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Do mRNA vaccines cause transfected cells to be killed by cytotoxic T cells?
Based on my research on how mRNA vaccines (specifically for COVID-19) work:
An mRNA sequence, that contains the sequence of the coronavirus spike protein, is absorbed by some cells. These cells now produce foreign coronavirus spike protein. These cells then present some of the produced foreign spike protein on their surface via MHC I complexes so that they can activate a cytotoxic T cell and cause it to produce lots of copies of itself (cell-mediated immune response). Some of the foreign spike proteins are also released from the transfected cells which allow for B cells to activate a humoral immune response and for professional antigen-presenting cells to present the foreign spike protein on MHC II complexes to activate helper T cells.
My Question:
As far as I understand it, once a cytotoxic T cell encounters a cell that has a foreign protein presented on an MHC I complex, the T cell kills the cell that has presented the foreign protein before it leaves. This means the cells transfected with mRNA through the COVID-19 vaccine (even though a coronavirus hasn't actually hijacked them) will eventually be killed by cytotoxic T cells that encounter them since they are presenting foreign spike proteins on their surface. Is this not toxic for the body since it is killing your own cells? Or does the fact that the mRNA sequences are not self-replicating contain these cell deaths to only the transfected cells and only a few cells die in this process so that the vaccine is not toxic overall?

There is a question on stackexchange that is not only related
Why cytotoxic T cells don't kill dendritic cells when they present antigen?
Your question refers to "some cells" (explanatory text) and "transfected cells". Thus, any cell that takes up the m-RNA-vaccine is referred to. However, any answer must be based on the different types of cells involved in immunization, vaccination and - in killing infected cells, in the end. There are the immune cells which present antigen, there are, as well, the body cells which present.
The explanatory text of your question speaks of "presentation".  The very first paragraph of Wikipedia on "Antigen presentation https://en.wikipedia.org/wiki/Antigen_presentation seems to even limit the term  "presentation" to presentation by immune cells, which would exclude any body cells, like muscle cells transfected with vaccine antigen.  This might illustrate that immune cells are different from body cells in respect of presentation of antigen that becomes target of cytotoxic t-cells.
Both immune and body cells  take up antigene, however the immune cells, by presenting prime naive T-cells, i.e. activate the T-cells. The related question  cited asks about the fate of the immune cells.
As for  the fate of body cells like muscle cells you refer to  in  the last paragraph of your question the video message you link to in your own answer seems to refer to those body cells: transfected cells will simply be killed, but not enough of them to cause harm.
Here are additional remarks, enjoy: I think  it is an open question if the transfection as such would lead to cell death (assuming some failure of cytotoxic T-cells, not doing their job). Think of vaccination that transfects with "attenuated", if not live virus: even if the virus is incapable of - natural - replication  it is unlikely that the host cell whose ribosome machinery has been usurped can keep up its metabolism. I would like to be allowed to mark the following as a new thought of mine: the fact that the antigen is being presented speaks in favour of the cell not being able to survive - which is counterintuitively (how can a cell infected by virus still be able to digest, process, transport and present antigen on its MHCs, at all? Looks like it will stay alive.)
From the very fact of antigen presentation it is possible to infere, in my opinion, that the cell will not survive transfection. Host cells may  have their  own, inner defence mechanisms which are able to beat infection without any presentation of antigen - think of "interferon", but also, nowadays, of double stranded RNA, dsRNA.  A cell that is successful in defeating the virus without engaging the adaptive immune response would cancel out its survival by presenting and attracting cytotoxic t-cells. So it is a possibility that cells in spite of being transfected by mRnA vaccine do not die.  However, that would be considered a vaccine failure.
So with effective vaccination transfected body cells will die.
Caveat: from my reading of textbooks it is a possibility that vaccination might be effective even if body cells are not transfected, but that is beyond your question. Premise of your question is that a cell is being transfected (then what happens?).
A reference on the  possibility  that a "transfected cell" might survive by self defence  would be  "RNA interference",
https://en.wikipedia.org/wiki/RNA_interference
Last not least - see  the video you linked to - there is "B cell immunity".
To my mind it is a possibility that B-cells become transfected by mRNA vaccine - if so, they should present the antigen as an endogenous on to cytotoxic T-cells which makes your question very relevant in respect to B-cells, in my opinion. However, B-cells produce antibodies, considered most important in vaccination. This speaks in favour of B-cells taking up antigen via their B-Cell receptor that should be among cell debris of transfected cells that died - for instance few muscle cells transfected by vaccine. What you need here, in respect of B-cells is authority on either cross-presentation of endogenous antigen by B-cells (if mRNA is being uptaken through membrane, if B cells are transfected) or, authority on B-cells "only cleaning" up dead cell's antigen as part of dead cells, killed by virus or immune cells.
My answer is in line with the answer you already gave -  elaborating on what is in fact causing the cell's death:
"Do mRNA vaccines cause transfected cells to be killed by cytotoxic T cells?"
Yes,  mRNA vaccines cause transfected cells to die.

"So it is a possibility that cells in spite of being transfected by mRnA vaccine do not die. However, that would be considered a vaccine failure."  Absolutely wrong. Further mRNA doesn't last forever in cells, so it's entirely plausible the intra-cell infection clears without the cell dying. It's not at all a given the cell will be killed before the exogenous mRNA inside it "runs out". https://medicalsciences.stackexchange.com/questions/25522/is-the-code-from-the-mrna-vaccine-executed-by-the-cells-as-a-one-off

Interesting you say "absolutely wrong" - as I cling to "would be considered" (a failure). Literally: to consider that way would be absolutely wrong? The faster, better the vaccine works the sooner T-cytotoxic cells will kill the transfected cells presenting. Conversely, any no showing up of killer cells might be termed a failure. Still, I will try to amend my answer. Thank you!

@Fizz re "It's not at all a given the cell will be killed before the exogenous mRNA inside it "runs out". -  Any reference I'd consider valuable. What happens to antigen once expressed on MHC? Your premise: antigen on MHC vanishes mRNA "inside runs out", correct?
Did you know that antigen presented on MHC is returned and recycled to the cytoplasm? Is it being "re-presented" then, again? Alternatively, "to recycle" includes hiding away from? P.S. Remove to chat is all right with me.

“Is this not toxic for the body since it is killing your own cells? ”

Yes, cytotoxic T cells do kill mRNA vaccine-transfected cells, but not to the extent of harming your body. This is because the mRNA vaccine cannot be not integrated into the host genome, mRNA then will be degraded after translation within hours, preventing spike proteins variants to be continuously produced. Meanwhile, these locally produced antigens will mark the cells as "transfected", and induce immune response against the virus, including the activation of cytotoxic T cells, which directly kill the infected cells without damaging healthy tissues [1]. In some people, this process might cause some degrees of inflammatory responses, including pain, redness, swelling, fever, etc [2].

Individual vaccine antigens induce innate immune responses that may differ qualitatively or quantitatively according to the vaccine composition, but that induce a good adaptive immune response.

Once all transfected cells are eliminated and the antigens are no longer present, the level of antigen specific cytotoxic T cells will return to baseline [3].
Resources

Wadhwa A, Aljabbari A, Lokras A, Foged C, Thakur A. Opportunities and Challenges in the Delivery of mRNA-Based Vaccines. Pharmaceutics. 2020; 12(2):102. https://doi.org/10.3390/pharmaceutics12020102

Hervé, C., Laupèze, B., Del Giudice, G. et al. The how’s and what’s of vaccine reactogenicity. npj Vaccines 4, 39 (2019). https://doi.org/10.1038/s41541-019-0132-6

DiPiazza AT, Graham BS, Ruckwardt TJ. T cell immunity to SARS-CoV-2 following natural infection and vaccination. Biochem Biophys Res Commun. 2021;538:211-217. doi:10.1016/j.bbrc.2020.10.060

Additionally: This happens as well to virus infected cells, but to a much greater extent.

cells transfected with mRNA through the COVID-19 vaccine (even though a coronavirus hasn't actually hijacked them) will eventually be killed by cytotoxic T cells that encounter them since they are presenting foreign spike proteins on their surface.

It's not a given that happens before the exogenous mRNA inside the cell runs out. There's a decay process for mRNA of any kind, and exogenous mRNA is particularly targeted by intracell innate responses like TLR7 (although mRNA vaccines try to counter this with nucleoside modification, which delays the process).
Further, MHC-I isn't a flag that goes up an stays like that forever until the cell is killed. MHC-I is subject to recycling.... and it's a darn complicated process whose duration depends whether the MHC-I is fully or sub-optimally loaded, but it happens regardless of whether any killer T cell shows up to answer the "suicide-by-cop 911 call" or not.
Both the question and the 3 existing answers to it apply the "deterministic computer model" to biology, taking processes that in reality happen with some probability (which may be pretty low) as being 100%.
And it turns out that nucleoside modification has a somewhat surprising side effect: it reduces killer T-cells leaving helper T-cell activations intact (which help with the production of antibodies). One review mentioned that

Comparative studies performed by
our research group and others demonstrated that nucleoside-modified mRNA LNPs
outperformed unmodified mRNA LNPs in translation capacity, but failed to elicit successful
CTL [cytotoxic T cell] responses due to the drastically reduced production of type I IFNs [119, 157].

The research group which wrote that review seems focused on cancer immunotherapeutics, and the two cited studies definitely are about that. The lackluster CTL activation is a big deal for cancer therapy, but not really a problem for priming your immune system against an infectious disease you haven't yet encountered "for real".
In the 1st of those two papers cited there's an interesting [pair of] graph[s], showing the point I mentioned previous about killer vs helper T-cells.

And since mRNA vaccines are normally injected in skeletal muscle, it's also worth knowing that

Muscle fibers do not normally express major histocompatibility complex class I (MHC-I) molecules, and their reexpression is a hallmark of inflammatory myopathies.

Last paragraph - so interesting! Let us know what did you Google to find that reference, please.
Isn't it common textbook knowledge that any i.e. all nucleated cells express MHCI?
So "overexpression" in that paper to be understood as "expression at all", as basic expression is zero?
And, this is in favour of any regular, non-immune-system host cell needs not be targeted for immuization, which is by dendritic, APC, cells and lymphocytes alone, to successfully occur?

Quote: "MHC-I is subject to recycling...." - I think you are right that recycling does not imply any "restauration" i.e. any "come back" of what has been "recycled". When watching  recycling of a motorcyle do no await any new"1", smile.  Quoting your quote at "darned":  "...removed from the surface followed by intracellular degradation or recycling to the cell surface, in a process likely involving ..." - Surprise: there is "no interdiction of reconstitution": is spike antigen presented on MHC recycled to surface or not? Again, what did you google, I'm out for even more reference, thanks!

Maybe of interest to you:  B Cao, "Muscle stem cells can act as antigen-presenting cells..." in case you do further research on muscle cells not expressing MHC.  There is more reference, stating muscle cells, under normal circumstances, do express "some" MHC, which wouldn't be zero. Of general interest, why not eleborate? Muscle cells are fused cells, multinucleated (textbook wisdom: "all nucleated cells feature MHC").

@PeterBernhard: thanks; the abstract doesn't say anything about MHC though. I'll have to look into the paper to see what mechanism (if any) is being suggested. The paper simply uses an Ad vector.... speaking of which there's a Q about those here (being effective vectors for expressing genes in muscles):  https://biology.stackexchange.com/questions/97523/how-do-adenoviruses-interact-with-muscle-tissue-that-it-makes-them-acceptable-as/

According to the person who made this video's response to my comment asking this question, the transfected cells are killed by cytotoxic T cells, but the amount of transfected cells dying is not enough to cause irreparable harm since the cells regenerate themselves fairly quickly through division. Plus, the acquired cell-mediated in addition to humoral immunity is well worth the risk of an mRNA vaccine over a standard protein vaccine (which only leads to humoral immunity). If anyone has a better answer than this please let me know.

muscle cells do no regenerate, and covid vaccine is done to muscle cells

@ManudeHanoi: true, which is why this can't be the major pathway by which mRNA vaccine eject their proteins. Killer T cells merely targeting (let alone killing) muscle cells is the hallmark of serious pathologies like inclusion body myositis, which is very hard to treat. With hundreds of millions of doses of mRNA vaccines administered, you'd expect significant reporting of long-term deltoid muscle strength loss, but nothing like that has been reported among the vaccine side effects.

@ManudeHanoi: also "Muscle fibers do not normally express major histocompatibility complex class I (MHC-I) molecules, and their reexpression is a hallmark of inflammatory myopathies" https://pubmed.ncbi.nlm.nih.gov/23850081/ Basically skeletal muscle cells are unkillable by killer T cells under most conditions.


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Visualisation of phylogeography
I am working on phylogeography on one model species and I am a beginner. You can imagine one species that came on locality more than 5 mya (million years ago). It was a good environment, so the species expanded very quickly. After climatic changes this model species split in two refugiums (isolated locations for a once widespread species) and evolved into two species. This happened several times and now we have from that one ancestral species six valid species.
I have data from MrBayes and BEAST molecular clock. Can you recommend some phylogeographical program which can consider also expansion and contraction of model species?
My input data:
molecular identification (sequences)
coordinates (lat, lon) for each species
geographical data of a continent (altitude, precipitation etc.)
My goal:
Create a map where will be polygons (areas) of each species. These areas will expand and contract (step-by-step not like a do not want create video).
My problem:
I am able to make polygons by MCP, or kernel density, but unable to incorporate barriers into model. For example, polygons of species which lives in mountain region created by MCP include areas of lowland inside...

You might want to consider asking this question on http://biostars.org as well. Just to be clear, it is completely on topic and welcome to stay here, but you could also ask it on biostars.

@terdon thanks for recommendation..I try it :)

I think Spread will be best for this work.
SPREAD: Spatial Phylogenetic Reconstruction of Evolutionary Dynamics

(source: kuleuven.be)
Authors: Filip Bielejec, Andrew Rambaut, Marc A. Suchard & Philippe Lemey
Homepage: http://www.phylogeography.org
License: LGPL

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

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

sort: votes


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What's the purpose of colorful mushrooms' caps?
What's the purpose for many mushrooms to have colorful caps? Is not it is in their interest to hide as well as possible? Or there are mushrooms that propagate by being eaten, like fruits?
Why not all the mushrooms are poisonous?

Mushroom is actually the reproductive organ of the actual fungal body beneath the surface. It have a high surface area to disperse or spread the spores.
If the eating predators are low or dispersing is not an option, then it will need other organisms to attract to that they can be spread, so they are not toxic. Analogous to fruits, they uses different colors which are non-toxic to attract.$^1$
Whereas brightly colored mushrooms are less toxic, whereas, most toxic ones are either brown or white.$^2$
Edible Mushrooms

Toxic Mushrooms:

Source:

Why do mushrooms come in so many shapes and colors?
Mushroom poisoning

Image Source:
https://www.etsy.com/listing/93680839/antique-1900-edible-fungi-print

Are you claiming all color is due to toxins??? Then you have to explain why non-toxic Russula has the red cap https://en.wikipedia.org/wiki/Russula and why the most toxic species such as the Amanita phalloides are usually uncolored https://en.wikipedia.org/wiki/Amanita_phalloides

@Anixx: Thanks for the pointer! I hope it is correct now.

It's possible some colored nontoxic mushrooms could be mimicking toxic mushrooms. Very interesting, though, that in some cases it by more advantageous to attract herbivores/potential dispersers.

galerina are orange and highly toxic

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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How many different protein coding genes are in the Human Biome?
There are approximately 20k protein-coding genes found in the human genome. This number is presumably very small when considering all the genomes found in the diverse microbes associated with the human body.
Is there an estimate for the total number of protein-coding genes found in human microbiome?

What is the relation between microbiome and human genome?

Sorry, I mean only the human microbiome.

Still?? Microbiome is the micor-organisms in human body. http://en.wikipedia.org/wiki/Microbiome

Yes, I'm asking how many different genes are associated with a human and its resident symbionts, i.e. the number of protein-coding genes in the human genome + the number of protein-coding genes in the human microbiota.

The Human Microbiome Project collected samples as shown in the image below from healthy volunteers:

They give an estimate of about 8 Million genes in the human microbiome, which is about 360x the number of genes in the human genome. See here for their press release with a lot of information. Additionally these two articles are as well interesting, if you want to dive deeper into the stuff:

A framework for human microbiome research
Structure, function and diversity of the healthy human microbiome

Human Microbiome Project
According to Published data on HMP website:

The human microbiome consists of all the microorganisms that reside in or on the human body.
They may cause illness but some are necessary for good health.
There total count is 10 times more than Human cells.
~800 genomes had been sequenced.
~5000 Human sample had been used.
Include 14 disease project samples.
Total data stored on the DACC resource is 14 terabytes.
Total protein(~8 million) coding genes found to be 360x of number of human genes

Source:
[1] http://en.wikipedia.org/wiki/Human_Microbiome_Project
[2] http://commonfund.nih.gov/hmp/index

These look like numbers for the human genome only.

If I had to guess, I'd estimate there are at least hundreds of thousands of different protein-coding genes associated with a human.

I know. Can you edit the question, it is actually confusing? You need to know the number of genes in human Microbiome which have an effect in human genome?

Thanks @Devashish I tried to clarify the question. I hope it makes more sense. And no, the genes do not have to be known to affect the human genome; they just need to be resident.

"360x more abundant than human genes" looks like a good answer. So, probably millions of genes.

Would you consider exactly same genes from different microbes as different genes? By gene do you mean the genes in the genome or gene products?

The main text of your answer is entirely copied from a Wikipedia article. While you mentioned the source at the end of your post, you didn't mark the text as a quote. This is still plagiarism and not allowed on this site. You have to make clear any place where you quote a source verbatim. Answers should also not be taken entirely from external sources, they should be in your own words and quotes should be only for support.

@WYSIWYG I think I would consider the same gene found in two different microbe species to be different as they operate within a different genomic environment. But I'm not sure. I imagine that there is a lot of mutualistic sharing of gene products between microbes, and probably some horizontal gene transfer as well. The answer I'm most looking for is some quantification of genetic and molecular information.


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Height and natural selection in humans?
I watched the documentary "Evolve" recently and in the segment on "size" Scott V. Edwards, Harvard evolutionary biologist mentioned the idea that humans might evolve to be 7' tall in 'hundreds of years'. (I think this may have been taken out of context... I have emailed him to find out, but do not expect a response from someone so busy)
The reasoning goes that the trend in the past 100 years has been greater height, and women show a strong preference for men who are taller than they are. (Though a large share perhaps all of this difference has been due to diets higher in protein at an early age)
I wonder, though, if this is only part of the story. The preference women have is not just for tall men, but for a man who is taller than she is. Likewise, men seem to prefer woman who are shorter than they are. There is even cultural pressure: the classic western image of a couple on wedding cake always shows a man who is about 4" (to scale) taller than the bride.
Thus, women who are short have an advantage as they have a greater pool of men to choose from. (Colloquially, simply ask any 6' tall woman if she feels her height helps her find dates.)
Let's say that men seek women who are shorter than they are, but no more than 8" shorter. Women seek men who are taller than they are but no more than 8" taller. Given that the current average height for men is 5'8" and for women it is 5'4" (and distributed normally SD 2.8") will we have selective pressure that leads to greater or lesser height? (This is, obviously, oversimplified, but it is a starting point.)

It is oversimplification to say that height is the only parameter that defines female preference. There are plenty of other characteristics in males that female will take into account.

I'm somewhat skeptical of the assumption that attractiveness is correlated with number of offspring (to the extent that any substantive selection will take place).

@kate has what is probably the more correct answer for the observed pattern.
But as an experiment, I set up a basic simulation to approximate the conditions that you lay out:

Starting mean heights of 5'8" (172.72 cm) and 5'4" (162.56 cm) with standard deviations of 2.8" (7.112 cm). I used cm, because it's easier than dealing with inches.
Males will not mate with females that are taller than themselves.
Females will not mate with males more than 8" taller.
Males will not mate with females more then 8" shorter (follows from #3 above).

The problem that I quickly ran into was that, by truncating part of the normal distribution, the variance in height at each generation gradually decreased. After about 20 generations, the means weren't evolving because there was so little variation in height.
Human height is one of the most studied quantitative traits, going back over 100 years to some of the very first statisticians (Fisher, Galton). Height is a polygenic trait with very high heritability (h2 = 0.8)1. Genome-wide association studies have reported 54 genes involved in determination of human height2.
Imagine that each of these 54 genes has just two alleles: a and b. a gives a +1 to height. b gives a -1 to height. So aa would be +2, ab or ba 0, and bb -2. The sum of all those alleles is correlated to height. So if all 54 were aa, then the height would be +108.
The problem comes in when people only mate with taller people. Over time, the proportion of b's will decrease, and the proportion of a's will increase, but only to a point. Once all the alleles are fixed at a, there won't be any room left. The genetic variation will be exhausted. Without the input of new alleles, height will cease to evolve.
1 Lettre, G. 2011. Recent progress in the study of the genetics of height. Hum Genet 129:465–472.
2 Visscher, PM. 2008. Sizing up human height variation. Nat Genet 40(5):489-90.

Directional selection nearly always reduces level of variation, but in case of 54 genes and population over 7*10^9 - mutations are not negligible.

Excellent answer (you did a simulation!). Marta is right: mutation generates variation, but also human mate selection is not driven by height.

(This should have been a comment, but I don't have enough reputation yet. Sorry!)
You asked an interesting question, but I'm not sure about your reasoning.
Firstly, the "trend" you describe, that in the past century humans grew taller that ever before, is a phenomenon known to most European countries, one of the so called "secular trends": a uni-directional change in height (or growth rate) over a period of time. It was established that adult hight increased by 1 to 3 centimeters for each decade until 1980 (except for the times of World War 2, which had an opposite effect in some places). Such changes, however, happened much too quickly to be of genetic origin; and are much better explained by an increase in quality of life. In line with this explanation is the increase in height and growth tempo we see now in Third World countries, clearly the effect of improving life conditions.
Secondly, in my opinion, womens' preference for higher men can be another manifestation of their wanting simply the best male. I don't see any particular advantage for a woman to want a man higher that she is, but, as you pointed out, anecdotal evidence suggests otherwise.

Based on:

Cole, T.J. Secular trends in growth. Proc Nutr Soc 59, 317–324 (2000), PMID: 10946801.

See more on secular trends in:

Cole, T.J. The secular trend in human physical growth: a biological view. Economics & Human Biology 1, 161–168 (2003), PMID: 15463971.
Sargent, M. Biomedicine and the human condition: challenges, risks, and rewards. (2005).

To answer the question with a complicating question, suppose the anecdotal preference for "tall" men and "short" women is really just an urge toward the norm? Suppose that women seek taller men in proportion to their self-perception as "shorter than average"--the closer a woman is to average (female) height, the less likely she is to seek a mate who is markedly taller?
In my unscientific experience, height matters less to people whose height is more or less normal.
Then, with some assumptions about the heights of offspring of couples whose heights are different, the tendency might be toward a stable average. As noted in other answers, nutrition is probably a big factor in recent gains in Europe, Asia, and Africa.
This would be hard to model mathematically and I am not convinced the result would shed much light on the question, especially (as noted above) in light of the polygenetic nature of the trait.

The tendency for mean height to be pushed upward is natural when you consider two facts
(that so far have been left out here):

With the higher costs to females in general for reproducing, they are the "choosier" gender, so when it comes to mate selection, females' preferences matter more.  Therefore, a tendency for males to prefer shorter females (if that is even true) would not have an equal and opposite effect.
There is not a 1:1 ratio between males and females who pass on their genes.  The standard deviation on number of children is higher for males, and a higher proportion of males than females produce 0 offspring, thus "truncating part of the normal distribution", every generation, more for males than for females.  Again, even if there were just as much preference for short females by males as there is preference for tall males by females, there would still be a trend upward in mean height.  This fact has more to do with the speed of the change rather than whether or not the change will happen, though.

Two facts that have been discussed already but not widely acknowledged here should be explicitly mentioned again:

Male and female height each influence height in both male and female offspring.  This matters because even if there were preference not for the male to be too much taller than the female, this would not stop the trend upward in height because females would be constantly be trending upward in height.  Thus, females would not serve as any kind of "anchor" for height.
Height changes are due to more than just genes (whose effects could "top out" in the absence of mutation, as kmm mentioned), but in any case mutation is not negligible for human height (as Marta Cz-C mentioned), so a lack of possible genotypes for the extreme height we are talking about is not an issue.  Actually, this is obvious from the fact that there already are (fertile) people taller than the threshold mentioned in this question.
(The only real reasons for an upper limit on human height, which have not be brought up here, are nicely presented in this video: How big can a person get?, and those lead to a maximum height somewhere above the 213 cm (7 feet) we are talking about.)

Some things that have been mentioned here, though true or possibly true, are not really relevant to the question:

A limit on how much taller the father is than the mother for the typical child (imposed by female or male preference) does not change the answer to the main question (direction of mean height change, if any), only the speed ("in 'hundreds of years'").  (This follows from the "anchor" comment above.)
The fact that there are many other factors than height for mate selection, and even that many of these factors are more important than height, also does not change the answer to the main question.  (That is unless the other factors which correlate with lower height put downward pressure on it.  I don't think anyone would argue this, but I will provide an example because I think it is interesting:  If shorter males were, on average, more intelligent than taller males, then even if females preferred taller males (intelligence being equal), if they also preferred more intelligent males then human height could go down (while mean human intelligence goes up).)

Of course, generalizing all of this to humans in the present and in the future (switching language from "males" and "females" to "men" and "women") is predicated on some assumptions:

that women, particularly the ones who have children, do prefer and get taller men.  This could fail to be the case in the face of competition from women who also prefer taller men but do not have children.  This could also change due to reversal of the preference for height or due to increased preference for other factors that correlate with lower height combined with a reduction in the lustre of male height for females.  As one example, the ever-decreasing importance of physical competition between males and the ever-increasing level of safety from unarmed attack in the modern world means that height (and other measures of strength) matters less and less.  As another example, the reduction in face-to-face workplace settings, which are no doubt at least partially responsible for taller men being paid more than shorter men, should lead to wealth (which is a factor on its own) being less of a correlate with height and therefore reduce selection for height.
that the preferences of women will continue to matter more than the preferences of men, for mate selection.  If women and men were completely rational actors, this one could already have changed due to recent decreases in reproduction costs for females (mostly due to medical changes, such as lower death rate associated with pregnancy) and increases in reproduction costs for males (mostly due to legal changes, possibly to the point where the costs for males are higher than for females).  The way women and men think and feel with regard to mate selection is very strongly biased toward the normal conditions in our evolutionary history, though (higher female investment), and are hard to act against.


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Source for Squirrels Dislodging Nuts to Drive-Off Predators
I was reading a recent article by the Boston Globe on Harvard's Arnold Arboretum and it off-handily mentioned something very interesting:

‶I love the hickory collection,″ [Michael] Dosmann admits. ‶You have these tall trees that reach up to the heavens. You’re walking under a tall canopy of almost pure golden yellow.″ But be careful, Dosmann jokes. ‶Sometimes the squirrels intentionally try to dislodge the hickory nuts while you are directly underneath, just to frighten you out of their territory. You might get knocked in the head by a hickory nut, but it’s worth that gamble to experience the hickory collection in autumn.″

The idea of squirrels being able to drive away a predator like this is really amazing, but I am doubting if it is true. On one hand, Dr. Dosmann has a PhD in Ecology from Cornell University and is the the head curator for the arboretum, so I don't think he is exaggerating to impress a reporter. On the other hand, this behavior would require a lot of intelligence and I question how effective it would be on any human-sized predator.
I could not find any other sources that mentioned this behavior, but that could just be because I am not sure what key words I should be searching for. Searching 'squirrel antipredator behavior' on Google Scholar mostly returns articles about when squirrels flee from a predator, but I can't think of another phrase that would describe this behavior.
Has anyone heard of squirrels driving possible predators off by dislodging nuts at them? If not, are there any similar behaviors in other organisms?

I've both heard of the hypothesis and experienced it (although their aim isn't that good). They don't do it every time you walk under a nut-bearing tree with a squirrel in it, though. It may depend on how habituated they are to humans in their territory. I am also struggling to find references.

One of the reasons I want a formal source is it is easy to see how this belief could come about through a bias in data collection. If squirrels drop nuts by accident at a constant rate, completely independent of humans' presence, then squirrels will only be observed to drop nuts when humans are nearby (since when there are no humans nearby, no one will observe the drops). Without video cameras or other equipment to measure how often nuts are dropped when humans are not nearby, I do not see how you could rule out this possibility.

Your thinking is correct, and I'm pretty sure the same point has occurred to Dr. Dossman. Maybe he can provide you with a source? I'm serious here; it's not that hard to reach scientists these days. Or you just may be correct.

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


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Real time PCR standard curve
As blunt as possible: when performing real time PCR it is a routine step to run one PCR in order to plot a "standard curve" with several decreasing dilution ratios from your sample. what is the real purpose of this?
how should results be used/interpreted?

You can use 3 or 4 dilutions- 1:1, 1:5, 1:25, 1:125
Purpose of doing this is to calculate the primer efficiency. Ideally primer efficiency should be 2 i.e. two molecules of DNA are formed in a round of PCR. So after n-rounds of PCR there should be $2^n$ DNA. However, this may not be the case always. You calculate primer efficiency like this:

Plot $Ct$ vs $log_2(Conc)$
Get the trendline (in excel) or use a linear regression command for other applications
Get the slope ($s$) of the trendline
Efficiency in this case would be $2^{-s}$.

Some people use base of 10 in the log instead of 2 (for which you have to do $10^{-s}$ instead.
This, you can directly use to find out how many copies are produced after n cycles i.e instead of $2^n$ it will be $x^n$  where $x$ is the calculated efficiency. This is particularly useful when you are calculating the fold changes using the comparative Ct method. For details see this article.

usually you would find a $log(conc)$ vs $Ct$ graph in examples for which the primer efficiency calculation becomes 2^(-1/s). Means the same but what I described looks neater to me :P

and why is normalization with housekeeping gene performed?

Because these are supposed to be stable in their expression. That way they can be used to normalize for differences between the cells in the experiment.

and may I normalize with housekeeping gene results of an "A" qPCR run and a interest gene results of another "B" qPCR run? (same experimental conditions)

it is not necessary that you should normalize with a housekeeping gene. The reference gene should be such that it doesn't get affected by the treatment. Usually housekeeping genes are not affected unless there is some global perturbation- in such cases you should use a spike in. You should use the same reference for replicates otherwise comparison is difficult- qPCR is not absolute quantification; it's relative.

you can do the qPCRs for the reference and the interest gene separately with the same DNA template. However, it is always advisable to run the controls and the samples in the same run.

I can only agree with @WYSIWYG. Additionally you have to test your reference gene for the experiments (preferrably a number of them) and choose the most stable one. It is not so that always beta-actin or GAPDH are the best choices.

Because the purpose of the standard curve (which actually results in a standard line) needs to be linear. If it is not linear (because of not enough values which are not linear distributed), then you quantification will be wrong.
Ideally the line should look like this:

This picture is taken from this website, which gives a nice introduction into the topic.

and why is normalization with housekeeping gene performed?


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gene expression fold change threshold limit
When interpreting qRT-PCR results, which results are acceptable as fold changes, which are acceptable for housekeeping genes? e.j. a values of 0.8 raw fold changes for a "housekeeping" gene is acceptable as such? and conversely which is the threshold to say that there was "fold change"?

What do you mean by "raw fold"? Values not normalized to the normalization gene?

yes, values not normalised to any housekeeping

Why not? This will make comparisions hard to impossible.

please clarify, what are you answering to

Why didn't you normalize your genes?

because my housekeeping gene got a 20% fold reduction under the experimental treatment

What is the difference in your gene of interest between treated and untreated? Fluctuations in housekeeping genes can (and do) happen and are not necessarily due to the experiment. Thats why I usually test two stable genes if possible.

as i already wrote i got a 20% reduction = 0.8 fold change treatment/control

Ahh, I thought this was only for the housekeeping gene. If both are reduced by the same amount, this will be difficult.

sorry i misread before. well i had 3 genes of interest and the results varied: 2 got upregulation of %20, other %100. the housekeeping nevertheless was downregulated at %20 under treatment

So now you have two possibilities to choose from: First it is very possible that your housekeeping gene varies a bit because of slightly different experimental conditions (cells a bit more dense, slightly more metabolism and so on). In this case you can correct for this and your values can be used. Second it can be, that your treatment also affected the housekeeping gene. If this happens you need to choose another housekeeping gene for normalization which is not affected. If the first is true (and I tend to think so) this correction can be done in a software like REST2009.

As I mentioned in your previous post. If your reference gene undergoes changes then replace it with another reference and if even that doesn't work out then use a spike in. You must normalize. Interpreting the raw values can be erroneous- there could be a loading bias. Don't think much- repeating RNA isolation and/or qPCR is not a very hard job. And as Chris said, use two references if you can.
BTW, if you are fine with it then can you tell what is the gene that you are studying and what is the treatment
w.r.t what is a significant fold change.
There is no hard and fast rule to determine what is an acceptable fold change. In some robust systems a minor perturbation in the gene expression will not translate to any great biological outcome whereas there can be sensitive systems in which minor changes can affect the cell state. These things depend on how the gene is integrated in the regulatory network.


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DNA degradation rate
Usually DNA sample manipulation is realized with an ice box at hand in order to avoid degradation, and also its storage is set at -20ºC. Nevertheless, DNA has been obtained from really ancient samples that were not in a cold environment and even our DNA is at 36ºC. Furthermore, when performing PCR, samples are put into a massive heat shock and at high temperatures.
Then how needed are those protocols in order to grant correct DNA quality? how much can a sample be left without need to worry? and how does this degradation happen (DNAse free environment)

Really awesome question !

DNA decomposition isn't a phenomenon that is too common.
In nearly all cases, DNA is broken apart to the accidental contamination with nucleases. Long-term storage of DNA in the -20 is also suggested in order to significantly lower the rates of these nuclease enzymes.
Additionally, DNA only truly fragments at very high temperatures (>90-100 degrees Celsius) due to the nature of the covalent chemical bonds that form DNA. Nearly any organic molecule will degrade at very high temperatures, and some will degrade at lower temperatures due to unstable structures or heat-labile bonds.
Of course DNA will deanneal at somewhat-high temperatures due to its double standedness , but allows for reannealing to the initial molecule once the temperature is brought down.
One additional reason for potential DNA degradation is DNA shearing, which will occurs when you tear up your DNA physically due to exposure to rigorous shaking, resuspending or other "violent" techniques.

and how common are nucleases?

Not that common, but just think about how it only takes one enzyme to destroy your entire sample. A "source" of nucleases can be from your fingertips too, which is why its very important to wear gloves when dealing with DNA directly.

DNA is a incredible stable makro molecules. It survives in out cells and we can do things like PCR (which need serial heating and cooling steps) with it without degradation. As long as you work clean, your DNA is not at risk. We usually keep our working stocks of plasmids or primers in the fridge at 4°C to avoid repeated freeze-thaw cycles.

@Chris, exactly. If you treat your DNA well, it would treat you well (experimentally, that is). :)

@JunkDNA One important source of DNAses and RNAses when isolating nucleic acids are the cells/tissues themselves from which the DNA/RNA is isolated. Pure nucleic acids in an appropriate buffer are very stable, in my experience RNA samples can be stable for years at 4°C or even above (small RNAs with stable structures).


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My dog and I are wondering: is this a biting midge, or another bug?
A week or two ago, my dog started scratching, and it only increased. Not long after, I started getting bit by something that itches something awful. I thought it was fleas so got some medication and moved my dog out of my room. He stopped scratching immediately. After deep cleaning, I let him back in my room the next day. He shortly thereafter scratched again, but not intensely or frequently. My bites have continued.
I set out a flea trap (water, dish soap, flashlight on the water) and it caught the bug you see in the pic (it has only caught four of them).
Is that a biting midge, or something else?
Also, I'm in New York City.

https://i.sstatic.net/GC0iL.jpg -- close-up pic, color and pattern
https://i.sstatic.net/CVgnl.jpg -- several from a distance to show size
https://i.sstatic.net/rQqp4.jpg -- same one as in the first pic

The size is maybe as big as the hole a small nail makes in the wall, a very small ant, or a freckle.

Please mention which country/region this photo was taken in.

Right. I'm in NYC, so it doesn't make a ton of sense, but I know there is a small presence. I have several houseplants and am on the second floor. I rarely have my window open, but shortly before this started, there was an entire day I kept my window open. It does have a screen, but midges would easily fit. Walking my dog could also be a way to pick them up, i guess

I added a section picture for scale.

Welcome to Biology.SE! Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible) — photos must be uploaded (not links) — this is both to ensure the post remains relevant (links can and do break) and for the convenience of other users; 2) an estimate of the size of the organism; and 3) the species-identification tag. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

@tyersome The photos were uploaded to the image hosting service that stack exchange uses.

@Brindle Cruncher, did you actually see the insect biting you or your dog? If not, the itching could be something totally unrelated. (As mentioned, you found these insects in a trap, not on your dog/yourself.)

@adhish I did not, so good point. My dog has stopped scratching like crazy, and my bites have gone away, so totally plausible. I did feel bites happening, but maybe that was in my head. Still curious about the insect identification though.

@tyresome thank you! When I uploaded the photos, they were automatically turned into stack exchange service links. I'll add the other two points.

It seems to be a Yellow-banded polybia wasp (Polybia occidentalis), a species of Potter wasp.

my doubts with this conclusion is that the abdomen of the insect in your photo is quite large compared to other observations of the species. Also, Polybia occidentalis is a species that exists in South and Central America, not up north in New York, Perhaps it is able to exist there due to the warm summer weather though I am not entirely sure.
It might be another species of potter wasp. Potter wasps are able to sting but rarely do so to large organisms and their stings don't hurt much. They usually prey on caterpillars and beetle larvae and use those to feed their own. They create these nests that look like a ceramic pot. each of these "pots" contains one larva of the wasp (along with all the food the wasp has collected for their larva when it hatches).
here's a photo of the pots (wasps seem to be willing to create these pots on pretty much any solid surface including under leaves):

Wasps are not parasites, they are hunters of other insects, if my identification of this species is correct, then you and your dog are likely not going to suffer any direct harm from this species let alone parasitic behaviour.

I don't think so. Its bites are painful, but most importantly my bugs are tiny (see the second picture I added).

I'm a bit confused, are you talking about the insect with yellow horizontal stripes? because that is the only one I have noticed.

Potter wasps are extremely tiny as well (as seen from the image i put which has multiple wasps easily fitting on the last joint). If you are talking about the same stripey insect, then perhaps I can post more images to make my identification more clear and possibly more convincing? I merely chose that photo because it has different angles of the morphology of potter wasps.

check out the three different pics.

Thank you for the clarification, unfortunately I cannot identify the species in the third picture. Perhaps taking it out of the water might help take a clearer picture of the more detailed characteristics of the insect?

It's the same insect. Just wanted to provide it for context on size.


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Why is thoracic breathing dominant in women while abdominal breathing is dominant in men?
In human males, lateral movement of thorax constitutes 25% of breathing while abdominal movement accounts for 75% of breathing. It is exactly the opposite in the case of women.
I got this piece of information Trueman's Elementary Biology.

Welcome to the Biology community. Please improve your question by: 1. Citing sources for the information you provided (i.e. differences in respiratory movements in the sexes), and 2. Describing what efforts you made to answer this question (e.g. reading books or journals, doing your own experiments). This will invite good answers to your question. Cheers!

Some workers (https://www.karger.com/Article/Abstract/87456 and https://journals.physiology.org/doi/abs/10.1152/jappl.1975.39.4.608) have observed that respiratory movements do not differ in males and females, at least in quiet breathing. That makes it even more important to cite your sources in this question.

I think that your question will be correct if you give a reference for the percentages. it is true though, otherwise just take the percentages away and cite this paper: http://rc.rcjournal.com/content/57/9/1442.short ... Upper thoracic movement was significantly decreased with age. There was less abdominal movement in females than in males, except during quiet breathing in the supine position.

@Meercat Here is a good article that should answer your question: https://breathe.ersjournals.com/content/14/2/131. (You can read and download it for free.)

Probably an evolutionary feature to prevent pregnancy from making breathing difficult.


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How many hematopeietic stem cells (in percentage) does the bone marrow contains?
I've found out that the body marrow of an adult weights about 5% of it's total weight. How much (%) of the bone marrow consists of hematopeietic stem cells and how much consists of other non-hematopoietic cells, i. e. "stroma" (%) ? I've also found that in adults, ~70% of bone marrow consists of adipocite cells.

What research have you done to try to find the answer? Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning.

Im not a biology student. My baby girl was diagnosed with AML - M5a (FAB) and I am trying to understand better What's going on in her bone marrow and how the hematopoesis works in a healthy organism. The doctors explains it, but they don't go so deep. It helps me psihologicaly to understand better the underlying mechanisms.

In the bone marrow usually, the amount of stem cells is very low less than 99% of cells. You can check that on the Williams haematology book. It shouldn't be hard to find online.


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Is a virus a poison?
I've understood that a virus is not a living organism (like e.g. a bacterium). From Wikipedia I get that a poison is a substance that reacts physically or chemically with molecules in the human body. Since a virus is a protein that binds to certain cells in the body and alters the cell's function in a harmful way (resulting in the production of more viral matter), why is a virus not a type of poison? (Or is it?)
Additional info:
I'd like to understand the difference between them—if any—on a chemical and physical level, as well as the consequences for treatment. For example: we all know by now that viruses can only remain harmful/intact on surfaces for a certain amount of time. However, I would think that a poison on a surface does not have such a time limit (but I may very well be wrong). What's the difference, if there is one? Why is licking a banister with viral load older than 4 (or so) days not harmful, but is licking a banister with poison older than 4 days?

Does poison have genetic material or can it divide like virus? Is it considered living when inside a cell, like viruses?

I am voting to close this question as it is about the use of the English language, not about biology.

@David I'm very confused by your attempts to shut down questions about viruses. Before posting I had also checked this relevant question and you did the same there. I initially wanted to post this to MED or Chemistry but according to WP, both poisons and viruses are in the realm of biology. Your suggestion of sending this off to a linguist is strange and absurd.

I see this as a valid question about terminology in the field of toxicology, which can be rather specific and sometimes inconsistent withing the field, and with common usage of similar terms in the English language.

Welcome to Biology.SE! Your question is about definitions — i.e. word usage. That seems sufficient to explain the comment by @David. As a new user please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. From that you will see that questions should be focused, that separate questions should be asked separately (not mixed together), and that we expect evidence of prior research, especially for something that meets the criteria for "homework". Thanks!

@MikeyC — The poster's doesn't mention that she is a student of toxicology, but I suppose that it is the question rather than the poster's intent (she doesn't make that clear) that is important. But if you regard this as question in toxicology, do you think it is of any importance to biology or the concerns of SE Biology? Is it related to some "actual problem she/you have faced"? And does some definition used by professional toxicologists (one no doubt you could link to) have any relevance to the average biologist, let alone person? Really?

Thank you all for the info. I still don’t really understand how we got to semantics but that may be my inexperience with both fields. I asked the question assuming scientific words have fixed objective meanings so different words denote different physical systems/objects/interactions. (Rather than denoting connotations etc.) I’m very surprised that does not seem to be the case for poison/virus but I guess this is part of an answer to the question then :) I don’t understand though why two fields of study exist (virology and toxicology) if the difference between them is purely semantic.

@David — Are you asking if the language used by biologists is of any importance to biology? "Really?" The fact that you suggest a formal definition used by specialists has no relevance to the average biologist/lay person underscores the importance of this kind question. Scientific jargon can obfuscate the intended message from non-specialists, especially when it overlaps with but differs in meaning from common parlance.

@Laura — I can see how it might seem like a purely semantic distinction, but it becomes meaningful in an interdisciplinary field like toxicology, which often overlaps with other biological fields like immunology and infectious disease. If we didn't have a convenient way to distinguish infectious biological agents (like viruses) from the poisons they sometimes produce, it would quickly get confusing trying to describe the mechanisms of disease etiology in a clear and concise way.

@MikeyC — No. I am asking about the one specific case of a word that long predated modern biological science and does not describe any biological process, and I doubt whether you will even find in a textbook of biology, except perhaps tangentially. This is a common word in the language of which everyone has an interpretation from centuries of usage. I am asking how knowing the particular definition a specialised field like toxicology has adopted will help with a real biological problem she has encountered, (A student preparing for an exam does not hack it. And her bio says she’s a physicist.)

Although "Virus" literally means "Poison" in Latin, it would be a great over-simplification to regard a Virus as a Poison.
Now, most poisons are chemical compounds that interfere in some chemical pathway in our body. For example:

Carbon Monoxide: Binds with Haemoglobin, rendering it unable to transport oxygen
Sarin: Indirectly inhibits degradation of the  neurotransmitter "Acetylcholine"
at the synaptic cleft.   Mechanism of action of Sarin

Hence most poisons are quite "simple" in their actions. However, viruses can be considered as a complex machinery of functions that interfere with a multitude of processes in our body including cell transcription, receptor-mediated endocytosis, et.c
Hence, the best analogy would be to consider a virus as a tactical poison.
Now, as for last question, viruses are fragile assembled structures.  Viral Self-Assembly

Environmental factors like heat, uv-light, oxygen, etc may damage the assembled structure. Hence, viruses have a self life, and so do may poisons.
  Sarin (self life)
However, poisons tend to have a longer self life because chemical compounds are more stable than the capsid of viral proteins with weak hydrogen bonds.
As per David 's suggestion, poison is defined as "...substances that cause death, injury or harm to organs, usually by chemical reactions or other activity on the molecular scales, when an organism is exposed to a sufficient quantity."  Wikipedia
Viruses do work at molecular level, but not in the same sense as poisons do. Hence, viruses do fit into the description of poisons but not precisely.
Hope you find this helpful.

What is your definition of "poison" and the basis for believing it is correct or universally applicable?

Thanks a lot for this and the examples. Sorry if this is a misguided question but are there any non-viral or ‘simple’ poisons that are transmissible in the same way a virus is? It seems to me a virus is unique in that one of its tactics is causing replication of itself, making transmission possible because of the sheer quantity of the substance in the body. Is there a toxin that can do the same?

The closest example that I can think of are Prions, which are just misfolded proteins molecules. Synthetic prions can be aerosolized and used as a slow poison . They cause a cascade of  protein deformation, leading to a slow neurodegenerative breakdown. They are naturally transmitted via cannibalism of eating infected mammalian brain in general.(https://www.defenceiq.com/air-land-and-sea-defence-services/articles/prions-as-bioweapons)

Is a virus a poison?
In toxicology, a virus is not classified as a toxic agent or a poison but as a biological agent (regardless of whether you consider it to be living or not). With the main distinction being the biological agents reproduce. You can find different definitions of "poison" in different sub disciplines of toxicology, but generally it's any substance capable of causing toxic effects in relatively small quantities. A "substance" in this case is considered to be a single agent. Just as salt-water is not a single substance but a mixture of substances, a virus is a structured organism made of proteins, nucleic acids, and other macro-molecules. Its often the case that none of these different parts are solely responsible for the toxic effects of a virus, but instead it's the action of viral replication which causes cellular damage leading to disease.
There are some biological agents which also produce toxins or poisons. One example is Clostridium tetani. This organism can infect an open wound, but it's toxicological effects are not a result of direct tissue damage caused by the organism, but of the tetanospasmin toxin it produces, which is a potent neurotoxin and the causative agent of tetanus. Again, in this case, C. tetani is the biological agent, but tetanospasmin is the toxin/poison.
we all know by now that viruses can only remain harmful/intact on surfaces for a certain amount of time. However, I would think that a poison on a surface does not have such a time limit
Neither statement is universally true. There are viruses that can remain infectious for months in the environment, and some bacterial spores that can survive for years. There are also some insecticides (poisons for insects) that breakdown in a matter of days in the environment. It just depends on the specific properties of each different agent, and on the environment they are in.

You mention the scientific discipline of toxicology, but — like the other answers — argue an opinion rather than cite a definition of "poison" and explain its practical relevance.

I provided a definition of poison, and discussed it's relevance to the question.

In that case, are prions poisons?

Virus is more complicated than just a protein. Rather it is a collection of proteins and nucleic acids (the viral genome), packaged in a certain way. When virus penetrates a cell, it hijacks the cellular machinery, making the cell produce many copies of the initial virus.
Unlike a cell, virus does not have all the necessary elements for reproduction, i.e. for copying its genome, generating all the necessary proteins, and ingesting food for powering this reproduction activity. This is why one says that viruses are not alive, whereas cells are alive. A cell can exist and reproduce without virus, but not vice versa.
A poison can a simply a small molecule (not necessarily an organic one) which is capable of disrupting normal functioning of a cell, e.g., by binding to some of its proteins.

What is your definition of "poison" and the basis for believing it is correct or universally applicable?

@David I wouldn't dare yo give any definition that is universally applicable


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When and Why does G0 phase occur?
I've asked this question, specifically because i've seen this question.

As we see in this diagram , G0 phase occurs after M phase and at a specific point within G1 phase.

Is there a meaning to saying "end" in this case?
What is the checkpoint for causing a cell to enter G0 instead of continuing with the cell cycle, in case of heart cells and neurons? (what exactly is "checked"?).

Regarding when, I would answer at the end of Mitosis (check also this link:  https://biology.stackexchange.com/questions/70323/what-determines-the-reversibility-of-cell-of-g0-phase-in-cell-cycle?rq=1 ).
I wouldn't know what to answer to your second question, but maybe the link I posted above will help.


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What's the exact species of this African Giant Snail?
We've got an African Giant Snail a few years ago but failed to identify the exact species so far. When we got it, it's been about 20 % smaller than now, so it's probably not been an adult snail, but we don't know the exact age.
We only got this single snail, so there's no way to check for the eggs.
Here's a picture (small version, about 400 KiB) and a link to a bigger version. If you need more detailed pictures of certain parts, please let me know.

Bigger version: https://i.sstatic.net/S9z2x.jpg (about 2.2 MiB)
This picture shows that the apex is about 12 centimeters (4.7") in length, while the foot is about 14 centimeters (5.5").

I am not sure how to handle this.
The answer is the content of this page, which (I guess) should not be entirely copy / pasted here for copyright reasons.
So based on the texture of the skin, you have a variety of Achatina.
If I receive advice about how to make this answer comply more with the rules of the site, I will edit my answer.


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Help identifying a part of a flower
I researched about floral diagrams and this is what I found:-
This is floral diagram of Theobroma cacao. I managed to identify others but this part near the stamens was not found anywhere.
Also the floral diagram includes some circular parts which I have highlighted.
So what exactly are these parts called?
https://en.wikipedia.org/wiki/Floral_diagram

Please could you include a link to the source of your image. Thanks.

Because the background is now black rather than the white in the original diagram you've lost essential information. It also looks to me like a careful reading of the linked wikipedia page answers your questions. One hint that may help you is to think about how the cross-section of a stamen changes along its length. That will help you recognize structures you've circled in green. ——— Please also read the "homework" guidelines. (Note that "homework" can apply to questions even if they are not assigned as homework.)

ok i have corrected but I couldn't find any information about these pars


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Can someone identify this flowering bush from the US?
This bush is in Tennessee, USA.:

@DevashishDas , red horse chestnut is a tree...the Q. refers it as a bush...

Not sure about the ID, but those are definitely flowers, not fruits. You can see some of the fallen blossoms on the leaves in one of the photos.

Red flowering Japanese knotweed.

Polygonum cuspidatum, common name Japanese knotweed. A notorious invasive species.
It's actually a herbaceous perennial (those stems grew in just one season, and will die back to the ground at the first hard freeze), not a shrub. The red things are ripening seeds, not flowers.

Can you please add some reference to support your answer?

It is quite showy as it booms in cascades of silver flowers in late August that turn an intense magenta and then to scarlet each year right at time of the solstice. --Bitter Orange and Japanese Knotweed


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What is this black insect (wasp-like?) South America?
I live in the Pacific coast of South America. Seems to have two wings, like a wasp's. The "tail" is a bit bulky but is only connected to the rest of the body by a thin part. It's black overall. The antennae in the photo are downwards but they just spring normally to the front...

Actually I took photoshop to help me find this little guy, Ensign Wasp(Evaniidae)
Google Images:

My Photoshop research:

How did you do that? Photoshop search?

Np, I actually used Photoshop to identify the color of it's eyes and Antenna. It was quite clear it was wasp after that.

@jleeothon: Welcome to Biology SE, Can you mark as answer if this is what you were looking for?


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Is humans' height ideal?
More or less we humans are around 1.70 meters tall.
My question is, would it be possible to scale us? that is, is it in principle possible having humans 1 cm tall, or 10 meters tall or is there some reason that makes our height somehow ideal?

I will go with the fact that BMI may be a factor.

Imagine what would happen to your brains when you're 10 meters tall and you stumble, fall and bump your head to the ground. Natural selection at its core.

I remember there is a vsauce video about that https://www.youtube.com/watch?v=DkzQxw16G9w

There's also limits due to the structural strength of atom bonds. Larger animals needs stronger bones to support their weight. The buildings that we create are static structures, which demands less strength than a constantly moving animal requires.

Humans can, to some extent, be scaled: While most humans are two meters tall; the human body essentially works throughout the entire range from around a meter to around two and a half meters, although you tend to run into problems at the extremes.
However, outside of that range you run into the tyranny of the square-cube law:
As you scale a creature (or, in fact, anything), it's mass increases proportionally to the cube of the scale, while its surface area increases proportionally to the square of the scale.
This means that as you scale humans down, their mass, and hence their ability to generate heat would drop faster than their skin area, and hence their ability to dissipate heat; meaning that if unaltered, smaller humans would rapidly run into problems of freezing to death.
(Small animals typically solve this through a number of methods: Higher metabolic rates, rounder bodies, and more fur. Small humans, i.e. babies also suffer under this, and solve it by having what is typically referred to as "baby fat", a blubber that, among other things, aids thermoregulation.)
Similarly, as the human body is scaled up, the opposite problem arises: The body becomes unable to dissipate heat quickly enough. Larger animals solve this problems with giant organs specifically suited to radiate heat, such as elephant ears; or through submersion in water, as seen is cetaceans and hippopotamuses; or simply through living in cold climates, such as the polar bear. (All of this is typically augmented by lower metabolic rates.)
Heat economy isn't the only problem with size, however:
Especially when scaling up, the strength of various structures in the body become problematic. Unusually (yet not even freakishly) tall humans generally have some manner of bone problems, and also often have problems with too small hearts, leading to low blood pressure, or too big ones, leading to heart failure.
If the change was gradual enough, with sufficient adaptation, this wouldn't necessarily be a problem. After all, giraffes and elephants get on perfectly well; but a pump-valve heart such as we have cannot be scaled up indefinitely.
With a continuous-flow heart, this limit could probably be stretched, but how that would even begin to work biologically I have no idea.
Further problems with very large humans include getting enough air flow through the lungs, the enormous chore it would be to stand up or sit down, and of course, just getting enough food to drive the enormous body.
The long and short of it is: Anything less than about half a meter would probably leave us freezing to death; and anything more than two and a half meters is quite frankly a stretch (if you'll pardon the pun).
(There are people alive now that are more than two and a half meters tall, but they are not generally speaking in good health, although some do get on.)
Of course, all of this is predicated on the specific gravitational and atmospheric conditions on Earth.
On another planet with a greater or lesser gravity, a different proportion of oxygen in the air, or just a denser atmosphere; many of these limits and limitations would be quite different indeed. (Which is why whales, living in such an alien world as the sea, can be an order of magnitude bigger than any animal that lives on land.)

Amphicoelias fragillimus disagrees with your last paragraph

@silvrfück: Indeed; last paragraph clarified. It is, however, worth mentioning that A. fragillimus itself lived under somewhat alien atmospheric conditions. There are of course also more vegetative beings on land, such as giant fungi and clone forests; many of the outlined limitations apply specifically to animals.

"While most humans are two meters tall..." I'm deemed tall at 180CM. Most people I know are not 200CM?

@James: I'm rounding; which is why I said 2 meters, not 200 cm.

That's a pretty big round up @WillihamTotland


text:
Books for beginners
I want to study biology. I have zero previous knowledge of biology but I know Physics, Chemistry and Maths. From which book should I start? I have heard about Campbell Biology, but it is very costly in India(more than my 1 month's earning). So please suggest books that:

 Are cheap OR  could be found on internet
Require no previous knowledge of biology
Contain no technical mistakes
Adequately explain the topics which they deal with
and also mention some history of the topics

Edit
I am not looking for online videos. I want books; my internet is slow and there are some other problems. You can also tell costly books--Perhaps I could find them in the library or could print it somehow. If Campbell Biology book is available online then please give me the download link.

Many previous editions of textbooks are available for free online. I don't have any recommendations though. Is there a specific area of biology you want to focus on?

@canadianer Once I read a school book, it says everything is made up of cells and various cells combine to form an organ or something like that. So in particular I want to know everything about cell, how they were made, how they combine etc etc. I want to study historically, i.e. how scientist discovered this and that etc etc.

@canadianer Once I was reading Nervous system, the book said that there is some kind of sodium impluse which sends the electrical signal to our brain. But I could not understand the sodium impulse. So I want to learn about that. But at first I want to make a solid background in biology so I will first read some introductory book.

@metacompactness thankyou very much for the link.

As @metacompactness said in the comments, the campbell (9th edition) is available and free in pdf online (here). This book is a classic that most undergraduate students know quite well.
Online resources
There are some very good online resources to get an introduction to biology. I think that online resources might have the drawback that they may miss the big picture that a whole book can give you and it may be complicated to really understand in what order you should look at the videos particularly if you jump from one website to another. Otherwise, it is often quicker to learn from someone speaking in a video than from reading a book. I learned lots in various field thanks to free online courses. I appreciate a lot reading books but I think that free online resource is the best option for you.
As I did my undergrad in biology, I never really needed this kind of resource but generally speaking I find Khan Academy to be very good for introducing students to new fields of knowledge. And there is a whole biology section on Khan Academy. The MIT courseware is also a very good free resource. Education portail might be a good starting point as well.
If you google "free introductory course biology" you will find many other resources.

Here is a ted talk by Salman Khan (from Khan Academy) for the fun.

Khan academy is amazing! That would be a wonderful place to start!

This is a low price edition available in India on flipkart.com, it covers all topics extensively. It costs around ₹ 570.
Biological Science (English) 3rd Edition by Taylor

Is this book for absolute beginners or for BS as many people wrote in reviews?

This book is equivalent book to Campbell Biology.Taking into account the prize of Campbell biology,this book is relatively cheap.

I didn't read this book, I can't judge but Campbell biology is available online for free and I am currently enjoying it :)

A great place to start is Khan academy. It is free and very easy to understand.

Also, another thing you could try would be Bob Jones Biology (books A&B). I don't know how much those cost in India. But, they explain things in great detail starting at the bottom and working upward. I  will let you know that they have a strong Christian influence which some people would disagree with. However, if you can look past that, they are excellent, well-written books!

https://www.khanacademy.org/youcanlearnanything?video=main


text:
In which phenomena does one gene pair hide the effect of other unit?
This question was asken in an exam,

The answer they are saying is "Epistasis". But I think "Dominance" fits better,  because it is not mentioned whether genes of same allele are to be considered or different allele. Also it is not told whether genes in same locus are being talked of or different.
Please give some reference if you can. I know only school level biology. I do not know even in detail what allele and locus are. As far as I could understand from wikipedea and other sources I think "Dominance" is correct.

The definition of "gene", according to The American Heritage Science Dictionary is:
"A segment of DNA, occupying a specific place on a chromosome, that is the basic unit of heredity. Genes act by directing the production of RNA, which determines the synthesis of proteins that make up living matter and are the catalysts of all cellular processes. The proteins that are determined by genetic DNA result in specific physical traits, such as the shape of a plant leaf, the coloration of an animal's coat, or the texture of a person's hair. Different forms of genes, called alleles, determine how these traits are expressed in a given individual. Humans are thought to have about 35,000 genes, while bacteria have between 500 and 6,000. See also dominant, recessive. See Note at Mendel."
So, when the question refers to genes, it must be referring to two different genes on two different loci. If the question was referring to alleles of the same gene on the same locus, the correct answer would be dominance, but since it is referring to two different genes, the answer is epistasis.

"So, when the question refers to genes, it must be referring to two different genes on two different loci". Why is that? It is not mentioned   whether same loci are being discussed or different.

When you talk about two separate genes, you are always talking about two separate loci ("specific places on a chromosome"). Two different genes cannot occupy the same locus. Different alleles can occupy the same locus, but different alleles are just different forms of the same gene.

Consider two different genes (call them two different loci, if you like). Gene A where + is a wild-type, functional copy of the gene, and a is a mutant, loss-of-function copy of the gene. Gene B where + is a wild-type functional copy of the gene and b is a mutant, loss-of-function copy of the gene.
An individual with this genotype:
+/+; +/+
Will be wild-type. And if the a allele of Gene A is recessive, and the b allele of Gene B is recessive, then an individual with this genotype:
+/a; +/b
Will also have a wild-type phenotype. In a diploid organism, dominance is when +/a individuals have a mutant phenotype.  The same holds true for +/b individuals, if one copy of the mutant allele causes a mutant phenotype then the b allele is dominant to the + allele of the B gene.
If both mutant alleles are dominant then this individual would have two mutant phenotypes:
+/a; +/b
Most mutations, however, are recessive to the wild-type allele, so you would not see a mutant phenotype until there are two mutant copies and no wild-type alleles. Either:
a/a; +/+
or:
+/+; b/b
The double mutant would have this genotype:
a/a; b/b
You cannot interpret, or make logical sense, of an epistasis experiment unless the alleles are recessive.
If this individual does not have a double mutant phenotype, but instead only shows the 'A' gene loss-of-function phenotype:
a/a; b/b
Then we would say that the A gene is epistatic to the B gene, because homozygous A gene mutants "hide" the B gene mutant phenotype.
If, instead the double mutant only has the 'B' gene mutant phenotype then we would say that the B gene is epistatic to the A gene.
If the double mutant has both phenotypes then there is no epistasis between these two genes, or loci.  Conversely, if the double mutant has a wild-type phenotype then the mutations are suppressing each other.


text:
Why can human viruses that can't infect chickens be grown in embryonic chicken cells?
Embryonic chicken cells are commonly used in vaccine production.  The viruses are grown in chicken eggs, or in embryonic cells taken from those eggs, and then inactivated or attenuated to produce the vaccine.   But why can human viruses—some of which are not known to infect adult chickens—infect immature embryonic chicken cells?
For instance, according to this WHO fact sheet (https://www.who.int/news-room/fact-sheets/detail/measles), "Measles is a human disease and is not known to occur in animals." Yet the the measles virus prepared for the MMR vaccine is grown in chicken embryonic fibroblast cells.
N.B.:  According to http://www.ogrod.uw.edu.pl/__data/assets/pdf_file/0010/2161/13a.pdf, while measles may have evolved from domestic animals, it is thought to have its origin in cattle rather than chickens: "Measles, for example, is closely related to two other morbilliviruses-canine distemper and rinderpest (a disease of cattle)" [1]
One guess is that, while a virus would normally require interaction with a species-specific surface protein to initiate membrane fusion (see https://www.frontiersin.org/articles/10.3389/fmicb.2011.00247/full [2]), and thus viral (or viral RNA) entry into the cell, the naive nature of undifferentiated chicken egg cells enables such fusion to occur without such species-specific proteins.
Another guess (in the opposite direction) is that the species-specificity of viral infection depends on species-specific cell recognition factors, and because the cells in chicken eggs are undifferentiated, or minimally differentiated, they possess a broad range of recognition factors (where the non-chicken-specific ones are lost as the cells differentiate).
It was surprisingly difficult to find information online about this.  According to the the following (https://www.jstor.org/stable/30105172?seq=1), chicken embryo cells do become more resistant to viruses as the embryo ages; but this doesn't explain the lack of species-specificity:
"Cells dispersed from young embryos were permissive to viral growth, while those from older embryos were restrictive in an age-related pattern similar to that observed in ovo. The mechanism of natural antiviral cellular resistance did not involve viral attachment or release from cells from older embryos, but apparently depended on intracellular events during viral replication. These observations suggest that increasing natural resistance is based partially on intrinsic cellular changes. Sensitivity of a given virus and responsiveness of cells to the action of interferon may be more important to antiviral resistance than the amount of interferon that the virus induces." [3]
[1] Dobson, Andrew P., and E. Robin Carper. "Infectious diseases and human population history." Bioscience 46.2 (1996): 115-126.
[2] Hashiguchi, Takao, Katsumi Maenaka, and Yusuke Yanagi. "Measles virus hemagglutinin: structural insights into cell entry and measles vaccine." Frontiers in microbiology 2 (2011): 247.
[3] Morahan, Page S., and Sidney E. Grossberg. "Age-related cellular resistance of the chicken embryo to viral infections. I. Interferon and natural resistance to myxoviruses and vesicular stomatitis virus." The Journal of Infectious Diseases (1970): 615-623.

Flu viruses are not adapted to only infect humans. In fact a lot of wild species of it show up in birds (ducks and chicken) first, before they jump to humans.

@Chris  Yes, some human viruses grown in eggs are also avian.  That's why I was careful to write, in the first paragraph, "some of which [emphasis added] may not infect adult chickens".   However the point, and the source of my question, is that eggs can be used to grow human viruses regardless of whether they can infect adult chickens or not.  For instance, eggs are used to grow the measles virus for the MMR vaccine, and measles is not known to affect animals (besides us).  [continued next comment]

[continuing....]  Thus the fact that some of the viruses grown in eggs may also happen to infect adult chickens doesn't logically affect my question, which is: What allows the eggs to be infectable, independent of whether the adult chicken is susceptible or not?

I would suggest focusing on a single viral pathogen of humans and providing references showing that that virus doesn't affect adult chickens. Alternatively, can you provide references that support your assertion that human-affecting non-influenza viruses are typically grown in eggs? I did a quick search and found two sources saying that MMR is typically produced using viruses grown in chicken embryonic fibroblast cell cultures (or human cell lines) not eggs.

@tyersome I've made it explict in my title and intro that the essence of my questions is not why viruses that can't infect the adult of the species can be grown in their eggs, but rather why they can be grown from immature, embryonic cells (irrespective of whether this is done in situ within the egg, or in such cells taken from the egg and grown in culture) . I've also given measles as an explicit example, since a WHO fact sheet (who.int/news-room/fact-sheets/detail/measles) says "Measles is a human disease and is not known to occur in animals." If I am able, I will post a primary reference.

The measles vaccine uses an attenuated virus: one that has been  modified to reduce virulence such that it is (hopefully) no longer harmful to the host but still retains the antigenic determinants to induce acquired immunity. Although in modern times rational attenuation by genetic engineering is becoming established [1], the traditional method involves simply growing the virus under conditions abnormal for it such that it must evolve to survive. This often involves culturing the virus in cell types (or possibly organisms) in which it does not typically cause infection. Due to existing variation within the viral population or novel mutations, the virus may, over time, adapt to infect these cells with some degree of efficiency. Importantly in the context of vaccine development, the genetic changes generated during this adaptation may also reduce the pathogens ability to causes disease in the host organism [2].
This effect was originally observed by Louis Pasteur in 19th century who subsequently used it to develop a vaccine against the bacterium Erysipelothrix rhusiopathiae, which infects pigs [3]. Pasteur noticed that propagating this bacterium in rabbits, in which it did not initially cause disease, increased its pathogenicity in rabbits while at the same time reduced its pathogenicity in pigs. The virus had evolved and this attenuated form was used as a vaccine in pigs.
The attenuated virus for measles vaccine was created by the same principle in the 1950s to 1960s. An isolate of the measles virus from an infected patient was successively passaged through human kidney cells, human amnion cells, fertilized hen's eggs [4] and chick embryonic cells [5]. This attenuated virus, which was now replicative in chick embryonic cells, was no longer infective in humans and was used as the basis of the measles vaccine [6].

References
[1] Bull JJ. 2015. Evolutionary reversion of live viral vaccines: Can genetic engineering subdue it? Virus Evol 1(1):vev005
[2] Badget MR, Auer A, Carmichael LE, Parrish CR, Bull JJ. 2002. Evolutionary Dynamics of Viral Attenuation. J Virol 76(20):10524–10529
[3] Bazin H. 2003. A brief history of the prevention of infectious diseases by immunisations. Comp Immunol Microbiol Infect Dis 26(5-6):293-308
[4] Milovanovic MV, Enders JF, Mitus A. 1957. Cultivation of Measles Virus in Human Amnion Cells and in Developing Chick Embryo. Exp Biol Med  95(1):120-127
[5] Katz SL, Milovanovic MV, Enders JF. 1958. Propagation of Measles Virus in Cultures of Chick Embryo Cells. Exp Biol Med 97(1):23-29
[6] Enders JF, Katz SL, Milovanovic MV, Holloway A. 1960. Studies on an Attenuated Measles-Virus Vaccine — Development and Preparation of the Vaccine: Technics for Assay of Effects of Vaccination. N Engl J Med 263:153-159

Thanks for the very informative post. I wasn't aware of the "passaging" technique in vaccine development. I'll need some time to look over the references before I reply in more detail. But my initial read of your post is that viruses grown in immature cells of species the viruses don't "natively" infect had to have been changed to enable them to grow in such cells, and that this change sufficiently attenuates the infectivity of the virus in humans to enable it to be used as a vaccine.

However, the passaging sequence you describe for measles (human kidney cells->human amnion cells->fertilized hen's eggs->chick embryonic cells) suggests that non-native infectivity is easier to achieve when you use immature cells than adult cells. I assume that's why they had to first get the virus to infect highly undifferentiated cells (fertilized egg) before it could infect slightly more mature cells (embryonic). This suggests the attenuated virus wouldn't be able to infect an adult chicken, so my question remains: Why is a virus that can't infect an adult able to infect immature cells?

A capsid is not a membrane. Viruses are acellular. Viruses are not karyotic and do not have membrane bound organelles.
If An envelope forms around the capsid, the virus buds. The envelope comes from the infected cell not the virus.

Welcome to the site. Please take a [tour] and visit the [help] for more information on what we do at this Stack site and what makes a good question and answer. In particular note that we value answers that provide (scientific) references to support the answer. I suspect that your answer should have been a comment rather than an answer as it doesn't actually address the question or any of the content in the question.

Yes it was supposed to be a comment. My apologies.


text:
if an SNP were edited using CRISPR What are the chances that, absent artificial selection, wild type alleles would reemerge?
I am researching a fatty acid amide hydrolase (FAAH) SNP RS324420 and FAAH out microdeletion that together lead to reduced pain sensitivity and reduced anxiety (Moreira et al 2008).

The causative mutations for this new pain insensitivity disorder are: the
co-inheritance of (i) a microdeletion in dorsal root ganglia and
brain-expressed pseudogene, FAAH-OUT, which we cloned from the
fatty-acid amide hydrolase (FAAH) chromosomal region; and (ii) a
common functional single-nucleotide polymorphism in FAAH conferring
reduced expression and activity. Circulating concentrations of
anandamide and related fatty-acid amides (palmitoylethanolamide and
oleoylethanolamine) that are all normally degraded by FAAH were
significantly elevated in peripheral blood compared with normal
control carriers of the hypomorphic single-nucleotide polymorphism.
The genetic findings and elevated circulating fatty-acid amides are
consistent with a phenotype resulting from enhanced endocannabinoid
signalling and a loss of function of FAAH. Our results highlight
previously unknown complexity at the FAAH genomic locus involving the
expression of FAAH-OUT, a novel pseudogene and long non-coding RNA.

Br J Anaesth. 2019 Aug; 123(2): e249–e253.
Published online 2019 Mar 28. doi: 10.1016/j.bja.2019.02.019
I would like to know, theoretically if CRISPR was used to edit these genes in humans to allow  reduced anxiety and pain sensitivity,  'what is the probability that a recurrent mutation would cause the wild-type allele to reemerge in this gene',

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. In particular, speculative questions lead to "answers" that are opinions (rather than factual) — this makes your question as currently written off-topic for this site. In addition, questions should be clear (e.g. abbreviations and acronyms should be defined). Finally, summarizing what you have already learned about your question will demonstrate that you've done the expected prior research. Thanks!

@tyersome I appreciate the question is worded in a speculative way. However, I don't agree that the question is fundamentally speculative in nature - I think it could be reworded to 'what is the probability that a recurrent mutation would cause the wild-type allele to reemerge in this gene', which could certainly be answered using a simple population genetic model. In that sense, I think it is an interesting and relevant question,

@MissEllieKarslake. I think your question is an interesting one, but we might need some more details to give it a proper answer. Please can you include a) what organism you are interested in, b) which particular SNP and deletion you are interested in, c) whether you are interested in a wild or lab population. Thank you.


text:
For how long can a person drink sea water?
How long could a person of lets say 18 years be able to drink sea water without getting too much into trouble ? Or can a person drink it without noticing that it is a very bad idea ? I don't mean in just 1 drink session but like can one manage a day or two ? Can one drink it and go to sleep and be still healthy (although very thirsty) in the morning ?
(this is just a hypothetical question, I'm not a scientist at all, I'm not sure what tags to use actually)

Additional brainstorming:

kidney failure
any other organ failure
dying of thirst
...

I don't remember were I read this. A shipwrecked man drank seawater to stay alive. He claimed that the seawater he decided to drink was to his surprise fresh water. He said that there was a pocket of fresh water floating about on the surface of the sea. Through a recent Google-scan I learned that saltwater is heavier than freshwater. After a a heavy downpour at sea the surface water would be less salty than the rest, wouldn't it? It was said in the article I read that sea water is 3.5 % salty and that the body can just deal with water that is less than 2% salty.

https://www.bbc.com/news/world-asia-45623130 This guy did it for 49 days involuntary .

It takes about 2 weeks under ideal conditions, and as little as a few hours under the worst conditions, dehydration is very strongly affected by things like environment and activity level. Your best bet is to just use information on dehydration as if they were not drinking anything and just use the shorter estimate since sea water is not helping at all.

(source: free.fr)
Alain Bombard
He is a french biologist who voluntarily tested how many days a man can survive drinking seawater and how?
Biologist point of view
Sea contains ~3.5% of salt$^1$. Our kidney separates the waste from water and excrete them in urine provided the salt content is less than ~2%.$^2$
So, it will take the water already present in the body. Causing excessive thirst and dehydration, eventually cause death.
Alain's Experiment

Just one spoon of seawater at 20 minute intervals, drinking very
  slowly and letting the saliva in your mouth reduce the saline in the
  water you have swallowed.

Though he survived 65 days (From and including: Sunday, 19 October 1952
to Tuesday, 23 December 1952, ~4,400km) of his journey and lost 25 kg of weight, this result is never successfully reproduced.
Source:

http://oceanservice.noaa.gov/facts/whysalty.html
http://paradise.docastaway.com/drinking-sea-water

The results of Bombard, are, nicely said, at least doubted.

@caseyr547 The accusations agains Bombard where that he was supported (also with food and water) by a ship during his time on the atlantic ocean.

Bombard had a rain harvesting system on his craft which he drank daily, he was NOT drinking only sea water. By his own admission without rain and fish fluids the sea water would have killed him, the media grossly exaggerates what he did.

After drinking 1 liter of seawater with 3.5% salt your kidneys need to excrete at least 1.5 liters of urine in order to maintain normal blood sodium levels, which leaves you with 0.5 liter of negative water balance. This occurs because the kidneys have a limited ability to concentrate urine; it's explained in more detail here.
When a negative water balance results in 1% loss of body weight (0.7 kg in a 70 kg person), which could occur after drinking of about 1 liter of seawater, you can already experience dehydration symptoms, starting with thirst, dry mouth, pounding heart and dark yellow urine, followed by fatigue, dizziness, nausea, headache and eventually coma and death, that can occur at about 10-15% loss of body weight (7-10.5 kg in a 70 kg person), which could occur after drinking 14-21 liters of seawater (Nature.com).
Death occurs due to acute kidney failure resulting in the accumulation of sodium, urea and other substances in the blood.
It is not time, but the amount of seawater that causes problems. One could drink 1 liter of water in the evening, need to urinate several times during the night, and be mildly dehydrated and otherwise "fine" in the morning. But what's the benefit of this?