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Sperm formation - Frequent Ejaculations
I have visited various authenticated websites and other materials and learnt that a complete sperm development takes approximately 64 days.
My doubts :

If sperm truly takes 64 days to develop, how can a man ejaculate multiple times (e.g., 4-5) in a day and still have sperm come out each time? Why don't all the sperm come out at once? And each time he ejaculates, the sperm are complete (i.e., the "head" and "tail" portions are always included), right?
Does frequent ejaculation, then, reduce the sperm count of each subsequent ejaculation? If so, do the sperms remain depleted for extended periods (i.e., 64 days), or are they replaced more regularly? At what rate are they replaced?

Comments are not for extended discussion; this conversation has been moved to chat.

The arithmetic of human sperm
A young, healthy man produces about 1000 sperms every second, which comes to about 90 million per day [1]. These sperms are stored in the epididymis and ductus deferens until ejaculation. With several days of storage, the number can easily become big enough to allow for multiple ejaculations on the same day.
The maturation period of 64 days does not matter here, because sperms form and mature asynchronously [1]. While one spermatogonium is on day 1 of its life, another is on day 2, another on day 3 and so on. Only those sperms that are mature are released from the testes (NOT directly in semen, but into the epididymis for storage).
Does semen normally contain sperm with abnormal morphology?
Yes. Even men in whom 96% of the ejaculated sperms have abnormal morphology can successfully conceive [2].
What happens on ejaculating repeatedly?
This has already been assessed in several studies [3–5]. Overall, the results have been that with repeated ejaculation in quick succession,

Semen volume decreases.
Sperm count decreases (pointing to sperm depletion) but not to zero.
The percentage of sperms with abnormal morphology remains unchanged.

Hope that answers your questions.
References

Mesiano S, Jones EE. The male reproductive system. In: Boron WF, Boulpaep EF, editors. Medical physiology. 3rd ed. Philadelphia: Elsevier; c2017. p 1092–1107.
Cooper TG, Noonan E, von Eckardstein S, et al. World Health Organization reference values for human semen characteristics. Human Reproduction Update. 2010 May–Jun;16(3):231–45. doi: 10.1093/humupd/dmp048
Oldereid NB, Gordeladze JO, Kirkhus B, Purvis K. Human sperm characteristics during frequent ejaculation. J Reprod Fertil. 1984 May;71(1):135–140. doi: 10.1530/jrf.0.0710135
Zvĕrina J, Pondĕlícková J. Changes in seminal parameters of ejaculates after repeated ejaculation. Andrologia. 1988 Jan–Feb;20(1):52–4. doi: 10.1111/j.1439-0272.1988.tb02363.x
Mayorga-Torres JM, Agarwal A, Roychoudhury S, et al. Can a short term of repeated ejaculations affect seminal parameters? J Reprod Infertil. 2016 Jul-Sep;17(3):177-83. http://www.jri.ir/article/674

Thank you for the answer!

Spermatogenesis begins in the seminiferous tubules.  In this process, sperm are formed from the processes of mitosis and meiosis from germline cells called spermatagonia.  Given continuous signaling from Sertoli cells, although the meiosis cycling takes about 64 days, all cell lineages are on their own schedule depending on unique signaling pathways they synergize.  Thus, there is no problem ejaculating 80-300 million sperm per ejaculation, several times per day, if the proper levels of testosterone and temperature are present to regulate the process.
This may seem like a lot of cells, but note one sperm is about 85000 times smaller than an oocyte (cell in an ovary).  A certain fraction of spermatogonium is always reserved no matter how much a healthy male ejaculates, thanks to Sertoli cell signaling.  Leydig cells that regulate spermatogenesis through testosterone production are also critical for spermatid maturation from the seminiferous valves to the epididymis. Further understanding the signaling pathways and genetic traits allowing the spermatogonia to be retained and replenished to form semen could have huge implications for regenerative medicine from a genetic engineering stand-point (aside from reproductive physiology).
Information pertaining to the rate of sperm production is highly dependent on individualized omic data. The 64-day cycle you mention is analogous to the circadian rhythm which repeats every 24 hours.  With a super healthy metabolism because you ejaculate three times in one day does not mean it will be impossible to ejaculate once or twice the next day, like if you run thrice in one day it doesn't mean you can't run twice again the next day.
Thanks for the interesting question!

Thank you for the answer. Could you also help by answering the questions of "fully developed sperm or the incomplete sperm during the ejaculations"


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

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

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

what research have you done to answer this question yourself?

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

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

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

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Why do patients with type 2 diabetes not show the body wasting seen in type 1 diabetics?
Type 1 diabetes results from the destruction of the cells in the pancreas that produce insulin, while type 2 diabetes is characterized by so-called "insulin resistance", presumably a reduced responsiveness of the body's tissues to the effect of insulin.  More succinctly, in type 1 diabetes, insulin is not produced at all, while in type 2 diabetes, insulin is produced, but it is ineffective.
Based on this description, one would expect that type 1 and type 2 diabetes would look similar, with maybe type 2 diabetes being a milder form of the condition.  This is not the case, however.  The diseases are markedly different, at least when it comes to their effect on body weight.
Type 1 diabetes results in wasting:

The images show a type 1 diabetes patient before and after insulin treatment.
In contrast, type 2 diabetes is associated with obesity, exactly the opposite scenario.
If the body does not respond to insulin in type 2 diabetes, why don't those afflicted waste away, in the way that (untreated) type 1 diabetes patients do?

Comments are not for extended discussion; this conversation has been moved to chat.

I have changed your title to reflect the content of your question. How obesity produces type 2 diabetes is a valid question — it could well be asked separately — but is not what you are asking.

The following is based on a conversation I had with a senior biochemist in my university who conducts grant-funded research on the relationship between diabetes and heart disease. It can be criticized for the paucity of external sources from which its veracity can be checked. However, although the question is based on a misconception I thought it should be addressed. Perhaps others could help improve the answer by supplying references etc.
The following points about Type 2 diabetes mellitus are relevant.

‘Type 2 diabetes’ refers to a disease which encompasses conditions
with a spectrum of severities.
This means that the description of it being “characterized by so-called ‘insulin resistance’” — alternatively expressed as cells being refractory to insulin — in fact means that there is a variation in the degree to which the cells are refractory. In many cases, although this leads to a higher blood sugar, it does not result in the complete breakdown of fat and muscle protein found in type 1 diabetes, where insulin is completely lacking.
Type 2 diabetes does not result in an increase in fat deposition and body weight. In many — but not all — cases it is caused by overweight.
In type 2 diabetes caused by overweight there is a gradual loss of fat. It is not apparent in a ‘snapshot’ of type 2 diabetics, many of whom have such large fat reserves that it will take a long time before these are broken down.
In severe type 2 diabetes the situation eventually becomes similar to type 1 diabetes as the beta cells of the pancreas can be destroyed. In these cases insulin injection is required.
Normally type 2 diabetes is controlled with drugs that reduce the glycemia — metaformin is currently the agent for the first line of treatment — and by lifestyle changes, especially in diet. (The treatment of type 2 diabetes was reviewed by Juan José Marín-Peñalver et al. in 2016 and considers their mechanisms of action etc..)

In starvation, the breakdown of both fat and protein starts at the same time as soon as glycogen stores are depleted (source - p.385). Why would an untreated person with diabetes 2 on isocaloric diet lose weight (fat or muscles)? Two important reasons for wasted appearance in diabetes 1 are 1) loss of glucose due to glycosuria and 2) dehydration due to polyuria triggered by glycosuria.

@Jan — OK. The fat reserves are usually completely depleted before the protein, but I will take the phrase (mine not my source's) out.

It is still a parallel process. Initially, more fat than muscle will be lost, but at the time when fat stores are depleted, there will be already some loss of muscle. But the question is why would a person with diabetes type 2 lose weight at all when on isocaloric diet?

@Jan — You will notice that I waited three weeks before answering this question because of extreme pressure of a project I am working on. I felt I should try to answer as I had said I would in a comment apparently transferred to chat. I am still interested in improving my answer and finding appropriate biochemical sources, but it will be a week or two before I have time to do more than add comments. (The answer to your point would seem to lie in the hormonal control of fat turnover. I had thought that this would be through glucagon, but my colleague thinks not.)

Type1 diabetes is an autoimmune disease where insulin producing cells are killed by the immune system. Many cells need insulin to be able to transport sugar from the blood. Without insulin they won't be able to use the blood sugar and people start to urinate sugar because of the high blood sugar levels. So the insulin levels will be low and the blood sugar levels will be high in type1 diabetes.
In the case of type2 diabetes the insulin production is not affected and cells cannot transport sugar fast enough, because they don't sense insulin properly. This results high insulin and high blood sugar levels. As the disease progresses, the insulin producing cells can die off and we can end up with a similar condition as we have in type1 diabetes.
Both have connections to weight. Insulin is a hormon that facilitates fat storage and fat conversion from sugar and it inhibits fat breakdown. So when insulin is low in type1 diabetes, then people have a hard time to gain weight. On the other hand insulin resistance is associated with obesity. So typically obese people suffer from type2 diabetes and they can lose weight as the disease progresses.

If the tissues are refractory to insulin, that includes the adipose tissue, so your statement that the increased concentration of insulin prevents them losing weight doesn’t make sense, and according to my source is untrue.

@David You are right, I tried to find a reference for it, but failed. Probably it is just an urban myth. I edited my answer.

@David If it is any truth in that high insulin + IR causes weight gain, then probably it has something to do with leptin. I don't have time to investigate this.

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Do technological developments terminate the evolution of human species?
One of the most agreed upon mechanisms for evolution is natural selection. Changing environmental conditions necessitates development of variations that enable the survival of that particular species. These genetically passed down variations later becomes the adaptive features which further result in the development of new species.
But with the development of technology we are finding newer ways to cope up with changes in the environment. Does this impact human evolution?

please search for similar questions before you post, this has been asked several times. https://biology.stackexchange.com/questions/20291/human-evolution-in-modern-times

"Natural selection" is a somewhat misleading term.  Evolution does not need "natural" selection to occur; it only needs selection.  Even the term "selection" is a bit misleading because it's often thought of as referring to the death of individuals or, somewhat more accurately, as reduced likelihood of producing offspring, due to lower fitness.
In fact, any process that gives individuals with particular genetically determined features - a reproductive advantage in a given ecological niche will drive evolution among the sub-population within that niche.
Addressing your question more directly: Suppose technology leads to people whose keyboarding talents are high having more children.  If so, it will tend to drive evolution among the sub-population having access to keyboards toward genotypes having higher keyboarding talents.  But if having keyboarding talents results in those individuals having less likelihood of producing children, evolution in that sub-population will be driven in the opposite direction.
IF it could be said that technology in general decouples human reproduction from "natural" influences like disease, resource availability, climate, etc., it could then be said that evolution will be less driven by those influences and more driven by, e.g., the cultural tendencies of particular sub-populations to produce more children.  But that would be a gross over-simplification.
It is almost certain that changes in technology have had significant influence on human evolution.  Agriculture, clothing, tool use, etc., have all had long-term consequences in human evolution.
Human culture is very complex, and separating out all the effects of technology on differential reproduction rates among sub-populations would be extremely difficult; but it's almost certain that there are such effects.

You might enjoy the 2006 comedy, "Idiocracy". The premise of this movie is that while technology allowed every person to survive, the smarter people study more, have a more demanding career, and have fewer children than the stupider people who just have a lot of kids - and the hypothetical result is that in 500 years, the human population becomes much less intelligent than it is today. Of course, this is just a movie :-)

It was a fun movie, and I refer to it often.  Just a movie, yes.

Evolution is not a path towards perfection/improvement but simply a series of changes over time.
Thus, as McGrew explained, technology can have an effect on what drives our evolution but cannot stop evolution: nothing can actually, because changes happen even by simple chance (see e.g. genetic drift).

Arguably it is possible that technology will stop human evolution.  Technology led to burning large amounts of fossil fuels, which causes global warming.  If carried to an extreme, this renders the Earth uninhabitable for humans (and most vertebrate life forms).  Thus technology renders humans extinct, and since extinct life forms don't evolve...


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Does antibodies get produced in female body against sperms?
Our immune system produces antibodies against any foreign particles entering our body.In female body  sperms are a foreign particle .Does females produce antibodies or some sort of chemical resistance against these sperms?If so how come sperms able to survive this?Is it because there a huge number of sperms entering female body?

https://en.wikipedia.org/wiki/Antisperm_antibodies Sperm can trigger antibodies production.Sperms are also killed by the low pH in the female genital tract


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How did the Spanish Flu disappear?
In 1918 through 1920, an Influenza pandemic colloquially named the "Spanish Flu", ravaged the world. It infected about half a billion people, and killed as many as 50 million people. But my question is - how did the 1918 flu virus disappear in 1920?
One can hardly believe that after infecting half a billion people, the virus was contained in any sense of the word. Why didn't the more than one billion uninfected people get infected? Why didn't we see some small epidemics continue to circulate the globe infecting the yet-uninfected as well as newly born people for many years - potentially until today?

What research have you done on the epidemiology of flu virus infections, before posting here? The Spanish flu was no different in that respect from the Asian Flu of the 50s, or last year’s flu strain. (Some would say that epidemiology is off-topic here, as it is some distance from biological mechanisms, but if you ask questions here you need to demonstrate that you have researched them first. )

I tried to see if there was any similar question on this site, and found none. I tried to Google a bit and didn't find any answer. I thought that even if an answer could be found on the Web, it wasn't obvious (at least to me) how, and it would be useful to have an answer here, on this site, for posterity. If "epidemiology is off-topic here", were is it not offtopic? Please note that I wasn't asking why the Spanish Flu is no longer a pandemic. I was asking why it went completely extinct. Is there something in the flu virus which makes it a particularly bad surviver compared to other viruses?

Another clarification: I know there is no reason why the Spanish Flu had to remain particularly common. It could remain one of hundreds different viruses going around - flus, "common colds" and so on, and reach a few people here and there. But the particular 1918 strain was very visible - it killed a large percentage of people infected. If this virus was still extant, wouldn't we see small deadly flu epidemics in various places over the last 100 years? What in the flu virus or the circumstances allowed that not to happen?

It's didn't disappear.  It's still around today, over 100 years later.  The 1918 influenza virus is the parent virus for all the human seasonal influenza viruses that are around today, as well as for most of the swine influenza viruses out there.
In fact, the presently circulating H1N1 viruses in humans are close enough to the 1918 virus that they probably immunize against each other (Seasonal trivalent inactivated influenza vaccine protects against 1918 Spanish influenza virus infection in ferrets.).
What did happen is that the 1918 virus mutated, becoming less virulent in the process, within a year or so of entering the human population. Why? Presumably because, after infecting virtually the entire human population in its first year, there was so much population immunity that it needed to mutate a little in order to continue to infect. That is, after all, what flu viruses do.
But it continued to circulate for decades, as a very similar H1N1 virus. Also, it almost immediately infected pigs and became endemic in the swine population, only to resurface  after 90 years to cause the 2009 influenza pandemic.

In 2009, persons who had lived through the first decades of the 1918 pandemic H1N1 era, especially those born before about 1950, were substantially protected from the 2009 pandemic virus by having acquired immunity to the antigenically similar H1 or N1 of the 1918 virus, or both, or to the descendant seasonal H1N1 viruses that circulated over subsequent decades. This is because the 2009 H1 gene was a 1918 viral progeny that had survived for more than 90 years, with minimal antigenic drift, in a domestic pig “time capsule.”

—The Mother of All Pandemics Is 100 Years Old (and Going Strong)! (Am J Public Health. 2018 November; 108(11): 1449–1454)
In 1957 and 1968, the H1N1 virus reassorted with avian viruses to generate first H2N2 and then H3N2 viruses (the great-grandchildren of the H3N2 pandemic still circulate today). But most of the internal genes in those reassortants remained the 1918 versions.
So the 1918 flu never went away. It’s still killing hundreds of thousands of people every year. It’s just that everyone has got used to it, and thinks it’s fine and normal to have hundreds of millions of influenza cases every year.

Thanks for the detailed and informative response! The reason why I'm still puzzled by all of this is that the 1918 strain was distinctive in that it killed a very large percentage of young, otherwise-healthy, of infected individuals. Somehow we're not seeing this phenomenon any more.  Even if the original strain mutated to create 100 different strains, if the original strain was still around as well, wouldn't we have seen small local epidemics of it from time to time killing large percentages of the healthy adults in certain towns, etc.?

We don't know in detail why the 1918 flu was so virulent; we do know that the surface protein hemagglutinin (HA) was a significant part of it, and we know that the HA of flu viruses changes very rapidly in response to population immunity pressure. The presumption is that virulence depended on a very narrow and precise sequence, that changed as a result of adaptation to human immunity - probably because virulence per se was not an adaptive  trait but was simply a side effect of other factors.

nice answer! Another related question: Before 1918, there were other influenza viruses circulating? The 1918 influenza was of a zoonotic origin? Where did it came from?

1918 was an avian influenza, perhaps passed through swine before infecting humans. Many strains of influenza circulated before 1918, but we don’t know much about them because we don’t have samples. There were many pandemics, presumably zoonotic, most probably avian origin but perhaps also equine

Check out the below link where I have put a graph on why it killed more young people. I have also linked there a PNAS article if you're curious. https://biology.stackexchange.com/questions/95652/when-someone-gets-infected-with-the-influenza-and-gains-some-immunity-is-that/95667#95667

worth noting that the war created nearly the perfect conditions to favor more virulent strains, since no matter how quickly it spread new solders were cycled in to feed it. eliminating at least one condition that normally disfavors virulence, running out of hosts too quickly.

Although the accepted answer is good and very possibly correct, I was never fully convinced by it. It describes a situation where less than a third of the world's population was infected, and yet for some reason the virus had to mutate to escape immunity to continue spreading, while the original violent strain died off. This would only make sense if the flu's R was so low that at 30% population infected, we reached herd immunity. I don't think this is plausible - unless the flu was grossly under diagnosed.
I recently read a different theory which I found more convincing:
The alternative theory posits that the flu virus often mutates in a way that does not evade immunity. In other words, being infected with one mutant protects you from the another. Now, consider that the violent virus (that appeared in the second wave of 1918) further mutated and a less violent mutant appeared.  It is likely that the new mutant will have a higher R than the original. This may happen both because of a-priori reasons (namely, a less violent strain would lead more people to go out and spread it) and for a-posteriori reasons (namely, we only noticed a new strain when it has an higher R than the original).
Now we have a less violent mutant with a higher R than the original violent strain. The less violent version would spread faster than the violent one, until more people are inected with the less violent one than the violent one.
Remember that we assume that catching any one of the two strains immunizes you to both, so both strains R number begin to go down, until the old strain's R is below 1 while the new one is above R. At this point the old strain goes extinct, while the new strain continues to spread for a while longer. Moreover, as the new virus is less scary, people relax all their prevention measures (masks, social isolation, etc.) so its R increases even more, allowing it to infect even more people before reaching herd immunity.

Re: " It is likely that the new mutant will have a higher R than the original." Isn't this just the same as the original answer? "there was so much population immunity that it needed to mutate a little in order to continue to infect." - that is, it had a higher R. Remember, some of the human population already had resistance to the 1918 strain, whether because of prior exposure to a similar strain, or because of some gene polymorphism.

The original answer posits that the new mutant has a R higher than the original's because the new mutant strain escaped immunity that the population had to the original strain. My question about this is why, under that assumption, they couldn't both serotypes continue to spread if you could get infected with both. So my new answer is that maybe you couldn't get infected with both - there was no immunity escape - getting the mild strain protected you from the violent strain (and vice versa), which can explain why today we see only the milder strain.

I think you are perhaps assuming that the "other" 2/3 of the population lacked immunity to the original strain. The working hypothesis seems to be that in fact they DID have some immunity already, whether because of past exposure to related strains or because of the versions of genes in their immune systems, and so the original strain petered out. My understanding is that in recent times we have not observed any individual strains persisting for more than a year or two, so I am not sure why the original Spanish Flu strain would behave any differently.

This review may be of interest: "The evolution of seasonal influenza viruses"  https://www.nature.com/articles/nrmicro.2017.118.pdf

@Armand "they DID have some immunity already ... because of past exposure to related strains" - that's an interesting reversal of the theory I mentioned. So it's not that the mild strain evolved after the violent strain, but perhaps the opposite - the mild strain evolved first, infected most people on earth until 1918 but nobody really cared because it was a mild flu, and when in the second wave of 1918 it mutated and became violent (but still with the same antigens), it could only infect about a third of the population before herd immunity was reached and the violent strain died out.

@Armand but then the question becomes - why didn't the violent strain do what all other strains do since - mutate their antigens to evade prior immunity. The theory I mentioned might solve this question - if the violent strain was first replaced by a less violent strain with the same antigens - and only then did the antigenic drift occur.

Sorry, I guess I'm not being clear.  Flu has been around for thousands of years, it mutates all the time, both on its own and by incorporating segments from e.g. animal viruses. I think you're overthinking this, focusing on one or two strains and ignoring the rest at a short moment in time and not considering the past exposure history of the population. Check out the reference I mentioned above.

Currently COVID-19 Omicron variant and its subvariants, each subsequent one with lower virulence, but higher transmissiblity, seem to provide real-time evidence in support of the "crowding out" theory. Note however, that the increase in transmissibility is not the only viral strain "success factor" here, because it is hard to distinguish from growing immune evasion causing re-infections.

Right, the COVID-19 pandemic is a good test-case for "my" (I didn't invent it...) theory: Before 2020, nobody had any prior immunity to COVID. Because of quarantines etc, and vaccines, when Omicron arrived, only 50% (say) had any prior (even partial) immunity. But Omicron had higher R and people who got Omicron had partial immunity for the previous strains - so the previous strains all died out.


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Can heterotrophs use anabolism to obtain energy?
With that question I mean: directly.
Please bear with me, as I don't know much about Biology or Chemistry (those are my main difficulties while studying).
I know that energy that biological beings use can be stocked in molecular bindings so that they can have it available later, when needed.
But in that process, if anabolic, it is not obtaining energy, but 'spending', stocking some energy in chemical bindings, so that it, through catabolism, can be liberated and used.
Wouldn't heterotrophs, then, obtain energy exclusively through catabolism?

@John — Please follow the instructions in the comment box and do not use comments to answer questions.  Your answer is incorrect imho, but I cannot vote it down or comment on it.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For this question, you should make sure you understand the terms you are using such as anabolism, which I think should make the answer self-evident. (See study suggestions in next comment.) Thanks!

I have found that learning about a subject is easier if you start with a relatively accessible and reliable source like Khan Academy. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

@tyersme Thank you so much for your replies and your help. I'm afraid I did some research on the topic. I started studying metabolism for a test and there it was given the definitions on both anabolism and catabolism. Anabolism would be the constructive part of the metabolism, in which we have the storage of energy and the catabolism we'd have the release of energy.
But later I came across a question in which the correct answer was : 'heterotrophs use both catabolism and anabolism to obtain energy". And I wondered why. (Continues in next comment) -->

I wondered why because if the energy is stored in anabolism, if anything, I would think the organism wouldn't be able to 'obtain' energy if it was spending it so it could be stored and used when needed. Later I came to think that if an organism synthetizes, for exemple, enzymes so that it can be more efficient in obtaining energy. Maybe the positive balance of energy would allow us to state that a heterotroph would use both anabolism and catabolism to obtain energy. Please let me know if that reasoning make sense.


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What are an internal and external exons?
I read the book: Essential Genetics and Genomics It has a table summarizing the properties of the "typical" human gene:

It has a gene feature Size of internal exon, what internal means in this context?
When I searched for it I found mentions about external exons, but found no definition.
I strongly suspect they mean:
External exons are the first exon right after the 5' untranslated region and the last exon just before the 3' untranslated region and all the other exons are internal exons.
As turned out this was almost right, but had a mistake which is wonderfully pointed out in the accepted answer.

Yes, the internal exons are those that aren't at the ends, which are often referred to as terminal exons1.
However, exons are sequences of nucleotides that are incorporated into the mature mRNA — i.e. they don't have to be (entirely) protein coding.
It is probably simplest to think of exons as being the transcribed regions that are not introns — i.e. they are the sequences that don't get spliced out during transcript maturation.
In other words, the 5'UTR is typically§ part of the first exon and the 3' UTR is typically§ part of the last exon.
§Note: I say typically, because sometimes introns are found within the UTRs2,3.
Reference:
1: Bolisetty, M. T., & Beemon, K. L. (2012). Splicing of internal large exons is defined by novel cis-acting sequence elements. Nucleic acids research, 40(18), 9244-9254.
2: Eden, E., & Brunak, S. (2004). Analysis and recognition of 5′ UTR intron splice sites in human pre‐mRNA. Nucleic acids research, 32(3), 1131-1142.
3: Paolantoni, C., Ricciardi, S., De Paolis, V., Okenwa, C., Catalanotto, C., Ciotti, M. T., ... & Giorgi, C. (2018). Arc 3′ UTR splicing leads to dual and antagonistic effects in fine-tuning arc expression upon BDNF signaling. Frontiers in molecular neuroscience, 11, 145.

Thank you for the precise answer and references.

You're very welcome!


text:
Why do gram-negative bacteria attack the digestive system more than gram-positive ones?
I was researching for a biology project on the subject of contagious infections of the digestive system (mainly the intestines) and almost all of the bacteria that came up (E.coli, Shigella, Cholera, etc.) were gram-negative. Is there is reason that that type effects the digestive system so often or is it coincidental?

Gastrointestinal infections can be caused by Gram positive and negative bacteria:
Gram-positive:

Staphylococcus aureus
Clostridium difficile, botulinum and perfringens
Listeria monocytogenes
Bacillus cereus

Gram-negative:

Salmonella enteritidis and typhi
Campylobacter jejuni
Shigella
Escherichia coli
Vibrio cholerae and parahaemolyticus
Helicobacter pylori
Yersinia enterocolitica

Any part of the GIT can be infected by G+ or G- bacteria:

Stomach: S. aureus (G+), H. pylori (G-)
Small intestine: Bacillus cereus (G+), Salmonella enteritidis (G-)
Colon: Clostridium difficile (G+), Shigella (G-)

Certain bacteria typically affect only certain parts of GIT: H. pylori and S. aureus affect mainly the stomach; C. difficile affects mainly the colon.
Anyway, infections of the gastrointestinal tract are much more commonly caused by Gram negative than positive bacteria (Stat Pearls, 2019).
From the pathogenicity viewpoint, the main difference between Gram-positive and negative bacteria is that G+ bacteria produce exotoxins (which are proteins that bacteria secrete into their environment), while G- bacteria produce endotoxins (which are lipopolysaccharides as parts of bacterial walls). The differences between endo- and exotoxins (microbiologyinfo.com):

Endotoxins are heat stable, so they are not destroyed by cooking, they don't need specific receptors, they don't trigger antibodies and there are no vaccines against them.
Exotoxins are heat unstable, they trigger antibody response and have specific receptors in the GIT.

More than 80% of skin infections is caused by Gram positive bacteria, such as Staphylococci and Streptococci (Clinical Infectious Diseases).
75-95% of uncomplicated urinary infections (Microbiology Spectrum) and most sexually transmitted infections (Clinical Laboratory Science) are caused by Gram-negative bacteria.
Respiratory infections are caused by both Gram-positive and negative bacteria (Lumenlearning).
So, the only pattern I see is that in dry/air-exposed areas (skin, respiratory tract), most infections are caused by Gram-positive bacteria, and in wet areas (gastrointestinal and genitourinary tract) by Gram-negative bacteria. This doesn't mean that there is any actual biological mechanism behind this pattern, though.


text:
the blue whale calf gains 200 pounds per day- amazing biotransformation
MY main research topic is TIME in relation to biology the blue whale calf CONVERTING mothers milk to fuctional bio-mass(up to 200 pounds/day) IS amazing-if this secret could be uncovered and used in relation to crops/livestock it woud be a game changer QUESTION does anyone have knowledge of ANY research pertaining to this  (delta time-biomass accumulation/growth genetics)?

MY main research topic is TIME in relation to biology the blue whale calf CONVERTING mothers milk to fuctional bio-mass(up to 200 pounds/day) IS amazing-if this secret could be uncovered

Wikipedia says they weigh 40,000 lbs when they finish nursing, so I think the "secret" is to be really, really large.  Relative to body mass, gaining 200 pounds a day is actually very slow for a mammal.  Human babies grow faster than that.

It’s the “relative” bit that is important here.

you need to slow down a bit and REALLY think  about this as a biologist (are you one?)the mothers milk goes into the calf gets  broken down then absorbed the calf is taking in "raw material"and digesting it and gaining weight of 200 lbs  per day(BIOTRANSFORMATION  from mixed protiens+sugars [lactose)per day the "raw material"  is transformed to bio active physiological cells YOU DON'T think this is amazing in a big picture stem cell world? how much does a human leg weigh?(axolotl/starfish/worms/lizard tails)20  lbs?  TAKE the PROOF of the blue whale calf and a human leg could be re-grown 1DAY

@hyperchronos12 Asking people's opinions is offtopic here.  Stick to biology questions.

your community lacks scientific imagination and fails to project into the future---which is in some way good i will be the one going to sweden and stand on the carpet

i am not "asking for opinions" i am attempting to make clear the original question of  TIME vs-BIOMASS  accumulation, i used the blue whale calf as a proof of the possible   hopefully the readers have an understanding of genetic engineering/pluripotent stem cells/axolotl(ability to regrow severed limbs THE genetics that enable the blue whale calf is my interest-and the transfer  of such we must have an imagination quality in science FIND proofs first axolotl  CAN REGROW LIMBS(concept proof)   blue whale calf gains 200 lbs/day(concept proof) genetic engineering to regrow limbs  NOT PROVEN/YET

@hyperchronos12 The developmental genetics of mammals is an active area of research.  If that is what you're interested in knowing about, narrow down your inquiry to some specific questions and then post them.

master question  # 1 have the blue whale    "growth genes been isolated and cloned" ?-QUESTION #1(a)--  have the genes for the stomach/intestines/liver been elucidated that enable these systems to up-take massive amounts of proteins/fats/sugars in a short period of time-? Q #1(b)[bio physics]  is this massive conversion of raw food to bio active cells, exothermic-for which a water borne creature could only withstand?


text:
Is one DNA molecule same as one chromosome
Is one DNA molecule = one chromosome or is one DNA molecule = all the chromosomes, ie, all the genetic material in our cells? I have googled it but  I am not getting clear answers ?

Considering the encyclopedic definition of a molecule...

Molecules are held together by shared electron pairs, or covalent bonds.

...one DNA molecule is one DNA strand.
Put another way, one DNA molecule is a polymer of nucleotides connected by phosphodiester bonds. This means that one intact double-stranded chromosome is composed of two molecules of DNA interacting by hydrogen bonds.
In practice, however, one piece of double-stranded DNA is commonly called a DNA molecule.
All of the chromosomes in a cell constitute a single genome.
To further add to the confusion, identical chromatids may be said to compose a single chromosome, such that one replicated chromosome composed of two chromatids may comprise four DNA molecules, by the definition outlined above.

Note, the same encyclopedia lists ionic bonds as being on the same "continuum" as covalent bonds...

Ionic and covalent bonding therefore can be regarded as constituting a continuum rather than as alternatives.

...so atoms held together in ionic interactions are also considered molecules, by this definition.


text:
Is there a conformal transformation that maps the skull of Panthera tigris to the one of Panthera leo?
While visiting the Museum of Natural History in Rouen a few months ago, I was stunned by the similarity between the skulls of Panthera tigris and Panthera Leo: the overall shapes were very similar and only distances between homologous parts seemed to vary. As I'm into math, I wondered if this similarity could be explained by some conformal transformation mapping the skull of one species to the one of the other. Are there clues about such geometric correspondences between related species?

Have a look at D'Arcy Thompson's work.


text:
The "truce of the watering hole" -- is it completely discredited?
In short, the idea comes from Kipling that animals observe a sort of truce around watering holes and prey animals do not have to be on guard (as much?) from predators in the vicinity.
I have read that this is false, that predators might even wait around watering holes for prey. However: Cleaning stations in the ocean seem to have rules and a truce (and a fish violating these rules, primarily not to attack other fish waiting to be cleaned is attacked by other fish of various species). So the idea of a truce at waterholes, perhaps only partially observed, is not that far fetched.
I wonder too if lions, for example, at some level understand that in order to survive they need prey to be able to eat/drink and breed. While this also sounds too sophisticated, is it any more sophisticated than the behavior of killing cubs so that females come into heat?

Comments are not for extended discussion; this conversation has been moved to chat.

Cleaning stations offer a pretty strong individual incentive not to attack, those that attack do not get cleaned and thus get riddled with parasites. Watering holes are just the opposite there is no advantage to not attacking and in fact a decent advantage for attacking, (a meal) many predators hang around watering holes just because the draw prey.
To put it another way the genes from lion A say hunt things at the watering hole, the genes from lion B say don't, Lion A is going to have more meals and thus more offspring than lion B therefore the genes to hunt at the waterhole will spread. Lion B gains no benefit from not hunting at watering holes that can offset the very large and immediate advantage lion A gets. This is a good general test to why group selection generally doesn't work, even if all lions were type B as soon as lion A occurs from a mutation it has a huge advantage and drives out lion B's genes.
There is quite a lot of evidence that predators often concentrate around watering holes, heck this is how crocodiles make a living. The idea that lions do not is an out dated and stems from early observations done only during the day (when lions are mostly inactive yet close to watering holes to hunt at night), spread by fiction writers and reinforced by advertising and poorly researched articles.
https://www.nrcresearchpress.com/doi/abs/10.1139/z77-235#.XkxeG2hKhPZ
https://academic.oup.com/beheco/article/23/5/970/232520
The Serengeti Lion: A Study of Predator-Prey Relations
By George B. Schaller
Seasonal Diet and Prey Preference of the African Lion in a Waterhole-Driven Semi-Arid Savanna

If you look at predators as being "farmers" of a sort, the lions, etc. realize that absolutely terrorizing their prey would result in probably their finding another watering hole where predators are more judicious about what they hunt.

@releseabe except watering holes are few and far between and there are many predators each using them, so prey have no choice, also if the prey can move so can the predators.  there is again no benefit.


text:
Can I execute/model a genome?
Hi I am wondering if we can execute a genome on the sub-cellular level by running it on the computer. What I mean is using the genome as data to examine by having the cells reproduce and see what happens as they grow.

Given that Nicolai has adequately answered the question, I vote to close this question.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, note that "speculative" questions are off-topic. ——— You might also want to make sure you have a good grounding in the basics of biology — that will help you understand why the answer is "No". I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful.  Thanks!

A simple genome can be modeled, however imperfectly, on a computer, where some have taken experimental genomics data and built simulations from it.
For instance, from the paper A Whole-Cell Computational Model Predicts Phenotype from Genotype:

Understanding how complex phenotypes arise from individual molecules and their interactions is a primary challenge in biology that computational approaches are poised to tackle. We report a whole-cell computational model of the life cycle of the human pathogen Mycoplasma genitalium that includes all of its molecular components and their interactions. An integrative approach to modeling that combines diverse mathematics enabled the simultaneous inclusion of fundamentally different cellular processes and experimental measurements. Our whole-cell model accounts for all annotated gene functions and was validated against a broad range of data. The model provides insights into many previously unobserved cellular behaviors, including in vivo rates of protein-DNA association and an inverse relationship between the durations of DNA replication initiation and replication. In addition, experimental analysis directed by model predictions identified previously undetected kinetic parameters and biological functions. We conclude that comprehensive whole-cell models can be used to facilitate biological discovery...
We have developed a comprehensive whole-cell model that accounts for all of the annotated gene functions identified in M. genitalium and explains a variety of emergent behaviors in terms of molecular interactions. Our model accurately recapitulates a broad set of experimental data, provides insight into several biological processes for which experimental assessment is not readily feasible, and enables the rapid identification of gene functions as well as specific cellular parameters.

(cite)
Also:

Given the vast behavioral repertoire and biological complexity of even the simplest organisms, accurately predicting phenotypes in novel environments and unveiling their biological organization is a challenging endeavor. Here, we present an integrative modeling methodology that unifies under a common framework the various biological processes and their interactions across multiple layers. We trained this methodology on an extensive normalized compendium for the gram-negative bacterium Escherichia coli, which incorporates gene expression data for genetic and environmental perturbations, transcriptional regulation, signal transduction, and metabolic pathways, as well as growth measurements. Comparison with measured growth and high-throughput data demonstrates the enhanced ability of the integrative model to predict phenotypic outcomes in various environmental and genetic conditions, even in cases where their underlying functions are under-represented in the training set. This work paves the way toward integrative techniques that extract knowledge from a variety of biological data to achieve more than the sum of their parts in the context of prediction, analysis, and redesign of biological systems.

(cite)
Gentle advice: Avoid answers from cartoonists, whose domain of knowledge does not include biology.

I think it's a bit of a stretch calling these sorts of models "executing a genome". They are using a whole lot more data than DNA.

I can't speak to semantics but the question directly asks if it possible to model the genome on a computer. Researchers have done this using sequencing data, as the cited articles show.

Shrug Whatever.


text:
How does the age of a parent affect the chances of occurrence of certain genetically transmitted diseases?
Do genetically transmitted age-related diseases (like hypertension, arthritis etc.)have the probability of occurring at an earlier(younger) age in the offspring if they are born at a later age to their parent(s)?

Are you asking if an increased age of the parents at the time they have children, increases the risk of developing symptoms of genetically predisposed diseases in the offsprings at an earlier age?

Yes. And  I am asking about the diseases like diabetes, heart disease etc. which usually appear after a certain age.

In some studies, they have observed either positive or negative association between maternal or paternal age (the age of mother or father at the time of delivery) and earlier development of genetically predisposed diseases, such as diabetes type 1 and certain cancers, in offspring.
Diabetes type 1
Maternal age and diabetes in childhood (BMJ, 2010):

...the risk of childhood onset diabetes [type 1] increases with
  maternal age: 5% for each five years of age...the main explanations
  are that biological programming of the child is in some way affected
  by the age of the mother, or perhaps the father...

Cancer
Parental age and risk of sporadic and familial cancer in offspring: implications for germ cell mutagenesis (Epidemiology, 1999)

We used the nationwide Swedish Family-Cancer Database to analyze the
  effect of parental age on cancer in offspring at ages 15-53
  years...Maternal age was associated with sporadic melanoma and
  leukemia, causing a 30% excess if mothers were more than 40 years vs.
  less than 20 years of age. A marginal effect of about 10% of both
  maternal and paternal age was observed for sporadic breast cancer.
Paternal age increased the RR of sporadic nervous system cancer by about 15%. Accumulation of chromosomal aberrations and mutations
  during the maturation of germ cells may be a mechanism for these
  findings. In familial cancers of colon, melanoma, and thyroid, higher
  age showed an apparent protective effect, which was also noted for
  sporadic cervical cancer and melanoma.

Rheumatoid arthritis
Ages of onset suggestive of genetic anticipation in rheumatoid arthritis multicase sibships can be explained by observational bias (Rheumatology, 2007)

There was no significant correlation between the age of RA onset and
  the maternal or paternal ages of conception.

Cardiovascular disease
In one study, they have found no significant association between maternal age and blood pressure in children. There seem to be no studies about the effect of maternal/paternal age on early-onset heart disease.
On the other hand, offsprings are at increased risk of developing a cardiovascular disease early if their parents had it early (PLoS One, 2016).

In another study, they have observed that maternal ages <25 and >45 have been associated with increased frailty index: a sum of 8 conditions (cancer, lung disease, mental health problems, diabetes, heart disease, stroke, blood pressure and arthritis)
Maternal Age and Offspring Adult Health: Evidence From the Health and Retirement Study (Demography, 2012)

In summary, net of some obvious confounders, only maternal ages below
  25 and above 45 are associated with negative offspring health
  outcomes. (see Fig 1 and Table 2)
The mechanisms thought to be responsible for the young maternal
  age–offspring health link are related to the physiological immaturity
  and sociodemographic disadvantage that often accompany young
  parenthood... On the other hand, the negative association between advanced
  maternal age and adult health is thought to be driven by the
  physiological reproductive aging of the mother.

In this study, they have not checked for the age of onset of diseases in offspring, though.


text:
Why do biologists judge intellect based on brain size?
I have seen many times, that scientists will say Species A is smarter than Species B due to a higher brain-to-body ratio.  I've even seen similar arguments made by comparing the sizes of specific regions of the brain.  For example, "Species A must have a more developed linguistic ability than Species B because it has a larger language center in its brain."
This doesn't make sense to me.  I don't think we can make these judgements because we don't know what "software" is being run in each brain.  I can run a merge sort algorithm on a weaker computer just as fast as a brute force sort on a stronger computer.  The raw computation ability of a computer doesn't necessarily correlate to how quickly it can solve problems.
What am I missing here?

What am I missing here? Brain mass is an easy to measure proxy for how much energy is being spent on computation. If that computation is not doing something of value, natural selection will tend to shrink the expenditure of energy, and thus the size of the brain.

In addition to the answers given here, I'd say there is a bit of a misconception here about the direction of inference. After adjusting for body size, it is an empirical observation that species with larger brains are more intelligent (and the same might be said for particular brain regions in different species). For species for which we cannot make observations (say, extinct species) or haven't yet, we can use this prior data to make informed guesses. The same is not generalized for brain sizes within species like humans so the same claim is not made there.

Your are confusing yourself with your analogy, brains are not like computers. The complexity of the "software" a brain can have is determined by how many cells and therefore connections it can have. In particular flexible (learned) thinking as opposed to instinctual "programs." Brains that are flexible need more cells to allow for more possible connections. Computers are not great analogies for brains they are just the best we have. but to use them a brain is like a solid block of ram, yes a large mass is not necessarily fast but it Can do a a far larger variety of tasks, intelligence is not a measure of speed (flies react way way faster than humans) but generally a measure of how many things you can be computing at the same time. the human brain is basically built to model the entire worlds around us including the brains of other humans, which is many many tasks happening simultaneously. Which is one reason brain size can also be used to predict how social an organism is, (at least in non-kin selected social behavior) social interaction requires modeling many complex things. You also run into the problem with defining intelligence, which is problematic to say the least.
And as another poster has pointed out natural selection will quickly eliminate unused brain mass, (neurons are super expensive to maintain, our brain eats about a third of the calories we consume) so they are strongly optimized for weight, so portions of the brain that are larger should, in general, be doing more to offset the cost, otherwise they will be quickly shrunk. So a portion of the brain that is large must be being used, and must be offsetting the caloric cost, also note many the parts of the brain are fairly basal to the groups being compared like mammals so the so the chances of drastically different fundamental ways of operating are fairly slim.  so if the same portion of the brain is very different in size between two related organisms chances are it is becasue that portion is doing more or less. It is even easier to see with sensory processing portions of the brain, if the olfactory bulb of the brain is huge it has to be due to an increased function in the the sense of smell because it really doesn't do anything else and how the sense functions has not changed. this is backed up by observation the brains of animals with poor senses of smell (like cetaceans) have tiny olfactory bulbs while animals with excellent senses of smell (blood hounds)have huge ones. Intelligence is associated with enlargement and complexity only in specific portions of the brain, not the brain as a whole.
That said brain mass is only a rough estimation.  It more done to control for body mass (which effects brain mass directly) as things like how folded the brain is can drastically alter the complexity without changing the mass much. No one assumes brain size is a prefect predictor for intelligence.

Correct me if I'm wrong, but aren't neural networks susceptible to getting stuck in local maximums?  So a species that found a good neural network will be stuck with it, while another may have found a different, much better neural network?

@Ryan_L Brains are networks of biological neurons, not neural networks.

@BryanKrause what about brains precludes them from getting stuck in local maximums?

@Ryan_L The answer to that question would both take a textbook to explain different ways biological networks can avoid local maximums, and also leave many examples where local maximums exist in brains (there are models of both depression and addiction, for example, that are probably best described as problems of being stuck in local maximums). But, note that I did not say that brains do not get stuck in local maximums, I simply said that brains are not neural networks. Your questions seem to be coming from over applying an analogy to the brain that does not fit.


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Examples of healthy lifelong asymptomatic carrier of a severe infectious disease?
I am curious, is there any known disease/infection that is very severe normally (patient suffers greatly and die easily without medical treatment), but ends up having little to no effect on the lives of asymptomatic carriers? I am asking this as I am thinking whether this means certain disease symptoms are mechanisms resulted from evolution to protect the "greater good", i.e. killing the patient to avoid transmission to another member of the species.

I think this question is probably strongly misguided. For now I've given it a downvote; better research and focus might encourage me to change my mind on that. But as-is, it seems too contaminated with misunderstanding of both evolution and disease.

Research needed aside, in what way it is misguided? Isnt it just asking for a possibility (a possible example and possible reason behind)? And I am not quite sure I like the way you are judging it by "probably" and "seem", without giving any actual reason.

@ychung What I meant is that there are underlying assumptions, not contained in the question, that are wrong. One important one is how evolution works, which has now been covered a bit in the answer by user1850479. Another is the relationship between symptoms and transmission. An asymptomatic individual may carry a disease longer, but that doesn't mean they transmit it more than someone symptomatic, even if that person dies.

You are generalizing my view, fighting a strawman. I said "certain" symptoms (in response to a particular infection/pattern of infection) that make an individual suffer and die, could have evolutionary advantage in stopping an infectious disease that could harm the greater good of the species.

@ Bryan I really dont get why you guys are saying my understanding of evolution is wrong? So, how are you disproving that it is not possible certain mechanism could develop within the population to stop infectious disease while sacrificing individuals (as a consequence I insist)?

@BryanKrause, I think you misunderstood the question.  The OP is suggesting that there may be an evolutionary advantage to displaying symptoms of severe infectious disease, (presumably because it would alert and thus benefit close relatives of the sick individual).

The current Covid19 plague may be an example: it appears that most carriers in certain slices of the population may be asymptomatic (young people in particular) but able to transmit the virus.

@Dirigible Please don’t answer questions in comments. There is a specific injunction against it in every comment box on every Stack Exchange site because doing so breaks the model on which Stack Exchange was founded.

I am curious, is there any known disease/infection that is very severe normally, but ends up having little to no effect on the lives of asymptomatic carriers?

HIV is an obvious example, where so-called "long-term nonprogressors" successfully suppress HIV replication sufficiently that they do not develop AIDS but are unable to clear the infection entirely [1].

patient suffers greatly and die easily without medical treatment

Since the comments below seem to suggest that HIV does not cause death without medical treatment, I'll point out that this is incorrect.  Over 30 million people have died from HIV infection.

I am asking this as I am thinking whether this means certain disease symptoms are evolutionarily wired to protect the "greater good"

It does not.  Selection happens on individuals and not whole species, so the greater good is irrelevant.  Asymptomatic infection is a point on the spectrum of possible responses to infection between sterilizing immunity and death. Individuals who are chronically infected mount enough of an immune response to control the infection but not enough to completely clear it.  In the case of HIV, they are typically people who have exceptionally strong immune responses to a normally lethal virus.
Edit
The comments below suggest a deep misunderstanding of evolution. Since I think these are really the core of your question, I'll address them here.

If traits really evolve only according to how much an individual reproduce sucessfully, it would be a different world today.

Which individuals reproduce is the sole determinant of which genes are passed down to the next generation.  This is because the genetics of each individual are determined at conception, and cannot be changed.  Hence, reproduction alone determines the traits of the next generation.
To quote wikipedia[2]:

Evolution is change in the heritable characteristics of biological populations over successive generations. These characteristics are the expressions of genes that are passed on from parent to offspring during reproduction. Different characteristics tend to exist within any given population as a result of mutation, genetic recombination and other sources of genetic variation. Evolution occurs when evolutionary processes such as natural selection (including sexual selection) and genetic drift act on this variation, resulting in certain characteristics becoming more common or rare within a population

Evolution is the process by which some traits are passed down to the next generation while others are not though the mechanisms of selection (e.g. individuals with harmful traits dying) and genetic drift (e.g. random chance).

Thank about a hypothetical super fast reproducing bacteria, using up all resources, which means extinction at the end, such traits would not be passed on. In fact some sort of "moderation" mechanism is needed to take care of the "greater good".

This is exactly what happens if you put a lot of fast reproducing bacteria in a closed environment with limited resources.  They will all eventually die.
You seem to be thinking of evolution as something that intelligently looks out for the wellbeing of species.  This is not the case.  Evolution is a random process by which different amounts of reproduction and survival between individuals alters the composition of the succeeding generations. As a random, emergent process it has no goals, no intelligence, and no sense of "good".  Rather, it simply happens as a result of individuals reproducing.  This frequently does lead to extinction, as evidenced by the fact that the vast majority of species no longer exist.
(1) https://academic.oup.com/cid/article/51/2/239/303856
(1) https://en.wikipedia.org/wiki/Evolution

Thank you for the answer! HIV is an interesting case definitely. However, the severity of AIDS as I understood come from accumulating infections from other pathogens, not the immune response/symptoms to HIV itself which is kind of chronic (I may be wrong). I also disagree with the notion "Selection happens on individuals" makes greater good irrelevant. Even if a stressor act on individuals apparently, it could produce a trait that improves greater good. You can argue the evolution of "dying" is exactly for the greater good. In some diseases, acute symptoms can definitely make you "die faster".

@ychung Long-term nonprogressors are so called because they do not progress to AIDS.

@ychung The greater good is irrelevant to selection.  Traits may or may not improve whatever you consider to be "good", but selection does not care about that. Some more reading about what selection is may help you understand that point better.

My first point is trying to say that HIV/AIDS is not really what I am looking for in the question (thank you for the answer tho). Second point I disagree. Just think about it, traits can definitely be selected in the direction to preserve greater good in the face of large-scale and amplifying stressor (based on population size). Whether "selection does not care about" or not is not important, the consequence is.

@ychung Edit your question to clarify what you're looking for.  Second point: selection is the process by which individuals either reproduce or do not reproduce. A trait might act on the greater good by accident (see genetic drift), but such traits cannot be selected for. Since you have questions, what selection can and cannot do may be a good topic for a second question.

Typhoid Mary is a good example I am looking for. 2) By-product/ accident or not etc., it is the result that matters. You are not quite understanding what I am trying to say. Think large-scale, think density-dependent stressor, if traits really evolve only according to how much an individual reproduce sucessfully, it would be a different world today. Thank about a hypothetical super fast reproducing bacteria, using up all resources, which means extinction at the end, such traits would not be passed on. In fact some sort of "moderation" mechanism is needed to take care of the "greater good".

Similar things can be hypothesized for a hypothetical infectious disease, the denser the infected individuals (which without the "immune reaction" would otherwise die slowly and able to infect many more people), the higher chance the population will go extinct in the long-run.

I dont think any of the point about evolution disprove what I say (I have never said  evolution as something that intelligently looks out for the wellbeing of species), I said it could happen as a consequence. So, how are you disproving that it is not possible certain mechanism could develop within the population to stop infectious disease while sacrificing individuals (as a consequence I insist)? I dont really get what you are trying to disprove me and saying I misunderstood evolution.

I meant HIV/AIDS patient die not because of things arise from HIV infection solely, it is complicated from infection of other pathogens. (Which makes it not exactly what I was trying to ask for.) Thanks for the answer but you seem to be misinterpreting me all the time...

@ychung If you don't want to be misinterpreted, you can edit your post above to reflect your intended question.

@user1850479, there are many, many examples to contradict your statement that " Selection happens on individuals".  Evolution of altruistic and cooperative behaviors are examples.  Warning colors on toxic butterflies and amphibians are also examples.  Yes, the bright colors of a poison frog deter predators from eating the frog.  But that didn't directly help the first frogs to display those colors: they were eaten and killed by predators who were not repelled by those colors.  It "trained" predators to avoid that frogs' close relatives.

@S.McGrew Selection is one process that can change the traits of an organism, but it is not the only one. Consequently, pointing out the existence of any particular trait doesn't disprove the existence of natural selection.

Where did you get the idea that anyone is arguing against the existence of natural selection?

Natural selection is the differential survival and reproduction of individuals due to differences in phenotype.  You listed examples that you believe "contradict" this such as the evolution of cooperative behavior. My point is that other processes can change phenotype besides selection, and so your examples are not necessarily inconsistent with natural selection.

"Yes" is the simple answer to the first part of your question.  HIV, "Typhoid Mary", maybe Covid19, and other examples have been given.
The second part of your question,

I am asking this as I am thinking whether this means certain disease symptoms are mechanisms resulted from evolution to protect the "greater good", i.e. killing the patient to avoid transmission to another member of the species.

is good, but doesn't have a definite answer as far as I know.  However, your idea is certainly plausible.  Although displaying symptoms (e.g., a rash, cough, odd behavior, or bad odor) will not benefit the individual, it will benefit individuals who are repelled by those symptoms.  In cases where individuals who have a tendency to be repelled by the symptoms also have a tendency to display those symptoms (and those tendencies are encoded genetically), close relatives of those individuals have a distinct selective advantage over other individuals in the population who do not have a tendency to be repelled.
A lot of literature relating to this idea can be found by searching "evolution of altruism" and "kin selection".

Thank you for your answer! Displaying horrible symptoms to repel other individuals in the species is definitely one plausible mechanism that can reduce the transmission of pathogens.

Take note though that the two (displaying symptoms and being repelled by the symptoms) need to become coupled through selective processes, of which kin selection is the most effective.

Here is an example of the opposite: tuberculosis apparently evolved the ability to enhance its own spread by inducing symptoms: coughing. https://m.medicalxpress.com/news/2020-03-tuberculosis-bacteria-trigger.html

Yeah, that's why I said symptoms killing the patient (which in itself constitute a severe warning to other members of the species) is a more "direct" mechanism to stop transmission.

That's not quite what I meant.  It can be a co-evolutionary process.  A microbe can evolve to cause symptoms that help spread it; a species can evolve to respond to a microbe by displaying scary symptoms;  it's even possible for a species to respond to the microbe by suppressing the symptoms that help the microbe spread.

Yes, I know what you are saying. There are many different possibilities indeed.  For all the different immune response-pathogen combinations possible, it is the end result of a co-evolutionary arm race with some trickery and mimicry mixed within.

But I tilt it to humans as the main subject of evolution here because I think early humans evolve mainly by being killed and survival given that prehistoric humans live in tribes or isolated populations, only the tribe that has the right traits perpetuate. Whereas virus evolution has a whole lot of other mechanisms (like its inherent high mutation), many cases a virus may just be an opportunist capitalizes on a human trait when it hasnt even co-evolved with humans that long. (that's why I insist it is the pattern of infection, not the actual virus that matters)

It's plausible.  You should put together a mathematical model (that's "falsifiable") and see how well it fits.  The model should allow for other answers too, and compare how well they fot relative to each other.  And, just to complicate things, all of the varoius evolutionary processes are probably going on simultaneously!

Well I can only hope I have the required expertise :( Unfortunately, I do biogeochemical modeling instead. Maybe someday an evolutionary biologist will stumble upon this thread :)

It might be a fun and educational exercise for you anyway, even though you don't have experience in this field.  Important contributions to a field are often made by smart people who come in from another field with a fresh perspective.


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Circulating Tumor Cell vs Circulating Tumor DNA
I'm a little confused about the wording of these two phrases and under which context the epithelial-mesenchymal transition occurs.
For example:
Is it the circulating tumor cell that releases the ctDNA so that it undergoes EMT?
Or
ctDNA from the CTC somehow creating new instructions for the EMT phenomenon to occur?
I think there is something I am fundamentally confused about and or I am mixing several or different concepts and phenomenon together and would like to get some clarification on this.
Thanks.
EDIT: So this is my new hypothesis / thinking..
So when EMT occurs, CTCs are more likely to develop in the context of cancer, and so when CTCs circulates throughout the blood stream CTCs may be apoptosed of necrosed as a by-product thus leaving ctDNA in the bloodstream and or possibly through out the body.
Is that a correct explanation to my confusion?

I'm not sure the relationship you are trying to build between EMT and cancer cells.
Yes some "healthy" cells undergoing EMT could (due to specific underlying mutations) result in cancer cells but such a phenomenon is not a "hard and fast" rule.
The majority of ctDNA would likely be (as you suggest) from lysed cells, however, should mutations occur that allow for the aberrant export of DNA, then the latter could occur (I would assume this is rare but based on the currently available literature this possibility cannot be discounted).
Thus your "new hypothesis" seems to be the most likely.

Okay thanks for your input!

Welcome to Biology.SE! This looks like a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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Can the human body store protein?
I am interested to know if a human body can store protein.
Absolutely for the bodybuilders, does it really matter if they divide their protein consumption during the day or eat all of it in one meal at anytime they want?
Is there any constrain on protein absorption per hour?
What will happen for the extra protein we eat?

The human body can not store Proteins (technically).
BACKGROUND :
PROTEIN is a very broad term and there are hundreds and thousands of proteins.[1]
Proteins are heteropolymers consisting of amino acids held by peptide bonds.
Amino acids :
There are 9 amino acids which we need to intake.

Phenylalanine, valine, threonine, tryptophan, methionine, leucine, isoleucine, lysine, and histidine.

Amino acids our bodies can produce:

These five are alanine, aspartic acid, asparagine, glutamic acid and serine.

These amino acids combine in different arrangements to give those thousands of Proteins. This process is carried out by Ribosomes (cook) and mRNA (recipe) inside every* cell.
Protein metabolism in humans :
During human digestion, proteins are broken down in the stomach to smaller polypeptide chains via hydrochloric acid and proteaseactions. This is crucial for the absorption of the essential amino acids that cannot be biosynthesized by the body.
Trypsin and Chymotrypsin as Trypsin and Chymotrypsinogen are the enzymes  necessary.
.
MAIN ANSWER  :
The excess Amino Acids are broken down into Glucose ( carbohydrate like stuff ) and the Nitrogen moiety is converted into Urea / Uric acids. This is then excreted by kidneys.

Amino acids can be broken down into precursors for glycolysis or the Krebs cycle.
Amino acids can also be used as a source of energy, especially in times of starvation. Because the processing of amino acids results in the creation of metabolic intermediates, including pyruvate, acetyl CoA, acetoacyl CoA and so on; amino acids can serve as a source of energy production through the Krebs cycle.

Therefore excess protein is simply used to make energy like carbs and the Nitrogen part is excreted. Now the excretion process can strain the kidneys due to increased work load, and prolonged stress can lead to malfunctions.
Also,
Our body is very concerned with conserving nitrogen levels, since our body can't fix nitrogen gas (N2) into ammonia (NH3). but, we can't just store huge amounts of ammonia because it's toxic. sugars and fats aren't toxic, so we can store them. because of this, our body either quickly utilizes excess ammonia to make nitrogenous compounds like amino acids and nucleotides, or it excretes it via Urea in our urine.
Problem with Protein storage :
If our bodies had to store proteins, it would need several sophisticated mechanisms and specialised storage cells.( Like we have adipose tissues short fats and lipids storage ).
if you examine the structure of amino acids, they are very similar to many of the carbon-hydrogen-oxygen metabolic intermediates. for example, alanine is an amidated pyruvate, glutamine is an amidated alpha-ketoglutarate, etc. many are easy to make, and most don't cost much to do so, so the body would rather use these intermediates to either:

Create acetyl-CoA, NADH, FADH2, and ATP for energy. this would happen during exercise or starvation.

Create glycogen, fatty acids, nucleotides, NADPH, and other metabolic compounds. this would occur after a big meal, during sleep, and when energy is not needed in high amounts. these compounds are very expensive ATP-wise.

So there's no need to store whole Amino Acids because they can be immediately used for whatever the body needs and then remade when necessary.
We do not store amino acids because we don't need to.
Right dose of Proteins :
Research shows:

A total of 80 g of whey protein was ingested in one of the following three conditions: 8 servings of 10 g every 1.5 h; 4 servings of 20 g every 3 h; or 2 servings of 40 g every 6 h. Results showed that MPS was greatest in those who consumed 4 servings of 20 g of protein, suggesting no additional benefit, and actually a lower rise in MPS when consuming the higher dosage (40 g) under the conditions imposed in the study.

Check here for the interesting results ( this is very relevant to your second question )
Therefore distributed intake of right amount of protein is important!
Scientific literatures :
Proteins:
https://en.wikipedia.org/wiki/Protein_(nutrient)
https://en.wikipedia.org/wiki/Amino_acid
Protein Metabolism:
https://opentextbc.ca/anatomyandphysiology/chapter/24-4-protein-metabolism/
Protein intake and storage:
https://newsnetwork.mayoclinic.org/discussion/are-you-getting-too-much-protein/
https://www.self.com/story/what-protein-does-in-your-body

I have written a long answer, do take time to read and understand

I'll add a more straightforward answer than the previous answerer (who was certainly more in-depth and informative than I will be), for the purposes of clarity. I think protein is stored in the body very much functionally, just not in reservoirs of reserve chemical energy such as adipose tissues do with fat.

I am interested to know if a human body can store protein.

The body cannot store dietary protein; it breaks it down into amino acids, which are absorbed and then turned into protein. One cannot repurpose dietary protein without breaking it down into its constituent monomers, the amino acids.
Amino acids are then used in a plethora of ways, the primary of course being protein synthesis (a kind of anabolism, or 'body-building' if you will). Amino acids are strung together to form newly made proteins for the body's needs, and this is a constant process of (re)building in the body. This is why protein intake is essential for survival, given that it's an essential macronutrient.

Does the body store protein in any meaningful way?

Certainly one could argue that you can store protein by making proteins which are long-lived and later available for catabolism, such as those that make up muscles. The muscle tissue can then be used up at a later time if there is need for energy. This is seen with muscle wasting in the elderly or those that are starved. Proteins are a source of gluconeogenic substrates (see this wiki about gluconeogenesis), and thus can be used as a held store of energy. However, please keep in mind that this phenomenon is rather minimal for dietary protein.
(As an aside: notice I am not talking about proteins that are unavailable for breakdown; many proteins are indeed long-lived, such as collagen, but these escape the ability to be re-used. I wouldn't consider this storage, since their function cannot be said to be one of storage.)

Is there any constrain on protein absorption per hour?

Yes, there is a constraint on amino acid (digested protein) absorption per hour by the GI tract. Most dietary amino acids (and some small peptides) are absorbed in the small intestine, though there is evidence the large intestine can also perform this task in humans.

What will happen for the extra protein we eat?

Remaining protein that is not broken down and subsequently absorbed by the intestinal epithelium, will pass through the digestive track and gets pooped out. Along with anything else that the body was unable to digest, such as fibre (like cellulose which makes up much of plant tissue). Not much more to it. Simple!

Additional interesting readings and protein turnover?

A suggested item if you like.

Does it really matter if [people who wish to be bodybuilders] divide their protein consumption during the day or eat all of it in one meal at anytime they want?

It is certainly possible to live on both regimes. This question is unfortunately off-topic for this SE. There are many different philosophies of body-building.


text:
Can wood frogs who have frozen and thawed remember their past lives?
Wood frogs (Rana sylvaticus) can survive being frozen for up to 7 months at temperatures as low as -16 °C. Their breathing stops, their heart stops and all signs of life disappear. (Source)
I have looked for research that shows that when these frogs thaw in spring, they retain memories from before they became frozen, but I haven't found any. Can anyone give me any insights?
Note: This research shows how butterflies can remember experiences they had as caterpillars, before their metamorphosis. Perhaps something similar can be done or has been done with wood frogs?

sweet experiment!  good luck.

Wood frogs are highly philopatric to their breeding ponds. And the fact that they return to the same pond after multiple winters, would indicate that, at the very least, they must retain at least some spatial memory after freezing.
It is worth noting that a frozen wood frog is not nearly the same scenario as a butterfly metamorphing. Butterfly metamorphosis involves complex reintegration of all bodily systems, whereas frog brains do not reform during the winter--they just cease neurological activity. Even frog metamorphosis is less complex since much of the chondocranium and brain morphology is retained from tadpole to frog.
I know it wasn't the original question, but it is relevant to note that tadpoles seem to retain their personality through metamorphosis (see Wilson & Krause, 2012; Koenig & Ousterhout, 2018), which also seems to indicate that they have neurological stability.
References:
Wilson, A. D. M., & Krause, J. (2012). Personality and metamorphosis: is behavioral variation consistent across ontogenetic niche shifts? Behavioral Ecology: Official Journal of the International Society for Behavioral Ecology, 23(6), 1316–1323.
Koenig, A. M., & Ousterhout, B. H. (2018). Behavioral syndrome persists over metamorphosis in a pond-breeding amphibian. Behavioral Ecology and Sociobiology, 72(12), 184.


text:
Expected $\mu$ and $\sigma^2$ for a phenotypic trait, given heritability h and known parental phenotypic measures?
Say a measurable phenotypic trait has mean $\mu =0$, variance $\sigma^2 = 1$, and heritability $h$, meaning that h*100% of the variation in the population is caused by genetic variation and (1-h)*100% is caused by environmental factors whether shared or unshared.
We define "standard environment" as an environment in which the contribution made by each environmental feature, whether shared and unshared, is at the population mean for the contribution made by that feature.
Clearly if we take individuals in the population at random their expected mean measurement is 0 and their expected standard deviation is 1.
But say we have two parents whose phenotypic measurements for the trait are respectively $p_1$ and $p_2$. Then what will the expected mean and standard deviation for their offspring be if their offspring's environment is standard? I am interested in the general case, but even an answer only for the case $p_1 = p_2$ would be helpful. I would also be interested to know whether the answer might reasonably be expected to vary according to whether the parental phenotypic measurements are or are not significantly different from what would be expected from their own genes.
From a "pure mathematical" point of view, the answer is "we can't tell", because for example the expected mean measurement might be 0 for all individuals except those who have both parents with genes determining an expected measurement greater than 3 or smaller than -3. So please make (and state if possible) whatever assumptions seem reasonable.

Is this a homework question? If so it should be tagged as such.

No, it isn't...


text:
Identifying this winged ant with big hind legs
I found this walking across my floor not too long ago. I am not sure if it is actually an ant, I just chose the best words I could find for the title. It has wings, but does not seem to ever fly. It has antennae and the hind legs looks much larger than I've ever seen on an ant. Moreover, they seem to have a red tint. Any ideas?
Area: U.S. East Coast

Welcome to Biology.SE! That looks more like a wasp of some sort than an ant. Please [edit] your post to include an estimate of the size of this insect since that can be an essential clue for identifications. ——— If possible clearer, closeup photos of the creature from multiple angles would also be helpful. ——— Finally, please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Yes, that is a wasp. The legs are distinctive of that family, butI've forgotten the name.

I think it might be some kind of Conura. There are photos at https://bugguide.net/node/view/18810/bgpage which resemble yours. And according to that page it's in roughly the right area of America. But there are a lot of wasp species in the Conura genus and I don't know if other wasps in the chalcid family have those large hind legs. So... inconclusive.

The expanded hind femora are a feature of the Chalcididae as a whole, but are not unique to that family within Chalcidoidea (the related family Leucospidae also have them, but are much larger and might be mistaken for potter wasps at first glance [at least in North America]).


text:
Do kids under a certain age not hear the warning beeps that smoke detectors make when they are running out of battery power?
I've always been very annoyed by those regular single beeps that smoke detectors start doing increasingly often as the batteries start to run out, to warn (and annoy) the user to replace the batteries. They drive me insane.
Lately, I've been observing how a bunch of kids seem to sit in a room and just ignore those beeps completely, even after I point it out and ask them to really listen. They can't hear them. I seriously believe that they just don't physically hear them. Kind of like those dog whistles.
Is this backed up by science? Do kids under a certain age literally not hear those "low battery" warning beeps? Is this maybe per design, even? If so, why? Isn't it important that as many humans as possible are annoyed by this so that they replace the old batteries with new ASAP?
It's really frustrating to me when they don't even hear it, but I hear it very well. I hate it so much.

Hi Leonard, I don't think this question in its current form is a good fit for Biology.SE. If you can add a reference to a notable claim then I think this question could be migrated to Skeptics.SE and answered there.


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What does it mean for there to be no correlation between phylogenetic independent contrast?
I am testing the correlation between two physiological parameters in plants using the pic function in R. I am a bit stuck on the interpretation of the phylogenetic independent contrast (PIC). Without considering the PIC, I got a significant correlation, but there is no correlation between the PIC. What does the absence of correlation between the PIC mean:

the correlation without PIC is the effect of phylogeny

OR,

There is no phylogenetic effect on the correlation.

Thank you

Welcome to Biology.SE! Can you add information about what tools you are using to do your analysis? ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Hello,  I am using the pic function in R

Comments are ephemeral, so in the future please edit your question to include that kind of information — that should increase your chances of getting an answer.  In addition, the Bioinformatics site might be a more appropriate place for this type of question, especially since it isn't getting any response here.

Your first option is the correct interpretation. The correlation you observe in the raw data is the effect of phylogeny.
Without using PICs, you might expect to see phylogenetic autocorrelation, i.e. your raw data correlate as a function of the amount of shared evolutionary history between different species. Using PICs is one way of testing whether the correlation still exists when the effect of phylogenetic autocorrelation is removed. This is exactly what you observe—you see the correlation in raw data (which are not phylogenetically independent) but it disappears when you use PICs. Without knowing any details of your study beyond what's in the question, it sounds like a textbook case of phylogenetic autocorrelation.
The PIC method originates with Felsenstein (1985). I'd encourage checking that paper out for further details on the method and interpretation of the results.


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What is the charge of (bacterial) ribosome?
Ribosomes are negatively charged and thus electrostaticaly repelled from DNA. However, I could not find a good reference that would allow me to estimate the magnitude of negative charge on a ribosome. Anyone could help with that?
This reference suggests it to be on the order of tens of e- or more.

@tyersome — Whoa! It's a fair question in itself if you look at the paper, even though it is not of interest to me, and the concern with DNA seems strange. The pH of the intracellular mileu can be assumed so that's not particularly important. In fact I am quite surprised that ribosomes are negatively charged, rather than neutral, as the negative charge of the RNA is balanced to a large extent by magnesium ions — you can't study ribosomes (as I used to do) without say 5mM magnesium. In all the  ribosome conferences I attended last century I never remember the topic coming up.