text:
Can threat to survival increase mutation rates in germline cells?
Can stress that is related to a threat of survival of a population of animals or plants in some environment, like due to hunger, thirst, fear from predators, etc..; results in an increase in average mutation rate in germline cells of individuals of that population, thereby increasing the likelihood of producing heritable trait(s) that might be beneficial to that population in combating those adverse survival conditions in that environment?
In bacteria this is known as "Stress Induced Mutagensis"
Is there something comparable to that in animals and plants?

Well... since I can't delete this accepted answer... it's going to be a reverse ferret, to some extent. One 2014 review by Ram and Hadany lists a fair number of SIM occurrences outside of bacteria:

Stress-induced mutagenesis (SIM)—the increase of mutation rates in stressed or maladapted individuals—has been demonstrated in several species, including both prokaryotes and eukaryotes. [...] SIM has also been observed in yeast, algae, nematodes, flies and human cancer cells.

The one for algae (Goho and Bell, 2000) appears/claims to have been the fist:

Cultures of Chlamydomonas were exposed to a range of relatively mild stresses for a period of 24 h. These stresses comprised high and low temperatures, osmotic stress, low pH, starvation and toxic stress. Fitness was then assayed as the rate of division of isolated cells on agar. We found that there was a strong tendency for stressed cultures to have lower mean fitness and greater standardized variance in fitness than the negative controls which had been cultured throughout in unmodified minimal medium. The same tendency was shown, as expected, by positive controls which received mutagenic doses of ultraviolet irradiation. We concluded that the most reasonable interpretation of these observations is that mild stress increases the genomic rate of mutation.  This appears to be the first time that this phenomenon has been noticed in eukaryotes.

The paper cited for Drosophila, Sharp and Agrawal (2012)

Our results show that mutation rates are sensitive to genetic stress, such that individuals with low-quality genotypes will produce offspring of even lower genetic quality, in a mutational positive feedback loop. This type of variation in mutation rate is expected to alter a variety of predictions based on mutation load theory and accelerate adaptation to new environments. Positive mutational feedback could affect human health by increasing the rate of germline mutation, and possibly somatic mutation, in individuals of poor health because of genetic or environmental stress.

Clearly this one is quite bold in extrapolating its findings.
And long story short, the paper on nematodes (Matsuba et al., 2012) finds a temperature dependant mutation rate.
What seems to be the weak point in these paper, and perhaps why a more critical review of Lynch et al., 2016 of SIM doesn't mention them, is that no explicit mediating mechanism appear to have been identified in these studies on eukaryotes. In bacteria (e.g. the paper linked by the OP) how SIM works inside the cell is pretty well understood, there are in fact several mechanisms that all respond (convergently) to various forms of stress.
There's an acknowledgement (in the Drosophila) paper, that such mechanisms in eukaryotes might differ from bacteria

The sources and mechanisms underlying this variation have been best studied in microbes, but the sources of variation in microbes may differ from those in multicellular eukaryotes for several reasons. [...]
In animals, mutation rate varies among genotypes, although the functional sources of this variation are unknown. [...]

It does go on into some theories how it might work.
As for yeast, Rodriguez et al. (2012)

Mismatch repair (MMR) is a major DNA repair pathway in cells from all branches of life that removes replication errors in a strand-specific manner, such that mismatched nucleotides are preferentially removed from the newly replicated strand of DNA. Here we demonstrate a role for MMR in helping create new phenotypes in nondividing cells. We show that mispairs in yeast that escape MMR during replication can later be subject to MMR activity in a replication strand-independent manner in nondividing cells, resulting in either fully wild-type or mutant DNA sequence. In one case, this activity is responsible for what appears to be adaptive mutation. This replication strand-independent MMR activity could contribute to the formation of tumors arising in nondividing cells and could also contribute to mutagenesis observed during somatic hypermutation of Ig genes.

I guess a weak point of this paper vis-a-vis of SIM (which they only mention in passing) is that it's not obvious in their setup what the stress was. Basically they saw (adaptive) mutation-rate change (in response to the environment), but they don't pinpoint what exactly they think the stressor was. So this paper is a way the reverse of the other three I, i.e. the mechanism is clear, but stress is not.

but in humans stress has been identified with abnormal sperm morphology, so this might be related to an increment in mutation rate in the male germline cells which would most likely have a bad side to it, which we happen to observe, since most mutations are deleterious. But that might not be the complete story, there may be a possibility of a beneficial aspect that escaped observation, i.e. a beneficial mutation that might arise from the possibly higher rate of mutation.

see: https://www.medicalnewstoday.com/articles/277543.php

@ZuhairAl-Johar: (psychological) stress at the level of organism doesn't necessarily translate in the kind of cell-level stress needed to produce [more] mutagenesis. At least I don't know of evidence for that link. The article you indicated talks about lower testosterone etc. as the effect of organism-level stress; it's not clear that that has any effect on mutagenesis, and I think it probably doesn't have such an effect.

I don't have access to the review, but are you sure it supports such a broad claim? For instance, we've known for several years that Alu translocation rate is increased in response to heat stress. I am not entirely sure if the OP would include this sort of stress, but still.

@terdon: they don't' mention/cite that paper. They do discuss SIM in some 35 bacteria that it was observed in. And they do acknowledge "large-scale topological" mutation-rate variation in eukaryotes with some examples. I guess they don't think that's SIM enough. I should also mention that this review is marked as "opinion/perspective", so perhaps the journal editors did see it as somewhat biased.

@terdon: of course heat stress is included.

@terdon: you were fairly correct, I should have checked one of the other review (more sympathetic toward SIM) which Lynch was citing. I've rewritten my answer based on that. Let me know if you think it's too skeptical.

Oh wow, that's what I call improving an answer, thanks! That's a much more nuanced position :)

@ZuhairAl-Johar What do you mean by heat stress? The feeling that your surrounding is too hot? Or the gametes being exposed to high temperatures? Because in your examples you describe stress as more psychological state of mind (ex. fear), but in these it's the latter i.e. I believe the cell upregulates or loses regulation of DNA mutation processes in direct response to heat.

@Cell, "stress" can be psychological or organic, thirst, hunger, excessive heat or excessive cold that threats survival are definitely stressors, even psychological stress can cause physiological changes, like hormonal or otherwise, that might cause a stressful conditions on the germline cells. Heat, cold, other stressors need not directly affect the germline cells, it can affect them via hormonal or other chemicals released in response to stress.

@ZuhairAl-Johar That's nice but I wasn't asking for an explanation of what stress means. I was just asking for you to clarify that you understand heat stress means something different mechanistically in lower organisms than what your question is implying (psychological).

@Cell, yes of course they are different, however heat stress in higher organisms need not be mediated via psychological stress, a physical stress can indirectly affect the germline cells through hormonal or other chemical changes without being related to psychological stress from that physical stressor, anyhow this is different form the direct effect of those stressors on lower organisms definitely.

Sure if you say so.


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Possible combinations in the Meiosis' Telophase 1
As you might already know

Meiosis is the process in eukaryotic, sexually-reproducing animals that reduces the number of chromosomes in a cell before reproduction $^{[1]}$

One of the reasons why meiosis has been so important in evolution is variation.
As my teacher used to say: Nature rolls the dice... - It's the magic of genetics; two completely different persons might share the same parents.
So here the question:

Suppose we have a cell with four chromosomes (two couples of homologous chromosomes) in the Prophase 1. I've drawn all possible combinations that could happen - these are chosen randomly - in the Telophase 1.

Is there a genetic disorder (not only regarding humans), in which the four initial chromosomes are split, in the Telophase, into two parts, each of them containing a couple of homologous chromosomes. I.e. (referring to the image) is the combination $(\color{red}{red}+\color{blue}{blue})(\color{green}{green}+black)$ in the Telophase 1 possible?

$$$$
$^{[1]}$ Quote from https://biologydictionary.net/meiosis/

Failure to properly separate homologous chromosomes during meiosis, either by including an extra copy of a chromosome or including zero copies of a chromosome, causes gametes that are 'aneuploid', and as a result, a zygote that results from that gamete will have an extra or missing chromosome as well.
For humans, most aneuploidies are completely fatal at some point of early development, so there is not an associated genetic disorder in live births.
One common aneuploidy that is not fatal to the embryo is an extra copy of chromosome 21; this causes Down syndrome.

Thanks, @Bryan Krause [+1]. However, what I meant with the question was, if homologous chromosomes (here red+blue and black+green) could stay together in Telophase 1 (which isn't normal (or even possible???) but might be a genetic disorder)

@Dr.Mathva I explained what the result would be if/when this happens for even 1 chromosome pair, which would lead to a genetic disorder in the offspring. A genetic disorder where all of your own germ cells failed to go through meiosis properly would effectively mean sterility because nearly all their gametes would be aneuploid, and most lethally so, so such a trait would not be passed to offspring.

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text:
How to derive the Equilibrium value $\hat F$ equation
In population genetics, there is a relationship between $\hat F$ and $Nm$.
$\hat F=\frac{1}{1+4Nm}$
In population genetics textbook, (i.e. Hartl, D. L., and A. G. Clark. 2007. Principles of population genetics. Fourth edition. Sinauer Associates Incorporated, Sunderland, Massachusetts.) it reads that using the equation below:
$F_t= \bigg(\frac{1}{2N}\bigg)(1-m)^2+\bigg(1-\frac{1}{2N}\bigg)(1-m)^2F_{t-1}$

Set $\hat F = F_t = F_{t-1}$. After expanding the squared terms on the right-hand side, and assuming
  that $m$ is small enough and $N$ large enough, and that terms  in
  $m^2$ and $m/N$ can be ignored, some rearrangement leads to:
$\hat F=\frac{1}{1+4Nm}$

I tried redoing it algebraically, without success. So do you know how to get to "$\hat F=\frac{1}{1+4Nm}$"
$(1-m)^2 = 1-2m+m^2$
$F_t= \bigg(\frac{1}{2N}\bigg)(1-2m+m^2)+\bigg(1-\frac{1}{2N}\bigg)(1-2m+m^2)F_{t}$
$F_t-\bigg((1-2m+m^2)-\frac{(1-2m+m^2)}{2N}\bigg)F_{t}= \frac{(1-2m+m^2)}{2N}$
$F_t(1-(1-2m+m^2)-\frac{(1-2m+m^2)}{2N})= \frac{(1-2m+m^2)}{2N}$
$F_t(-2m+m^2-\frac{(1-2m+m^2)}{2N})= \frac{(1-2m+m^2)}{2N}$
$F_t(\frac{2N(-2m+m^2)}{2N}-\frac{(1-2m+m^2)}{2N})= \frac{(1-2m+m^2)}{2N}$
$F_t(\frac{2N(-2m+m^2)-(1-2m+m^2)}{2N})= \frac{(1-2m+m^2)}{2N}$
$F_t= \frac{(1-2m+m^2)}{2N} * (\frac{2N}{2N(-2m+m^2)-(1-2m+m^2)})$
$F_t= \frac{1-2m+m^2}{(-4Nm+2Nm^2)-1+2m-m^2}$
Then $m^2= 0$
$F_t= \frac{1-2m}{(-4Nm)-1+2m}$
$F_t= \frac{1}{(-4Nm)-1+2m} -\frac{2m}{(-4Nm)-1+2m}$
??
$F_t= \frac{1}{(-4Nm)-1+2m}$
Magic
$\hat F=\frac{1}{1+4Nm}$

Sign problem
When you go from
$F_t(1-(1-2m+m^2)-\frac{(1-2m+m^2)}{2N})$
to
$F_t(-2m+m^2-\frac{(1-2m+m^2)}{2N})$
You make a mistake in the sign. It should be
$F_t(2m-m^2-\frac{(1-2m+m^2)}{2N})$
Approximations
I will assume this error of sign propagate to inverse your end result. You hence should get
$F_t= \frac{1}{4Nm+1-2m} -\frac{2m}{(-4Nm)-1+2m}$
$\frac{2m}{4Nm+1+2m}$ is negligible compared to $\frac{1}{4Nm+1+2m}$, so you can indeed remove it. You get
$F_t= \frac{1}{4Nm+1-2m}$
Also, $2m$ is negligible compared to $4Nm$, so again you can remove it. You end up with
$F_t= \frac{1}{4Nm+1}$
Tadaa!

Yup! Good old sign problems. Thanks for the help.

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If DNA methylation inactivates genes, does DNA demethylation activate them?

DNA demethylation can be passive or active. The passive process takes place in the absence of methylation of newly synthesized DNA strands by DNMT1 during several replication rounds – for example, upon 5-azacytidine treatment [23]. These pharmaceutical demethylating agents act via inhibition of DNMT1 and favoring its degradation by proteosomes [24]. This approach is currently used in cancer to demethylate tumor suppressor genes [25].

If we’re demethylating a tumour suppressor gene for cancer curing doesn’t this mean that we’re activating it (to stop the tumours)? I can’t seem to understand the function of DNA demethylation. I came across it when reading about genomic imprinting and haven’t been able to wrap my head around it. Please help.

Here is a series of articles explaining DNA Demethylation from Sience Direct.
In the most broadest of senses, DNA methylation adds methyl groups to DNA preventing the transcription complex from forming and transcribing the gene into mRNA. By demethylating the DNA, it allows the transcription complex to form and mRNA to be transcribed for translation.
When it comes to cancer, Most of the tumor suppressor genes are down regulated to allow for genes like stat3 to be upregulated. Ideally, by removing the suppression of these genes, they can reduce the levels of oncogenes and slow the growth of the cancer.
Think of it like this A -| B. Cancer decreases A so B can increase in expression A↓ -| B↑. By demethylating A, we  A↑ -| B↓.


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Are Males the main evolutionary tool for production of genetic variation necessary for evolution?
What I'm saying here is just a personal reflection, that might turn to be gravely erroneous, actually I'm asking that because I didn't see it presented elsewhere.
Evolution is propelled by two directions. The first one is a process that is novel in producing genetic variation, which includes: Mutation and Migration. The second is a clearing up process, something that wash out results from the first process, and those are: Natural Selection and Genetic drift.
Natural selection is more functional in the sense that it only preserves traits that are adaptive to the environment. Genetic drift is not discriminating in that sense, so it can wash out any result of process 1 whether its harmful or beneficial.
It's clear that the primary source of evolution is the first process (i.e.; mutation and genetic migration), since the second process (i.e.; natural selection and drift) only acts on what results form it.
[Note: by primary "source" of evolution, its meant here to be what's responsible for producing the basic material upon which evolution works, since evolution is change in genetic variation over generations, then "genetic variation" is the basic material for evolution, and this is produced by mutation and migration. Natural selection and drift don't produce genetic variation, they change it by an act to decrease it, and a process that acts to decrease something, can hardly be viewed as a producer of that thing. A butcher is not the primary "source" of meat, the cow is!]
Now in principle the more we have production of genetic material the more is the chance of getting a genetic change that is useful. Of course increase in mutation rates can result in injurious traits, those would be washed out by selection and drift, however its the higher probability of having a beneficial mutation that is the primary concern here.
The male spermatogenesis in mammals supplies the impression that it is the MALE sex that is the Ore of evolution. The incomparably high cell production rate of all stages of spermatogenesis as compared to Oogenesis, tends to make one think that the chance of mutation arising in spermatogenesis is ought to be much higher than that arising in Oogenesis.
The testis seems to be the Oven in which genetic variation is baked. The rapid turnover of spermatogenesis, whereby each primary spermatocyte finally results in 4 sperms (Compared to One Ovum resulting from each primary Oogonia), that's beside the very large number of sperms produced daily, that continues for years and year. While with the Oogenesis everything really finishes at the foetal life, the remaining is just maturation steps, nothing is new as far as change of genetic material inside the Oocytes is concerned, this is the state throughout most of the female's life.
When I look at the seminiferous tubules, and see all those layers of spermatocytes leading to sperms, I tend to think that there is even some small scale natural selection, that bad mutated germline cells would die off, and only the ones with good genomes would survive all the stages of spermatogensis, and possibly the ones with beneficial mutation might have an advantage in survival in that milieu and even might have better chances of fertilizing the ovum?
Not only that, the testis seems to be more exposed to stressors inside the body and even to direct external environmental stressors, while the Ovaries lying deep inside, seem to be more protected. The Oocyte actually "selects" one sperm, so it's rule is selective rather than productive of change.
All of that makes one think that it is the male germline cells that could mediate high mutation rate in response to stressors, or even without stressors by virtue of the very high production rate of germline cells for very long periods of time. It seems that this is the real source of beneficial mutations that would ultimately drive evolution.

Four connected questions:

Is the mutation rate in male germline higher than in female germline?

If Yes, then doesn't this mean that Males are more likely the source of most beneficial genetic mutations, which is the main drive for evolution?

If 1 and 2 are true, then are we justified in inferring that "being the main source of beneficial genetic mutations" is the main purpose behind evolution of a Male sex?

Was this idea proposed before?

I read until It's clear that the main source of evolution is the first process, since the second process only acts on what results form it. It depends upon what you mean by "evolution" in this sentence. And even when well defined you are likely to fall into both semantic issues in decoupling the effect of each (see for example shifting balance theory) and also into issues of estimating the relative effects of each. In any the relative importance of these two processes have been a long lasting debate in the field.

@Remi.b, possibly you mis-understood me. By the first process I meant "mutations and migration", and actually mutations mainly, it is those that are the SOURCE of genetic variation. Natural selection is not the source of variation, it acts to cut down a pre-existing variation. A butcher can hardly been seen as the source of meat. The cow is. By source I mean what manufacture the basic material of some process to be possible in the first place. Neither natural selection nor genetic drift manufacture genetic variation, evolution is change in genetic variation over generations... to be continued

..continuation, so by definition without "genetic variation", evolution is not possible, so the 'basic material' that is needed for evolution to happen is 'genetic variation', processes responsible for manufacturing this variation are mutation and migration. Natural selection and drift do not manufacture genetic variation, they actually act to de-limit it, i.e. disposing of some of it. A process hat act to decrease some material cannot be deemed as the source of this material, it is a source of change on this material yes, but not of this material itself.

I'm voting to close this question as off-topic because this is the presentation of a theory disguised as a question by the well-worn “am I right ?”

@David, but this is not a theory?! its an impression.

@David, I've edited the question.

@ZuhairAl-Johar You should focus on one question at a time. Otherwise your post would be considered too broad. While a good background is appreciated, an extensive one just becomes too much and buries the main question. Be terse and include all the relevant background but nothing more than that.

If I actually understand your premises, which is a big if, you're asking if the genetic material in the sperm has been subjected to more mutation than its counterpart in the egg... by the time of mating. In case of humans, where's there's a lot of research and the answer is almost certainly yes.

Recent [GWAS] studies have shown that 76% of new mutations originate in the paternal lineage and provide unequivocal evidence for an increase in mutation with paternal age.

The general theory how this works (which you seem to repeat) goes back to...

Haldane (1947) suggested the following general mechanism for the sex differences in mutation rate: “The primordial oocytes are mostly if not all formed at birth, whereas spermatogonia go on dividing throughout the sexual life of a male. So if mutation is due to faulty copying of genes at a nuclear division, we might expect it to be commoner in males than females.”

As for [your] choice of terminology...

Subsequent estimates of a higher mutation rate in males from molecular genetic data led Miyata et al. (1987) to suggest that evolution is “male‐driven.”

And a more contemporary term is male-biased mutation:

The concept of male-biased mutation has been thoroughly analysed in recent years using an evolutionary approach, in which sequence divergence of autosomes and/or sex chromosomes are compared to allow inference about the relative contribution of mothers and fathers in the accumulation of mutations. For instance, assuming that a neutral sequence is analysed, that rate heterogeneity owing to other factors is cancelled out by the investigation of many loci and that the effect of ancestral polymorphism is properly taken into account, the male-to-female mutation rate ratio, am, can be solved from the observed difference in rate of X and Y chromosome divergence. The male mutation bias is positively correlated with the relative excess of cell divisions in the male compared to the female germ line, as evidenced by a generation time effect: in mammals, am is estimated at approximately 4–6 in primates, approximately 3 in carnivores and approximately 2 in small rodents.

Finally one needs to be careful what one means by variation because...

The creation of genetic variation by recombination can be a much faster process than its creation by mutation.

If we could somehow turn off mutation, in a large population meiotic recombination would still result in new combinations in offspring for quite a while. Eventually, after this combinatorial space is exhausted, we'd only see organisms that repeat something that is already living or has lived in the past.

So, I've dealt with your 1 & 4. As for theories why we see this male-bias in mutation... (your 2-3) it gets more complicated:

A general theoretical perspective is that level of mutation is a balance between deleterious mutations reducing fitness, advantageous mutations increasing fitness, and cost in fitness from mutation repair mechanisms to reduce the mutation rate (Sniegowski et al. 2000). The relative importance of these factors may vary but because most mutations are generally less fit than the present wild type, selection generally should act to reduce the mutation rate by improving the repair mechanisms. However, the strength of indirect selection changing the mutation rate, either increasing it or decreasing it, is quite low and is on the order of the change in the mutation rate caused by a modifier locus (Sniegowski et al. 2000).
Using the context above, sex differences could be the evolutionary result of selection for a more efficient lowering of the detrimental mutation rate in females, a retention of a higher advantageous mutation rate in males, less cost for lowering the mutation rate in females, or a combination of these factors. One evolutionary hypothesis for sex differences in mutation rates is that there may be different selective optima in the two sexes balancing the deleterious mutation rate and the cost of efficient repair and replication (Ellegren 2007). More specifically, if we assume that the major impact of selection on mutation rate is to minimize the mutation rate per replication as much as possible to reduce rate of deleterious mutation, then any sex differences observed in mutation rate may be related to the different number of replications in the two sexes. In other words, if the major impact of selection is to reduce mutation rate as much as possible, it has been generally more successful in females, either because of more male replications or because repair mechanisms are more efficient in females than males for some reason. Consistent with this, Crow (2000) suggests that an increase in mutation rate at later reproductive ages is not surprising. His reasoning is that until recent times few men would live into their forties so there would have been little selection pressure to reduce the detrimental effects of mutations from older men. Or, the sex differences in mutation rate may not have a strong evolutionary basis and are primarily the result of sex differences in gametogenesis.

As you can see, like most theories regarding the evolutionary reason for some mechanism that itself affects evolution... it's not settled science.
So, regarding 2-3. I think I get your point that if we pick a mutation that has survived until today, there's higher chance it came from a male (2). Even if this is true, it implies little about the evolution of sex-bias in mutation.
You infer (3) that

"being the main source of beneficial genetic mutations" is the main purpose behind evolution of a Male sex

I think the discussion is getting more into philosophy than science at this point. As previous long quote says, it could simply be that natural selection was bad at reducing something that is, on-average, detrimental, but was worse at reducing it one group, i.e. in males, e.g. because it's harder to reduce there. So, assuming that's the case, the "main purpose" of evolution could have been this reduction, and the fact that beneficial mutations (like all mutations) are more often traced to males, is just a statistical artifact of the (mutation reductive) "main purpose".

Yes recombination is a source genetic variation which is why sex is there for, and Migration also acts by adding recombination, however as you said once its exhausted, it cannot push further. However as far as recombination is concerned male and female contribution seems equal. Its mutations that seem to be male driven. Not only that the conditions for a sperm to be produced, live and travel are pretty much harsh condition, as if a kind of small scale natural selection occurs, only those sperms with genetic contents that enable them adapt to the sexual tract environment would survive, cont...

continuation... this small scale natural like selection might be a kind of selection for sperms with beneficial genetic material, so it appears as if all of this is made deliberately to make the male system a machine of producing beneficial mutations to push the wheel of evolution forwards. Of course a side effect to that, is that it can be harmful as well. It appears to me form that, that the male sex from evolutionary  biology point of view is meant to be the Ore of genetic variation necessary for evolution.

I didn't say that mutations are always beneficial! On the contrary I've explicitly said that there is a side effect to that, which is production of harmful mutations. However, I see the complexity you are referring to.

@ZuhairAl-Johar: indeed, I should have said "on average".

Well your addition, seem to even further support the view point presented here, that males are primarily meant to be the source of beneficial mutations! The female sex plays the part that reduce harmful mutation rates, i.e. it plays selective role, and the cost in fitness regarding repairs is related to females.

even on average definitely mutations that are deleterious are much more than the beneficial ones, the male seems to be the source of both kinds of mutations the good ones and the bad ones, and the latter ones are of course more! The point I'm raising is not that. I think that of all beneficial mutations the proportion of those that comes from the male is much much higher than those coming form the female. Therefore as far as the source of good mutations that fuels evolution is concerned, the male seem to be the main producer! But it comes at a cost of course, hereditary disorders!

I don't know why you say "some of my premises is wrong", which ones? what you wrote in the two brackets is what I said actually?

@ZuhairAl-Johar: I've moved that discussion to the end and gave it a bit more thought.

@I see the point of view present there, as you said it becomes complicated. But I get the feeling that it is not correct. Its a little bit twisted. But of course its a possibility.

@ZuhairAl-Johar: Here's another possibility: If we assume we are at mutation-drift balance (a big if), and in males it's harder to reduce mutation, then the average mutation rate (male + female) /2 would be optimal. But it would not have this value in either group.

@Fizz How would the hypothesis that a selection on mutation rates is behind the observed differences explain why oocytes are only produced early in the female life amd stay quiescent rather than generated continuously but with a slow generation rate?

@Fizz, I'm afraid I cannot comment on your last possibility. I don't know what you mean by optimal?

@Cell: I don't think it tries to explain that.

I should have mentioned that the female has mitochondrial DNA. which is a source of genetic variation that males do not supply. However I think the higher mutation rate of males germline out-weights that. Actually even regarding richness due to recombination, its the male that is the source of sexual difference, so in some sense it contributes a little bit more to genetic variation that females even through re-combination.

The argument you've cited in the last lines, would culminate as you commented in the result that the males being the main source of beneficial mutation is just an artifact of failure of the main purpose behind sex evolution in males. I don't like that. However even if we assume this, still it doesn't change anything, still the primary source of evolution is the male sex whether that was an artifact or not, I tend to think that it is not an artifact, the artifact and the cost paid to gain these beneficial mutations is the inevitable occurrence of the harmful mutations.

Yes. The rate of de novo mutations has been found to be higher in paternally derived DNA from several papers. A recent paper from a quick search [1] found that ~80% of 15,746 de novo mutations in 225 families were paternally derived.
Based on the total mutations yes, but they are also even more likely to bring deleterious mutations. So per base probably not.
That doesn't make much sense. Consider a lowly prokaryote organism that replicates asexually. The replication process is not much different than spermatogenesis. So it doesn't explain why sex differentiation occurs. More likely sex differentiation occured to promote genetic diversity (by preventing self-replication) and rather than the male sex evolving towards increased gamete replication, the female sex evolved towards decreased  gamete replication due to selection against pregnancy at older ages (when the body is more fragile and sensitive to giving birth). This is just my speculation I have no references.
Yes. It's called Male-Driven Evolution. [2].

[1] Parental influence on human germline de novo mutations in 1,548 trios from Iceland. Jonsson, H, et al. 2017
[2] The rate of spontaneous mutation of a human gene. Haldene, J.B.S.1935


text:
Near-zero water loss in a closed hydroponics system?
I know there are a lot of factors that would impact this...

Plant type.
Plant neediness (i.e., even sibling plants will possess different needs, defects, etc).
Automation efficiency.
Water & nutrients quality.

And that is barely touching the surface, but assume that...

We only have 1 healthy adult (meaning fully grown) plant who transpires 90% of absorbed water. The other 10% fuels photosynthesis, cell growth, etc..
Its nutrient levels/requirements are (somehow) perfectly monitored/satisfied.
The hydroponics system is enclosed s.t. nearly all the transpirated water is reintroduced into the water supply, rather than evaporated.
The recycled water is kept clean & nutritious by an automated system.

So my questions are...

Is it possible to create a system where the aforementioned 10% accounts for the only loss of water?
Am I missing any other significant source(s) of water loss?
Are there implementation factors which would jeopardize the plant's health?

don't forget photosynthesis removes water from the system by converting it into oxygen and sugars. thats is why finding the right symbiotic fungi can be important too, they are creating the oxygen and sugar back into co2 and water.

@John "The other 10% fuels photosynthesis, cell growth, etc.". Introducing fungi is an interesting idea but I am not sure that it would be able to reclaim any of that 10%. Glucose gets converted to sucrose, cellulose, & (in times of excess, stored as) starches/oils/etc. Leaking anything back into the water wouldn't be in the plant's best interests. Also, fungi (like all living things) requires water so, if anything, its presence would hasten the rate of water consumption, no?

it would require more starting water, but fungi like animals coverts oxygen and sugars into water, it will never account for all of it but it will reclaim some of it.  You need to make differentiation between water that is lost from the system by being converted into other compounds vs water that is simply absorbed. I may be getting confused by what you mean by "closed system", Is water being lost to the atmosphere or is it an air tight system?

@John "The hydroponics system is enclosed s.t. nearly all the transpirated water is reintroduced into the water supply, rather than evaporated". I will read more about the fungi concept but would you like to take a shot at answering the 3 questions?


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How is it possible for phosphate to form two ester bonds in DNA replication?
I understand that in phosphodiester bond formation, two hydroxl groups on the phosphate molecule bind to the 3' and 5' OH groups on two independent pentose sugars. This is a condensation reaction, so two molecules of water are released.
I am just confused about the hydroxl groups on the phosphate. From what I know, the phosphate molecule looks like this.

How is phosphate able to do a condensation reaction with two pentose sugars if it has no hydroxide groups?
Thanks a  lot

It's catalyzed by a ligase, e.g. DNA ligase It's not a one-step process.

Orthophosphate is not involved in phosophodiester bond formation, but deoxynucleotide triphosphates and the 3'-OH on a deoxyribose of a growing polynucleotide chain. Consult a text book to see the actual reaction, as you are expected to do before posting here.

@David I read this resource https://teaching.ncl.ac.uk/bms/wiki/index.php/Phosphodiester_bond which stated that "In phosphodiester formation, two hydroxyl (OH) groups on the phosphate molecule bind to the 3’ and 5’ carbons on two independent pentose sugars." But isn't there only one hydroxide on each phosphate? Thanks

I said a text book. Berg et al. on NCBI Bookshelf is a reputable source. Read about the DNA Ligase reaction there, especially Figure 27.28 and 27.29. The DNA polymerase reaction (which forms most of the phosphodiester bonds) is described in terms of the enzyme mechanism, but the reacting species are shown correctly in Figure 27.12. Explore the rest of this book if you need more context.


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How do veins's valve pocket sinus tend to become hypoxic?
For context, this question relates to the formation of deep vein thrombosis as I read that hypoxemia in vein can trigger coagulation cascade and cause a thrombus to form in vein.
I read that vein's valve pocket sinus tend to become hypoxic due to vortical flow. The diagram I attached below has oxygen tension color coded with a gradient from red to blue; the darker the blue is, the greater the hypoxia.
However, how exactly does vortical flow have to do with hypoxemia in those regions? From my understanding, the lack of blood circulation in vein's valve pocket shouldn't affect the amount of O2 bound to the haemoglobin stucked in the vein's pocket? As veins are not permeable to O2 thus O2 can't escape into surrounding cells.
References:
Bovill EG, van der Vliet A. Venous valvular stasis-associated hypoxia and thrombosis: what is the link? Annu Rev Physiol. 2011;73:527–545. doi: 10.1146/annurev-physiol-012110-142305.
Mackman N. (2012). New insights into the mechanisms of venous thrombosis. The Journal of clinical investigation, 122(7), 2331–2336. doi:10.1172/JCI60229
https://www.jci.org/articles/view/60229

As veins are not permeable to O2 thus O2 can't escape into surrounding cells.

Veins are not like impermeable rubber tubes, they are 'living' structures requiring, like all cells, Oxygen and glucose to survive. Smaller veins get the O2 from diffusion, while the larger veins need help from vasa vasorum, small blood bessels that bring blood to the walls of the veins.
The innermost cells lining veins are epithelial cells. They also line valves.
In the picture you posted, blood is not circulating well behind valves. The cause of hypoxia is that epithelial cells are continually removing O2 from the blood.
When enough O2 is removed to cause hypoxia, the endothelial cells may become damaged by the lack of O2, causing inflammation and (possibly) potentiating clot formation.

Activation of endothelial cells by hypoxia or possibly inflammatory stimuli would lead to surface expression of adhesion receptors that facilitate the binding of circulating leukocytes and microvesicles. Subsequent activation of the leukocytes induces expression of the potent procoagulant protein tissue factor that triggers thrombosis.

Mackman N. (2012). New insights into the mechanisms of venous thrombosis. The Journal of clinical investigation, 122(7), 2331–2336. doi:10.1172/JCI60229


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Is Wikipedia a good source of taxonomy?
I have been quite interested in biology lately,and I would like to know whether it is a good choice to look up taxonomic information there.

totally depends. Depends on 1) if you want Linean vs phylogenetic taxonomy, 2) organism of interest, 3) taxonomic rank of interest, 3) area of the world, 4) how well-known/studied/interesting a taxonomic group is, 5) how complex or unclear the phylogenetics are, 6) how up-to-date or accurately stitched together the Wikipedia page is, 7) what sources (and their age + reception) are used to inform the Wikipedia page,  etc...

Perhaps equally important is: why do you care? If this is for any formal, professional, academic, or research-focused interest, then I'd say no. If you're simply curious how the world is all organized or learning about different groups of organisms then I'd say Wikipedia is more than adequate most of the time. Just go into it realizing it's not perfect or consistent, so sometimes you need to use outside (reputable) sources to help better inform what you're looking at.

Thank you! I am only a 15 year old student,so it is not for formal interest.:)


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Leaf-curling type spider southeastern US
I have a spider in my backyard in Mobile, AL.  It seems to have sewn itself up inside of a living water oak leaf.  I tried googling it but only came up with this Austrailian spider that does a similar thing, but not exactly.  Notably, there is no attendant web, just the folded leaf container.  The leaf has been folded twice into a perfect little tetrahedral home.  Here is a picture... I didn't want to disturb her too much:

What species is this beautiful geometer?

Scott, please try to get another image of the spider -- one in which we can actually see the spider :p. Thanks

I would expect this to be an orbweaver, as I've seen numerous examples of leaf shelters for these spiders.  Usually, they're associated with a big orbweb, though.  It's not going to be anything with an unpleasant bite, though, so it should be fine to gently open up (maybe have a bowl underneath to catch the spider when she drops out) and expose the occupant for a photo.


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When is really necessary to visit field to observe sample collection process?
I know this could be a bit generic question, but for the sake of providing context this applies to a Transcriptomics Thesis.
Yesterday I've seen two researchers discussing about if it was really necessary for a post-doc geneticist to visit the place where the blood, weight, height, hair (and other) samples are taken.
From your experience, it is really necessary for a post-doc to travel and visit the field? Does that add real value to a Thesis? Shouldn't the sample collectors report everything like their name, how they measured a sample, etc?

This may be better on Academia.SE

After being a lab tech, just because they should report everything, doesn't mean that they are doing exactly what you think/wish. I would say it is important so you can see if the process of sample collection and processing is exactly what you need for your thesis. I had to follow a written report on how to feed a certain insect, after a few nights the post doc came in and realized there was something missing from the report and we were feeding the insects one the wrong side of the leaf. May not happen to you, but I think its always good to verify.


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Why is urea not converted to ammonia in the body?
After the liver processes metabolites to produce urea and other by-products, these travel in the blood to the heart, then they are oxygenated, and some travel through the renal artery to the kidneys.
Urea in water can decompose into ammonia which is toxic, as mentioned in a textbook page no 170 (6), under production of ammonia.
Reactant and product are at equilibrium. Also a gaseous product, CO2, is present which could potentially escape during oxygenation of blood. Hence, according to Le Chatelier's principle, an equilibrium shift towards  the product is possible
NH2CONH2 + 2H2O → (NH4)2CO3 ⇌ 2NH3 + H2O + CO2
The chance of urea decomposing into ammonia is high while travelling in the blood (i.e taking long route) and in the bladder, but it still does not happen. Why not?

best to ask 2 different questions. Just ask this: Why does urea not decompose into ammonia inside the bladder? 1 phrase, simple, easy to read. urine degradation is also decomposition.

I tried to rewrite it very concisely. It's an interesting question. Apparently uric acid is responsible for half of the blood's anti-oxidant potential, despite the blood having a pH of 7.35. At that pH and temperature, ammonia can become gaseous and toxic. Urine has a pH of 6, so it has excess H+, so the ammonia would mostly become ammonium NH4, which is 100 times less toxic than ammonia. The nitrogen cycle in aquariums and in plants is something that helps to understand ponds, tap water, plants, aquariums, so i am always interested in the nitrogen cycle.

it's worth noting that the white substance from bird and lizard poop is uric acid. Fish produce a lot of ammonia, and they also have bacterial symbiosis in their gills to absorb it, and water based animals can produce ammonia directly because there is an excess of water, whereas most land animals have had to adapt to nitrogen waste with limited water.

Another info is here, from reading about fish, that secrete 90% of nitrogen as ammonia/ammonium. it sais: most of the ammonia in fish blood is ammonium ion. side note: pK of NH3 = 9-10; fish blood = pH 7.4) i can't explain that though.

@com.prehensible Can you write your comments into an answer?

I don't know the real answer, perhaps it's from the acid dissociation constant, the blood plasma, the time of urea conversion? and I don't know the real reason, I don't know biochemistry. Apparently NH3 ammonia can go through cell walls and NH4 can't.

The answer to this question is quite simply this:

The activation energy for the uncatalysed reaction is such that the
  amount of decomposition of urea in aqueous solution at blood temperature and
  pH is negligible in the time taken for the transfer of urea to the
  kidney.

The literature supporting this is very old, so I shall first cite a relatively recent (2004) and (I think) freely available paper by Robert P. Hausinger on urease in which he writes:

The substrate [i.e. urea]  is highly resonance stabilized (30 to 40 kcal/mol), thus
  decreasing the reactivity of its carbonyl carbon so that spontaneous
  hydrolysis of urea has never been observed. Rather, urea decomposes
  in solution (with an estimated half-life of 3.6 years at 38°C) by
  the slow elimination of ammonia to form cyanic acid (17)

Reference [17] is a paper by Zerner in Bio-organic Chemistry from 1991 which requires a library subscription. In effect it quotes the same half-life:

The urea molecule is very stable. Between pH 2 and pH 12, the
  nonenzymatic decomposition of urea in aqueous media is independent of
  pH and has a half-life of 3.6 years at 38°C (36-38).

References 36 is a book written in 1923, and references 37 and 38 date from 1942 and 1955, respectively. I have not checked the latter, but can if anyone demands it.
All of which is not surprising, as the purpose of the urea cycle in mammals (etc.) is to eliminate toxic ammonia, and, as @Fizz points out, the enzyme urease is needed by bacteria that utilize the compound.

[Partial answer]

[OP claim:] Urea in water can decompose into ammonia which is toxic.

Probably not as easily as you think. If Wikipedia is correct:

Urea alone is very stable due to the resonance forms it can adopt.

Some bacteria use urease to catalyze the reaction by 14 orders of magnitude (says Wikipedia).
There are some primary sources from the 1930s on the resonance forms of urea; I've not read them just yet.
From experimental data in solutions (not blood), urea would be close to its maximum stability in blood, pH-wise at least:

The stability analysis shows that urea is more stable at the pH range of 4-8 and the stability of urea decreases by increase in temperature for all pH values. Within the experimental range of temperature and initial urea concentration values, the lowest urea degradation was found with lactate buffer pH 6.0. The urea decomposition rate in solution and pharmaceutical preparations shows the dependence of the initial urea concentrations. At higher initial urea concentrations, the rate of degradation is a decreasing function with time. This suggests that the reverse reaction is a factor in the degradation of concentrated urea solution.

As for the reaction speed in terms that even I can understand:

The urea molecule is very stable. Between pH 2 and pH 12, the nonenzymatic decomposition of urea in aqueous media is independent of pH and has a half-life of 3.6 years at 38°C.

(This review cites data from older papers, so presumably they had less sensitive methods, so they concluded a wider pH range where it's most stable.)
For the chemistry experts, there exists a lot more information on the kinetics of the reaction.

In effect you are saying the question is based on a false premise, a point of view I imagine is correct, in which case I would vote to close. However neither you or the poster have given any figures for the rate of the uncatalysed reaction. Could you find some so we can resolve this definitatively please.

@David: I'm trying. The best I found is not in blood, but in solution. https://www.ncbi.nlm.nih.gov/pubmed/25043489 I'll have to access the full paper for the details...

@David: I found more urea chemistry than I can handle right now: https://hal.archives-ouvertes.fr/hal-01449373/document

Blood is likely to be irrelevant. Water will do. I’ll have a look later if you can’t find the info yourself. However the poster should be made to justify his claims or withdraw.


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Do orcas react differently to swimmers in orca-like dresses?
Question on animal behaviour. This video shows the trainers of the orcas in swimming pool with them. Why do they use orca-like dresses? Is it just for the show, or do orcas then treat them more peacefully? :)

there is an "ethology" tag already :)

To close-voter(s): this question can definitely be answered without the use of opinion, so I disagree regarding the VTCs. I vote to keep open.

This is hard to answer and doesn't seem to have been directly studied anywhere. However, my guess is that it's just for the show. Orcas readily eat penguins and Commerson's dolphins, which are both at least as 'dressed like' them as the humans are in this picture.


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The effect of salt, pH and temperature to the salivary amylase
If I prepare the following set of tests, incubate for 15 mins, then add 2-3 drops of iodine solution to each test tube:
Salt test (1ml starch solution + 0.5 ml enzyme + 1ml 1M NaCl, incubate at 37 oC
Acid test (1ml starch solution + 0.5ml enzyme + 1ml 0.5HCl), at 37oC
Alkaline test (1ml starch solution + 0.5ml enzyme + 1ml 0.5M NaOH), at 37oC
Temp test (1ml starch solution + 0.5ml enzyme + 1ml H2O), place in water-bath
(75oC)
What is the effect of salt, pH and temperature to the salivary amylase? I don't know what exactly how salt effect.
high temperature will denature the enzyme.
How about salt?

Sounds like a homework question to me. 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.

At extreme pH (too acidic or too alkaline), the salivary amylase will be denatured.
At salt, the addition of salt will affect osmolarity and hinder the reaction.


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Reasoning for Stomatal Distribution Between Monocot and Dicot
When you compare the stomatal arrangement of bean and corn plants under a microscope, you notice that the corn's stomata arrangement is much more organized and linear then the beans. I am wondering whether there is an evolutionary explanation for why that developed?
One thing to note is that the morphologies of the epithelial tissue cells are very different, so maybe it is a natural consequence of that?

Wouldn't this be a natural result of the differences in veining in the leaves?  The parallel veins in the corn leaf would constrain the placement of the stomata to the rather linear area between the veins.

Sounds plausible, can you provide some reference?


text:
Can flow-FISH be used on metaphase cells?
I know flow-FISH can be used on interphase cells but was wondering if it only works on interphase cells or can work on cells regardless of stage in the cell cycle.

Don't know if this will help but Maurizio Carbonari in cytometry A in 2016 published on methods which allow for cell cycle analysis.
The abstract

Formamide has long been one of the most widely used reagents in the study of nucleic acids. However, the use of formamide for treating cells to be analyzed by flow cytometry is a recent development and is restricted to measuring telomere lengths by flow‐FISH. In this field, we have published several papers in order to observe the effects of formamide treatment on cells at room temperature. We therefore discovered that, with suitable modifications, a short and simple incubation in this ionizing solvent facilitates cell cycle analysis by flow cytometry, equivalent or superior to that obtained with treatments in alcohol, acetone or detergent in hypotonic solution. Even using a bulky and problematic stain (low quantum efficiency and G‐C base preference), such as 7‐aminoactinomycin D (7‐AAD) which, on the other hand, has the advantage of being excited at 488 nm and does not bind to the RNA, it is possible to obtain excellent coefficients of variation and (G2–M) mode/(G0–G1) mode ratios. These parameters, especially if stained cells are washed before acquisition, arrive at optimal values. It is noteworthy that the ability to wash the cells stained for DNA content analysis without affecting the stoichiometry of the staining has not been described elsewhere in the literature. With formamide treatment the doublets are practically absent, sample recovery is efficient, as well as the preservation of physical parameters, and the stained cells can be stored for at least 10 days at room temperature before acquisition.

As for Flow-FISH, it is a method used to measure telemore lengths.
Vyacheslav I Borisov et al. in Current Protocols in Cytometry. 2014
Published on applying flow-fish to look at M phases.


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Tiny light-colored bug ID in Amman-Jordan
Can you please help me identify this bug I keep finding inside my home in Amman-Jordan. Mostly on the wall and once on the bed sheet. Too small to be noticed and too light colored. I used my flash light and zoomed with my mobile camera to be able to take photo.

Hi, for proper identification you should provide, the region / country you saw it, and ideally the season and the habitat (in the wild, in a house, etc...). Apart of this the pictures should be in a good resolution and focus, your latest pic is not perfect but the two others are probably useless as too blurred. I recommend you to edit your question.

That's the est best photo I could take with my mobile. Is it by any chance bed bug nymph?! I live in Amman-Jordan

@Rashah it is not a bed bug of any kind. See Insect identification - Is this a bedbug? for more info for IDing a bedbug. Your insect is a psocid (or book louse), which you can read more about in the post that yours has been marked as a duplicate of. (See the link at the top of the page)


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A speculative question about sensation
I know this is rather speculative and I am not a biologist, but I have womdered about this for a long time.
I have always been able to pinpoint the central line of any part of my body exactly as if there were some nerve running through it. For example, given a pen, I could trace the line dividing one of my toes precisely. I, in some way, sense that the pencil is exactly at the middle?
 Is there any physiological reason for this? Is this true for everyone or is this an illusion peculiar to me?

given a pen you can trace a line anywhere on your body. This is becasue humans have Proprioception.  we can sense the movement of our muscles, tendons, and joints and track the location of every element of our body. Using this we can control our body precisely without other sensory input. It takes time to completely master this but most people have done so by the time they become adults.


text:
Trophic levels and energy loss
Just a general question about trophic levels. Traditionally, it's thought as much as one order of magnitude of energy is lost as one moves from trophic level to trophic level. I am confused here since it seems to me the energy content of certain primary consumers is more if not equal to an equal number of producers. Take a 1 acre lot of grass vs a 1 acre lot of cows; surely the calorie content in the cows is more than that in the grass no? A one ounce cut of beef has more calories than an ounce of grass. I could imagine for plankton or insects, maybe the energy content is not as conserved since they can store less energy and eat less. So my question is whether this one order of magnitude drop is a rule or just a 'rule of thumb' or if I'm framing the whole thing wrong.
Thank you

1 acre of grass will not feed 1 acre of cow. in fact 1 acre of grass feedson good grazing on average 1 cow.  An acre of grass produces about 10,000lbs of grass dry matter in a year. which feeds 1000lbs of cow for the same time.

To second @John, standing biomass $\neq$ to production. Grass production is $>>$ consumer production. Because grass is consumed and turned into consumer biomass (in this case, cattle), and because the cattle aren't being consumed, the standing biomass is greater in the cows than the grass.

Also equal cuts of grass and beef have about the same calories, humans just can't access most of the calories in the grass.


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Animal reproduction when resources are scarce
(This question is aimed at animals that take care of their young, e.g. dolphins.)
As I understand it, most animals reproduce if possible. The only way they don't is because they run out of resources. I'm wondering how this shows up in practice:

Do they simply not have sex? If so, does this mean they don't have sex drive?
Do they conceive and then let their children starve to death?
Do they fail to conceive (that is, are there biological changes to a mother who's not getting enough food such that she is no longer fertile)?

Option #2 seems the least likely to me because presumably pregnancy involves a cost to the parent, and with resources already scarce this would be a waste; however the plot of White Fang does indeed involve this situation (I have no idea how scientifically accurate that book is however).

Rabbits reproduce when resources are scarce. They then eat their young. There are many more options than the three you present. Consider, for example, that nutritionally challenged females might not have an estrus cycle, which would prevent pregnancy. Humans reproduce when resources are scarce as well, and it does indeed take a great toll on mothers and children. But it happens anyway.

@anongoodnurse by the second law of thermodynamics, wouldn't it be more resource-intensive to produce children and then eat them? Not having an estrus cycle would be similar to option #3. As for humans ... I'd say that's out of the scope of the question.

Humans are animals, too, and where sex is concerned, dolphins are like us. So, not outside of scope imo.

Different animals use different strategies and all the three mechanisms are valid and there possibly are even more. Moreover, the laws of thermodynamics are applicable to particles and not organismal behaviour. Organisms need to choose the "theoretically most optimal" strategy for different reasons.

I think this is probably too broad to be answerable, for the reasons pointed out in the comments. From a selection standpoint, you have to consider that resource scarcity can fluctuate, and an organism that fails to mate today does not have an opportunity to take advantage of an increase in resources in some future months. There are also a limited number of opportunities to ever reproduce: for some animals, even those that raise their young to some extent, there is only one chance ever. Consider that, on average, a given individual will produce ~2 offspring that grow up to successfully breed.

@BryanKrause I'm not thinking about that though - in this question I'm flat out assuming scarce resources, and wondering how that translates to lack of population growth.

This is actually a comment, but was not allowed to comment.
I think what you're interested is more in population dynamics and I think what you're really asking about is more in line with what system of  differential equations explains a network of animals and how their populations grow and decrease with the amount of resources and the species population.
I think the problem is that, there's actually no good model, because there are so many factors which seem to contribute to shifts.
@ MIT this year, they had a visiting prof from Tufts give a talk on this, and they're working on models, to try and describe this, and even HE- the prof said, yeah, it gets complicated even for two species.
I would recommend, that if you have time to read up on this?
https://sites.tufts.edu/hening/publications/ <--- a link to his publications
https://arxiv.org/abs/1710.01220
Also, this is probably more a question for the mathematics stack.

I'm not more interested in population dynamics unfortunately. This is a biology question, not one about differential equations.

@Allure - It's kinda sad that you don't recognize a good and helpful answer when given one. You think the user who answered isn't giving you a "biology" answer?

ThermoRestart, thank you for this insightful and helpful answer. I hope we get more answers from you.

@anongoodnurse considering I asked the question you'd think I'd know what kind of answers I'm looking for. They are of the kind that "so-and-so species adopts strategy #1, this one does #3, nobody does #2, and there's #4 which you haven't considered". This answer is inapplicable to what I had in mind. I'm not going to downvote it, but I'm not going to accept it either.


text:
How many nutrients do trees process daily?
Is this tree fact below that I have found on social media sites true? I don't know the source of the quote. It's pretty amazing. I'll be glad if someone can provide the source too!

Natural Wonders
Every day, a 40 foot tree takes in 50 gallons of dissolved nutrients from the soil, raises this mixture to its topmost leaves, converts it into 10 pounds of carbohydrates and releases about 60 cubic feet of pure oxygen into the air.

There are 1000s of tree species that all vary in anatomy, morphology, & physiology; so, this type of generalization seems inappropriate & misleading. 2 trees of the same size but of different species would surely absorb/process nutrients at variable rates & in varying quantities. Further, even 2 trees of the same species would not experience consistent nutrient uptake & processing if environmental conditions (e.g., temperature, water availability, humidity, soil type, etc.) varied b/w each. Finally, trees of the same size aren't necessarily the same age, & age would impact these processes, too

I don't know much about trees, but I was very skeptical about this post at first. If this web page is correct, then the post is actually not so far-fetched.
Trees are amazing. According to the page, the average tree absorbs 10,000 gallons of water and uses 1000 gallons, evaporating the rest. 24 gallons of water contains one pound of dry matter. That means that the average tree would accumulate almost 42 pounds of dry matter in a single day.
Now, I certainly cannot vouch for the credibility of the website, but it was difficult to find a page that showed the numbers, so take it with a grain of salt and try to find other sources that back it up or counter it.
Here's the link: https://www.thoughtco.com/process-of-using-water-by-trees-1343505

We found the following link when search on the quote, the information is cited there:  http://gibneyce.com/tree-stats---classics.html
Cristina Hubbard, Executive Director
Forest Web

It's vague and hyperbolic.
The USGS water page says that a big oak tree can evaporate 40,000 gallons per year, that's 400 gallons per day for the growing season.
This page also disagrees with the quote, giving less than half the figure, about 400 gallons per day for a 40 foot tree.
A 10x10 meter square of forest gains about 4 tons of weight per year, 11kg per day, so that fits in with the quote's estimate of 10 pounds per day.
So there is some truth to the quote for a hot day, it's overly generalized and vague.


text:
When are neuropeptides loaded into vesicles?
It is well known that small neurotransmitters like monoamines (dopamine, serotonin, etc), acetylcholine, glutamate, etc are loaded into vesicles at the axon terminal. Stated differently, synaptic vesicles,SVs (which are the name of the vesicle type that store small neurotransmitters), are made locally within the axon terminal, and then ultimately loaded with small neurotransmitters.
However, I cannot seem to find when larger molecules, like neuropeptides, are actually loaded into their vesicles. I know that neuropeptides are made in the soma, but I am unsure of when they are loaded into their vesicles.
Are neuropeptides loaded into their vesicles at the synapse?
" Small-molecule neurotransmitters are synthesized locally within the axon terminal" https://web.williams.edu/imput/synapse/pages/I.html
"As a rule, the synthesis of small-molecule neurotransmitters occurs within presynaptic terminals" https://www.ncbi.nlm.nih.gov/books/NBK11110/
"SVs are made locally at the terminals and are regenerated after exocytosis"  https://www.sciencedirect.com/science/article/pii/B9780080450469013929

Can you cite your sources? There are major errors in your question, almost all of the things you say you "know" are incorrect.

here are the citations. If the small molecules are synthesized locally within the axon terminal, they are clearly being stored in the vesicle within the axon terminal. This is the general dogma of vesicular packaging.

What about the rest of your statements? You've cited only the things are correct, you haven't corrected anything that is wrong.

I am unaware of any of my statements being wrong. Could you please enlighten me? I am not trying to promulgate false information. These are my understandings of concepts.

" Stated differently, vesicles are made in the soma, shipped down to the axon terminal (via motor proteins), and then ultimately loaded with small neurotransmitters." is wrong.

Thank you for catching that. I was unaware that synaptic vesicles were strictly produced from the recycling process at the axon terminal.

This paper is very interesting: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4194108/
and wonderfully highlights how motor proteins and endocytosis work together to create the SVs that are ultimately loaded with small neurotransmitters

Neuropeptides are packaged in the soma via the Golgi into dense core vesicles, similar to how other types of secreted proteins are packaged.
These vesicles are transported to axon terminals where they await release signals.

Sossin, W. S., Fisher, J. M., & Scheller, R. H. (1989). Cellular and molecular biology of neuropeptide processing and packaging. Neuron, 2(5), 1407-1417.
Wong, M. Y., Zhou, C., Shakiryanova, D., Lloyd, T. E., Deitcher, D. L., & Levitan, E. S. (2012). Neuropeptide delivery to synapses by long-range vesicle circulation and sporadic capture. Cell, 148(5), 1029-1038.

Do dense core vesicles also have all of the traditional synaptic transmembrane proteins in them like synaptotagmin and synaptobrevin? Or are those specifically unique to the "synaptic vesicles"

@S.Cramer At least some of them do. Some are not released by calcium so I'm not sure what machinery they have for membrane fusion.

Interesting. I ask because the one article that I mentioned in the comments above (about "synaptic vesicles") explains that the specific transmembrane synaptic proteins are only incorporated into the vesicle once the components have FIRST merged with the axon terminal. Then, via an endocytosis process, these transmembrane proteins are somehow selected to be included in the synaptic vesicle during its assembly. If you're saying that "at least some of them do", then clearly these transmembrane proteins are being incorporated in to the vesicle membrane in a very different manner. Cheers~

Can you point me to where in the article you see that?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4194108/
In figure 3, it looks as though the particular proteins that will be used for synaptic vesicles are first shipped to the synapse via a standard trafficking vesicle. Then, upon arriving at the axon terminal, this trafficking vesicle fuses with the axon terminal. Thereafter, an endocytotic process incorporates these "deposited" proteins into the synaptic vesicle. That's how I am interpreting the figure, at least.

Ah I see, well for the small molecule vesicles of course that is the case because they do not come pre-packaged and are recycling membrane from the synapse. It's possible that dense core vesicles undergo some merge with an endosome at some point, I'm not sure though, I'd have to research that separately. I just know that at some point some of them will contain synaptotagmin.


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How do I homogenise a small pellet of 10 to 50 cells within less than 50 µL?
I have a problem with declumping/ homogenising bacterial cells in small volumes (10 to 50 µL). I know that I can get all of my cells out of the tube, but they are still stuck together and won't form separate colonies on an agar dish.
I know that because when I take the last 50 µl from a 1 ml tube and put it in a new tube and mix the 50 µL with a larger volume (e.g. 100 µL), we get a higher CFU count.

Just to be sure: is it really 10-50 cells in your pellet? Or is this a typo and its rather 10-50 x 10^6 cells  or similar?

Thanks for the quick answer! Yes, there are only 10 to 50 colony building units in the 50 µL pellet!

What homogenisation method(s) did you already try?


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Coronary circulation
It is said that the coronary artery that gives the posterior descending artery(PDA) determines if the heart is right dominant(most cases) or left dominant. Is there any reason to this? Why PDA?

Where/ By whom is that said? Could you please provide a reference?

source, please...

This is purely an anatomical definition: right dominant is defined as coronary circulation where the PDA (posterior descending artery) is a branch of the RCA (right coronary artery) and left dominant is defined as coronary circulation where the PDA is a branch of the LCX (left circumflex artery). The Wikipedia article on coronary circulation is a reasonable reference for this question.
There's nothing else special about the statement "dominant" and it doesn't have any other importance for cardiac function, except that someone who is left dominant would have more serious issues if there is a blockage in their left main or LCX.
Typical human coronary artery anatomy consists of two ostia off the aorta, right and left. The "left main" branches fairly early on into the LAD (left anterior descending) artery, which follows the septum between left and right ventricles down the anterior side, and the LCX, which follows the 'top' of the left ventricle counter-clockwise (if looking down at the top of heart and rotating the heart so the atria are on top; in an actual human heart the atria actually point towards the midline a bit more than other species). The RCA travels in roughly mirror fashion, following the 'top' of the right ventricle in clockwise fashion. The RCA and LCX nearly meet on the other side of the heart, at the posterior septum.
In a majority of people, the RCA continues and follows the septum down to the apex (kind of like the LAD but on the opposite side). In a non-negligible minority, the supply of the posterior descending artery is either shared by RCA and LCX or is completely supplied by the LCX.

Thank you for the answer. Could you elaborate on 'someone who is left dominant would have more serious issues if there is a blockage in their left main or LCX' Please?   For wouldn't someone right dominant have equally serious problem with a blockage in left main artery?

@ADP Of course a complete left main blockage is pretty much fatal already, but I meant it just as to a matter of degree: the more of the heart is supplied by that vessel the more severe a blockage is. The same goes on the other side: someone who is right-dominant would have more severe impacts from a RCA blockage than someone who is left-dominant.


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How much does biomagnification affect human beings?
It is known that the effect of biological magnification increases with higher trophic levels. Since, we are at the top of the food chain, how much are we affected by it? Is there any proof of humans affected by biomagnification? And should we be worried?
Thank you, for your attention!
Edit: Before posting here I had searched on Google Scholar about 'effect of biological magnification on humans'. Not only I couldn't find anything specifically about humans, whatever I found were too complex for me to comprehend. (I'm not a student of Biology). Yet, some of those which I understood stated that, accumulation of substances upto hazardous levels poses health risk. What I am trying to know is that, have there been cases where we know biomagnification to have hurt humans?
Thank you again!

Short answer: yes. What has made you think otherwise? Your question suggests that you don't fully understand the concept of biomagnification -- the magnification takes place as you move up trophic levels . Being at or near the top would suggest we are strongly impacted by this phenomenon.

For an example, see warning labels about mercury in seafood.  (Seen recently on packages at the US Whole Foods grocery chain.)

@theforestecologist I understand the concept and I know it to be real. Neither am I thinking otherwise. Only I want to know should we be worried about it?

@TheDude What would you differently if you were worried about it?

@BryanKrause Honestly, I was curious and just wanted to know. But after seeing your question, I guess, depending on its level of impact, I may tell my family and friends to become vegetarians (so as to stay in a lower trophic level and be less exposed to it).

What is biomagnification?

Biomagnification is the process by which chemical contaminants increase at a far greater rate than thermodynamics would predict. Specifically looking at organic / lipid soluble compounds. A very basic explanation is that as food is digested and the lipids are absorbed, chemical concentration (see Fugacity) within the food increases as it travels along the gastro-intestinal tract. As we consume more of the contaminated food it accumulates in our bodies, and if a threshold is passed can result in negative physical effects in our bodies.

Have humans been affected?

Agent Orange - the US sprayed a significant amount of Vietnam with agent Orange, which contained dioxin. The persistent nature of the compound caused it to accumulate in the soil and vegetation, and eventually the contaminated vegetation was either consumed directly by the people, or by wildlife which in turn, could be eaten. The result was that even though the compound itself was relatively harmless to humans, as it travelled up the food web, the concentration increased via the mechanism described above. The same mechanism is what resulted in pesticides like DDT being banned in the 1970’s.

Should we be worried? (Opinion)

Of course it is something that we should be aware of, and there are some guidelines with eating seafood / fish. Aquatic and marine systems typically can support a higher number of trophic levels and as such we should pay much more attention to seafood. For example, around where I live we have Fish Consumption Guidelines ) that encourage people to limit the number of fish meals per month, especially for women who are or planning to get pregnant. This allows time for our bodies to remove the accumulating compounds before reaching dangerous levels. Therefore, you do not need to eliminate higher trophic organisms from your diet, just enjoy them in moderation and not excess. Knowing where your food comes from also helps in making these decisions.

Your wiki link mentions both the negative human impacts as well as biomagnification, but it doesn't explain in what way biomagnification of agent orange has impacted people. Please consider finding a source that supports your claim more directly. Thanks.

@theforestecologist - there is an entire section regarding health effects on the Vietnamese people. Are you asking for a more mechanistic approach?

Yes. Most people know (and your link provides evidence) that people are negatively impacted by agent orange. But we're also harmed by nuclear bombs and malaria. How exactly does biomagnification play a role in the harm that agent orange causes humans? I did not see anything from your article that explicitly made that link.

Minamata disease is another. https://en.wikipedia.org/wiki/Minamata_disease?wprov=sfla1


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Are SNPs always in linkage disequilibrium with other SNPs
Is it possible to have a SNP that is not found is be non-randomly associating with any other SNP?

Linkage disequilibrim is a result of two SNPs both appearing after a cross (e.g. in offspring).  As such even at great distances two SNPs could both appear in offspring 50% of the time.  Linkage refers to a non-random odds that two SNPs (or any other marker) will both appear together in offspring. (Equilibrium being essentially random linkage).
By this definition, SNPs on different chromosomes should have no linkage.  Typically linkage reflects that there is a chance of a crossover between the two SNPs that would cause them to not co-migrate.  The closer together in general the linkage is very strong - a crossover appearing between two mutations that are just a few bases apart is nearly impossible.

There can be a number of reasons for Linkage Disequilibriunm (LD). Here is a non-exhaustive (non-referenced also) list.

Random LD happens
Epistasis
A recent selective sweep
Hybridization
Population structure
Genetic drift can also create negative LD (see Barton and Otto, 2005)

Of course, in all cases, reduced recombination rate will help to create an LD and to retain it for a longer period of time.


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Why are babies rarely born with cancer?
Childhood cancer is fundamentally a disease of dysregulated development. Why does it rarely occur during the fetal period, a time of enormous growth and development?

"Childhood cancer is fundamentally a disease of dysregulated development." Can you please clarify what you mean in stating this? I'm a bit confused why you say this; I can think of lots of 'childhood cancers' that seem to be no different than those occuring in older adults. In fact, a number of cancers have a bimodal presentations, one in childhood/adolescence and then again in adults.

Nature tends to turn against cancer not towards it. Cancer exists when cells begin to multiply with abnormal features, without correction. Cancer is the consequence of many many harmful mutations, which inhibit the correct reading of DNA.
Cancer takes time to develop, not months, but years. Also, babies don't have old tissues, so there haven't been as many divisions, or as many opportunities for mutations, as a 5 yr old or a 10 yr old has gone through.
Although rare, Neuroblastoma is a cancer that babies CAN be born with. Nerve cells develop early, week 5 of fetal development.
Perhaps someone else could talk more about the biological mechanisms which really make cancer more a reality for older organisms, but probablistically, it doesn't make sense that a newborn baby would have cancer.
I looked up these links, to try and address your question.
cancer in general
https://www.cancer.gov/about-cancer/understanding/what-is-cancer
why cancer takes time to develop
https://sites.duke.edu/missiontomars/the-mission/cancer/why-do-most-cancers-take-so-long-to-develop/
cancer in babies
https://blog.dana-farber.org/insight/2015/02/can-babies-be-born-with-cancer/


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How to do a nucleic acid or genome and amino acid search
I have been looking to find a database where i can search for genome and amino acid search. Are there any open source databases available for the same.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

In my experience the most popular sequence database is https://www.ensembl.org/ (other databases are available, eg. NCBI).  If you have a sequence of either nucleotides or amino acids that you want to find matches for then the BLAST/BLAT search is probably what you want.

Really? Primary in what sense? Ever heard of NCBI?

I thought about that when writing.  I work in Europe, and I do not know anyone who uses NCBI rather than ensembl.  I shall alter my answer to indicate others are available.

I work in Europe too and have worked at EMBL. However I do not know anyone who uses ENSEMBL for database searching. Part of the reason is that the ENSEMBL interfaces have always been so much worse than those at NCBI because the latter had the money to make it a priority whereas I suspect EBI had neither the motivation nor the money. The worst on-line experience I have ever had was trying to submit RNAseq data to ENA.


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How are drugs distributed in regards to bone marrow?
I know that as volumes of distribution increase they correspond to the blood, then the vascular rich group (heart, kidneys, liver, brain if BBB permeable), then muscle then adipose. But things like flow should also be taken into account. So are drugs usually distributed in a similar manner to blood, vascular rich group, etc?

I guess this is about the distribution of a drug within the body?

Volume of distribution is a property of the drug and not the tissue. Your question is unclear.

Thank-you for letting me know, but can you explain further? I know that the volume of distribution is unique to a drug, but high volumes of distribution indicate the drug is preferentially stored in adipose; and that low volumes indicate it is retained in the blood. I am asking where the bone marrow would fit in the progression above. i.e. Are low Vd drugs stored in blood AND bone marrow? or Does the bone marrow retain drugs with a similar capacity to the VRG?

@RobyVicary Vd is an indicative of the drug solubility. Drugs with high water solubility are enriched in blood whereas the ones high lipid solubility (and hence low water solubility) end up in adipose. There are other factors too apart form solubility. However, pharmacodynamics is not simply determined by drug solubility. Your question should be rephrased and perhaps you should ask how much percentage of a certain drug in blood is present in bone marrow. Most bone marrows have good vasculature; so I would guess that bone marrow should have almost the same concentration as the blood.

How are drugs distributed into any tissue, and what affects it?
Note that there are no general answers, and that this is highly dependent on the drug in question.
Active or passive transport
Is your drug a substrate for any uptake or efflux transporters that may affect the distribution?
Solubility
Lipophilic drugs will generally have a greater volume of distribution, as there is more passive diffusion into tissue.
Blood flow
How much drug is presented to the area in question? Tissue with greater perfusion (e.g. kidneys) will have a greater exposure to the drug. Look up the well-stirred model.
Relating this to the blood marrow
So what should you research in order to answer your question?

What are the physiochemical properties of the drug in question? How are these compared to other drugs where the bone marrow is a target?
Is the drug a substrate for any relevant transporters in the tissue of interest?

You should also look up if there are any physiologically-based pharmacokinetic (PBPK) models for your drug or drugs with similair physiochemical properties. Some of these are free, and allow you to make general assumptions about the distribution of the drug.


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After how many hours water drunk is expelled from the body?
If one drinks a liter of water at 7 am when (in what span) will that water be eliminated through uresis?
Is that process influenced by any factors such as empty stomach, sleep or other?

The time from drinking to urination depends mainly on your hydration status and the presence of food in the stomach.
Scenario: You have drunk enough fluid in the previous days, so you are normally hydrated. In the morning, you get up from the bed, urinate, drink 1 liter of water in 5 minutes and eat nothing.
Some water can come through the stomach and can be absorbed in the small intestine in about 5 minutes; the entire liter may need more than 2 hours (sweatscience.com).
When some water is absorbed into the blood it can immediately trigger diuresis - the excretion of the urine through the kidneys into the bladder. It may take about 3 hours for the entire amount of water drunk to be excreted. So, the approximate time span (from start to end of water excretion) could be 5 - 180 minutes. But not likely the entire liter of water will be excreted, because, in the morning, you are in a slightly negative water balance, so some water will stay in your body.
If you are dehydrated before starting drinking, much less urine will be excreted in the first few hours.
If you drink after eating, the food in the stomach can delay water absorption and excretion by more than an hour. This also happens when you drink nutritional fluids, such as milk or juice.
This is from my experience and understanding basic physiology. I'll try to find some references.

Thanks for your exhaustive reply, I regret I cannot upvote your or any answer, but I'm sure others will see to it.Can you clarify one thing for me, since what you say clashes with my experience: waking up at about 7:30 am I drink in the excess of half a liter water and at breakfast I have some 30 cl of milk, then at dinner at supper little more water, yet 80% of diuresis takes place during the night between 10 p.m and 7:30 am. I thought it took at least 15 hours to excrete all the water !!

If I take literally what you said about 80% diuresis happening at night, does this mean you urinate 4 times at night and once during a day? The most common reason for frequent urinating at night in healthy people is drinking in the evening. Another reason is that when you lie down, some fluid shifts from your legs toward the heart and the heart detects this as an increase of blood volume, which triggers diuresis. Also, diuresis does not occur only due to drinking but because the kidneys constantly remove waste from your blood in the form of urine.

It is a hypothetical question which is not a true scenario I would try to explain the process of water absorption and excetrtion.
when a person consumes water it is absorbed into blood stream (liquid as well as in the form of water in food consumed). The amount of water absorbed in the stomach and how quickly water is absorbed depends, in part, on how much has been eaten. If someone is drinking water on an empty stomach, they are more likely to experience a faster rate of water absorption – as quick as 5 minutes after taking a drink. Whereas, if a person has eaten a lot of food before they drink water, the speed of absorption will slow down accordingly and absorption could take up to a few hours.
Approximately only 20% directly makes to the bladder remaining water would be utilized for performing vital function of the body.
Once the human body uses up all the water it needs to function efficiently, it begins the process of removing excess water.The water is not only excreted solely through uresis (urine is only 95% water), the other routes for water excretion is sweat, fecal route and saliva.Small droplets of water also exit the body via the breath.
As water is not excreted thought sole route is not possible to calculate the exact time taken for removal from the body.


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What is the best argument for maximum parsimony method in phylogenetic tree construction?
Beside the fact that maximum parsimony is computationally cheap, what other good arguments are there for it? Is there any model behind this principle? Why would one expect this principle to provide right phylogeny in any situation at all ?

I've programmed a phylogeny tree data parsing program which uses standard tree of life OTT files. I had never heard of maximum parsimony and the topic on Wiki exceedingly complex. They just say it's popular because it's simple. computationally speaking the data in pylogeny tree file can't actually be wrong if the tree does not contain errors unless you skip some nodes, a tree can easily be checked by counting the branches up and down from a species and into their shared nodes, and a check can't present an error. that said I don't know if the OTT even has taxon and information of that kind.

The idea of parsimony is that when constructing phylogenetic trees a simple hypothesis (e.g., four evolutionary changes are necessary to connect two taxa) is more likely to be true than a more complex hypothesis (e.g., 15 evolutionary changes) (source: Berkeley University).
The reason is that for a certain taxon to evolve, there must be a certain number of evolutionary changes. In the end, this happens by more or less stochastic processes (Dingli & Pacheco, 2011) that randomly generate genetic changes (mutations). The characteristics of better fit individuals survive, while those of the least fit are terminated from the gene pool. Hence, every additional change that must be adopted to create a new taxon from another means that the chance that that happens decreases exponentially; it's all a matter of statistics. The less the number of changes needed, the higher the chance that that might have actually happened.
Reference
- Dingli & Pacheco, BMC Biology (2011);9:41

Generally speaking, parsimony consists in not making unnecessary ad hoc hypotheses.
In the case of phylogeny, parsimony can be used at two stages: when inferring the number of character changes for a given topology and then when choosing among topologies.
One does not expect parsimony to provide the right phylogeny in any situation. It is just the most sensible we can do when no further information about evolutionary processes is available. This is why parsimony is a popular choice when it comes to deal with morphological data: models of character evolution are not as easy to devise for morphological data as for molecular data.
In the case of phylogeny based on molecular data such as protein or DNA sequences, models of evolutionary changes exist, which are not based on ad hoc hypotheses, but on reasonably good knowledge gathered from disciplines such as molecular biology, biochemistry, etc.
Under these models, "hidden" multiple character changes are expected along long enough branches. This may lead to differences with respect to the most simple parsimony criterion, when inferring the number of character changes in a topology.
In such a case, simple parsimony may not be the most sensible approach to phylogeny resconstruction.


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PCR in different cell line
I developed a PCR cycle to amplify a 5.5 kb genomic DNA region in HEK cell line. When I tried to use the same protocol in A375 cell line I had no results but only smear. Can you help me?
Thanks in advance

Are you running a housekeeping gene? how does that look like?

No, it's an intron of a gene upregulated in this cell line

And in this intron there is an enhancer region

Do you have a positive control run with your sample?

I use HEK gDNA as positive control

@Annalaura Your positive control should be some region that would be amplified in both samples. A test of whether the gDNA prep is good.

@WYSIWYG Yes, i have amplified 2 smaller amplicon using this gDna sample


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What is the outer boundary of oligodendrocyte myelination?
The sensory and motor neurons comprising the spinal cord and brain stem have the interesting property that different structural components belonging to the same neuron can occupy both the PNS and CNS.
Here are several examples:

Motor neurons' somas are in the CNS while the majority of their axonal projections are in the PNS
Sympathetic preganglionic neurons' somas are in the CNS while the majority of their axonal projections are in the PNS.
Pseuduniopolar sensory neurons' have part of their axons in the CNS, but their somas and other part of their axons are in the PNS.

The general dogma of myelinating cells states that Schwann cells myelinate the PNS axons while oligodendrocytes myelinate the CNS axons. However, I'd like to know which cells are responsible for myelinating the segments of axons that are just exiting or entering the spinal cord. Does there exist an abrupt demarcation point where the myelinating cells suddenly cease to operate / exist?
Referring to the provided picture below:
Does this picture reflect what is truly observed? Is there really a distinct "outer limit" of oligodendrocyte myelination?


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Does the molecular composition of human body change after a period of time?
I was discussing change in human biology over time and my two in-laws charged in saying, "we're molecularly different after x". I didn't pay attention to what time period they exactly mentioned (hence x).
I am familiar with how mainstream media warps research data to be entertaining. So would serious researchers and scientists consider bold statements such as "we (humans) are completely different after 6 years!" as nothing more than anecdotal?
I'm not talking about decomposition after death but rather about processes in the live body.


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what is the integral of PAR radiation over total solar radiation
This paper say 48%: What is the maximum efficiency with which photosynthesis can convert solar energy into biomass? -Zhu 2008
Also why does Zhu use 740 nm at high end of PAR wavelength!
My calculation says 43% (also using 7440 nm)
Have you done this integral? What did you find

What paper?  Could you give a name and / or link, please?  Thanks!

Yes the paper is: What is the maximum efficiency with which photosynthesis can convert solar energy into biomass? (Zhu,2008)


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What happens with the nitrogen in blood in membrane oxygenators?
The air we breathe consists of about 80% nitrogen and 20% oxygen. The oxygen gets diffused into the blood and CO2 out of it, the nitrogen does mostly nothing, as there isn't a partial pressure of nitrogen between the air and your blood.
In membrane oxygenators the blood flows arround small tubes which contain pure oxygen. The oxygen diffuses in your blood en the CO2 diffuses in the tubes, basically doing the same thing lungs does. However, since it's pure oxygen that flows through those tubes, the nitrogen in your blood should get diffused into the tubes.
So is this what happens? Does the nitrogen simply diffuse untill there's nothing left? Isn't that then bad for your body if all the nitrogen is out? Or can't nitrogen pass through the membrane the tubes are made of? Or does it differ wether you use 'true' membrane of microporous membrane?

You are not considering the fact that nitrogen has low solubility in blood. There isn't a lot of nitrogen in the blood anyway and it performs no physiological function. I don't understand why you assume that loss of nitrogen will have any negative effect on the body?

I was actually asking what happens with the nitrogen in your blood in membrane oxygenators, wether it gets diffused in the tubes or stays in the blood or... The "isn't that bad for your body" is more of a side question which you now answered, for which thank you.

It gets diffused out, like you expected.  Grist (2013) writes about this in relation to "the bends," which has already been mentioned by user1136.  He writes:

Cavitation of blood containing normal oxygen and nitrogen levels by mechanical heart valves after implantation generates bubbles that can be detected in the brain using transcranial Doppler ultrasound (2). These bubbles are mainly nitrogenous. Nitrogen is less soluble in water than oxygen. So during excessive turbulence, temperature changes, or pressure changes, nitrogen is the first gas to come out of the solution. (Ask any knowledgeable diver about the physiology of the bends.) We know these bubbles are mainly nitrogen because when the nitrogen in the patient’s blood is off-gassed by breathing 100% oxygen, the cavitated bubbles go away. In one study, the administration of 100% oxygen by facemask reduced the cavitation generation of GME by 98% (3). [Emphasis added]

Can't say it a lot better than that and the rest of the article.  When people are breathing de-nitrogenated air, it simply results in nitrogen being diffused out of the blood.  So yeah, basically the amount of N2 goes down to 0, at least if they are on it for long enough.
As for it being bad for you, not really, at least not perceptibly: though nitrogen is critical for body function, it's practically useless to the body in the N2 form; it has to be "fixed" to a more reactive form such as ammonia / other nitrogen oxide.

Sources

Grist G. 2013. Oxygen or Nitrogen: Which Is the Lesser of Two Evils? J Extra Corpor Technol 45(1): 61-63.

Sprent JI, Sprent P. 1990. Nitrogen fixing organisms: Pure and applied aspects.