text:
Is it possible to simulate tetrachromatic vision in a trichromat?
Suppose we are able to stimulate the whole matrix of cones of a human retina, targeting each cone individually¹. Normally we would project an image in the LMS color space onto the cones, in such a way that each sub-image of particular color channel would get to cones of corresponding type. As the eye moves, this image would be adjusted so as to create an illusion of real surrounding (similarly to a VR headset).
Suppose now we think up a new spectral sensitivity function $P(\lambda)$. We choose a subset of e.g. M cones to represent this type of sensitivity, making sure that this set is scattered enough around the M cones so as to avoid clumping the same color channel cones. And then we try to simulate tetrachromatic vision by replacing the M-channel sub-image in the projection by a special sub-image that an actual sensor with $P(\lambda)$ would capture.
Would this result in a sensation of a new color having appeared in the image, or would this be simply a lot of noise in the visual field?

¹The technology is not quite there, but on the way: see e.g. this answer.

I think your question would be better if you provided more background information — at a minimum adding links for things like "LMS color space" will make your question somewhat more accessible. In addition, the material about eye-tracking seems superfluous and to me distracts from the question. Finally, my (non-specialist) understanding is that people with tetrachromatic vision have been identified, which perhaps obviates your question?

@tyersome OK, I've added the link to LMS color space@Wikipedia. Regarding the existing human tetrachromats, no, this doesn't obviate the question: I still wonder whether the people who don't have corresponding phenotype are able to have tetrachromatic-like sensations, and whether the choice of the type-four cones makes it any different. Moreover, there might be some limitation in the brain, restricting, if not potential for tetrachromacy,then maybe for pentachromacy—or there might not be—which is what I'm also interested in.The eye-tracking material was a description of the thought experiment.

I think the thought experiment contributes to this questions seeming too speculative (i.e. any answer would be primarily opinion and thus would not meet the criteria for this site). ——— Are really really interested in whether adults can adjust to new color inputs? If so, there are reports about people acquiring UV vision after cataract surgery.

@tyersome well, UV vision is not a new color: basically, just an extension of S cone sensitivity. Namely, those people see UV simply as violet, which isn't a new color (the same cones are stimulated by 370 nm light as by 400 nm). I'm not looking for opinions, but rather an answer from the position of modern neuroscience theories about how brain functions regarding the processing of the input signals from cone/rod cells.

And finally, I'm interested in how color vision works from the POV of my thought experiment: e.g. whether the neurons connected to different cone types are predefined to particular color channels, or it's possible to repurpose them for a different sensitivity curve by some kind of modification, so as to get completely new colors and higher-dimensional color gamuts.

The experiment on squirrel monkeys is much closer to my idea than aphakic human UV vision, but it still leaves some doubts because the species already has large percentage of trichromats (77%of females), so the male brain may be genetically prepared to handle third cone type thus enabling the success of this experiment. In humans, OTOH, only 12%of females have 4 cone types, and only a small fraction of these are actually tetrachromats.That does leave some doubts on whether every trichromatic human can be made tetrachromatic,more so penta-.

I think it's an interesting question, but there are 4 sub-questions that share little overlap in some cases. It's best to ask focused questions. Feel free to split them up in multiple posts

@AliceD OK, I've removed the sub-questions that depend on the first one. However, I think there's no use in asking them in multiple posts until this one is answered, exactly because they depend on the first question.

Surely a great thing to wait with asking a fellow up question. Good luck!

How is this different than what is done now with false-color photography?  If I understand correctly, all you're doing is mapping the (R,G,B,UV) color space into (R,G,B), which doesn't result in any "new" color sensation.

@jamesqf the difference here is that e.g. you repurpose part of the set of e.g. M cones to another sensitivity curve. This could result in two possible outcomes: 1) The human sees a noisy image, as if looking at raw undeveloped Bayer-pattern image, but with the pattern following the direction of looking akin to an afterimage. 2) Due to fine dispersion of one set in the other, the signal from the retina is somehow demosaiced by the brain, resulting in a smooth new color. I wonder which of these outcomes would actually happen.


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Can anyone (urgently) tell me if this is a bed bug
We just arrived in a place where a lot of people were living before.
This is what we found on the mattress and we are curious to see if this is a bedbug, or some harmless species; To know if we go out right away or not :)
Location: Poland. ;  Size: ~13mm long

Here is a photo with a measuring tape next to it:

Closeup:

Does this answer your question? Insect identification - Is this a bedbug?

Have you tried searching on this site for "bedbug" — there are several very good answers already posted that should put your mind at ease ...

The shape looks different but, not knowing anything about bugs, I have seen a variety of pictures online with different shapes, etc so I would feel at peace confirming what it is :)

By the way, the different shapes you've seen online are just insects being misidentified as bedbugs. In my experience, bedbugs are one of the most often misidentified species on the internet.  Bedbugs have 1 of 2 consistent shapes (hungry vs full), both of which are demonstrated in the post Insect identification - Is this a bedbug?

Since it's clear you still have the specimen, could you try taking a clearer picture under any type of magnification?

@theforestecologist: I added a close up photo; since we're moving right now, I didn't have a way to make a better photo

This is not a bedbug. This is a hemipteran called a leaf-footed bug in the Coreidae family. (Note: bedbugs are also in the order Hemiptera, but in a different family).
Species similar to yours found in Poland include Coreus marginatus (or "dock bug"), which [according to Wikipedia], is found throughout Europe.

 Adult male and nymph shown from dorsal and ventral views. Source: Wikipedia
C. marginatus is typically 13-15 mm long (which matches your updated length) and has a widened abdomen as does your specimen. Additionally, the antenna of C. marginatus is typically red-orange with black ends (as is also seen in your specimen). A more complete description from Wikipedia:

The head, pronotum and abdomen of an adult dock bug are speckled reddish brown. The antennae are composed of four segments, red-orange in colour except for the final fourth segment which is black. Between the antennae are two small projections, known as antenniferous tubercles, which can be used to distinguish this species from other superficially similar species.[6] The pronotum has angular upward facing projections and the scutellum is clearly visible. The rounded edge of the abdomen has lighter coloured markings. Adults are between 13 and 15 mm long and males are typically smaller than females but have longer antennae.

See here for an additional picture showing a specimen with less prominent abdominal markings as in your specimen.
C. marginitus tends to be found in thick vegetation, so unless you've bee around hedgerows, wasteland, or other densely-vegetated areas, it's possible you have some other closely related species.
I haven't been able to find a better matching specimen, though it seems likely I have only gotten you to the right family without being certain of the genus or species. I'll update if I can find more info...
Notes:

Your specimen does not appear to be another common hemipteran found in Poland:  Leptoglossus occidentalis, which is native to the western United States but has invaded Poland for over 10 years [Surce: Lis et al. (2008)1]

You can find a guide to this family of insects (with pictures) for the neotropics (not immediately useful to you, but a good resource) by Fernandes et al. (2015)2

 1 Lis, J.A., Lis, B. and Gubernator, J., 2008. Will the invasive western conifer seed bug Leptoglossus occidentalis Heidemann (Hemiptera: Heteroptera: Coreidae) seize all of Europe?. Zootaxa, 1740(1), pp.66-68.
2. Fernandes J.A.M., Mitchell P.L., Livermore L., Nikunlassi M. (2015) Leaf-Footed Bugs (Coreidae). In: Panizzi A., Grazia J. (eds) True Bugs (Heteroptera) of the Neotropics. Entomology in Focus, vol 2. Springer, Dordrecht

source: Stack Exchange

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

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Apoptosis related
I have two questions
1. Is it possible for a cell undergoing apoptosis to induce apoptosis in
     a surrounding cell?
2. If we induce apoptosis in a normal cell surrounding a tumor.
     Is it possible for the molecules released during apoptosis to
     differentiate between normal and cancerous cells?

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


text:
Where do methyl groups in the human body come from?
Where do methyl groups in the human body or other mammals come from? Do we synthesize them (where?) Do we get them from our diets (in what? anything beside methionine?) Do our gut microbes produce them for us (and are we dependent on them for that?)

Well, as it's Christmas, I'll play Santa and give you some S-adenosylmethionine for your biochemistry Lego set. You'll need to consult the instruction page to see how to use it and what other pieces are needed. Another time you may find the biochemistry manual useful for the research you are expected to do before posting.

Thank you for your response.  I am new here and did not see instructions about what I was supposed to do before posting a question.  Regarding the question itself: the methionine-homocysteine cycle does not CREATE methyl groups--it only passes them around and activates/deactivates them.  I am trying to find out where they are synthesized, whether we have endogenous production of them or are reliant on exogenous sources, and if so, what are those sources. (I find it hard to believe that we can get enough solely from ingestion of methionine.)  Anyone else?  Thanks.

Read the whole section. The methyl group for the cycle comes from methylene tetrahydrofolate, which is produced by the reaction of serine with tetrahydrofolate. And serine, as you should know from your studies of the central metabolic pathways, is not an essential amino acid, but is synthesized from an intermediate of glycolysis. You wouldn't be thinking that methylation only happens to the amino acid residues of histones, or that you can understand its bichemistry without actually studying basic biochemistry, would you?


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Evolution of recurrent laryngeal nerve in a giraffe
Do natural selection and survival  of the fittest explain the divergent length of the recurrent laryngeal nerve...centimeters in the human, 15 feet in the giraffe?

Are you suggesting the length of the nerve evolves independent to the length of the neck? That's not how development works at all

I don’t understand what you’re asking. The divergence of all ancestral traits can be explained by evolution. I’m aware that the laryngeal nerve’s path under the arch of the aorta has been used as an argument against intelligent design; based on that and your comments on some of the answers, it appears to me that you’re just trying to start a discussion on intelligent design versus natural selection. For that reason, I have voted to close your question. Perhaps you could clarify why the divergence in length you mentioned is confusing to you.

I am expressing a fact. I find plausible that finch charateristics diverge on isolated islands. I don't find plausible that natural selection explains the lengthening of the r.l. nerve to 15 feet. Within the province of discussion of natural selection an appropriate scientific skepticism is  not possible. Is it because the theory of the r. l. nerve by natural selection is "not falsifiable". This criterion of science seems to have been forgotten. I am entitled to doubt it and not be thought to entertain intelligent design. There nay be some agency in the genome  which governs tandem association

You are expected to show some attempt to research questions before you ask them, what research have you done. Clarity in what exactly you are asking would also be a desired improvement.

I have research Darwinian explanation. I wrote a book about. If you would like I can send you the google drive link since I am trying to get feedback on it. I've read Popper.  And I don't find that appropriate scientific skepticism is permitted in the field of natural selection.

This has a lot to do with how development works, there is no gene that makes the nerve this long. Instead, there are genes that tell the nerve where to grow and what path to take using other tissues as landmarks. At each step of the neck getting longer letting the nerve follow this path is more beneficial than the complex evolution of pathways necessary to change how it grows. At each step the added length of the nerve is a small detriment while a large number of simultaneous mutations would be needed to change the developmental pathways. Since these mutations are extremely unlikely to occur together and produce the desired results, they are instead a major/lethal detriment.
Based on fish it is likely that in the early common ancestor the nerve took a straight path. As necks evolved the heart moved down into the body and away from the gills the nerve originally connected to. Thus, the nerve is trapped by its own developmental pathway, it runs behind the gill arches which in tetrapods have become the aorta which is essential and the Ductus arteriosus which is developmentally vital. The nerves uses these as developmental landmarks for how it develops and grow in long before the neck develops. In an embryo (which has no neck) this is still a short straight trip, but as the embryo continues developing it has to grow longer and longer as the neck forms. Keep in mind the larynx and heart develop in very different location then where they end up in the body. Elongation of nerves as the tissue elongates does not need to be programed individually there is a general process that makes it happen in all nerves so no new mutations are needed. This is plasticity at work. The right and left nerve are actually different lengths because different gill arches are lost on the right and left side of mammals.  Simply letting the nerve get longer is less detrimental than not having the nerve which are the two options. As I mentioned above rerouting the nerve is unlikely to happen due to the improbability of the co-occurrence of multiple mutations to completely reorganize developmental pathways. There is a cost (extra tissue and calories and some signal lag and even rare developmental errors in the most extreme cases), but since it controls most of the larynx not having the nerve would prevent vocalization or or even breathing properly. Given those two options it is fairly easy to see why evolution favors individuals that maintain this pattern.
Evolution is full of kluges and "good enough" solutions/compromises like this.

https://www.evolutionarymodel.com/apps/photos/photo?photoid=56959380
https://arxiv.org/pdf/1901.01560.pdf
https://web.duke.edu/anatomy/embryology/cardiovascular/cardiovascular.html
https://www.sciencedirect.com/science/article/abs/pii/S095943880500187X

This is good answer, but I think it would be even better if you could provide some more references for particular statements (e.g. tissues being used as landmarks for nerve growth, number of genes involved in guiding this nerve, the movement of the heart during evolution & development, etc.) within the text and also indicate within the text where the figures are relevant. ——— I also took the liberty of editing in way I hope improves the clarity of your argument, but since this is out of my field it would be great if you corrected any errors I inadvertently introduced!

The improbability of multiple simultaneous mutations is pretty basic I any link will just be to a textbook. but I can add some more references.

I'm not sure how to address this question so that we may arrive at a suitable answer, but I'm sure that the recurrent laryngeal nerve is an example of bad design. Evolution works from traits already possessed by the parents. Mammals evolved from fishes in our evolutionary past and fishes do not have a neck. As a result the recurrent laryngeal nerve of giraffes loops under the aortic arch instead of over the arch.
Offspring of giraffes that are born with a longer neck have more chances of surviving and passing on the trait because they have an easier time to access food sources in higher places and an easier time to watch out for predators. Simultaneously, by natural selection the nerve is gradually lengthened in tiny increments. As Richard Dawkins said in his book Outgrowing God, "evolution cannot go back to the drawing board. Evolution has no foresight.”1
References:
1: Dawkins, R. (2019). Outgrowing God: A Beginner's Guide. Random House.

The idea that varieties died out because their r.l. nerve was not long enough (for my poor brain)  passes the bar of implausibilty.

Also if I may add, there is the rare variation in which the left r.l. nerve is non-recurrent, direct from vagus n. to the innervated tissues. The tenets of natural selection would imply that this uncomplicated variation should have gained ascendancy

Welcome to Biology.SE! This is a good start, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. In addition, your answer could be interpreted as saying that the looping is giraffe specific. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!

I also think that elaborating on how mammals (Is it really only mammals?) ended up with a recurrent laryngeal nerve would improve your answer. Finally, if you have a quotation from a book a complete reference to that work is best including a page number. (I've edited your post to improve the wording a bit and added the book reference, but don't have time to figure out the page.)

I wanted to delete one final comment and it looks like others were deleted. It was not intentional. If you want to pick up where we left off or restore them I would enjoy it. Thank you for your elaborate answer and comments. Natural Selection explains. Intelligent Design does not explain in the way that scientist love.

have research Darwinian explanation. I wrote a book about. If you would like I can send you the google drive link since I am trying to get feedback on it.

Sure I'd love to have a look.


text:
What is this fruit (round, 3 cm diameter, yellow outside, 1 black seed, found on Easter Island)?
What is this fruit (round, 3 cm diameter, yellow outside, 1 black seed, found on Easter Island)?

Some fruits may have more than one seed:

I think you are looking at Syzygium jambos in the Myrtaceae.  The first link at Wikipedia has a number of pictures which are quite similar to your pictures.


text:
Appropriate model to test if environmental variable is significant between two species?
I want to know if a given environmental variable has an effect on the range of two species/two groups of species. Specifically, I am interested in testing if one species has a "preference" for higher/lower ranges over the other (for example, do blue frogs prefer colder temperatures than red frogs?). I have occurrence data for my species as well as environmental data in a grid over the area. Can anyone point me in the right direction?

Welcome to Biology.SE! This question seems like it might be a better fit for the statistics site. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Do you want to test of they have different environmental preferences (in relation to a set of environmental variables), or if there is a positive/negative relationship between their ranges? Your Q seems to have bits of both, but they are not the same thing.


text:
Is a wet-mount needed to use Immersion Oil?
When I prepare my slide to use immersion oil, do I really need to wet-mount the specimen?  Can I do it with just the coverslip?
I am preparing fungus spores.
Using water for the wet-mount gives you a sort-of time limit.  You have to do your work before the water evaporates else you get little rivers at x100.

The answer is that you cannot use the Immersion Oil without water-mounting the coverslip.
I tried it.
The water-mount "glues" the coverslip to the slide, effectively anchoring it in place.  Without doing this, when you add the Immersion Oil, the coverslip will slide around because the oil "grabs" the coverslip.  When you pan the stage, the coverslip is stuck to the lens and the slide on the stage is moved around but the coverslip doesn't move because it's adhered to the lens.
When you water-mount the coverslip, it is anchored so solidly that it is actually even difficult to push it with your fingernail.
Conclusion:  No Immersion Oil without a water-mount!

I’ve done plenty of bacterial smears without a cover slip; the oil is applied directly to the specimen. I don’t know if that would be applicable in your application.

Really? Without a coverslip, that means the oil-immersed bacteria would be right on the lens.

The bacteria are fixed to the slide.

Ah, okay.  I can't do that with mushroom spores.

When I prepare my slide to use immersion oil, do I really need to wet-mount the specimen? Can I do it with just the coverslip?

Ideally you shouldn't use either with immersion oil. You should match the mounting media index as closely as possible to the immersion oil index, otherwise you'll reduce the resolution and contrast of your image. See:
http://www.microbehunter.com/the-importance-of-mounting-medium-refractive-index/

Using water for the wet-mount gives you a sort-of time limit. You have to do your work before the water evaporates else you get little rivers at x100.

There are lots of options for higher index mounting media that will also preserve your specimen at least as well as air.


text:
Is it true that ethanol can have some positive effects?
I recently was reading this inforgrafics about excessive alcohol use. It is written:

No one should begin drinking or drink more frequently based on
  potential health benefits

I am surprised. Is there any potential health benefits of drinking alcohol?
To check this information, I made a little research and found this article of the Medical Daily: 7 Health Benefits Of Drinking Alcohol. Apparently, a moderate alcohol consumption (no more than 2 drinks a day for a men) can lower the risk of cardiovascular disease, lengthen the life, decrease the chances of demantia and diabetes, ...
But, for all of these facts, only one study is provided. So, I want to know if it is a well established fact that alcohol can have positive effects on health. And, if so, what is the corresponding dose to get these benefits?

After a quick googling - should be relevant: Piano. 2017. Alcohol’s Effects on the Cardiovascular System. Alcohol Res. (a review). See e.g. “The associations between drinking and CV diseases such as hypertension, coronary heart disease, stroke, peripheral arterial disease, and cardiomyopathy have been studied extensively and are outlined in this review. [...] Low-to-moderate alcohol use may mitigate certain mechanisms such as risk and hemostatic factors affecting atherosclerosis and inflammation”

The classic j shaped curve associated with alcohol consumption is discussed in this answer

Based on your comment to @Willk I think this question (and the title in particular) would benefit from you editing it to be more focused. As currently written their answer seems like a valid answer as would an answer that focused on how alcohol can reduce spoilage.

Alcohol can be used as a disinfectant, and can preserve water. I ate a bad egg in a Dehli restaurant in 97 and vomited for 8 days and survived on rehydration salts. On the 8th day, I went to buy a bottle a Gin, 30% alcohol or something, and I had a good dose of it straight. it must have gone through my body pretty vigorously because after the gin, a coal colored flegm came out the other way and within 24 hours of drinking the Gin i was 100% fine. perhaps it was even salmonella considering it was an egg.

Different studies result in different answers, but in general there seems to be a small beneficial health effect of small amounts of alcohol.  An example study is The association of lifetime alcohol use with mortality and cancer risk in older adults: A cohort study.  The results are summarised in this figure:

From this image we can see that it appears that less than four drinks a day is accosiated with a reduced risk of death, this effect being mostly cardiovascular related.
All these studies are observational studies rather than controlled studies.  This always leaves the possibility that what is being observed is correlation but not causality.

Alcohol has caloric value.
First worlders today have a wealth of high calorie food choices which make the caloric value of alcoholic drinks either irrelevant or detrimental.  But it was not always this way. In circumstances where other caloric sources were limited or unpalatable, alcohol supplied calories needed to supply the energy demand of workers.  Persons working energy-intensive jobs (such as field labor or factory work) have historically supplemented calories from food with calories from ethanol.  The below excerpt discusses the dietary habits of metalworkers in the late 1800s.
Drink, Temperance and the Working Class in Nineteenth Century Germany

Despite the overall improvement in dietary standards of the previous
  two or three decades, the situation of these Manheim workers suggests
  that alcohol remained an essential part of the working-class diet. If
  provided necessary calories in palatable form. The sharp flavor of
  alcoholic beverages could add spice to otherwise monotonous fare,
  providing a sense of warmth and fullness even when meals were cold and
  unsatisfying. Perhaps most important, alcohol provided energy in
  concentrated form. Alcohol, whether in the form of beer or spirits,
  enabled workers to reduce the sheer quantity of food that had to be
  gotten down each day. The distinguished physiologist Max Gruber
  calculated that a worker who consumed even a 10th of a liter of
  schnapps with the meal could come up with no energy loss, reduces
  potato and rye bread consumption but some 288 and 122 g
  respectively.”Try eating a kilo of black bread or two or more kilos of
  potatoes day after day”, Gruber told his well fed middle-class readers
  in 1888, “and you’ll discover what a relief it can be to substitute a
  pungent and stimulating beverage for a 10th of this mass”.

The health benefit of alcohol consumption here would be that of not starving in situations of high caloric expenditure.   calories are concentrated as compared to carbohydrates and distilled spirits also have an indefinite shelf life - not true of grains and potatoes.

My question was more about health and disease rather than the nutritional aspect.

Also, I would expect that since beverage alcohol is produced by fermentation, the beverage would have fewer calories than the grain it is made from, since some of the energy would have been used by the yeast.  That's even before considering that in most such beverages, a lot of the original material is often discarded as waste, or used as fertilizer or animal food.

@jamesqf - you are right that there is a net loss of calories on converting starch calories to alcohol.  In exchange you get alcohol calories that will not be used by fungi or rodent pests.  For Pierre - not starving is a positive effect on health last time I checked.

The energy provided by ethanol provides no other form than heating which is typically not needed because it is in abundance already.

@DavidJonsson - care to check your biochemical pathways again? Pretty sure that ethanol can be metabolized into the citric acid pathway or into lipid biosynthesis...

@bob1 I wrote typically. There is typically no need for more lipids in humans either. Regarding citric acid I will return on the subject if I coincidentally get to know more. Maybe citric acid cycle affection can explain why some feel ethanol increases body heat.  I think the most suitable way to investigate this is to find out how people react if intestinal creation of ethanol is lowered or if the alcohol dehydrogenase synthesis is overexpressed. Why don't you ask a new question regarding this?

@DavidJonsson my point was that the ethanol doesn't just produce heat it also produces lipids and energy in the form of ATP (if I remember the citric acid cycle correctly... it has been more than 20 years).

Psychological benefits
Alcohol allows to relieve stress, makes people friendlier, and establish closer social contacts. For this reason wine constitutes an important part of national culture in many countries: vodka in Russia, wine in France, beer in Germany and Belgium, wiskey in British islands, etc.
Protection from pathogens
Disinfecting properties of alcohol, mentioned in the comments, have actually played important role in human history: indeed, massive drinking of wine and beer in the Middle Ages largely protected population from water-borne disease, such as cholera. It is only with advent of drinks like tea and coffee, where microbes are eliminated via boiling, that the consumption of wine began to be considered unhealthy.

Protection from methanol.

@DKNguyen not sure what you mean. Please give more details.

Ethanol treats methanol poisoning because it competes with the methanol reducing how much of it is metabolized into toxic compounds before it can pass through you.

@DKNguyen this is true, but is there anything like natural methanol poisoning? (I.e., apart of mistakenly consuming methanol instead of ethanol.)

Eating a lot of fermented fruit? But I looked and it up...interesting...methanol is produced by the human digestive system. Toxicity is in the dose I guess.


text:
What is this insect? 6 legs and black spots
What is this bug?

Details:
 - Georgia, (Southern) USA
 - Maybe 1-4cm in size
 - Seen near an open area/crack between an outer door-frame and door where it could have come from outside, or going from inside to outside since the temperature difference was noticeable in this area.
Thanks in advance!

Deffo isnt a grasshopper. A window louse?

It's almost certainly a harlequin ladybird (Harmonia axyridis). Well, that's the usual name for it in British English, I think Americans would refer to it as the Asian ladybeetle or Asian ladybug. The spot patterns for that particular ladybird species vary quite a bit so I'll need to do some googling to confirm.

(Note: I'm going to be using the British English "ladybird" instead of the US English "ladybug" in this answer.)
This is a clearly a species of ladybird. Going by the number of spots, their size and not-perfectly-round shape, the positioning of the four central spots relative to the others, and the fact that its background colour isn't bright yellow... I'm pretty sure it's Harmonia axyridis, the species that us Brits refer to as a "Harlequin ladybird". I think Americans refer to it as an "Asian ladybug" or "Asian ladybeetle".
The spot patterns for this particular species vary a lot, as to some extent do the colours, so I've googled for images to support this answer. The below picture was posted to:
https://en.wikipedia.org/wiki/File:Harmonia_axyridis01.jpg
and is the IP of a user or organisation called Entomart. On the Wikipedia page and on their homepage, Entomart grant permission for the use of the image as long as they are given proper attribution, so I'm able to include it in this answer:

For more pictures of the Harlequin (again, showing how much the spot pattern and colouration vary), see:
https://scx2.b-cdn.net/gfx/news/hires/2018/amechanismof.jpg
For pictures of other ladybird species to compare the Harlequin with - as also one more of the Harlequin:
https://www.naturespot.org.uk/taxonomy/term/19357
Thanks for posting this question! I didn't expect to see a ladybird on Christmas Day :-)


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Can men with Klinefelter syndrome produce chromosomally normal sperm?
Individuals with Klinefelter syndrome are XXY. Even though sperm counts are low some individuals can generate enough to be used in IVF and have offspring.
Does this mean that when sperm are formed, the process works correctly to separate all 3 of them and only sperm with a single sex chromosome are formed?
(Excluding same genetic issues happening again of course)

Welcome to Biology.SE! I've edited your question in a way that I hope improves clarity — please re-edit if I've changed your meaning. Note that we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Seems like there are some hypotheses about this mechanism. This might be interesting: https://www.fertstert.org/article/S0015-0282(12)00654-1/pdf


text:
How does a "chromogenic mixture" produce such pronounced color differences in this Agar Art?
The Forbes.com article Bacteria Become Art Tools In Annual Agar Art Competition says:

...People’s choice winner Zita Pöstényi, a microbiologist at SYNLAB Hungary Ltd, used three agar plates and four different bacteria to create a pattern inspired by Hungarian folk art.
[...]
Pöstényi used another trick to create her colorful plates. “I used a special media for this drawing,” she says,  “It contains a chromogenic mixture which enables the detection of activities of specific enzymes.” Thanks to this special mixture, the four bacteria species she used all showed up in different colors, which allowed her to create the traditional folk art pattern.
Usually, these unique colors tells researchers something interesting about the bacteria, but for the ASM Agar Art competition, these colorful features have become the medium.

Question: How does a "chromogenic mixture" result in different bacteria showing up in different colors in such a vivid way?

American Society for Microbiology Agar Art 2019 Contest, People's Choice. "Hungarian Folk Art," Zita ... [+]ASM / ZITA PÖSTÉNYI

She is referring to a mixture of chromogenic substrates: molecules which are more or less colourless until cleaved by a specific enzyme, releasing a coloured product.
For example X-gal is colourless until the enzyme beta-galactosidase hydrolyzes it, releasing a blue coloured product. If you spread a mixture of bacteria onto a plate, with some expressing beta-galactosidase and some not, you will see both blue and colourless colonies, as seen here:

[source]
Chromogenic substrates are often used to create differential media that allow the differentiation of different species of bacteria. This plate, for example, contains several different chromogenic substrates (a mixture, if you will) for identifying the bacteria commonly found in urinary tract infections:

[source]
If you wanted to make a picture with this plate, you could “paint” with Enterobacter spp. for blue, Staphylococcus aureus for yellow and S. saprophyticus for pink. Each species produces a specific enzyme that acts on a specific chromogenic substrate in the plate, changing its colour.
Alternatively, you could express the desired enzymes recombinantly in one species.

Thanks for the authoritative, well-sourced and colorful answer! With a CMY mixture and bacteria with variable expression rates of three enzymes one could make quite a palate.


text:
Was there ever a very first Homo sapiens?
My friend keeps saying that there was a first Homo sapiens. Meaning, there was a very first human being that was ever born.
I can't really understand what she means to say from a selection/gene mutation perspective. I can't understand how there would be anything that could be considered the very first human being.
Was there ever a very first, singular human being that could be discerned as such?

Perhaps she is referring to mitochondrial eve or a "common-ancestor of all people alive today" which is popular with journalists, although it's thought that the human population has never had less than a few thousand common ancestors.

She means to say the quite literally "someone had to have given birth the the first human baby," just as a logical deduction. There are humans, therefore the must have been a first human baby. So, something gave birth to the very first homo sapien.

perhaps ask her who made the first car? what was the first pet dog that wasn't a wolf?

Is there some reason you uncorrected the spelling and capitalization of Homo sapiens to "Homo Sapien"? If you insist that is correct please provide a reliable reference that supports that usage. Thanks!

I didn't realize it was corrected since no one posted an edit comment. Since I have other misspellings (doing this from my phone), I assumed I had accidentally left it in the lowercase. I didn't realize that the term is lowercase

Yes, for binomial names the genus is always capitalized and the species (and subspecies) are not. ——— On a phone you should still be able to see that a post has been edited and the word "edited" will be a link that takes you to a page that shows you the edit history. ——— You might find it helpful to take the the [tour] and then go through the help pages starting with [Ask] questions effectively on this site to become more familiar with how the site works.

No. It is important to distinguish "species" as a human system of classification, and "speciation" as a biological process. Except in cases like chromosomal speciation (changes in ploidy), speciation takes a long time. Probably thousands of years between some initial restriction of gene-flow, and fixation of a specific identifiable trait, present in all individuals of a species, and not present in any others. As a human system of classification, the taxonomists who define species would all understand that speciation is a process that occurs over time, although they may make some arbitrary distinction for convenience. For example, a node on a cladogram symbolizes an instantaneous process of species bifurcation, but this is understood to be an unrealistic simplification.

Thank you. While I didn't have the background, I was pretty sure that was the case.


text:
What subspecies of Iberian Ibex and what subspecies Golden Eagle are in this video?
In the nature documentary El Hombre y la Tierra, there is a scene featuring golden eagles and apparently some kind of Iberian ibex. The scene should be in some part of Iberia. This is the video which features the animals and location: https://www.youtube.com/watch?v=Yz7FFlFy8eM
Goats:

Eagle and Goats: 1: https://i.stack.imgur.com/3RHSs.jpg 2: https://i.stack.imgur.com/eBh2d.jpg Several other images: https://i.stack.imgur.com/Wpare.jpg
However, these Ibex have small horns and there are none with large horns. I'm not used to seeing this with ibex. Surely it can't be a flock made entirely of females and juveniles? So I would like to ask what subspecies of Iberian Ibex these are.
I would also like to ask, if I might, what subspecies of golden eagle is shown in the clip. I suspect the one which carries off the goat will be the female of a larger subspecies.
If it is not acceptable to ask about both species, please edit the part about the eagle out of my answer. Know that I would be happy with an answer to either question. Thank you very much.

The golden eagle is just one species:  (Aquila chrysaetos) is the most widely distributed species of eagle, it's on all the northern hemisphere.

@com.prehensible My mistake, meant to say subspecies. Do you know what subspecies of aquila chrysaetos is common to Iberia, and which might be present in the video?

Welcome to Biology.SE! Please edit your post to include an image from the video in question — posts on this site should be stand-alone and not require users to click through to links on another site. One reason for this is that links can break (e.g. the video could be taken down) and thus reduce the value of this question and any answers. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

@tyersome Thanks tyersome. I tried to add some images, but it wouldn't let me upload them from imgur.

The upload links must be to files rather than webpages — if you open the imgur images in a new tab (or window) you get a file with ".jpg" extension. I've uploaded the goat images for you, but you should probably put the eagles into a separate question.

Aquila chrysaetos homeyeri: Iberian Peninsula; nw Africa to Arabia and Iran ... don't know about the ibex, it has small deer horns?

@com.prehensible Thanks! The ibex is pretty confusing. I was wondering if it might be a different kind of goat, like some wild breed of a Spanish goat. They have horns more like that.

The eagle is Aquila chrysaetos homeyeri or chrysaetos. Homeyeri comes from the Iberian Peninsula; nw Africa to Arabia and Iran. Chrysaetos chrysaetos comes from the Alps to Sibera and the Iberian Peninsula.
They weight up to 7kg and they can carry a bit less than 3 kilos, big prey includes baby bears, coyotes, foxes, ibex, seals, badgers, dogs, cats, they can attack anything up to 1 meter in width, generally on the neck and the back:

It can defeat anything that can't withstand the powerful talon gripping and slashing, the hullux talon is 4-6.5 cm:
The Ibex subspecies is difficult to tell from the pictures,  although the ibex males and females always live in different herds and congregate once a year, all subspecies adults have horns 40-70cm in length,. The horns grow 8cm per year for 15-20 years after the first year, with females having slightly smaller horns, about 40-50cm.
The group of iberian ibex there are all 2-3 years old.
Groups of ibex entirely with small horns can be found, with other herds of ibex with 55 cm horns living elsewhere, although normally it's a bit more mixed with 4-5 year old individuals mixed in. At the time that the video was made, hunting laws were less strict than today, so it's possible that the bigger individuals of the herd had been shot.


text:
What insect is this? Found this at home, India

Found this insect in Kolkata India. Has a sting at its rear end. The wings are shiny.

Welcome to Biology.SE! Please edit your post to add an estimate for the size of this insect and the nearby environment as those factors can be helpful clues for identifications. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

That is a parasitic wasp in the family, Ichneumonidae. You can tell by looking for a cell in the forewing that looks like a horse head. The "stinger" is an ovipositor. These wasps lay their eggs in the larvae of other insects

I've been trying to work out which species of wasp in that family it is. Going by photos on https://www.projectnoah.org/spottings/17352592 it looks like this could be a female Xanthopimpla punctata ("Yellow Ichneumon Wasp"), but there seem to be a lot of very similar looking Xanthopimpla species it could also be.


text:
Eagles carrying off a goat to its nest: How heavy is the young goat? How strong is the eagle? Here is my guess:
I posted a related question, here, trying to identify the exact subspecies of animals. In the documentary El Hombre y la Tierra, a golden eagle carries off some sort of juvenile(?) goat.
The Japanese golden eagle male weighs as little as 5.5 lbs, while the largest subspecies female weighs around 14 lbs. However, the largest species lives in Central Asia, and this footage is from Iberia, I believe. Therefore, it is more likely the subspecies is the one that lives in North Western Europe (I presume they reach south to the Iberian Peninsula), which weighs 7.7 lbs and 11 lbs on average for males and females respectively.
The question is how heavy a juvenile goat is likely to weight. The goat in the video does not look much smaller than the adults, though it is a little hard to tell. The Iberian ibex, which the goat supposedly is a member of, ranges in weight from 65 to 265 lbs.
If we estimated the goat to be a fraction of that lower estimate, say a quarter, that would be 16.25 lbs. If we took the 11 lb estimate for the golden eagle, that would mean it carried 147% of its body weight back to its nest. Wow!

The goat attacking the eagle in picture 2 must be an adult, either a male or a female. It does not seem much larger than the goat that was carried off in the first picture, however. This might mean the eagle carried off a goat significantly heavier than itself!
I would appreciate your input on my investigation into this matter. I feel this would be worth academic study.
Thank you.
PS: It was a lot of work to research and post this, so please don't delete it. I will repost it somewhere else if this is outside the scope of this stack exchange. Thank you for your understanding.

You may find this link to be of interest ...

@tyersome That is very interesting, thank you for sharing it!

The weight of the eagle is not the deciding factor, it is its lifting power of flight ie the “wing” power... which has to overcome the total body weight...


text:
A question about cancer antigens and their mechanism
Can you name the most common antigen that cancer cells in general can't live without?

Are you referring to a certain type of cancer?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— Thank you for taking the [tour], but please also go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

@tyersome I actually have searched on internet and read books but all the answers wasn't convenient

I think that you would benefit from making sure your have a firm grasp on the basics of biology. I say this because you appear to not be using the correct terminology (e.g. You seem to think that antigen is a synonym for protein, which is not correct.) This makes your question unclear and creates the impression that you won't have enough background knowledge to understand the answer to your question assuming it was made clear enough to be answerable. ...

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

This is a hard question to answer because each type of cancer is a whole different game at the molecular level, however there is something you might be interested in called "hallmarks of cancer" (image 1) which are key features for cancer to thrive. They were originally described by Hanahan and Weinberg (2000) and have been revisited by Fouad and Aanei (2017) in an updated review. The hallmarks of cancer aren't specific genes themselves, but rather broader categories that englobe certain types of genes.
If you want to look at specific genes, we could talk a bit about what more purely data driven approaches have found. There is a very interesting work by Kandoth and collaborators (2013) that presents data from The Cancer Genome Atlas (TCGA), which is a database of different kinds of genomic features from several different cancer types. Among the results of this work (specifically on figure 2 which I include here as Image 2) you can see a table of 127 significantly mutated genes across 12 different cancer types. One gene that is well known in medical literature for being frequently mutated in almost any cancer type (situation which is also observed in the aformentioned table) is TP53 which encodes a protein that is key for genome maintenance in normal cells by participating in DNA damage and repair (which is a cancer hallmark under the "altered stress response" category). In the table you can also spot tissue-specific cancer genes such as APC in colon/rectum cancer and VHL in renal cell carcinoma.
Just to make sure you can understand the table, the gene names are presented in the right (rows) and the names of the cancer types are presented at the top (columns). The description for the cancer types abbreviations can be found here. To the left of the table there is a functional classification of the genes so you can know more or less what a given gene does in a quick manner. The values presented are simple frequencies (divide the number of samples of a particular cancer type that have the mutation over the total number of samples of that same cancer type) expressed as percentages (so they are already multiplied by 100). The final column (Pan-Cancer) shows the same idea, but taking all samples from all cancer types into consideration for the frequency calculation.
So for answering your question regarding if there is a common feature in all types of cancers: strictly speaking at the gene level no, since even the TP53 mutation which is the most common amongst all cancers might not be present in some cancers; however, looking at it by categories of genes (as one or some of the 7 hallmarks) reveals that all cancers apply similar strategies to thrive (they exhibit different mutated genes, but these genes frequently belong to the same biological pathways and participate in similar functions). I hope you find this useful (:

Image 1: 7 hallmarks of cancer (2017 review).

Image 2: frequency of mutation by gene and cancer type.
References:

Fouad, Y. A., & Aanei, C. (2017). Revisiting the hallmarks of cancer. American journal of cancer research, 7(5), 1016–1036. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5446472/
Kandoth, C., McLellan, M. D., Vandin, F., Ye, K., Niu, B., Lu, C., … Ding, L. (2013). Mutational landscape and significance across 12 major cancer types. Nature, 502(7471), 333–339. doi:10.1038/nature12634
National Cancer Institute. TCGA Study Abbreviations. Retrieved from https://gdc.cancer.gov/resources-tcga-users/tcga-code-tables/tcga-study-abbreviations

This looks like a good answer and you've done a nice job of providing supporting references. However, please include the complete reference information since links can break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. ...

In addition, since answers here "must be comprehensible without reference to external sources" it would be helpful to insert the figure and table you refer to into your answer Thanks!

oh ok I wasn't sure if pasting the literal image of the resource was ok. I'll modify the answer soon enough

That looks much better! +1

Thank you so much, you're answer really helped me


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Where are all the seagull nests?
Seagulls are common. I live on the shore of New Jersey (U.S.), but I have never seen a seagull nest. Where are they?

Seagulls in urban areas tend to build their nests on rooftops instead of ground nesting. I'm not sure if that's New Jersey's case. I've also seen gulls' nests in sea cliffs but the area wasn't as populated as New Jersey.

Breeding season
Chances to see nests will be higher during breeding season which normally occurs once a year. Eggs will be laid in early May but they will be built in the previous months.
Area
In densely populated urban areas gulls may build their nests on rooftops instead of ground nesting. In the case of New Jersey I found the following brochure:
https://www.nj.gov/dep/fgw/ensp/pdf/bnb_brochure.pdf
If you mean seagulls as in all Laridae, then you have two members of that family (black skimmer and least tern) in that brochure that actually use NJ's beaches and even have their own designated space for that.
Googling 'seagull rooftop nests' brings a decent amount of pictures of rooftop nests. 'Seagull nests' brings a lot of cliff-placed nests, rooftop and ground nests. I assume the choice depends mostly on food availability and predator population density. I remember in Spain a few years ago there was a big enough problem to appear on local TV news related to seagulls attacking people. They would nest on every roof and attack people that would go out on the balcony with a sandwich.

Sources:

Habitat Selection and Nesting Biology of Roof-Nesting Glaucous-Winged Gulls
Kees Vermeer, Damian Power and G. E. John Smith
Colonial Waterbirds
Vol. 11, No. 2 (1988), pp. 189-201 https://www.jstor.org/stable/1521000?seq=1


text:
What's the evolutionary benefit of stress and cortisol?
Stress and cortisol lower immunity and increase hard disease.
But why is it that way?
If that's true then we shouldn't be stressful at all.
What's the benefit of stress then?
Why do we (and most mamals) response to stress by lowering immunity? How do people that lower their immunity due to stress survive "better" in the gene pool?

Acute stress occurs. It is impossible to enter the world without it. Cortisol is part of the physiologic response. This question could be improved by researching the role of cortisol in response to acute stress and explaining what you don't understand.

Consider a stress:  you have been bitten by a wolf, and it wants to bite you more.
Your body responds (among other things) with a surge of cortisol.
The cortisol
1:  Blunts immune response.  That inflamed hip you have needs to not slow you down.  That chronic cough needs to go away.  That stuff can wait.  You need to RUN.

Blood sugar goes up.  RUN!
Platelets go up.  You need to stop bleeding.
Repair / anabolic mechanisms are suppressed.  That stuff can wait too.
Testosterone levels plummet. Do not try to impress the ladies, you with your bleeding wound.  RUN!

The idea is that a stressor warranting a surge of cortisol is temporary.  Once you have found a safe cave the cortisol wanes and you can lick your wounds and build back your body.  Artificially elevated corticosteroid levels (from pills, or a steroid secreting cancer) are indeed tough on the body because of suppression of immunity and anabolic processes.
When people today talk about "stress" with jobs and grumpy roommates, it is not stress on the same level as a wolf attack.  Serious heavy duty stresses are what the glucocorticoid system evolved to handle.

The requirement for cortisol in response to acute stress remains important today. Illness, surgery, injury, and childbirth require high levels of cortisol.


text:
What evolutionary advantages does a longer muzzle have against a shorter muzzle and vice versa
Basically I'm curious as to why when it comes to mammalian predators that some like say bears and canines tend to have longer muzzles than those like big cats.
aside from their ancestors/evolutionary line and such, what advantages or disadvantages do short muzzles and long muzzles have against each other and which is better?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Note particularly that "which is better" is probably the wrong question — I suggest starting with the assumption that varying traits (e.g. different muzzle shapes) have costs and benefits with optima that depend on the circumstances.  ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

This paper, The biomechanics of foraging determines face length among kangaroos and their relatives might provide some insight, but very likely misses a lot of factors that would apply, e.g., to wolves vs cougars.  In the case of carnivores or omnivores, hunting strategies, prey capture methods, and even tearing & chewing techniques are likely to interact synergistically with muzzle length via the Baldwin effect (Wikipedia). Another paper The Baldwin Effect and Genetic Assimilation compares the Baldwin Effect to the Waddington effect, which can have similar results.
Edit:
In response to the suggestion by @Willk and @tyersome, I've added the following explanation:
The Baldwin Effect is widely accepted among evolutionary biologists.  The Waddington Effect is not as widely accepted and is sometimes (incorrectly) interpreted as a form of Lamarckism.
In essence, the Baldwin Effect works like this:

a population is subjected to a new environmental challenge or opportunity
a few individuals learn a new strategy that overcomes the challenge or exploits the opportunity
natural genetic variation makes some individuals in the population more capable of learning the new strategy
Individuals whose genetic makeup makes them more capable of learning the new strategy have a fitness advantage and produce more descendants, so over time the proportion of individuals in the population who can are genetically equipped to learn and use the new strategy, increases.
Individuals whose genetic makeup gives them a physiological advantage in regard to using the new strategy will have a further fitness advantage, and will consequently produce more descendants than others in the population.

Let's say the environmental challenge for two different kinds of carnivore (let's call them Bogs and Dats) is to catch Mophers.  Both Bogs and Dats initially have the same medium-to-short muzzles.  Some Bog individuals figure out that they can dig  Mophers out of their burrows, and some Dat individuals figure out that they can catch Mophers at night when the Mophers leave their burrows.  Both strategies are successful.  Some Bogs happen to have longer muzzles than their cousins, and find it turns out that longer muzzles work synergistically with the digging strategy, allowing Bogs to stick their noses into the Mopher burrows to grab escaping Mophers.  The resulting fitness advantage results in an increase of the long-muzzle trait in further generations of Bogs.  Note that in this scenario it is the adaptive behavioral strategy that creates selective pressure that favors a particular genetic adaptation.
Dats on the other hand, because of their nocturnal hunting strategy, benefit from improved night vision; and long muzzles don't provide any fitness advantage to Dats because Dats don't dig Mophers from their burrows.  As long as Bogs and Dats don't hybridize, they will most likely end up with long and short muzzles respectively.
The Waddington effect, also called “Genetic Assimilation”, is somewhat more direct:

An environmental stress causes a proportion of a population to develop one or more abnormal traits, by interfering with embryological development.
If there is a selective pressure in the environment that favors some subset of those traits, individuals whose genetic makeup makes them more likely to develop that subset of traits, those individuals are likely to produce more descendants than other members of the population.
If being “more likely to develop” that subset of traits results from a weakening of genetically determined development controls that would otherwise prevent development of that subset of traits, then the subset of traits can eventually become the normal phenotype.

An explanation of how the Waddington effect might influence muzzle length requires a bit more hand-waving, largely because there is no evident environmental factor that would cause perturbations in the embryological development of, e.g., dogs.  However,  I'd assert that an abrupt release of a strong selective pressure can have a closely analogous result.  Wolves really have to look and act a lot like wolves in order to survive in the wild (partly because of their survival strategies), so they are subject to strong selective pressure.  Domestic dogs, on the other hand, are subject to much weaker selective pressure.  Moreover, when a variant shows up (a pug, for instance which has a very short muzzle), it is often considered “cute” and is bred separately to fix the trait in a subpopulation.  Although the "release of selective pressure" mechanism isn't quite what Waddington contemplated, the process is closely analogous.
Note that the Waddington effect and the Baldwin effect are not mutually exclusive.  Relaxation of selective pressure that reduces fitness of variants, and environmental factors that cause disturbances in embryonic development (a la Waddington) both produce a rich source of variants upon which the Baldwin effect depends.
However, It is very difficult to prove that any specific phenotypic trait in an existing species was caused by a particular selective pressure. At best we can only make plausibility arguments supported by models and rather sparse environmental & ecological data from the geological record, from analyzing genotypes, etc. In the case of canines vs felines (which split off from a common ancestor perhaps 42 million years ago), we can really only guess what the environmental challenges & opportunities might have been, and what behavioral strategies may have been adopted by different individuals and populations.

Curious to know why this was downvoted.

Because that is what happens on the Biology Stack.  Fleshing out the Baldwin effect so save me the wikipedia click would be nice.  Upvote from me, though.

I think your answer deserves better than anonymous downvoting, but I would guess that the down voters felt like that this wasn't a good answer. I don't have time right now to read the links you've given, but a superficial scan of the Wikipedia article on the Baldwin effect left me unconvinced of its appropriateness in an answer to this question. If you elaborate on the Baldwin effect and its relevance, I would expect you to get a more favorable response.

Thanks for that advice.  I'm not looking for favorable responses per se; just want to be helpful to the OP.  I will elaborate on how the Baldwin effect and Waddington Effect might be relevant.

The problem you have is it does not answer the question, which is what functional aspects of muzzle length favor different relative lengths. I get that you are saying it is difficult to answer but you need to say that explicitly, basically you need to say your not answering becasue it can't be answered (which is wrong but hey its your answer)

Its mostly due to different forms of predation.
Longer jaws are deeper and can reach farther around a prey item, it also increases the chances of catching a moving target in the jaws becasue the area the jaw covers is larger, all things being equal it should always be favored but things are rarely equal, everything has a cost. It is common to see longer snouts in animals that hunt primarily with the jaws. There two ways to do this which depends on how big the pery to are after is, for predators going after relatively small prey they favor long thin snouts, is really noticable in aquatic predators like gharials, it makes for a very fast bite with a wide attack range. Alternatively if they are going after large prey they need to balance strength with speed so you see long, but not as long, more robust snouts. Think alligators, hyena, wolves. Whereas cats who attack with their forepaws can use a smaller head and jaw and favor a more precise bite, becasue they are moving with the prey becasue they have grabbed it, the arms are absorbing most of the stresses. Cats favor grabbing and strangulation for which a small short jaws works fine. Energy and material saved here can be used elsewhere. A longer snout would be weaker unless they add a lot more muscle to stabilize it. In terms of resources it is a lot of cost for little gain, whereas in wolves it is worth the cost becasue they need that strength anyway, becasue they jaw is where all the stress of the struggling prey is being transmitted.
You see the same thing in dinosaurs, predators that can attack with the claws have weaker bites/smaller heads. In the case of dinosaurs however snout length varies less because the small heads favor slashing bites, which favors a longer snout (thus a longer cutting row of teeth) there heads get narrower and weaker more than shorter.  Mammals can't use this strategy because they don't get replacement teeth, and they would quickly not have a tooth in their head, so instead you see strangulation favored instead.
Of course an animal can try to balance a range of strategies and there are all kinds of specialized forms like saber teeth, venoms, ect. Of course this is also simplified a lot of other things effect snout length as well, things like climate (long snouts cause less heat/water loss through breathing), sense of smell, or even vision.
https://www.cambridge.org/core/journals/paleobiology/article/dinosaurian-and-mammalian-predators-compared/BE3492DA7E0A103C6F6E77B9611D86A9
https://link.springer.com/chapter/10.1007/978-1-4615-0161-9_14
https://www.cambridge.org/core/journals/paleobiology/article/constraint-and-adaptation-in-the-evolution-of-carnivoran-skull-shape/77B1591461066F9D0E30F309F6C495C6
https://www.sciencedirect.com/science/article/pii/0034568770900757


text:
How to calculate percentage of DNA that ancestors contributed?
In David Reich's book "Who we are and how we got here" there is a graph explaining that more we go back in our ancestors generations, the least we have chances to have any DNA inherited from one of these ancestors because the number of ancestors is doubling every generation while the number of stretches of DNA is only increasing by 71.

In the left side of the graph, there is a percentage indicating how many ancestors contributed to our current DNA. For example : 50% of 1024 ancestors after 10 generations.
I don't understand how this percentage is calculated and it is not explained in the book.
Could someone help me understand it please?

The answer I'm going to give is more or less copied from Graham Coop's post, but I'll try and summarise it here.
A single generation ago, we have 2 ancestors. If we go another generation back, we have 4 ancestors (your 4 grandparents). If we assume that there is no inbreeding within the ancestral population, every time we go back a generation, the number of ancestors doubles.
On the other hand, the amount of your DNA you inherit from each relative halves each generation. You get ~50% of your DNA from your mother and ~50% from your father. These are inherited in large blocks which are split up by recombination events. If you go back a generation, you inherit ~25% from each grandparent.
However, because of stochasticity in how recombination occurs, you don't inherit exactly 25% from each grandparent. What you really inherit is a value distributed around 25%. There is a nice discussion of the ins and outs of it here. As an extreme example, if your parents and grandparents transmit entire chromosomes without recombination, then it is possible not to inherit any DNA on that chromosome from the other grandparent.
It's quite unlikely ($p=4$ x $10^{22}$) that you don't inherit anything from a single grandparent. However, as you go back through generations, it's increasingly likely there are some relatives who don't contribute anything to your DNA.
For example, 8 generations back, there's around a 20% chance that any given ancestor didn't contribute anything to your genome. Therefore, we can say that the number of genealogical ancestors a given generation back is one minus the number of ancestors who contributed nothing. This is why, even though 10 generations back we might have 1024 ancestors, perhaps only around 50% of them will have contributed anything to your DNA.
I'm not entirely sure about how the figures in this book were calculated; whether it was from simulation or not. However, the results should be more or less the same as how Graham Coop calculated it in the above post.

Yes that's right, if we look at the Graham Coop's plot, him and David Reich seems to find the same chances to get ancestor's DNA (like 50% for 10 generations ago). But I don't understand how do we get from 1024 ancestors and 757 stretches to a 50% chances when 757/1024 = 74%.


text:
Is it possible to distinguish between coding and template strands from the sequence?
Let’s say you have the following DNA sequence fragment:
5’-ACCAGTACTTCGT-3’
3’-TGGTCATGAAGCA-5’

Is there any way to determine which strand is the template strand and which is the coding strand for RNA synthesis solely from the above information?

There are two main problems with your post. First it lacks any sort of context: why this sequence, is it eukaryotic or prokaryotic, are you looking for promotor sequences, is it a homework question and what research have you done yourself to try to answer your question? It sounds very much as if you don't really know what you are asking and have made no effort to read about the topic, otherwise you would know that the answer is No. The second problem is terminology. Template for the mRNA transcript of a gene meaningful, but unusual terminology;  coding strand is ambiguous. Please clarify.

For reference, this question has been the subject of discussion on biology.meta

Given a DNA sequence alone, you can annotate open reading frames (ORFs) in order to identify the coding strand, with the caveat that not all ORFs are genes.  ORFs are sequence segments that begin with a start codon (ATG, though see my note below) and end with a stop codon (TAA, TAG, TGA) when read from 5' to 3' in 3-base codons.  There are no start or stop codons in either strand of the short sequence you provide, so I've appended a new example sequence:
DNA :

    5' - AGGATGCAGGAGTGGTACGATTTATCCTAGGAACCT - 3'  <-- Coding strand
            ^^^                     ^^^
            Start                   Stop
    3' - TCCTACGTCCTCACCATGCTAAATAGGATCCTTGGA - 5'  <-- Template strand

RNA :

       5' - AUGCAGGAGUGGUACGAUUUAUCC - 3'

Note that the start and stop codons given are part of the standard nuclear genetic code shared by eukaryotes, and there are alternative genetic codes used in prokaryotic and mitochondrial DNA transcription.

I don't know about your specific example (perhaps look for triplets that code start codons?), but machine learning has been used to predict promoters from sequence information (from promoter regions, you get downstream initiation of transcription of DNA to RNA). You would probably need more sequence to predict a promoter with more certainty. Cites: https://en.m.wikipedia.org/wiki/Promoter_(genetics) and https://academic.oup.com/bioinformatics/article-abstract/35/16/2730/5270663

The answer is simple : promoter
the promoter is a non-coding sequence of DNA found on one strand of the DNA when reading from (5'->3') which is to be the template strand .
For example the (TATA) box is found in prokaryotic cells DNA (also named  prinbow) and in eukaryotic cells DNA .In eukaryotes, It has the following sequence (5'...TATAAA....3') and is centered (-20-30 bp/20-30 bp upstreaming away from the coding sequence of the gene)  it is the sequence to which the transcription factors  and RNA polymerase II bind initiating the transcription process.


text:
Genetic variance for a behavioural trait among human populations
From this article from The Guardian:

We instinctively assume that differences in behaviour that are in fact due to culture must be linked to – even caused by – characteristics of appearance. That is what the traditional notion of race is all about. But genetics has found no such innate origins of behavioural differences between “races” – and it is highly unlikely, given what we know about genetic variation, that it would. (my emphasis)

Because the term "race" is so poorly defined and because this categorization has been and still is an immensely important source of hate and discrimination, I will use the term "human populations" (despite the term being at least as vague). The fact that the term categorization into "races" does not make in any way a good representation of the partitioning of the genetic variance in human populations (e.g. see this post) is irrelevant to our discussion.
Are there any study who investigate the partitioning of genetic variance for a behavioural trait (e.g. drug dislike, aggressiveness, agreeableness, openness, reading performance, etc...) among "human populations" (defined one way or another)? Did they find a significant correlation? What is their correlation coefficient?

The article I refer to says

We instinctively assume that differences in behaviour that are in fact due to culture must be linked to – even caused by – characteristics of appearance.

In no way, do I expect that the phenotypic variation used to define races could "cause" much of an eventual genetic structure for a behavioural trait. I know it is a politically sensitive topic. Let's raise above it and discuss the evidence.
Estimating partitioning of genetic variance
If need be, see this post for a definition of heritability.
I realize that estimating the partitioning of genetic variance is a difficult endeavour and can easily be confounded with other sources of phenotypic variance such as the ones caused by social and educative systems. Any article that does its best to estimate a correlation coefficient between a behavioural trait and "races" is welcome.
Behaviour
Of course, the term "behaviour" is not perfectly defined. This has never prevented us from massively using this concept in biology and I don't think it should prevent us from using this vague categorization of phenotypes to answer the current question.
What behaviour am I interested in? ... pretty much anything that one might want to call behaviour. I am not particularly interested in behavioural differences that might be directly cause by a difference in the prevalence of a specific disease.
In the book IQ and the Wealth of Nations, Lynn and Vanhanen attempts measures of IQ among countries. These methodology has been highly criticized. I double that IQ could be considered as a behaviour but, while I would welcome anyone to include such work in an answer (along side its criticisms on their methodology; e.g. Witcherts et al., 2010; see also Rindermann 2007), I would rather like to focus on evidence that are not directly focused on IQ. I am fine with evidence that are on behavioural traits that somehow relate to our intuitive notion of intelligence (e.g. reading performance, spatial abilities, ...). This answer in the post Genes and Intelligence is very relevant and lists three articles that looks for loci that explain some variance in IQ.

Obviously, this is a politically risky topic.  It might be safer to approach it from a perspective on dog breeds.   It should be possible to model evolutionary mechanisms that might cause genetic linkages between physical and behavioral phenotypes to emerge.

Is there any evidence that (outside of a few pathologies) there is any genetic component to behavior?

My understanding was that variation within the so called races of humans was much larger than that among the "races". I'm also sure that I've read that there is more genetic diversity among "Africans" than among the rest of the worlds peoples. To me that suggests this question isn't actually scientifically based since it presupposes that the culturally based (i.e "made up") category of race has a genetic basis. See for example this Scientific American article.

@jamesqf Thanks for your comment. I tried to address it by extending the long follow-up to my question. Let me know if you think my question is unclear.

@tyersome Thanks for your comment. To me that suggests this question isn't actually scientifically based since it presupposes that the culturally based (i.e "made up") category of race has a genetic basis. I think we can all agree that there is some genetic structure for skin color and hair straightness among Nigerians and Japanese. I do not want to state that such phenotypic variation have been more important that cultural differences in defining races but the existence of some non-zero (yet eventually very small) genetic structure exists.

@tyersome I do not state either that races are in any way a fair partitioning of the existing genetic structure in humans (I have now added a link to a post that discuss the impressive genetic diversity among modern day Africans compared to the rest of the world). I am asking whether any such structure has been investigated for a behavioural trait. If you still think my question isn't scientifically based, please let me know why and how I can improve it. Thank you

I guess the problem I have with this is that "race" is known to not be a valid categorization. Consequently it seems to me that any question based on "race" is inherently problematic. There are genetic factors that control traits like skin color and hair curliness, but there are also genetic factors that control ear lobe attachment — you could define ear-races based on that, but it also wouldn't be meaningful. It isn't clear to me how to fix this problem — maybe you could substitute "human populations" for "races in humans"?

@tyersome I rewrote the post using the term "human population" instead of "race". It allowed me also to shorten the post as I don't have to clarify that I understand how meaningless the concept of race is in explaining the partitioning of genetic variance among humans. Thanks


text:
Do we excrete waste in same order of food intake?
Obviously I do not expect we poop out molecule by molecule in exact order. All I am  asking is, is it possible for us to pass stool's of today's food before we poop yesterday's food. Does our GI tract act like a First-In-First-Out pipeline always?
Otherway to frame the questions is, If we consume hard to digest food 'A' first, easy to digest food 'B' next, is there a chance of B to come out before A?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources).  ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

It depends on the food you have eaten. Some foods are more difficult to digest than others, and will take longer to pass through your digestive tract. Once your waste has accumulated in your colon and formed a semi-solid/solid stool, then it's likely no material can make it past that, or combine with it, but until that point, it makes sense that material from items could intermingle and get jumbled up.
The following provides rough guidelines for how long it can take to digest food:
https://www.mayoclinic.org/digestive-system/expert-answers/faq-20058340


text:
More efficient method of calculation genotype or phenotype ratios rather than doing a trihybrid punnett square or forked-line method?
Is there any other more efficient method of predicting ratios of offspring phenotypes or genotypes than doing a trihybrid Punnett square or forked-line diagram? Or are those two methods really the only solution. This is for a question dealing with unlinked traits.


text:
Is this some kind of parasite crawling about in my yard?

I've been living in Jamaica 25 years now and never seen something like this until recently they started popping up around my house at nights by the dozens.  They appear to be blackish purple or maybe just black (I think my light has something to do with it), but I recall seeing a grey one once and longest one I've seen so far is about 3 inches long.

It looks like a terrestrial ribbon worm.

https://upload.wikimedia.org/wikipedia/commons/a/ad/Terrestrial_Ribbon_Worm_%28Nemertini%29_%2822799575773%29.jpg
Nemertean worms are not leeches, but a different group of worms.  Most are marine but there are a few terrestrial ones.  This depicted worm is from Borneo and other terrestrial nemertean worms are from South Asia also.  But I have read that these can stow away in plants and are turning up in other parts of the world.  I found some small ones in San Diego that I thought were terrestrial leeches but were nemertean worms.
I would be very curious where you are in the world that big ribbon worms are partying in your yard.


text:
Is there a measure of human genetic variation, where human genetic variation can differ more than 1%?
According to this
Neardenthal genetics

The proportion of Neanderthal-inherited genetic material is about 1 to
  4 percent[12] [later refined to 1.5 to 2.1 percent[11]] and is found
  in all non-African populations

And according to this
Interbreeding between archaic and modern humans

Neanderthal-derived ancestry is absent from most modern populations in
  sub-Saharan Africa

Now, human genetic variation is usually said to be between 0,1% to 0,5%
Genetics

While the genetic difference between individual humans today is
  minuscule – about 0.1%, on average

Why are the genomes of humans 99,5% the same

Human's DNA sequence is said to be roughly 99.5% equal

But here,
Human genetic variation
There are at least 6 different ways to measure human genetic variation and

human-to-human genetic variation is estimated to be at least 0.5%

Does this last affirmation and the first two articles tell us that the difference in human genetic variation, according to some measures of variation, it's actually more than 1% ? (larger than some ways to measure our genetical differences with other animals like chimps for example that are usually mentioned to highlight our similatiries) Or are there things missinterpreted in all this?

The question makes it clear that the poster is aware of the different ways of estimating human genetic variation, and he is also no doubt aware of the fact that Wikipedia is written by “people like you” who may not be experts in the field or have updated an old entry based on limited data. Let me address what appears to be the cause of confusion in this question — certainly in other questions on this topic.
For simplicity let us take a suitable round number for the Human/Neanderthal relatedness. Then the poster’s first quotation can be simplified as:

The proportion of Neanderthal-inherited genetic material in modern Europeans is 2%.

and his second quotation simplified as:

Neanderthal-inherited genetic material is absent from modern Africans.

A common conclusion drawn from this is:

The genetic variation between modern Europeans and Africans must therefore
  exceed 2%, rather than being only ca. 0.5%.

Why is this wrong?
This conclusion is wrong because the 2% and 0.5% are measures of different things.
For simplicity, a value of human genetic variation of 0.5% can be regarded as the extent by which the DNA of the coding regions of the genes of two humans differ because of single nucleotide polymorphisms (SNPs) — single base changes in the same gene (that may or may not affect the gene function). This assumes all humans have the same 20,000 or so genes.
Now let us make an overall comparison of the genes of humans and Neanderthals. Since they diverged from a common ancestor their genomes underwent changes due to point mutations, but, as far as I am aware, they maintained the same set of genes. Even if I am wrong on this latter point, the vast majority of genes — and the ones that we are concerned with are common: they both have/had a gene for myosin, for hexokinase 1, for chymotrypsin etc.
Examination of the majority of such homologous genes reveals single base differences, which must have arisen since the divergence. A combination of such Neanderthal variants in one gene — never seen as human SNPs — and the converse situation allow one to designate a chymotrypsin gene, for example, as human or Neanderthal, even though the overall DNA sequence of the chymotrypsin gene may be 95% identical (to conjure a figure out of the air).
Now consider the European/Neanderthal comparison. It turns out that a small number of genes show no (or almost no) variation between the two, but that most of these show the standard ca. 95% difference between Africans and Neanderthals (and hence between Africans and Europeans). These, then, are the 2% of genes that arose from interbreeding of Europeans and Neanderthals, after the exodus from Africa.
But 2% of genes of different origin which still retain 95% sequence identity would only add 0.1% to the modern human variation, cited at ca. 0.5%.
Disclaimer
I do not know the actual extent of variation between most human and Neanderthal genes or the details of the non-African genes of Neanderthal origin. I will be happy to edit this answer if anyone has that detail. I apologize for the geographical generalizations not present in the question, but my concern was to convey the argument without burdening it with continued qualifications.


text:
How can the organic mercury compound Thiomersal be not dangerously toxic?
My intuition tells me that organic mercury compounds are absolutely toxic. Unimaginably, fundamentally, extremely and uncompromisingly toxic.
I know that is not true for all doses.
Thiomersal is the organomercury compound that was used in vaccines as preservative. It's use has been controversial outside of the scientific community.
I am not asking whether the use in vaccines is dangerous, to be clear:
The use of mercury as Thiomersal in vaccines it is not dangerous.
That is well-established beyond reasonable doubt. Far beyond.
My intuition tells me that any organomercury compound it so mind-blowingly toxic that I feel cognitive dissonance if I try to accept that, at some dose, it's not.
I'm totally aware that toxicity depends on dose, that the compound is toxic at higher doses, and the dose used is just low enough that it is not toxic.
But the dose used is still antiseptic and antifungal, and having anything in my body that contains mercury and carbon in a dose high enough to kill a form of life feels just not right.
I would not worry at all to get vaccinated with a vaccine containing Thiomersal, and if a physician would ask me whether I prefer a vaccine with or without it, I would answer "Whatever you think is best."
But still, on the abstract level, the feeling of "That can't be right" to have an organomercury compound in my body it pretty strong.
I know it is not dangerous, but:
How is that even possible?

How is it possible to have highly toxic chemicals like sodium and chlorine in the body?  Or how can harmless carbon and nitrogen form highly toxic cyanide?

@jamesqf I understand what you mean, and my intuition has no problem with that, even cyanide itself can be used as medical drug. But organomercury compounds are much worse than even cyanide: For example, methylmercury goes into the brain and stays there, going on to kill brain cells until there are not enough to live, some month later. Cyanide makes getting oxygen not work, either you die, or feel bad until the next day and all is fine, roughly. Methylmercury is just unimaginable toxic.

I think you missed my point, which is that chemical compounds have chemical properties that are usually entirely unrelated to the properties of the elements that compose them.  The properties of CN, including its toxicity, are nothing like those of elemental C or N.  NaCl (necessary for life) is nothing like elemental Na (probably bursts into flame in contact with body fluids) or Cl (used in WWI as a poison gas).  So why should any particular mercury compound be toxic?  See answer regarding the difference between ethylmercury &  methylmercury.

You might also ask why it is that literally hundreds of millions of people can spend large parts of their lives with mercury-containing dental amalgams in their teeth, without showing any sign of mercury poisoning.

@jamesqf And why sailors used to ingest large globs of pure metallic mercury, aka quicksilver, to clear intestinal blockages. Not that it's recommended as it can cause long-term mental effects, of course...

@jamesqf I see what you mean, and agree, the elements in a compound have no relation to the toxicity. But there are classes of compounds that are typically toxic. For example the lower alcohols. And with mercury, the organic compounds are such a class. It's enough to be toxic if only minor amounts of a high dose of a compound is metabolized to methylmercury, and as it's not a particularly comfortable way to die, it's not worth trying.

@CJDennis - Yes, it is not about mercury in general, but about organic compounds containing it. (I know somebody who ate metallic mercury just for bragging.) Exposure to metallic mercury is over longer time because it vaporizes slowly. I think the problem with fillings is different: The filling is created using a mercury alloy, which is eutectic. That means the amounts of the alloyed metals have a specific relation. If one of the metals is too much, it stays unalloyed as particles in the alloy bulk. If the mixture contained minimally to much mercury, that can diffuse out over long time.

@jamesqf I think your "obvious" relativising comparisons are not warranted. The OP obviously knows more about chemistry then what you are trying to make him look like. Organo-metalic compounds are often extremely poisonous when the metal itself is not and the OP points out exactly that. Take lead and tetraethyllead (gasoline additive) as an example. Methyllead is extremely poisonous and the OP points that out. It should not be dismissed so lightly, if not even offensively, that ethyllead is just something else. It should be explained scientifically.

@CJDennis - To illustrate the toxicity of an organic mercury compound: A scientist doing research specifically about the toxicity of methylmercury died from mercury poisoning. She was clearly aware what she was dealing with. She was protected. Some drops fell on her latex gloves, nothing more. There was no hole, just what went through the gloves by diffusion poisoned her. She died a few month later.

[citation needed]. Did she die from mercury poisoning, or methylmercury poisoning? There are so many compounds made of mercury. Some will be highly toxic, some mildly toxic, and maybe even some not toxic at all.

@CJDennis - It was Karen Wetterhahn, professor of chemistry at Dartmouth College. The toxic substance was dimethylmercury. She died in 1997. See https://sites.dartmouth.edu/dujs/2008/05/16/remembering-karen-wetterhahn/ .

@CJDennis There are actually several referenced cases.  Ceccatelli S, Daré E, Moors M. 2010. Methylmercury-induced neurotoxicity and apoptosis. Chemico-Biological Interactions 188(2): 301-308. doi:10.1016/j.cbi.2010.04.007

@Volker Siegel: Re lower alcohols being toxic, that brings up what seems to be a pretty direct analogy to the relative toxicity of methylmercury and ethylmercury.  Methyl alcohol is quite toxic (https://en.wikipedia.org/wiki/Methanol_toxicity ) while ethyl alcohol is regularly consumed by a large fraction of the human race, and is toxic only in large amounts.  So obviously all alcohols are not equally toxic, so why should we expect all mercury compounds, or lead compounds, to be?

Thiomersal is broken down into two compounds, thiosalicylate and ethylmercury (Ensink 2015).  The thiosalicylate it is relatively non-toxic, and there is even some evidence that this compound could counteract some of the effects of mercury poisoining (Asadi et al 2010), though the mechanism of this inhibition has yet to be elucidated.
Although they have similar names, methylmercury and ethylmercury have very different levels of toxicity.  Methylmercury has long been known to be highly toxic, producing high levels of cell death in the brain, particularly in the cerebellum and the visual cortex (Ceccatelli et al 2010).
Unlike methylmercury, ethylmercury appears unable to cross the blood-brain barrier as fast as it is eliminated in the stool.  Consequently, small quantities of ethylmercury have been shown to be non-toxic, resulting in the relative non-toxicity of thiomersal (Pichichero et al 2002).

Sources:

Asadi S, Zhang B, Weng Z, Angelidou A, Kempuraj D, Alysandratos KD, Theoharides TC. 2010. Luteolin and thiosalicylate inhibit HgCl(2) and thimerosal-induced VEGF release from human mast cells. Int J Immunopathol Pharmacol 23(4): 1015-1020.

Ceccatelli S, Daré E, Moors M. 2010. Methylmercury-induced neurotoxicity and apoptosis. Chemico-Biological Interactions 188(2): 301-308. doi:10.1016/j.cbi.2010.04.007

Ensink E. 2015. Preservative or poison? The science behind Thimerosal. The Substrate (online): http://substrate.asbmb.org/2015/05/15/preservative-or-poison-the-science-behind-thimerosal/

Pichichero ME, Cernichiari E, Lopreiato J, Treanor J. 2002. Mercury concentrations and metabolism in infants receiving vaccines containing thiomersal: a descriptive study. The Lanclet 360(9347): 1737-1741. doi:10.1016/S0140-6736(02)11682-5

is the toxicity of mercury in general primarily focused on its effects in the brain, then?

Primarily; see Ceccatelli et al 2010 if you have access to a library which contains it.

So its still nasty stuff but we simply poop it out fast enough to survive?

@PTwr That really describes a very large number of toxins. Everything has some minimum dose required for it to actually be dangerous, and below that it's usually a case of the body getting rid of it (either through excrement or through some form of decomposition) faster than it can do anything dangerous.

Just as a curiosity - what prevents the body from breaking it down into the more toxic or the two, or one being converted into another (like how Ureic Acid breaking down into ammonia) by the body?

@Pureferret If you examine the structures of thimerosal, ethylmercury and methylmercury, you'll discover that breaking thimerosal down into methylmercury doesn't make sense, structurally; you'll also discover that reactions that turn ethylmercury into methylmercury don't really make sense energetically.

There is a considerable number of toxins that work by building strong complexes with vital molecules or cell mechanisms.  If you start out with already complete complexes that the body will neither break up or accumulate, the toxicity is, so to say, already exhausted.  Cyanide is like that: it builds strong complexes with iron, but something like potassium ferrocyanide is even commonly added to table salt.
Things are different with enzymatic poisons like Amatoxins or Botulism toxin since their toxicity is not used up while they are effecting their damage.
"Not being used up" refers to the idea that the toxins are active and can cause damage catalytically, over and over. Consider diphtheria toxin, which enzymatically inactivates proteins necessary for protein synthesis. Even a single molecule of that toxin (well, technically it's a complex of more than one) can kill a single cell by inactivating every single one of its targets and causing protein synthesis to grind to a halt. Cyanide, on the other hand, binds to its target and doesn't let go, so one molecule of cyanide can inactivate one molecule of (say) cytochrome c oxidase (complex IV).

The case of "toxicity not used up" is interesting.

@VolkerSiegel "Not being used up" refers to the idea that the toxins are active and can cause damage catalytically, over and over. Consider diphtheria toxin, which enzymatically inactivates proteins necessary for protein synthesis. Even a single molecule of that toxin (well, technically it's a complex of more than one) can kill a single cell by inactivating every single one of its targets and causing protein synthesis to grind to a halt. Cyanide, on the other hand, binds to its target and doesn't let go, so one molecule of cyanide can inactivate one molecule of (say) cytochrome c.

Thanks, that's worth adding it to the answer - which I just did.

authors: Vladimir F Героям слава