. The numbers are just way, way off. Serum glucose levels are kept between ~70 and ~110 mg/dl between meals. Above that, we're making glycogen, below, we use it. It's a constant balance. All of it, though, is homeostatic in mechanism. (2 seconds of max exertion? What's kreatinine? Do you mean creatine? 8 seconds?) It seems we'd all be dead after 10 seconds of hard exertion. If it's for a game, use any numbers you want.

Your focus is on glycogen and athletics. Can you clarify whether you are concerned specifically with skeletal muscle glycogen by editing your question. At the same time, after reading my answer, please reconsider your use of the word energy.

@anongoodnurse Yeah, it seems that blood normally has just 4g of glucose in it in total and yeah, I do mean creatinine. The 2 and 8 seconds I fished out of some research done on weight lifters, apparently they hit similar "wall"s as marathon runners do after exhausting a particular store of energy and were unable to perform on the same level until recovery, all though these "wall"'s are easier to miss as it takes just 10 seconds to rebuild the ATP stores and around a minute for creatinine.

@David Its not just about athletics, though it does make up a large portion of the  expenditure if you're a sword wielding game character. My goal with the model is to meaningfully limit the amount of exertion one is capable of, as well as introducing fluctuations in a persons muscle, fat and other tissues. I want my knights to be able to get fat as well as have them starve over a long campaign and the consequences that come with it. I use the word energy because by my impression, anything converted to sugar by digestion ends up as usable energy at some point regardless of the path taken.

Creatinine is a waste byproduct, and has no role in energy. I'm sorry, but your claims just don't fit with reality. Molecular Biology and Physiology don't live in these tiny compartments you've put them in.

@anongoodnurse I mean phosphocreatine

It is hard to be sure what the poster is asking exactly, but my best effort is the following:

It takes 24 hours to replenish muscle (?) glycogen after carbohydrate
intake, therefore the “energy” from the digestion of the latter must
exist in some form in the intervening period. What and where?

There are several problems with this question which need to be clarified so that it can be recast in a form suitable for answering.

There is a failure to distinguish between energy and
molecules.

Certain molecules have the potential to release biologically utilizable energy when subject to particular chemical transformations, or have the potential to be converted into compounds capable of such transformations and which can be stored in the body. This distinction must be made in a scientific discussion of the topic.

It is not clear whether the question relates to muscle or liver
glycogen. From the reference to the (atypical) human beings termed
athletes, I assume that skeletal muscle glycogen is intended.

This is important, because the functions (and regulation) of liver and muscle glycogen are quite different.

The question seems to assume that muscle glycogen is major end-product of ingested carbohydrate in mammals.
The question seems to assume that mammalian metabolism prioritizes
the replenishment of muscle glycogen over other metabolic fates for ingested carbohydrate.

Neither of these assumptions are true. The skeletal muscle has a limited capacity for glycogen storage. Despite the plethora of irrelevant and undocumented figures in the question, this is not mentioned.
Likewise, the question does not consider whether there is any difference in replenishment of glycogen in the normal recovery after muscle exercise compared with that combined with a large intake of carbohydrate. This is relevant to the second point. The mammalian liver is the organ most involved in distributing glucose and fats to the body, and as far as glucose is concerned its first priority is the brain and nervous tissue, not skeletal muscle. The way the liver and its target tissues handle glucose depends on the hormones of feeding and starvation — insulin and glucagon, the latter of which does not affect skeletal muscle.

Finally, the actual question seems to have been obscured by scientifically meaningless assertions such as “I'm treating glycogen as our main "battery"”, and recitation of figures that are largely irrelevant to the actual question — when you unearth it.

Rephrasing the original question, removing the use of the term energy and its implicit, but erroneous, assumptions, actually gives us two questions.

What, quantitatively, is the metabolic fate of glucose following a high-carbohydrate meal in an average (e.g.) Western adult male.
Why does it take 24 hr to replenish muscle glycogen?

The quantitative answer to the first question can, I imagine, be found in the literature, although more thoroughly in laboratory animals. There must be radioactive tracer studies on rats exhausted in treadmills. In general depending on the physiological state of the organism and the tissue it can be oxidized via glycolysis and the tricarboxylic acid cycle, generating the ATP currently required for various anabolic reactions, converted to glycogen, fat or creatine (depending on the tissue) or its metabolites used in synthetic processes. I presume an excess can even be excreted in the urine.
If it really takes 24 hr to replenish muscle glycogen, I assume that is because the integrated regulation of cellular metabolism does not treat it as a priority. It may be that, even in the fed state, the combination of blood glucose and insulin concentration only drives a slow replenishment. It would be interesting to know the actual rate of replenishment.

I think the question was perhaps not asked with the specificity or precision that a biochemist would expect, but I think it's a reasonable question if you interpret it more from an exercise physiology standpoint. In that case, what OP describes as "energy" might ultimately come down to "(potential for) ATP". My interpretation is that they are not asking so much about "what happens" in terms of biochemical pathways of digestion but rather in resolving what they have found as some inconsistencies with the estimates they have learned about for different reservoirs of "potential ATP".

+1 one for the expanded answer, but one word of caution on the comment: "questions are written in English which has a scientific vocabulary of precise terms which may be understood unequivocally" : this website attracts interdisciplinary audience (of which I am). Most physicists would feel more at ease with the usage of the word "energy" in the OP than in your answer. This said, again, I am of the opinion that your answer is also very good for a non-biologist reader and that's the real point.


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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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Does DNA ligase have any role to play in replication on leading strand?
Actually I developed this doubt while solving some questions(they are poorly framed I suspect). According to my notes and my institute modules, 1 RNA primer is required on the leading strand as well to start DNAP activity, and at the end repairing enzyme will remove the primer and add the complementary nucleotides. Now, here's the problem i am facing, will the DNA ligase join the newly added nucleotides by the correction enzyme or it is not required? The questions that created this doubt say in the solutions that DNA ligase is not a requirement in replication on leading strand but i think it should be required to join the nucleotides added by the correction enzyme as is the case on lagging strand. Am i correct?

The work of DNA ligase is to form "phospho-ester bond" or  "phospho-diester bond"(bond joining phosphate of one nucleotide with OH of another nucleotide).
by forming this bond the DNA ligase seals gap b/w 2 nucleotide sequence.
Now in case of lagging strand okazaki fragments are formed and gap b/w two okazaki fragments are filled by DNA polymerase and then the final joint is done by DNA ligase by forming phospho-ester bond b/w a nucleotide(last nucleotide which was placed by DNA Polymerase)and another nucleotide (which is the first nucleotide in the nucleotide sequence of second okazaki fragment which is being joined together)
now there is no need of all this mechanism in case of leading strand because there is no okazaki fragment present in leading strand. So DNA ligase is NOT required in case of leading strand.
hope this helps!!
EDIT-->
as discussed in the comments below, the DNA ligase might be required in joining two leading strands of two replication fork of a replicon

Thanks bro, actually i talked to my teacher also about this and he admitted that actually DNA ligase IS required on leading strand when the nucleotides are finally added in the place of one Primer that is required at the starting of leading strand. However since its role is so small it is usually neglected and NCERT also has mentioned DNA ligase with only lagging strand so that's why...

@Vaibhav Agarwal yes bro i got your point , DNA ligase might be required in joining the leading strands of two replication fork
correct?

Actually the DNA ligase kinda works like this- we know everytime DNA polymerase has to start its activity, RNA primase is added . RNA primase consists of a few ribonucleotides added complementary to the DNA strand which serve as kind of a launch pad for the DNA polymerase . now when the DNA polymerase is done with its work after replicating the entire strand , the DNA polymerase 1 ( mainly, however other enzymes are involved as well) comes and removes the ribonucleotides and adds the complementary deoxyribonucleotides instead. Now the DNA ligase comes and seals the newly added deoxynucleotides

As a primer is added on the leading strand , some DNA ligase activity is required there. However it is generally ignored (as NCERT has done and we will follow for NEET) due to the very small role it plays there.

@Vaubhav ya bro you are correct in explaining that how DNA ligase and DNA polymerase work.

According to me too DNA ligase contribution is required for joining leading strand of two replication fork but this contribution is neglected in NCERT Textbook.
bro if you found my answer useful then pls upvote my answer. And thank you so much for accepting my answer as best the answer. : )


text:
Why is Heart Rate Recovery after exercise reasonably well described by a mono-exponential decay?
I have been measuring my heart rate recovery after exercise and I see that it can be fit reasonably well using a single exponential:
$HeartRate(t) = HR_{max} \times e^{-t/\tau}  + HR_{resting}$
This observation is further supported by this paper:
https://pubmed.ncbi.nlm.nih.gov/24494748/
From Wikipedia: "A quantity is subject to exponential decay if it decreases at a rate proportional to its current value"
So, the exponential decay suggests that the ability to slow down the heart depends on the heart rate itself. A faster beating heart somehow produces more of the signal to slow down the heart.
Is this the case? What is the mechanism that allows for such a feedback loop of the heart rate? Is the signal sent through the nerves as the heart muscles contract, or is the blood flow that allows a signal to travel?
Is there another way to explain the mono-exponential decay?
Here is an example from yesterday's run. I sprinted and then walked very slowly a few times. My heart recovery lifetime ($\tau$) including only the first three decays is 53 +/- 4 seconds. The last decay is after I ran up the stairs and then sat down, and its lifetime is of only 22 seconds.

Exponential decay is characteristic of a first-order reaction, and where the exponential factor arises because the integral of 1/x (dx) is ln(x). Radioactive decay is a great example. For any first-order reaction, we can calculate the half-life, once the first-order rate constant is known. This is independent of concentration ...

... The half-life is usually expressed as ln(2)/k but in your case, it will be ln(2)*τ which I calculate to be about 36.7s. Thus after 36.7 seconds, HRmax will have decreased to half its original value (no matter what that initial value was), and after a further 36.7 seconds it will have decreased to half that value again, and so on

I think most people would take exponential decay in a circumstance like this to be the null hypothesis. That is, if you had something not exponential decay, that would be curious and interesting and worth understanding better.
Exponential decay is a pretty fundamental concept in the universe in general and biology in particular.

So, the exponential decay suggests that the ability to slow down the heart depends on the heart rate itself. A faster beating heart somehow produces more of the signal to slow down the heart.

I would not think about it quite this way, and maybe that's why you're thinking there is something profound here about "ability to slow". Rather, I would think in homeostatic terms and consider the "set point". If your "set point" for heart rate is high during exercise and low during rest, you'd expect exponential decay if the physiological signal being acted on is a difference between the current rate and the set point. When the rate is much higher than the set point, you'd generate a bigger error signal and this would result in a faster decay.
More concretely, you could think in terms of regulators of heart rate like CO2 and catecholamines, as both of these are likely to follow an exponential pattern, CO2 because transfer out of tissues into the blood and out of the blood into the lungs are both going to be faster when CO2 concentrations are higher. Catecholamines are going to decrease by exponential decay through enzymatic degradation: when there are more molecules around to react, the rate of degradation will be faster.

Thank you! The precise nature of the "error signals" in homeostasis will keep me entertained for some time. I study the kinetics and dynamics of very simple chemical systems, and it is quite easy to take simple systems out of mono-exponential behavior. Even the systems that you mention - diffusion of CO2 and enzymatic degradation will often show non-exponential behavior unless special conditions are met. The emergence of mono-exponential behavior from a complex combination of dynamics over different time and size scales is quite fascinating, even if trivial!

The answer by Bryan Krause is right on point from a system's perspective.
From a cardiology point of view, heart rate recovery (HRR) post-exercise has been a significant consideration in cardiopulmonary exercise testing (CPET) in recent years.
Put succinctly, heart rate is influenced by the sympathetic and parasympathetic nervous systems. Increased sympathetic activity increases the HR and increased parasympathetic activity decreases it.
The response of both systems to the cessation of exercise is a huge determinant of the  behavior of HR post-exercise. So, abnormal HRR can potentially reflect imbalances between the sympathetic/parasympathetic systems.
In Chronic Heart Failure, the failing cardiac muscle prompts inappropriate neurohormonal activation of both systems, which is sometimes described as "flooring the gas pedal and the brake pedal at the same time". This can be directly observed (see Figure) in the HRR patterns of CHF patients, which is blunted because both the sympathetic and parasympathetic systems exhibit more inertia to change. Note that a lower HR is also achieved.

In fact, blunted heart rate recovery in CHF patients confers very poor prognosis.
Another interesting tidbit: In heart transplant recipients, one can essentially observe the behavior of a "denervated" heart, as all nerve connection have been severed*. In pediatric heart recipients, heart rate recovery (defined as peak HR - HR post 1-minute) was extremely slow compared to normal controls:

This finding highlights the significance of neural input to achieving a "normal", exponential HR decay.
*some innervation can be observed months-years post-transplantation
References

Zweerink et al. Chronotropic Incompetence in Chronic Heart Failure: A State-of-the-Art Review. Circulation: Heart Failure. 2018 Aug;11
Singh TP. Longitudinal changes in heart rate recovery after maximal exercise in pediatric heart transplant recipients: evidence of autonomic re-innervation? J Heart Lung Transplant. 2007 Dec;26

Welcome  Anastasios. Please take our [tour] and refer to the [help] as and when for guidance. Great first post. Enjoy Biology.


text:
Why do humans have sex for recreational purposes?
It never made sense to me why human beings crave sex other than for reproducing. It controls our society. It causes heartache, jealousy, anger, low self-esteem etc.  Sometimes humans will have sex over and over again even though they have no intention of producing a baby. I know it feels good but it doesn’t make sense to do something that risky unless you want a progeny. Why is this so?

I’m voting to close this question because it is posed in relation to the author’s philosophical opinions, rather than as a biological problem such as comparison with animals that only copulate when the female is “on heat”.

"I know it feels good but it doesn’t make sense to do something that risky unless you want a progeny"

This right here is where you are tripping up. It's not about what one wants. It's about the continuation of the human race and not risky at all from that perspective. In that case, anything that increases those chances is a good thing.
Just like eating. How often do you think "I better eat something so I don't die" instead of "I want to eat that thing because it tastes good" or "I want to eat to get rid of this unpleasant hungry feeling."

Yeah you make a good point…….


text:
In this aquponic tank, what are these three plants and could they be killing my beta fish?
I have a small aquaponic fish tank. In the tank there are two unknown types of water plants from a local pet store and the top there are three air plants from a local garden center. This tank was setup ~2 months ago and at this point tests low for ammonia, nitrate, and nitrite it also is within limits (as set by the aquarium water test strips) for PH (~7.9), hardness, and alkalinity. As far as I understand it, the nitrogen cycle and bacteria bed of this tank is alive and well. Both the water and air plants grow voraciously.

Here are the plants themselves along with their root systems. The best I remember the left was labeled as "Decorative Pepper (Hot)" and after eating one the first day I can confirm they are extremely spicy.

The second day after setting up this tank I added a single male beta to the tank. Provided it is a hardy air breathing fish I assumed it would do well while the bacteria bed setup. Though, after ~1 week the fish had died. I assumed it (Bubble Bob) was just a sickly fish from the local pet store. I wanted a few more weeks just to ensure the bacteria bed had set up and recently added another beta (Beta Bernie). I bought Bernie from a local tropical fish store and made sure to select the most lively one I could find. I assume this store takes much better care of their fish than the local big chain pet store.
A day after adding Bernie to this tank he became very sluggish and layed on the bottom, only moving to get air, not wanting to feed. This went one for a second day. Two days ago I got a small cut, added some tap water (the same water used to fill the tank), some dechlorinator, and put Bernie in it and floated the cup in the tank (which is heated). After a day Bernie popped back to life.

From this (same water, only difference being the plants) my assumption is that one of the air plants I purchased is potentially poisoning my betas. Can you identify these three air plants? Are there any species of air plants which are known to release chemicals that hurt fish?

Consider posting this to https://pets.stackexchange.com/

I went back and fourth between here and pets. I figured if anything I could identify the plants here. Then ask pets if the types of plants are known to hurt fish.

this is a good fit over at pets but you will need to give a lot more information about your water and tank setup.like the results of your last water test, PH-AMMONIA-NITRITE.i will need information about how long you cycled your tank before adding fish.if anybody here can identify the plants you have it will help diagnose your problem.a better plant to use in your filter is watercress it is one of the best plants for removal of exess nutrients and it is eddible.

you say in your question"The second day after setting up this tank"does this mean you did not cycle the tank at all? please take a look here https://www.fishlore.com/NitrogenCycle.htm

If I'm right, the middle plant looks like some kind of croton plant. Every part of a croton is poisonous, including the roots. Capsaicin (from pepper) is a strong topical irritant, but I have no clue how much is released by the roots. If it is, I don't doubt it could kill a fish. The remaining plant is a begonia, which is (iirc) edible and pretty tasty, but does contain oxalic acid in flowers and stem. Don't know about roots. So, you have two definitely suspicious plants and a maybe. Not good.


text:
Does a brown Pieris brassicae chrysalis indicate it is dead?
I have been breeding Pieris brassicae larvae in a glass tank indoors for my own personal observation. One of them, after the fifth instar, has moulted into a chrysalis. After 5 days of development in which the pupa changed colour accordingly to the information I had researched, going from a vibrant green to a paler green with black, white and yellow dots, the chrysalis has turned light brown on the sixth day.
I have found no correspondence of this in any of the sources, articles and videos I have studied. Does it indicate that the pupa is dead / stressed? (I am keeping the larvae at room temperature, i.e. 22°C and under a bright led light that is used to light up the whole room)

Did you do a google image search? I found this and others like it.  But time will tell. When my chrysalises die (different butterflies), they do turn brown, but they also appear dehydrated. IOW, they look dead.

Thanks! Do you think I should move them to a cooler space, (e.g. outside)? Or perhaps the bright led lighting I am using has a role in all of this?

I can't help you with that. I can tell you that most of the chrysalises that die for me were unrelated to the conditions in which metamorphosis was occurring. The caterpillar could have been stressed into pupating early or infected/parasitized (it's pretty awful to see a wasp come out of a Monarch chrysalis.) As I said, time will tell, and it's more likely than not that it would have died anyway.


text:
Best way to estimate wolf density through camera traps
I would like to know the most suitable sampling strategies and analytical methods (possibly, with relative bibliographical references) to estimate the populational density of wolves through camera traps, without single individual recognition.
So far, I've  only consulted this publication (https://besjournals.onlinelibrary.wiley.com/doi/10.1111/j.1365-2664.2008.01473.x), but I'm a beginner in the field, and I would like further advice.

Without being able to identify and count specific individuals, I would think any methods you find would be suspect. Are you able to identify differentiating characteristics between individuals?

@theforestecologist, nope, no differentiating characteristics available.

I can think of ways you might be able to do it with cameras placed in a grid over area and analyzed with time-stamped co-ordination of when counts take place, but I have no idea whether that would be something feasible or not and even if it would be considered statistically reliable.

Wolves are pretty lean animals, so I'd guess their density is in the range of 0.95 - 1.05 kg/L ;-)

Density estimation can be reliable without identifying individuals. Check out the resources  from St. Andrews Centre for Research into Ecological and Environmental Modeling.  https://www.creem.st-andrews.ac.uk/ They regularly offer workshops and are friendly, helpful, top-notch scientists.

Population estimation of wolf is a decade long challenge. Since wolves are wide ranging species, detection rate is very low in the camera traps. As they are difficult to identify at individual level it increase the chance of bias. However, with modern technologies we can estimate the wolf abundance using camera traps. I found two studies relevant to your question, 1. Estimation of pack density in grey wolf (Canis lupus) by applying spatially explicit capture-recapture models to camera trap data supported by genetic monitoring- here they have identified packs and estimated the pack density. This method can be applicable over larger areas where atleast 10 packs exists.
2. Estimating wolf abundance from cameras- here they have used motion triggered cameras and used Space Time Model (STE) to estimate the abundance of wolf.
Both the method have catch in it. Wolf packs are very dynamic and chances of avoiding camera traps (trap happy/trap shy) can cause possible bias. The main challenge is to extrapolate the data at landscape level.

Mattioli, L., Canu, A., Passilongo, D. et al. Estimation of pack density in grey wolf (Canis lupus) by applying spatially explicit capture-recapture models to camera trap data supported by genetic monitoring. Front Zool 15, 38 (2018). https://doi.org/10.1186/s12983-018-0281-x
Ausband, David E., Lukacs, Paul M., Hurley, Mark, Roberts, Shane, Strickfaden, Kaitlyn, and Moeller, Anna K.. 2022. “ Estimating Wolf Abundance from Cameras.” Ecosphere 13( 2): e3933. https://doi.org/10.1002/ecs2.3933

You could look into using a version of point - sampling distance sampling [1]
Also, [2] might help a bit to be more flexible than using a grid (even if it is on spatial capture recapture).
[1] Howe, E.J., Buckland, S.T., Després-Einspenner, M.-L. and Kühl, H.S. (2017), Distance sampling with camera traps. Methods Ecol Evol, 8: 1558-1565. https://doi.org/10.1111/2041-210X.12790
https://besjournals.onlinelibrary.wiley.com/doi/full/10.1111/2041-210X.12790
[2] Durbach, I, Borchers, D, Sutherland, C, Sharma, K. Fast, flexible alternatives to regular grid designs for spatial capture–recapture. Methods Ecol Evol. 2021; 12: 298– 310. https://doi.org/10.1111/2041-210X.13517
https://besjournals.onlinelibrary.wiley.com/doi/10.1111/2041-210X.13517

I edited your post to add full citations (in case those links ever get changed/break)


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Arrangement of Amino Acids in the Protein alphabet
I am a software engineer with little knowledge of molecular biology. However I am trying to understand some bioinformatics computer code where the protein alphabet appears to be represented as the following string, with each of the twenty amino acid constituents of protein:
ACDEFGHIKLMNPQRSTVWY

The code appears to define a second string in which the first is reordered as:
DEKRHNQSTPGAVILMCFYW

I am not sure of the biological significance of this. Does this reordering represent some specific interaction between these molecules?

Welcome to Biology.SE. Have you looked at a table of amino acid properties? There are many ways of grouping amino acids, so if it isn't documented why that order is being used I doubt anyone can give you a definitive answer beyond the trivial 'ordered by physicochemical properties'.

@tyersome But the mapping given by the OP doesn't appear to be based on physicochemical properties at all?

@user338907 — What makes you say that? DE = "acidic", KRH = "basic" etc. (see also acvill's answer), you seem confused there is no mention by the OP of this being a mapping ...

What is the context? HPLC? Mass spectrometry? 2D gels? Sucrose gradients? Protein folding? What kind of analysis?

OP is probably referring to this.

That is exactly right @voile
I have been looking at the DeepSequence paper and its implementation where you have related protein sequence aligned with each other and one is trying to develop a statistical model over their distribution.

I rephrased the question to align it to the accepted answer and to avoid a biologically misleading title. Although not a Python devotee, looking at the code in the link given by @Voile it would appear that I am incorrect in my comment that these are not strings. The answer would seem to be that the second string has been reordered on the basis (better a particular assignment) of amino acid properties. Why strings are being used in this way is not evident to any molecular biologist, or anyone else without analysing the code.

@Luce Thank you for your contribution. As the algorithm for the paper you refer to is neither standard or self-evident, I for one would find very useful if you could provide an answer explaining it.

@David So I analyzed the code a bit and this reordering thing seems to be a red herring. Must be hangover of some old code as it does not seem to be used anywhere...

@Luca — Strange. I'll have a look at it myself perhaps. I am having to work on someone else's Django code at the moment, so I might as well try to suss out the Python. If it beats me I have friends I can lean on. This whole thing would have probably been better on SE Bioinformatics, although I don't go there much.

Ah right...yes, did not know about that SE!

As suggested by tyersome's comment, the amino acids are grouped by their physiochemical properties. Let's add some commas:
DE,KRH,NQ,ST,PGAVIL,MC,FYW

aspartic acid (D) and glutamic acid (E) are acidic
lysine (K), arginine (R), and histidine (H) are basic
asparagine (N) and glutamine (Q) are amidic
serine (S) and threonine (T) are hydroxylic
proline (P), glycine (G), alanine (A), valine (V), isoleucine (I), and leucine (L) are aliphatic
methionine (M) and cysteine (C) are sulfur-containing
phenylalanine (F), tyrosine (Y), and tryptophan (W) are aromatic

My source is this graphic.

Thank you! Lots to take in!

I am the person who came up with that reordering and I can confirm that acvill is correct. Specifically, the hope was that in heat maps relating the sequence to other properties like colours would show up in clusters. It actually does not work that great but it's the best you can do arranging them in one dimension.

I have deleted my previous comment about strings as it transpires, to my surprise, that the computer code contains the two 20 amino acid sequences as strings. So your answer might be modified to say that "the second string contains the 20 amino acids arranged so that those of similar physiochemical properties are grouped together". The reason for constructing such strings can only be discerned from an understanding of the computer algorithm.

@David I will contact the authors and update the thread.


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Fixing the cell with 4%PFA and staining with PI to observe cell cycle?
I am wondering whether we can replace 70% ethanol to fix and perm the cells with 4% PFA to observe the cell cycle. Do I understand correctly that 4% PFA can permeate the cells, thus the PI will intercalate DNA?

PFA can also cross-link DNA, interfering with intercalation.

Thanks, I will search more details.


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The village of Twins — Mystery behind and Scope
With the presence of more than 200 twins,  Kodinhi , a village situated in Malappuram District in Kerala , India , is popularly known as the "Village of Twins".This phenomenon of large number of twin births is not only unique to Kodinhi.It has also observed in : (a)  Cândido Godói , a municipality of 6,151 inhabitants in the state of Rio Grande do Sul in Brazil , (b) in Igbo Ora in Nigeria and also (c) in Hiệp Hưng in Vietnam .
a) Kodinhi/Kodinji : The village of twins in Kerala

The village entered the international spotlight when a survey done by locals found an unusually large number of twin births in the region. A report by The New Indian Express Staff Correspondent Mithosh Joseph from Malappuram had brought the attention of several people outside India to the attraction of the spot. His report had featured well the ongoing researches in the area, the total number of twins, the peculiarities of parents and a few other comments by doctors who studied the strange phenomenon. Though initial estimates put the instance of multiple births at 100 pairs, follow-up surveys found the figure to be closer to 204 pairs (408 individuals) of twins, and two sets of triplets.Despite several studies being conducted, the exact cause of this phenomenon is yet to be ascertained. Women from Kodinhi married off to far away places are also known to give birth to twins.According to doctors, this phenomenon is due to chemicals present in water in the Kodinhi area .According to locals, the oldest known twin pair in the village was born in 1949. The number of twin births in Kodinhi has been increasing over the years, with surveys showing over 79 pairs of twins within the age group of 0–10 years.
In 2008, around 30 pairs of twins from Kodinhi, along with their parents, got together to form The Twins and Kins Association, the first such association of twins in India.The forum, according to its founders, aims to bring to wider attention problems peculiar to people of multiple births, such as those concerning their education and health.

b) Cândido Godói in Brazil

The rate of twin births in Cândido Godói is 10%, significantly higher than the overall 1.8% rate for the state of Rio Grande do Sul. This rate is unusual, exceeding the highest observed national twinning rate (4.5 to 5% for southwestern Nigeria).Nearly half (8 of 17) of twins examined in one study were monozygotic (identical) twins, a few more than the average of 30%.Twin births were noted from the early twentieth century, when the first immigrants included seventeen sets of twins, and have been observed through several generations in the latter part of the twentieth century.
The population is largely of Polish or German ancestry, with many tracing ancestry to the Hunsrück region of Germany, which has a higher than average twinning rate. The rate in Cândido Godói could reflect genetic founder effect: rare genetic traits occurring by chance among a small group founding a community will be more common among their descendants than in the population at large.

Note : Founder Effect
c) Igbo Ora in Nigeria : The Twin Capital of the World

In Igbo-Ora, research has suggested that the multiple births could be related to the eating habits of the women in the region.Though no direct relation between dietary intake and twin births has been proven, a research study carried out at the University of Lagos Teaching Hospital has suggested that a chemical found in Igbo-Ora women and the peelings of a widely consumed tuber (yams) could be responsible.
A possible explanation that the large number of twins being born here could simply be a matter of genetics

d) Hung Loc Commune in Vietnam
From the article: The hamlet of Twins ,

The high rate of twins in this area is not due to marriages between families who produce twins.In many families with twins the parents come from different regions of country with no background of twins in the family. It is a rumour that the water in this region consists of a special mineral that helps women get pregnant and produce twins.

What can be the reasons for such a phenomena? Is it just genetics or may because of some chemicals present over that particular area (what chemical)? What all ways this phenomenon can be beneficial (scope) ?

More Reference :
A Case Report : A Non-Identical Twin from the village of Twins with identical occlusal characteristics — A Non-Identical Twin from the village of Twins with identical occlusal characteristics
Website : International Journal of Health Sciences and Research (IJHSR)
Volume : 6 ; Issue : 10 ; October 2016
Pages : 260 - 264
Date of Publication : 05.10.2016
Corresponding Author : Praveen Jodalli
Abstract : Abstract of the case report
Accessed on : 20.11.2021
(Note : Based on Kodinhi/Kodinji village of Kerala only)

it's related to dulebobvulation.

This is interesting, and it's nice - lovely actually - to see sources. But what about research into a possible answer? What did you find when you googled why some areas are blessed with so many twin births?

some info here: https://www.google.com/search?q=factors+that+increase+chances+of+indentical+twin+birth&biw=1213&bih=645&sxsrf=AOaemvLCw958js4B4SfLX2XiVMhuRh-1aQ%3A1637570137571&ei=WVabYdOvIoO7lwTewoPYCQ&ved=0ahUKEwiTwOCSyKv0AhWD3YUKHV7hAJsQ4dUDCA4&uact=5&oq=factors+that+increase+chances+of+indentical+twin+birth&gs_lcp=Cgdnd3Mtd2l6EAM6BAghEApKBAhBGABQAFi6QmCqRmgAcAF4AIABkgGIAdokkgEEMS4zN5gBAKABAcABAQ&sclient=gws-wiz and general science https://www.google.com/search?q=hormes+that+affect+twin+birth&oq=hormes+that+affect+twin+birth&aqs=chrome..69i57j33i22i29i30.4538j1j4&sourceid=chrome&ie=UTF-8

@LifeInTheTrees Your links relate only to general factors increasing the likelihood of women conceiving twins, not the reason why there should be an abnormal geographical concentration of twins. If you know a source relating this please provide it.

You really need to examine the null hypothesis: that a few villages (out of perhaps millions on Earth) having a higher than average number of twins is simply due to chance.

Comments have a habit of doing that. Did you manage to find a more apt reference?


text:
Biomechanics of cells (stress, strain, tension..)
I am confused about the difference between stress, strain, tension, pre-strain and prestress in cells (especially in in-vitro experiments, like cell spreading on a substrate, cell doublets, cell rearrangements in epithelial tissues).

How are these 5 physical terms different or related?
Is there a reference or a book that can explain them in a good way, I got lost usually when they use in an article the terms ("they transmit tension" or "they impose stress")

@RogerVadim already mentioned an excellent book on biophysics (Phillips, Kondev, Theriot). Furthermore, since you are interested mostly on the mechanical aspects, I can recommend David Boal: Mechanics of the Cell.

Strain and stress are two essential quantities in elasticity theory, corresponding to the deformation and the forces appearing in response to this deformation. Tension or tensile stress is a particular kind of stress appearing in elongated objects, such as ropes, filaments, etc.
One could recommend any of the existing books on the elasticity theory, but these may turn out to be a bit of too "hardcore" in terms of the level of the math and the background physics knowledge required. I therefore suggest the reading more adapted to biologists (although not necessarily easy):

Physical biology of the cell
Mathematical biology I: An introduction

or similar books on mathematical biology and biophysics.

Thanks, you have a quick idea about the difference between stress and pre-stress in cells and how is that related to the cytoskeleton and actomyosin cortex?

@ALi Pre-stress is the inherent stress that exists in the material even before you load it. Prestressed concrete  is a good example - it seems far from biology, but most of the ideas is directly transferable to cytoskeleton. Unfortunately I cannot say more - the best I can do is google, which you also can do yourself (see, e.g., this one).


text:
Can antibiotic resistance cause problems for the microorganisms producing them?
My understanding is that antibiotics are naturally produced by microorganisms as a defensive measure against certain kinds of bacteria. For example, some Penicillium molds produce penicillin.
Clearly, antibiotic resistance has direct negative effects for humans because it makes certain infections more difficult to treat. But could this resistance also lead to problems for the microorganisms that produce antibiotics in the first place?
If this were the case then could there be additional negative "second order" effects for humans?

Does this answer your question? Will all bacteria become resistant against all antibiotics in the long term? Specifically, see the first paragraph of my answer.

I depends on what you mean by "problems." Antibiotic resistance mechanisms have probably existed in the wild for nearly as long as naturally occurring antibiotics. It's certainly possible for an antibiotic resistant organism to have an antagonistic effect on an antibiotic-producing organism, for example by competing for key nutrients or niche space. It's also possible for positive interactions to occur where one or both organisms benefits from symbiosis with the other.  Also not sure what kinds of second order effects for humans you have in mind.


text:
Newts in a rodent larder. Limits of regeneration? (NSFSqueamish)
Observation.
In the Surrey woodland of southern UK mainland I chanced upon a piece of corrugated metal. Lifting it up I found a bare patch of soil except for what appeared to be a nest of dry plant material and two palmate newts.
The newts had suffered traumatic removal of most of their heads leaving just the back-most portion of the skull and a dry wound with an airway/oesophagus present, little or no sign of a lower jaw or orbital sockets was present.
The newts showed rudimentary reflex withdrawal from gentle prodding, confirming that basic life-functions continued.
Supposition.
This was a rodent's nest and larder (food-store), the newts being preserved (and immobilised) in this way for later consumption.
Question.
Assuming sufficient body-mass and internal resources to draw from (and not being interrupted by being eaten), might these newts be able to regenerate to become fully functional again? (The question of resource limits within a newt might be mooted, but not the primary focus of my question).
Research.
Sciencedirect:

perfect adult regeneration of many other important tissues and
structures as diverse as heart, brain, spinal cord, jaws, retina and
lens, has also been described

Daniel Berg:

Experiments have been done on newts, in which a 70% of the optic
tectum is surgically removed. A  proliferative response was observed
in these animals and after 8 months the tectum was  almost  fully
regenerated,  but  the  origin  of  the  new  neurons  was  not
investigated  (Okamoto et al., 2007).

Here, it's later indicated that the origin of the progenitor cells for the regeneration is not known.
I'm unable to find or access any more recent or advanced research

Have no fear for the newts, they'll get better.


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Why is the partial pressure of oxygen in blood same as that in alveoli
The partial pressure of oxygen in alveoli is about 104 mmHg, after gas exchange it becomes 40mmHg. I understand that during gas exchange, the pressure gradient drives oxygen into the blood and Co2 out. My issue is that: since the partial pressure of oxygen in the alveolus is 104 mmHg and that of blood in the pulmonary capillary is 40mmHg, why would the partial pressure of oxygen in the blood after gas exchange also equal 104 mmHg and not 72mmHg since as oxygen leaves the alveolus the partial pressure drops and and increases by the same amount in the pulmonary capillary. At equilibrium shouldn't they both be at 72mmHg?  Mathematically speaking:
104-X(Alveolar PO2)=40+X(blood PO2)

There are three unfounded assumptions in your equation that I can see.

You're treating partial pressure as a concentration. Partial pressures are not concentrations, though they're convenient representations of concentration for gases because the behaviors of gases, especially with respect to diffusion between gases and liquids, behave according to partial pressure via Henry's law. For oxygen in blood, partial pressures are even more distinct from the "amount of oxygen per volume", because most of the oxygen carried in blood is bound to hemoglobin rather than floating freely/dissolved in the liquid.

You're assuming there is a finite amount of oxygen present in the alveoli, as if 104 mmHg of oxygen is present in the alveoli, and then blood comes and takes some of it away. That isn't the case; blood is constantly coming in through the capillaries, and there is constant diffusion and bulk flow of gases throughout the lungs (resupplied with external inspired air).

Following (1) and (2), it seems you're assuming the blood and gas are the same volume. This need not be the case.

Instead, to understand why the partial pressure of oxygen in blood leaving the lungs is the same as the partial pressure of oxygen in the alveoli themselves, it's important to realize that the surface area of the alveoli is absolutely massive, and that gases diffuse quite freely across distances the sizes of capillaries. They're the same for the same reason that if you put some water soluble dye in a glass of water and shake it up vigorously for a few seconds, you're going to find the dye evenly distributed. If it weren't evenly distributed to start, it's going to be very close when you're done. Same with blood through the lungs. If you put a little more oxygen into the alveoli, then a little more would flow into the blood; both concentrations would be higher, but they'd still be the same.
So, that tells you why the number is the same, but why is this number about 104 mmHg? Well, that exact number is going to vary by specific conditions, but you can be certain that the number will be an equilibrium somewhere between the atmospheric concentration of oxygen and the oxygen of blood entering the lungs. That averaging has already happened and is happening constantly all the time.

@ Bryan Krause; if the pressure in the alveolus is constant, then why is it that after the diffusion of O2 into the capillaries( in external respiration) the PO2 of Alveolar air reduces to 40 mmHg. Also, in internal respiration, the PO2 of blood reduces to 40 after Oxygen diffuses into the tissues, if pressure was constant there should be no reduction. BTW, I would appreciate if you could give me another analogy, the "dye" one was difficult to imagine.

I read somewhere that the difference between the vol of air in the alveoli and the vol of blood in the capillaries also plays a role in why the partial pressures are the same. And you also said it in your explanation, so I was wondering how they could be related

@Taofeek "the PO2 of Alveolar air reduces to 40 mmHg" - it doesn't. If you stopped breathing for a long time perhaps it eventually would, but not for normal breathing. "the PO2 of blood reduces to 40 after Oxygen diffuses into the tissues, if pressure was constant there should be no reduction" - I never said pressure was constant everywhere. There is low oxygen in tissues due to cellular respiration. Blood leaving the tissues has lower oxygen than blood entering the tissues, but blood leaving the tissues has about the same pressure of oxygen as the tissues themselves.

Another factor to consider is that oxygen is not (primarily) dissolved in the blood, it's chemically bound to hemoglobin.  So partial pressure may not be all that relevant.

@jamesqf Added that as an additional point under (1). It still remains that you can't treat partial pressures as concentrations for any solution, but it's particularly true for blood and oxygen (or CO2) as these are primarily carried by hemoglobin, so even if you used the partition coefficients for water or plasma you'd come up with some very wrong numbers.


text:
Why isn’t prokaryotic mRNA modified post-transcriptionally like eukaryotic mRNA?
Eukaryotic mRNA is subject to addition of a methyl-guanosine cap at the 5’ end, addition of 100-200 adenosines to the 3’ end, and splicing. Why don’t these occur in prokaryotes? Is it because there is no exonuclease and intron in prokaryotes?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

Before posting a question it is important to make sure it is scientifically correct and clear. Your title referred to post-translational modification and there was no mention that you are talking about mRNA. Having corrected that, we see that 1. you are asking about three distinct post-transcriptional processes, 2. It is not clear what you mean by "why" — do you want to know the function of each (which are described in any text) or some basic reason why mRNA (and its translation) has evolved differently in eukaryotes or prokaryotes? The latter can only be speculated on.

Does this answer your question? Why do some bad traits evolve, and good ones don't?


text:
What organism is this? Repetitive, long thread, double spikes, ... (from a human sputum sample)
Link to video

Collected in Portugal.

Welcome  André. Please take our [tour] and refer to the [help] for guidance as to our ways. Enjoy the site. I don't know about anyone else, but I'm not convinced that it's an organism. Did you ask the person what they'd eaten recently? Could you give us some idea of scale (how big)?

Thank you! The small cells you see next to it are neutrophils. So, it's thin but quite long. Goes on and on, coils, etc. And the double spikes repeat along the way. And it has that darker, nucleus-like, area near the level of the spikes. It must be a living organism or something made by one.

Why's this off-topic?


text:
Can hydroponically grown plants selectively uptake nutrients, or return excess water?
If a plant is growing with the roots in the water but the rest of the plant above water, does that plant have to absorb all of the nutrients in the ratio that they exist in the water or can it absorb what it needs and reject/return what it doesn't? My (quite basic) understanding is that plants use transpiration to create the pressure difference needed to suck up the water and all the nutrients it contains. This process doesn't allow an obvious way for the plant to either select for certain nutrients, return extra water to its roots, or reject nutrients it already has too much of. Is this because the plants actually can't, or because my understanding is flawed and too simple?
For background, I am asking because I keep aquariums. Like many people in this hobby, I grow pothos (Epipremnum aureum) in several of my tanks with the goal of removing nitrates, which can be deadly to fish in high concentrations, from the water. However if the plant is just taking in water and whatever nutrients are already dissolved into it, without any way to concentrate those nutrients or return excess water, then it stands to reason that having a pothos in the tank will not directly affect the concentration of nitrates. After all, taking a glass of 50/50 water and vinegar, and splitting it into two glasses doesn't give you one half full glass of water and one of vinegar; it just gives you two half glasses of the same mixture. There is still going to be some net effect from me refilling the tank more often with nitrate-free water to account for the water lost via transpiration, but is that it?
I have read through several questions here, but none seems to directly answer my question, or at least not in a way that I understood. While this could potentially be asked on the pets stack, I am hoping it is still on topic here. If I need to refine my question to make it fit better, please let me know.

A good search term is aquaponics .

I think most nutrients are actively transported in the roots, not dependant on transpiration rates.

I found a study from 2003, It very vaguely addresses your query, although it's not simply written: http://www.esalq.usp.br/lepse/imgs/conteudo_thumb/Mechanisms-and-Control-of-Nutrient-Uptake-in-Plants.pdf

Thanks for the pointers! @LifeInTheTrees, that does look rather information-dense. I'll do my best to work through it over the next few days and see if I can't pull out an answer


text:
In what sense is PCR a "nuclear-derived" technique?
The International Atomic Energy Agency (IAEA) has launched an initiative, ZODIAC, to combat pandemics that originate in animals. In part, this involves the deployment of kits utilising real-time reverse transcription–polymerase chain reaction (real time RT-PCR), which is described here as a "nuclear-derived" technique.
Nothing about the description, or my understanding of it from Wikipedia makes it clear how nuclear technology, isotopic composition, decay, etc. are involved in the real time RT-PCR technique, but the involvement if the IAEA implies a connection: what is this connection?

“Nuclear” here could be referring to a biological nucleus, though it is unclear from the linked website.

Nuclear-derived? DNA in eukaryotes is derived from the cell's nucleus, maybe that's what they're talking about? Alternatively, you can use radionuclide-labeled bases to do PCR-based sequencing, although that has been almost entirely supplanted by using the much safer fluorescence-based techniques.

I’m voting to close this question because it doesn't seem like it's really a question of Biology.

From what I can tell from other press releases involving IAEA it seems that they're referring to the use of radioactive labels historically used in quantifying PCR products. These days it's principally done using fluorescence rather than radioactivity. Why this is at all relevant to IAEA seems like more of a political question rather than anything involving biology. My guess is that there is some UN policy that gives IAEA jurisdiction over "nuclear-derived techniques" and they're using this umbrella to include PCR, perhaps so they can spend IAEA money on COVID-related initiatives.

That’s very interesting and I dare say you’re right. As a moderator, I suppose you get the final say on what is and is not on topic, but have to say I’m surprised that the history of PCR isn’t.

[HSM.SE] is the appropriate venue for that type of question, but I don't think this one would fit there either. The problem that I see is that this is opinion based (and thus off-topic for this site) since it is asking about why a non-scientific claim is being made.

@user924308 I'm open to other views and expect my actions to be reviewed by others in the community, but I think the question as asked is not particularly close to being about the history of PCR. That is, I don't think a biologist would think of PCR as a "nuclear-derived technique", that designation is only really of relevance to the IAEA as a political entity. As you can see in the comments from acvill and Matt, for a biologist, "nuclear" means "related to the nucleus of a cell". Radioactive compound are "radio-" to us biologists, not nuclear.

I think "why does the IAEA consider PCR to be a 'nuclear-derived technique when modern PCR does not use radioactive materials" could be a good Politics.SE question, though.


text:
What does equilibrium curve signify?
While learning about gas exchange, I came across the haldane effect. Then i came across the CO2 -dissociation curve. Apparently the curves are "equilibrium curves". Does it mean that the curves were plotted when the system of blood was in equilibrium? Otherwise what does it signify?


text:
Effects of mRNA vaccines on human body processes
I would like to understand the effect of an mRNA vaccine on more complex processes in the human body.
To what extent does this "artificial", external addition of mRNA interfere with the body's processes? It seems naïve to me to think that it cannot set processes in motion that can be passed on - positively or negatively - to future generations.
Do I have a wrong idea about "artificiality" or the processes in the body?
As far as I know, there are (permanent) processes going on in the human body to modify the genetic information that will be passed on to future generations.
I also wonder to what extent this "reprogramming" of the immune system places a (too) strong focus on COVID-19 and whether this can weaken the immune response to other diseases. I have a naive idea of a "point system" where only a certain number of resources are available for different disease control.

I can address some of the points made in the post.
One point about the "artificiality": I think there's one fact that's often overlooked in the discussion of mRNA vaccines. SARS‑CoV‑2, for example, is a positive-sense single-stranded RNA (+ssRNA) virus. That means, the information that the virus uses to replicate itself and which describes the "blueprint" of its components, is stored as a single RNA. This RNA can more or less directly be translated into corresponding proteins by the ribosomes outside the nucleus, just like the mRNA used by mRNA vaccines. So, during a "natural" infection with such a virus, the virus's RNA also gets inside the cells and is translated into proteins, just like with the "artificial" mRNAs by vaccines! But the way this RNA enters the cell is somewhat different.
With viruses, they dock onto the cell and release their RNA into the cell. With mRNA vaccines like the one by BioNTech/Pfizer and by Moderna, this RNA is packaged into lipids (the stuff cell membranes are made of), which integrate more or less directly into the cell membrane and release the RNA. With vector vaccines like the Sputnik V or the Oxford–AstraZeneca vaccine, a different virus is used to carry the RNA load and infect cells (in the case of AstraZeneca, an adenovirus is used which usually infects chimpanzees and is normally harmless to humans). RNA in any case is degraded by the cells within a short time and leaves no traces.
Regarding the permanent modification of genetic information in humans: the genetic information in humans is stored as genomic DNA in the cell nucleus. DNA has a structure similar to RNA, but they do not work together, so RNA can't be simply integrated into the DNA. For DNA to form proteins, which make up most of the parts of a cell, it needs to be transcribed into RNA, which then is further processed into mRNA. This mRNA is tagged with a molecular export factor, which it needs to pass through the nuclear pore complexes, which are the highly specific transporters between the nucleus and the cytosol. After an mRNA has been exported from the nucleus, this tag is cleaved, so it can't return to the nucleus. Additionally, only if genetic information of egg or sperm cells is altered, this change is actually passed to the next generation.
So in summary: mRNA from vaccines behaves pretty much like the RNA inserted by RNA viruses into cells. And it can't find its way into the nucleus, where the genetic information is stored. And even if that happens by some way, it would first need to get "reversely transcribed" into DNA to be integrated. Some viruses can in fact do that, like HIV, which can also break into the nucleus in some instances (or wait for a cell division). Simple, "naked" mRNA of a vaccine however can't do that, only in extremely rare circumstances where the cell is already infected by another virus like HIV, I suppose.
But maybe you were talking about what is called "epigenetic modification", which is the molecular modification of the genomic DNA, where the actual stored sequence information is not altered, but the way it is read is modified. This process however is mediated for example by methylation of parts of the genome, for example, and does not intrinsically have anything to do with mRNAs in the cytosol. It should be noted that epigenetic modification is usually also reversible, not permanent, but it can be passed to the next generation, just like the genome itself.
What you said concerning the immune system focussing too much on another disease: I don't know a lot of immunology, but usually, building an immune protection against one pathogen also strengthens resistance against others. However, problems concerning the immune system most often arise when the immune system "overreacts" to an antigen and starts attacking parts of its own organism (autoimmune reaction). This can in fact be triggered by vaccines, even by only mRNA (and its protein products), as well as "natural infections", of course. Clinical studies are in place to analyze these occurrences.

A nitpick - The Sputnik vaccine uses Human Adenoviruses (HAd26 and HAd5). The Astrazeneca/Oxford uses Chimpanzee Adenovirus (ChAdOx1, based on ChAd25).

The last point may be about the (effective) "memory capacity" of the immune system (a zero sum thought). This could maybe be addressed in the answer by stating (and comparing) the number of different pathogens (both new and already recognised) we are exposed to every single day. I don't know the number - in the thousands per year? Thus the "memory capacity" of the immune system must be at least on the order of 100 times that.

Thank you @bob1 for the correction, I fixed it!

Also thank you @peter-mortensen for fixing typos and adding Wikipedia links. I'm not sure if I'm qualified to comment on the "memory capacity" thing, maybe someone else could chime in to amend the post.

As @panda-byte writes in great detail, the mRNA processes in our cells are a one-way street and there is no conceivably relevant way for an externally introduced mRNA to modify your DNA.

Do I have a wrong idea about "artificiality" or the processes in the body?

Very likely, yes, if you (like me) do not have much more than general public knowledge, maybe as provided in a few short lessons in school if you were lucky.

I also wonder to what extent this "reprogramming" of the immune system places a (too) strong focus

The immune system is vastly complex and has many different layers and components. There is no way for a layperson (including myself) to have any luck in applying our intuition to these things - we must trust the scientists on this.
One of the best resources I know of which gives you a view of the insane complexity is the video How The Immune System ACTUALLY Works – IMMUNE from the excellent "Kurzgesagt" channel.  They provide the scientific sources as well if you wish to learn much more than appropriate for an answer here.

The information is passed to future generations mainly via egg cells and spermatozoa - as long as the genomes of these cells are not modified, there is no high risk (and, contrary to some antivax claims, mRNA vaccines do not modify any genomes). There may be some environmental effects on the immediate offspring, due to their contact with mother during pregnancy and breastfeeding, but these are also very limited.
On the other hand, the immune system of the vaccinated person develops new antibodies, which hypothetically might cause potential (over)reaction to other pathogens or manifest in new allergies.
Disclaimer: this is not an expert opinion, but a placeholder answer to motivate a deeper discussion. I will be happy to remove it as soon as the experts chime in.

The (unfounded) concern may be epigenetic changes (even if it wasn't directly mentioned in the question). Perhaps address that as well?

Re "new antibodies, which hypothetically might cause potential (over)reaction": Isn't the cytokine storm caused by something else than antibodies? (Not a rhetorical question.)

@PeterMortensen It might well be, but the cytokine storm is not the only concern. There are many kinds of autoimmune problems that include light harmless allergies and severe syndrommes.

authors: Vladimir F Героям слава


text:
What plant species generate the highest amount of bioelectricity?
I just want to ask which plant species produces a high amount of electricity. I'm very confused with the units that's why I don't know which species produce the highest amount of electricity. Also, can someone help me do differentiate each unit? It's just I don't have enough knowledge about it. By the way, the picture shows the species and produces power density through Plant Microbial Fuel Cell (PMFC)   Thank you...

Welcome to Biology.SE. Please take the [tour] and consult the [help] starting with [ask] for details about using this site. Your question appears to be about converting between various units, which is off-topic as it is not about biology as defined in the [help]. Have you tried searching for "power density unit conversion"? In general, we expect you to make an effort to understand the site and learn what you can on your own before posting. Please do this and then delete or [edit] your post accordingly. ——— Also don't post text as images.

I’m voting to close this question because it doesn't appear to be about biology as defined in the [help]. It is also poorly formatted (text as an image) and contains unreferenced material from an outside source.


text:
Where could I find biology-specialized transcription services for my conference?
I'm a conference organizer for various conferences in the field of biology. Just recently, I stumbled upon this Nature article: https://www.nature.com/articles/d41586-021-03487-2 and I have difficulties in finding biology-specific expert transcription services for my conferences. The generally well-known transcription service providers do not have people available that are familiar with the ubiquitous scientific terminology used by speakers on my conferences. Where could I find scientific experts that are capable of transcribing terminology-heavy talks across various fields of biology and willing to do so?

I’m voting to close this question because it is not about a problem in biology.

Short answer
To provide accessible conferences for the hearing impaired, automated artificial intelligence (AI) based captioning services are a good and affordable substitute to live captioners these days.
Background
I took the liberty to outsource this question to a giant in the field I work in (Auditory Neuroscience and specifically auditory prosthetics) and they wrote me the following back, and I quote (web links and comments in square brackets added by me):

'We previously used a remote live transcription service that cost
about $5000 [USD] for the [conference] week.  But the AI based automatic transcription
service is now so good we didn’t think there was enough difference in
quality to justify the expense of live captioners.  The institutional
version of Zoom has AI captioning built in – there’s a cc button at
the bottom of the screen, and the captioning built in to youtube is
excellent for prerecorded videos.  We used these two for the recent
[conference].'


text:
Is this a Northern Black Widow?
I’m in Florida and my 5 year old spotted a spider on an old watering pale toy. It looks like a widow in shape and color, and has red spots down it’s back. Most black widows here don’t have anything on their backs, so I took to the web to try and be safe, and found that the Northern variant has spots, but all the pictures I found have the spots blended towards the back end and they don’t seem to have the outline around the spots like this spider.

Also, I didn’t flip it over to check for the typical hourglass on the abdomen as I didn’t feel confident that I could do so without harming the spider or potentially myself.

A jar would have be handy. Honestly, if a black widow can have a grey velvety abdomen with no red spots? I'd wager 200 it isn't.

Your spider has red circles outlined in white (it is visible if you zoom in). This, indeed, looks like a dusty Latrodectus variolus

@LifeInTheTrees it was covered in dirt so that would explain the velvety grey color, and the red spots are surely there, you'll need to view the full image and zoom in a bit, apologies for the poor quality. Also, didn't have a jar available.

@JimN just glad my 5 year old didn't disturb it enough to cause any issues! Thanks for the help!

Yes it appears to be a male Norther black widow covered in dust. Here's an image using different color balance:

These species of black widow are found in Florida: Latrodectus mactans (Southern black widow), Latrodectus geometricus (brown widow), Latrodectus bishopi (red widow), and Latrodectus variolus (Northern black widow) (Edwards 2002).
quote:
Only the bites of the females are dangerous to humans. Despite their notoriety, Latrodectus bites rarely cause death or produce serious complications.(wiki)
male
https://upload.wikimedia.org/wikipedia/commons/c/cd/Black_widow_post_dorsal_1370.jpg
female:
https://upload.wikimedia.org/wikipedia/commons/thumb/a/a5/Latrodectus_variolus_%28Northern_Black_Widow%29%2C_F_Theridiidae.jpg/580px-Latrodectus_variolus_%28Northern_Black_Widow%29%2C_F_Theridiidae.jpg


text:
What is static compliance?
If static compliance is change in volume with respect to change in transpulmonary pressure, when there is no gas flow. My question is; if there is no gas flow, how would volume Change?

First of all, the definition that you have stated, is absolutely true in all sense.
Static compliance, theoretically, is indeed the change in volume with respect to change in transpulmonary pressure, when there is no gas flow. Here gas flow means air should remain static at the time of measurement. Hence it is literally about taking snapshots at varying volumes and noting the transpulmonary pressure.
Here is a diagram (source: https://derangedphysiology.com/main/cicm-primary-exam/required-reading/respiratory-system/Chapter%20031/static-dynamic-and-specific-compliance) i.e. identical to the original diagram from -

Rahn, H., Otis, A.B., & Fenn, W.O. (1946). The pressure-volume diagram
of the thorax and lung. Federation proceedings, 5 1 Pt 2, 82 .

For the above study, they acquired normal men, occluded their nostrils with cork stoppers, and measured their airway pressures at different fractions of their vital capacity (the subjects exhaled fully and then inspired a known volume of gas from the spirometer before performing a breath hold). With these manoeuvres, the above relationship was demonstrated.


text:
Are snake capable of love? (social bond in a male/female couple)
I'm wondering whether it has been noticed that some species of snake form male/female couples for life (or at least multiple reproduction cycles) like other types of animals do (penguins come to mind).
I understand that there is no such thing as chemical love, so that is out of the question.
I also know that most reptiles are loners or even attack/eat each others when they happen to meet. At the same time, there are snake pits with at times over 100 snakes living together.
So have we observed social bonding ("love") between a male and a female snake?

Could you please split this question up? Ideally, you'd ask these two separate questions in two separate posts. As a matter of personal preference, I would like this question better if you didn't bother with the term "love" - just ask "do any snakes form long-term pair bonds"?

@BenBolker I made an edit to restructure the point about the pit. It was not really a question only an example of possible socializing between snakes.

Not as far as I can tell. The closest example I can find is within-season pair bonding in copperhead snakes (defined as a male-female pair remaining together for some time, in this case defined as longer than a quarter of the breeding season).
Smith and Schuett (2015)'s abstract says:

Pair-bonding between sexes is common in vertebrate taxa, yet it has been noted far less frequently in some groups such as reptiles, and snakes in particular. Evidence to date indicates that many snake mating-systems are polyandrous, with both males and females having multiple partners in a single breeding season, and thus unlikely to exhibit lengthy pair-bonds. Wittenberger and Tilson (1980) suggested that pair-bonding exists when pairs remain intact for a consecutive period equaling at least 25% of the breeding season. Using this criterion, we present evidence of pair-bond formation in a North American pitviper, Agkistrodon contortrix (Copperhead), a species with a polyandrous mating system.

They observed one male-female pair that were found together over the course of 26 days out of a mating season of 70 days.
Uller and Olson (2018) say "in fact, multiple paternity in lizards and snakes is extraordinarily  common  and  reach (sic) higher  levels  than  that documented for any other vertebrate group": in their Table 1, the minimum level of multiple paternity observed in studies in snakes is 1/6. (Multiple paternity implies that females are mating with multiple males over the time scale associated with producing a single set of offspring. Genetic non-monogamy does not necessarily imply social non-monogamy — social monogamy + genetic non-monogamy is called extra-pair copulation — but it does suggest it ...)

Smith, Charles F., and Gordon W. Schuett. “Putative Pair-Bonding in Agkistrodon Contortrix (Copperhead).” Northeastern Naturalist 22, no. 1 (March 2015). https://doi.org/10.1656/045.022.0104.
Uller, Tobias, and Mats Olsson. “Multiple Paternity in Reptiles: Patterns and Processes.” Molecular Ecology 17, no. 11 (2008): 2566–80. https://doi.org/10.1111/j.1365-294X.2008.03772.x.


text:
What animal has the strongest immune system?
I'm wondering what animal has the strongest immune system. It can be defined as the most evolved immune system or the immune system that can eliminate or tolerate most number of (different) viruses/bacteria/diseases/pathogens/poison (some of which can kill most or many other animals or make them really sick).
I've done some research and found some animals that can be the answer but I couldn't be sure which one. There might be smaller animals that I've missed. There might be studies with more clear results that I've missed. Here are the animals I've found:

Shark
Ostrich
Bat
Alligator
Vulture

Here are some relevant quotes from the articles I've found:

Shark:

The shark's "antiviral defenses have been extraordinary," Zasloff said. "It has adapted a very remarkable immune system and stayed with it." In the study, squalamine thwarted infection of the dengue fever virus in human blood vessel cells and of hepatitis B and D in human liver cells—and with little harm to sharks.
 https://www.nationalgeographic.com/culture/article/110919-sharks-drugs-medicine-viruses-science-health-squalamine

Ostrich:

It is said that ostriches have the strongest immune system of any animal in the world. Because of this, they have shown great promise in preventative healthcare in humans and the beauty industry.
Ostriches strong immune systems make them highly resistant to viral infections. Japanese researchers have discovered how to mass produce natural ostrich antibodies that are effective against influenza, avian flu, MERS, Zika and even the Ebola virus. “The antibodies are resistant to higher pH levels and can remain active even when exposed to heat of up to 100 degrees Celsius.”
 https://pharmaboardroom.com/articles/ostrich-antibodies-a-health-and-beauty-elixir/

Bat:

The mammals can carry many viruses with the potential to cause serious diseases in people, including rabies, Ebola, Nipah, severe acute respiratory syndrome, or SARS, and others. Bats rarely get sick from those viruses. Why these pathogens tend to be so dangerous when they infect other animals has been a mystery.
Previous work suggests that a bat’s immune system is especially adapted to tolerate viruses, thanks in part to its ability to limit inflammation. Now a study using cells grown in a lab hints that to counter a bat’s immune defenses, these viruses have gotten good at spreading rapidly from cell to cell.
https://www.sciencenews.org/article/bats-immune-system-viruses-ebola-marburg-people

Alligator:

American alligators have an enviable innate immune system, the “primitive” first line of defence that is shared by all vertebrates. In 2008, chemists in Louisiana found that blood serum taken from the reptiles destroyed 23 strains of bacteria and depleted reserves of the HIV virus.
https://www.newscientist.com/article/dn27059-germ-killing-molecules-identified-in-alligator-blood/#:~:text=American%20alligators%20have%20an%20enviable,reserves%20of%20the%20HIV%20virus

Vulture:

Vultures' faces and large intestines are covered with bacteria that is toxic to most other creatures, but these birds of prey have evolved a strong gut that helps them not get sick from feasting on rotting flesh, according to a new study.
"On one hand, vultures have developed an extremely tough digestive system, which simply acts to destroy the majority of the dangerous bacteria they ingest," Roggenbuck said. "On the other hand, vultures also appear to have developed a tolerance toward some of the deadly bacteria — species that would kill other animals actively seem to flourish in the vulture lower intestine."
https://www.livescience.com/48899-vultures-bacteria-microbiome.html

this all depends on how you define strongest, A blue whales immune system can eliminate way more bacteria than a mouse just due to mass.

@John The question has details regarding "strongest immune system" already and the quotes I provided give an idea as well. I've also added: "immune system that can eliminate or tolerate most number of viruses/bacteria/diseases/pathogens". There are studies regarding immune system of animals. I might have missed studies that can provide an answer.

I've added the word "different" in parenthesis before "viruses/bacteria/diseases/pathogens" to make it more clear. I thought It was clear when the word "diseases" was there already and the quotes give a clear idea what the strongest immune system can be.

which really does not help, we don't measure immune systems by how many things they can fight because any immune system can fight a theoretically infinite number of organisms plus how many things an immune system is exposed to varies wildly, terrestrial organisms for instance are subjected to orders of magnitude fewer bacteria.

@John "Fighting" is different though. Immune system can fight many things but might not overcome. We are talking about eliminating or tolerating pathogens that can make animals really sick or kill them. More details are in the examples I gave. For example, vultures seem to be not affected by the bacteria that causes Anthrax which can kill many other animals, so the answer is likely an animal that can eat carrion. It is hard to find studies that compare animals though.

@0.. What if it's not even a matter of fighting? Not all viruses need to be fought because they are incompatible with the host to begin with. To me, this question is like asking who is the strongest fighter when everyone specializes in different styles of combat with dissimilar types of opponents where you can't pit the fighters against each other or the opponents against each other for comparison.

the problem is most infections diseases are specialized to their host very few diseases can infect a very wide range of organisms, anthrax for instance is very rare in predators it mostly infects herbivores. and is extremely rare in birds in general. a disease good at infecting one group of organisms my fair very poorly in another without the immune system coming into play. anthrax again for instance only infects endotherms.

I understand it is not an easy to answer question (hence asking) and might require comparison between studies. Anthrax was just one example of disease that a scavenger can eliminate. We are talking about many diseases/toxin where sum of them can kill many or most animals. Opossum might be the right answer as it is a scavenger and a snake hunter so it is immune many diseases and toxins where sum of these pathogens/toxins can kill many or most number of different species.

Though not strictly pathogenic in nature, Opossums (Didelphis virginiana) are well known to be able to recover from broad range of deadly toxins/venoms due to -- at least in part -- lethal toxin-neutralizing factor (LTNF).
According to Lipps (1999), who tried putting LTNF into mice:

Death due to intraperitoneal (IP) injection of a predetermined lethal dose of venom from major families of snakes, for instance Crotalidae, Elapidae, Viperidae and Hydrophiidae, is prevented in mice by subsequent IP inoculation of LTNF. Furthermore, LTNF neutralizes the lethality of scorpion and bee venoms and toxins from various animals, plants and bacteria. Thus, natural LTNF from opossum serum has potential as a universal therapy for envenomation caused by animals, plants and bacteria.

Also, because of their low body temperature, opossums rarely if ever get rabies unlike all other mammal species.
Opossums have also been known to eat a wide variety of foodstuffs including carrion, bones, and even garbage without getting sick -- suggesting they have strong immune systems associated with their gut.

Thank you, great answer. I've seen opossum mentioned when I searched before but didn't know the details about their immune system and LTNF.

I'm going to accept this answer (till something better comes up). Opossum, as a scavenger and a snake hunter, evolved to be immune to many diseases and toxins/poison where sum of these pathogens/toxins can kill many or most number of different species. Here is a relevant quote also: "They are nearly impervious to rabies because their body temperature is too low to host the rabies virus. They also rarely catch Lyme disease from tick bites, and are immune to the stings of honeybees and scorpions, botulism toxin, and snake venom." https://www.wildlifehc.org/in-defense-of-opossums/