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Can vaccines drive viruses to evolve? If so, how?
Obviously, destroying vaccine-vulnerable strains of a virus will leave the vaccine-resistant ones to represent an increased fraction of the overall viral population.  I'm asking, though, whether/how vaccination can allow a particular strain of a given virus to reproduce more than it would do without vaccination against another strain of the same virus, or to infect more hosts than it would infect without such vaccination.
If only vaccine-vulnerable strain A exists, might application of an anti-A vaccine somehow directly cause the mutation that creates resistant strain B?  If so, how?  Or are such mutations only random (in which case strain B might randomly arise even if the vaccine it was resistant to was never even invented)?
If strain A and strain B both already exist before any vaccine is developed, and then strain A is perfectly eradicated by a vaccine that strain B happens to perfectly resist, then of course strain B will remain - but will it actually benefit, in the sense of becoming able to increase its own population or its host population beyond what the respective count would have been without the anti-A vaccine?  If so, by what mechanism?

Mutations are random.  Also, I think it would help clarify your question if you considered whether you are interested in virus "benefit" as absolute number of virus particles vs. percentage of total virus particles, particles in one individual vs. in a population, and at one point in time vs. dynamic change over time. Finally, "vaccine-vulnerable" is not yes/no, but a dynamic continuum involving many factors and portions of the virus lifecycle.

"absolute number of virus particles vs. percentage" - this should be clear already. "particles in one individual vs. in a population" - in a population (of potential and actual hosts), unless the other option is highly relevant in a way I'm not aware of. "at one point in time vs. dynamic change" - whatever is most relevant. I don't know much about this; that's why I'm asking. "'vaccine-vulnerable' is not yes/no" - in my A-and-B example it is, for the sake of simplicity. In reality: One case in which vulnerability of any sort helped a less-vulnerable mutant would suffice to answer the question.

Antibodies/serum escape mutants are better studied (in-vitro and mice). Usually one escape mutation is not enough, the virus must accumulate 10 of these to be "resistant" and if each of these 10 mutations would have occurred anyway, the combination of the 10 would have been very unlikely without the selective pressure of the serum, making the 1st mutation rapidly fixed, then the 2nd and so on, with the neutralization by the serum decaying a bit each time. Change of selective pressure: some deleterious mutations becomes fit and conversely.

@reuns "the combination of the 10 would have been very unlikely without the selective pressure of the serum," - but why? How is the pressure exerted? If the mutations are random (meaning vaccination doesn't encourage or cause them), then vaccination shouldn't directly make that combo of 10 more or less likely to arise. Does it allow that rare mutant to flourish and become common by vanquishing the competition that would normally have kept the mutant in check? But in that case, HOW do viruses compete? Or is there some mechanism for application of pressure other than competition among viruses?

Isn't it obvious? Mutation 1 is likely to arise without selective pressure but it will likely stay at a very low frequency and eventually disappear, with the selective pressure its frequency rapidly increases which gives a lot of chances for mutation 2 to appear in the background of mutation 1, and so on, the fit mutations accumulate. This process works as soon as the vaccine/serum pressure is not too high, so that the virus doesn't get extinct before finding the good combos of mutations. It's easier to study in lab with antibodies cocktail, decreasing the titer until the virus can proliferate

@reuns "but it will likely stay at a very low frequency and eventually disappear," - why? How?  THAT is my entire question here.  If it can rapidly increase without the unmutated virus around, then why couldn't it do so with that original virus still around?  Would the original virus hold it back?  If so, how? If it does so, then yes, the rest seems obvious.

Because the virus with the mutation replicates better, it evades the Ab a bit. This mutation will often be not fit without the Ab.

In what way does the presence of antibodies it can evade a bit help it to reproduce more than it would without any of those antibodies to have to evade at all?

OK, if you insist on the vaccine vulnerability being yes/no, then you've essentially got a situation where A and B are totally unrelated viruses. Here's a real-world situation:
Let's call A "COVID" and B "RSV". Before we had a COVID vaccine and during the lockdowns, RSV (respiratory syncytial virus), had dropped to very low levels because little kids were not mingling and transmitting it due to the school shut-downs, etc. This allowed the pool of non-RSV-exposed kids to grow and become a larger fraction of the population than normal. Once COVID vaccines began to be administered, society began to re-open and just recently, mid-2021, there have been many RSV outbreaks, with larger numbers of symptomatic individuals than typical, and more serious cases than normal.
In thinking about what you wrote a bit more, it seems like your "benefit to B from a vaccine against A" would require:

Infection with A at least partially protects against later infection with B.
The Anti-A vaccine provides less protection against infection with B than does previous infection with A.
The Anti-A vaccine reduces the number of people who are infected with A before being exposed to B.

Items 1) and 3) together mean that the anti-A vaccine reduces the number of people infected with A, thus reducing the number of people at least partially protected against B because of earlier infection with A. (1) and (3) seem plausible to me.
However, the "benefit" for B would then require (2), that the anti-A vaccine provides less protection against B than does earlier infection with A.  That is, those people who now are not infected by A would have less protection against B even after vaccination.
Although theoretically possible, this seems quite implausible to me, given the real-world data we've seen over the past year. What tests have been done seem to show that the Moderna and Pfizer vaccines provide better protection against variants than does previous infection with another variant.


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If a small population left one continent and sailed to another, would the genes of the population that left show relation to the original population?
This question has a specific context, a religious one, and so I'm not sure this is the right place to ask, but I can't think of a better place. I would like as objective and unbiased an answer as possible. I hope the religious context doesn't make this an unsuitable question. I'll explain the religious context:
There is a religion that believes that a small number of Jews left Israel circa 600BC and sailed to the Americas, where they multiplied and built their own new civilization(s). This religious organization also has a history of teaching Native Americans that they are the descendants of this population, so therefore that their ancestors are Jews from 600BC.
But we're quite lucky in the modern age that we can do genetic testing! And they have done, and of course they've found no signs of a genetic relationship between any Native American tribes and any known Israeli or Jewish populations. The organizations response to this is that, after 2600 years, you wouldn't expect any genetic similarities between the two populations - if they've been physically separated for so long, all genetic markers of a relationship would have disappeared.
Is that correct? Would 2600 years be enough time to erase all genetic evidence that this population originated from Israel Jewish people?

Related: isolation by distance

You may be interested in recent research about migration between Polynesia and South America 800 years ago that left a genetic signal. It's only a fraction of your time span but still. The New York Times had reported about it.

Related: Genetic history of indigenous peoples of the Americas and Haplogroup

If we assume a population of 100 individuals migrated from the Middle East to Central America 2600 years ago and, even if they underwent admixture from the local population, then there would be extremely clear genetic signal that those individuals were from the Middle East and not 'native' to Central America. Native Americans and individuals from the Middle East are sufficiently diverged that they are easily distinguished from one another.
For example, you could plot all the populations on a Principle Component Analysis and the migrants from the Middle East would cluster with other Middle East populations and not Native Americans. The fact that 2600 years had passed since the migration event doesn't change this. In the context of distinguishing between populations, that amount of time doesn't erase genetic differences.
A very similar event to what you mention has been shown to have occured when migrants from Persia moved to India with their Zoroastrian religion, forming the Parsee community in India. Clearly Middle East and Native Americans are much less genetically similar to one another than Indians and Iranians, so it would be similarly much easier to disinguish them genetically.

That's a fascinating example about Zoroastrians! Thank you.

I've marked this as the answer, but I want to note that the answer of @RogerVadim below  also gives reasons to be skeptical of the idea that any genetic tests of Native Americans would necessarily conclusively prove that they are not Jewish (or at least Middle Eastern) of origin.

I think it would be more accurate to say “migrants from Persia moved to India with their Zoroastrian religion, forming the Parsee community in India“ rather than “… forming the Zoroastrian religion [in India]”. The Zoroastrian religion originated before this migration, probably in Persia.

@KrazyGlew thanks - edited.

@TKoL I’m afraid that your takeaway from the other answer isn’t correct: the evidence is, in fact, pretty damning. I think both you and I may have misunderstood the other answer; alternatively, the other answer is flat out wrong. Either way, it’s pretty misleading.

@TKoL KonradRudolph is correct. Comparing the genome of the religious group to i) Native Americans and ii) Middle Easterners (either ancient or modern DNA) would conclusively and unambiguously show whether the individuals were local or not.

@user438383 I'm curious what you make of this article then: Nearly one-third of Native American genes come from west Eurasian people linked to the Middle East and Europe, rather than entirely from East Asians as previously thought, according to a newly sequenced genome.

That article does show a genetic link to the Middle East, however it potentially still contradicts the LDS story, since the path to the Americas was via Siberia and presumably the Bering Strait. I'm not sure if that makes this evidence for or against the LDS origin story...

@Tkol Native Americans may derive ancestry from those sources, but they are still entirely distinguishable from the sources based on their unique combination of alleles.

@user438383 derive ancestry from those sources would be sufficient for LDS purposes. They've remained (deliberately) unclear if they believe ALL native americans are exclusively descended from from this group of Israelites, or if there may have been other Natives in the Americas prior to the events in the LDS holy book.

@KonradRudolph I don't see the contradiction between the two answers. On the one hand, the genetic signal would be unambiguous in such conditions, as this answer states. On the other hand, genetic signal is not sufficient for proving the point in the OP, since we do not have many genomes directly available form the 2600 ago, and comparison will be indirect, likely relying on non-genetic evidence. It is a problem of scientific study design.

@RogerVadim You don’t need a genome from 2600 years ago to perform comparative genetics. Phylogenies are routinely established based on comparison of leaf genomes, without the presence of ancient genomes.

@RogerVadim we do have ancient DNA from Caanites - only a single sample would really be necessary to show whether the Native Americans were/weren't related to it.

'@KonradRudolph interesting. How do you add geographic metainformation to your phylogeny? What do you use for time labeling? I suggest that we take a context more familiar to you - ancient British island population from 2600 years ago, instead of Israelites.

@user438383 Canaanites is one of many ethnic/cultural groups that populated the region - I doubt that comparison with Canaanite genome proves much. Note that Jews even in those times included such ethnically diverse groups as Ethiopians and Yemeni, from Sabaean kingdom.

From the point of view of genome comparison the signature would be unmistakable, as @user438383 has pointed out in their answer. There may be however other methodological issues undermining this study:

Scientific - one need an attested representative of a Jewish genome from 2600 ago or their attested ancestors
Political/religious - genetic testing is not recognized as a valid proof of Jewishness/non-Jewishness by Jewish communities (see, e.g., here)

While the scientific issue that I mention might not seem as much of a problem, the experinece shows otherwise. E.g., the highly controversial hypothesis of the Khazar ancestry of the Ashkenazi Jews has been a subject of much debate, with many studies both proving and disproving it. Khazars were a people and an Empire to the South of (modern) Russia that were an important political power throughout a few centuries. They are known to have converted to Judaism (or at least their elites). However, as this culture had vanished about fifteen hundred years ago, one cannot attest which people are descendants of Khazars and what genetic signal is an evidence of such a descent. Affirming or disproving this hypothesis is thus dependent on what is taken as a Khazar genome, and arbitrariness of such a choice produces equally arbitrary results.

Update
This is to bring precision regarding some of the remarks made in comments.

Firstly, to quote the OP:

Would 2600 years be enough time to erase all genetic evidence that this population originated from Israel Jewish people?

To summarize my answer in more plain terms:

[..] comparing two genomes proves nothing, if one cannot attest their origin. Jewishness issue was mentioned in passing, as a kind of things that a scientist needs to take into account, when posing an answerable research question.

In more expanded terms, as requested by the author of the OP themselves:

This would not prove that they are Jewish, since there were many other peoples present in the region at the time. 2) Over the two-and-a-half thousand years the region has been subject to many mass migrations (note that this is a land bridge between Europe, Asia and Africa), so it would be likely controversial and dependent more on historical than genetic evidence. Each can have his/her own point of view, but proving something beyond any doubt is next to impossible.

Finally, discussing "what/who is Jewish" would take us far away from biology, since it involves intertwined religious, ethnic, cultural, and historical aspects. The only reason to mention this in this context, is that a scientific question should avoid such complex and ambiguous notions, since they may render it unanswerable.

Update 2
Seeing the number of up- and down-votes to my answer, as well as the comments, I would like to add a bit more rigorous discussion regarding the difficulties involved in such a study. There are three points that one needs to address:

Do genomes of relatives separated by 2600 years still resemble each other?
What are the genomes that one needs to compare?
What does the positive/negative results of such a comparison proves

Point 1. is easiest to answer: yes. One could do a back-of-the-envelope calculation that 2600 years is about 100 generations, which means about the same number of new mutations in a 3 billion nucleotides long human genome. Recombination poses a greater challenge, but we still expect to be able to compare chunks of genome of tens or even hundred thousand nucleotides long. This perhaps already answers the OP, and this is why they accepted the answer by @user438383
Point 2 can be addressed in (at least) two ways:

Proxy genome @user438383 pointed out that a Canaanite genome is available. If we do find the similarities between this genome and those of our target group, this counts as a result. But if we don't, it again proves nothing, since the ancestors in question could be from a very different ethnic group. Note that we are talking here about a land bridge between Africa and Eurasia, through which the ancestors of most of the non-African human populations passed at least once.
Phylogenetic reconstruction @KonradRudolph mentioned phylogenetic reconstruction, but didn't elaborate. To implement such an approach we will need to

sample genomes from the populations that we believe to descend from the Middle East

build a time-labeled phylogenetic tree, to prove that the most recent common ancestor is located somewhere around 600 BC.

Prove that this common ancestor actually comes from the Middle East

Point 3
A correctly posed scientific question of this type should not make any reference about Jews and should not draw any conclusions about them. Doing so is just bad science. Indeed, Jews is a complex term that may refer to

certain ethnic groups (more than one) - vision widespread due to some sad historical events
religion - anyone can become a Jew by converting to Judaism, and such conversions are known to have happened on a large scale - e.g., the Sabaean kingdom, occupying a part of Arabian peninsula (modern Yemen) and parts of modern Ethiopia is known to have practiced Judaism, and some of their descendants in the region are continuing to do so till these days.
Cultural, political, and other attributions (e.g., Soviet Jews had it written in their passport, even if being non-religious and having rather remote Jewish ancestry.)

It also has a more direct bearing on our question, since it doe snot allow us to attest the ethnicity of the founders of the community in question, nor do the members of thsi community need to be descendants of its founders.

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

A good answer, but wouldn't it be sufficient to prove that no admixture has occurred to the Native American gene pool of any group from the larger group of Middle Eastern populations? Jews, however they are defined, were part of that larger group, after all.

@j4nd3r53n One cannot say reliably that one has sampled all the groups. One could prove the converse, that the population in question has common ancestors with some populations that are attested to have lived in the Middle East. I see several possible study designs here, but I don't want to be more specific than the OP. Jews is that the word has multiple meanings: ethnic, religious, cultural, historical - e.g., one can become a Jew by converting to Judaism, but oen can also be a Jew by birth while being non-religious. This word shouldn't be a part of the research question in my opinion.

Molecular Phylogenetics
You may have seen a "tree of life" image like this:

While this particular image only shows amphibians, such trees have been constructed for more or less every known species, using the morphological and genetic information available to us.  The field responsible for studying and constructing such trees is called molecular phylogenetics, and it is predicated on the idea that such a tree may be uniquely constructed with nothing more than the genome of each species.
Although we certainly do not have genomes for every species in history (or even every extant species), it is believed that the "tree of life" is a single tree.  That is, there are no "disconnected" subtrees which have no relation to the rest of the tree.  The notion of a group of organisms which descended from some ancestor, and then became so isolated as to "erase all genetic evidence" of their relationship would imply that some subtree exists which cannot be connected to an ancestor node on the full tree.
It's Possible
Now, we need to be careful here.  It is possible for two groups to only appear genetically related by a common ancestor which is older than their real common ancestor.  For instance, suppose we have that group A begets group B begets group C.  We want to know if C is really descended from B.  It may be the case that, based on the molecular record, we can only say that B and C are both descended from A, because B is only modestly different from A, and C has changed all those differences, even though it was actually descended from B.  So, I would say that it is theoretically possible.
Reality
However, there are a large number of "ancestry-informative markers" (AIMs) which allow us to determine from which continent a person's ancestors most likely originate.  For a given individual genome, we can say with decent confidence whether their ancestors came from Europe/Asia or the Americas.  Note that there are no concerns about populations which might have "bred out" all of their AIMs to confound a determination of their "ancestral continent(s)".  Perhaps that's because some AIMs have 100+ markers which would need to disappear in just a few hundred generations (the most extreme example would be a 13-year generation, which would give 200 generations over 2600 years).  AIMs are far too stable to simply disappear at a rate of nearly 1 per generation (if they did, then we couldn't reliably use them to determine ancestry in the first place).
Now, if we look at the specific example of a central Asian population seeding the Amerindian population, we have the problem that Amerindians are most closely related to northeast Asians (Siberians, in particular).  If Amerindians were really established by Jews, why don't they have strong matches to the Middle Eastern markers common among Jews?  So this claim fails in both directions: First Nations peoples are not genetically similar to any recognized/acknowledged Jewish population, but are similar to the north/east Asian population which almost certainly crossed the Bering land bridge after the end of the last ice age.  So much for Atlantic canoes... (or did the Jews take the long way around, travelling through Asia and Siberia to the Americas?)

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Is there a biological term for an activity period that is determined by temparature
In general we refer to the activity period of organisms in terms of the period of the day that they are active.  Diurnal, crepuscular, nocturnal, matutinal, and vespertine, for example.
There are certain desert animals whose activity patterns seem to match a temperature range more than they do the day/night pattern.  Is there a term for this type of activity pattern?

I doubt there is such term.
Note that diurnal and seasonal are likely pretty well correlated with the temperature cycle. The temperature cycle is, I would presume, mainly affected by the daily and seasonal cycle.
You can talk about a behaviour that is dependent upon the temperature which fluctuates daily and seasonally. Looking for specific keywords on Google Scholar, it appears that most authors go through short phrasing of the kind to express this concept.

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How long can algae survive with no air recycling (closed bottle)
In a small bottle nearly filled of Chlorella in water and grow medium, how long would it take for them to die (with or without light).
Thanks in advance ;)

Calculate the oxygen in the bottle, calculate how much oxygen the Chlorella will use all together per second = time.  Best I can give you with no specifics provided.

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Best data repository to publish a large 'plotly' table containing all annotations on a transcriptome?
I want to publish a transcriptome paper, along with interactive materials enabling readers to peruse the data behind the discussion. The R package 'plotly' enables rendering online-publishable tables that can be filtered & searched for specific entries.
I would like to publish such a table as supplementary to a paper (e.g. preprint version) however usually data repositories allow for uploading files and text. I intend to deposit the first version of my main manuscript to Bioarxiv, where they primarily publish .pdf files.
Would anyone here know an official data repository with a format such that would enable publishing online an interactive table?
A good example of such a table is given here.
Disclaimer: I have also asked this question at SE BioInformatics. Like me, they are unsure which would be the best fitting SE Community.

Your example seems to be hosted on the website of an institute. Is there any reason you can't do/try something similar?

Journals and services where you can submit your script and manuscript and get DOI:

PLOS One
F1000
Zenodo
CodeOcean

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Is there any system how genes are spread across chromosomes?
Every chromosome being a wrapped DNA molecule contains thousands or more genes.
Now, is there any system why a gene A goes to a chromosome K and gene B to chromosome J?

To a first approximation, it is "not too awful" to state that genes are randomly spread. In a more detailed view, it is a little more complex.
Homochromatin vs heterochromatin
Genes are not evenly spread within chromosomes. Typically, gene density is lower at the centromeres.
Supergenes
From wikipedia > Supergenes

A supergene is a group of neighbouring genes on a chromosome which are inherited together because of close genetic linkage and are functionally related in an evolutionary sense, although they are rarely co-regulated genetically

To my understanding, such supergene may come to existence via chromosomal rearrangements or via repeated proximal gene duplication.
Supergene and synteny
From Wikipedia > synteny

In classical genetics, synteny describes the physical co-localization of genetic loci on the same chromosome within an individual or species. Today, however, biologists usually refer to synteny as the conservation of blocks of order within two sets of chromosomes that are being compared with each other. This concept can also be referred to as shared synteny.

A classical example of supergene with highly conserved synteny among vertebrates is the case of Hox Genes (Amores et al., 1998).
Sexual chromosome
A sexual chromosome is some kind of a massive supergene! Consider, for example, the mammalian case.
Consider a locus that affects sex determination (SD) such as the SRY gene (coding for TDF) in mammals for example. Any male-beneficial, female-detrimental genes would gain at becoming closely linked to this SD gene. Over time, hence genes rearrange and recombination is reduced (mainly through chromosomal inversions if I am not mistaken). As recombination is reduced, deleterious mutations can accumulate through Muller's ratchet and eventually pieces of chromosomes are being lost to get rid of these deleterious mutations. This is how a Y chromosome (to consider the mammalian case, a W chromosome in birds) evolve to become so small compared to the X chromosome (or Z chromosome in birds).
Other Y-like chromosomes
Other massive supergenes can lead to Y-like chromosomes. For example, Wang et al. (2013) report a Y-like social chromosome in fire ants.
Additional source of information on the evolution of sexual chromosome
The post Do males of all sexual species have Y chromosomes? might be of interest to you. Charlesworth (1991) and Charlesworth et al. (2005) might also be a good reads.

In prokaryotes, genes of a single pathway genes are often next to each other, and are transcribed together as a single unit.  So for those genes, their position is quite important.


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Reversal form of endosymbiotic theory?
Cell's organelles give us evidence that they might have been independent organisms on their own.
Are there any single-cell microorganisms known to have gone so to say this way back as well, i.e. having some evidence to have their past as part of a larger organism?

It's not exactly what I've asked.. Slime molds same do not qualify. Still, good to know.

An organelle who did not come from an endosymbiosis does not contain DNA. It cannot just go away and leave on its own without hereditary material. A piece of DNA can however eventually leave a genome and become its own thing!


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Why don't we consciously know how our bodies work?
Our brain is responsible for regulating our entire body. However, we don't consciously know how our bodies work — our brain has to learn about biology, medicine, and so on.
Since our brain controls our bodies at the cellular level and below, why do we still have to learn about these processes to become doctors, biologists, etc.? Shouldn't we born knowing about them?

We aren't even conscious about most of what goes on in the brain; consciousness is still a poorly understood phenomenon, but we know that lots of brain activity happens without conscious awareness. Most of the regulatory functions of the body are included in that unconscious activity, but so are some processes closer to what we do in day to day life.
For example, if you are experienced driving a car, you are able to do most of the general functions (staying in a lane, for example, or starting to brake at an intersection) without much conscious input, allowing you to have a conversation simultaneously. You only need to be strongly aware of what's happening in an unexpected situation.
Similarly, muscle movements come from executed programs that are learned through experience (especially for humans; some of these movements are innate). When you raise your arm above your head, for example, there are muscles in your arm that move, but also muscles in your back and legs have to adjust to prevent you from tipping over with the new weight distribution, you might lean your head out of the way, all of this is done without you thinking about each one of those individual muscle movements: you are just conscious of the whole general movement.
Regulatory control of things like your heart rate or digestive system is even less out of conscious control.
Brain-computer analogies are often fraught with peril, but in this circumstance I think it is reasonable to use one. Your computer is able to perform all sorts of calculations, it even has software that allows you to communicate with a network of other computers to bring you StackExchange. But even if you download computer science books onto your computer, it has no idea how to assemble a new computer from scratch. It can display the text that could allow someone else to do it, but it is completely unnecessary for its day to day functioning to know how to replicate it.
So back to your original question: why don't we consciously know how our bodies work? Because it's completely unnecessary to know this for normal day to day operation in the context in which animals evolved.


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Neurons competing for survival
I was reading in a book that in the process of neurogenesis - when new neurons are born -  neurons compete for survival. Or in other words they have to make themselves useful to the brain otherwise they die and become processed as brain food.
To what extent is this real and how often does this happen?
i think that in the book I was reading it the author mentions it happening in early life, but I'm not entirely sure.
Would be great to know.
Thank you!

Welcome to Biology.SE and thanks for your question. Could you please provide a reference to the book you've read this in (and a direct quote of the claim would also be much appreciated). Thanks!

It's definitely real ;)
Depending on your previous knowledge, this review from 1987 might be a good starting point.
http://science.sciencemag.org/content/237/4819/1154.long
To give you an idea of recent developments this article is an easy read. Be sure to browse the references.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/

Welcome to Biology.SE! Could you include some relevant text from your sources, both for ease of reading and in case those links die?


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Using nanodrop for analysing biological samples other than nucleotides
I am a 3rd timer postdoctoral fellow with some experience in molecular biology and biochemistry, but major skills in Zoology and Natural History. I am studying some natural extracts, and isolating compounds.
Some biological samples come in limited amounts (e.g. invertebrate haemolymph), hampering analytical methods that rely on larger amounts. For instance, establishing UV-Vis spectra of extracts is a usual non-destructive method for approaching unknown samples and estimating general parameters, done with a spectrophotometer.
The microvolume-scaled spectrophotometer system popularly known as 'Nanodrop' has been around labs since almost two decades now. Its use has been usually limited to fast purity & concentration estimations for DNA & RNA in molecular biology labs.
I am considering using the nanodrop to estimate parameter of other biological and chemical samples. The manual says most commonly used solvents are compatible with the system. I have however yet found no-one else who has tried using Nanodrop for different applications.
Please, anyone here who has experimented using a Nanodrop system with other biological samples and extracts could comment on the experience?

The Nanodrop is a generic UV-visible spectrophotometer. According to the manufacturer, the latest model can measure absorbance from 190 to 850 nm. Its dynamic range is also very good: from about 0.1 to about 60 in absorbance. Therefore, as long as you don't use an incompatible solvent, you can measure anything that absorbs in this wavelength range. I use it very often for purified proteins. It also works well for turbid suspensions (like bacterial cultures; reading optical density at 600 nm gives an idea of turbidity).
It is easy to use, and of course the low volume requirement is a big advantage. One drawback is that it won't let you fine tune certain parameters like a "real" spectrophotometer would allow (bandwidth, gain, etc.). But you can definitely get decent spectra for characterization of mixtures and concentration estimation of pure samples.

'you can measure anything that absorbs in this wavelength range' -- Yes, I have been trying out for the first time recently. But have you officially done it? My peers seemed revolted as they state a nanodrop should be used only for DNA/ RNA/ protein standards. They sounded so dogmatic.

Yes, I have measured absorption of fluorescent dyes that is nowhere near absorption wavelength of proteins or nucleic acids.
Using a Nanodrop only for proteins and nucleic acids seems like a lab policy (in my opinion, too strict and not justified), but it is definitely not a technical limitation of the instrument.

I used the Nanodrop for the measurement of the absorbance at 600 nm of bacterial cultures, as well as nucleic acid preparations. However, I switched to using another spectrophotometer (Spetrophotometer, Ultrospec 2100 pro, UV/Visible Spectrophotometer, Amersham Biosciences) for my bacterial cultures because I trust it more due to using a cuvette containing 1 ml of bacteria instead of just 1 microlitre of culture.

In fact some nanodrop models do have a special pedestal for measuring OD600 of microbial growth. I ought to have mentioned that in my brief intro for the question. My main issue is, as soon as I mentioned to peers I'd be using nanodrop with other biological samples they got revolted, stating 'a nanodrop should be used only for DNA/ RNA/ protein standards'. I was wondering why they sounded so dogmatic about it, and how readers would receive if I employed it otherwise.

Maybe some people measure their sample and retrieve afterwards and you are contaminating the system. They might be concerned that their sample gets contaminated?

Perhaps. Nanodrop is naturally unstable, and people may blame anything for a weird result. But if samples are soluble in compatible solvents, I see no logical point, and they really declared they believe it is designed solely for nucleotide analysis (which is not what it says in the manual).

After completing my tests, I have decided to come back to answer my own question.
A Nanodrop machine has served my purpose quite efficiently, as far as I can judge. I used have used it to evaluate the degree of purity of a natural alkaloid extract from insects, using synthetic alkaloid analogues as controls. See our published paper discussing the method here, along with raw data.
We have noticed no alterations nor cross contaminations to colleagues' DNA/RNA samples running in parallel, highlighting on the fact that I properly cleaned the equipment between use.
Therefore, yes: I recommend using the Nanodrop as a cheap & quick method to scan biological samples, provided chemicals and solvents used in cleaning the pedestal are compatible with the manual.
Hope this discussion help others dare!

@WYSIWYG I reckon we did what you describe, no? On using synthetic compounds as standards and doing a wavelength scan?

Sorry. I did not see it. Also, if you use the "UV-Vis" mode (I have nanodrop 1000), you can choose two wavelengths (in other assays, the wavelengths are fixed). I assume you used that.


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How do I cover Cellstrainers?
I‘m doing some experiments for my bachelors thesis and I‘m using some Cell strainers by Roth for it (https://www.carlroth.com/com/en/accessories/cell-strainer-easystrainer™/p/cly9.1). My problem is that the setup is supposed to stay in an incubator at 37 °C for up to 3 weeks and it needs to be covered the entire time. Sadly I didn‘t find a proper way to cover the cell strainers which sit on top of a regular 50 mL Falcon tube. Does anyone of you have an idea or can speak from experience?
P.S.: Parafilm doesn‘t work since it gets sticky at those temperatures.

What about just setting the cap of the 50 mL tube on top of the strainer? It'll still allow some airflow, but should protect against contamination settling into it.

@MattDMo I‘m affraid the pbs solution inside the Falcon tube would evaporate. Air flow isn’t important to me since I just misuse the cellstrainer as a sample holder for a nanocomposite hydrogel I synthesized. But you just gave me an idea that might just work out. Thanks a lot!!


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Bug identification
Germany, cca 0.6mm, dead Bug, i haven't see before

This is an immature cockroach, possibly Planuncus vinzi.
Here is a map of the observed distribution of the Planuncus genus:

And here is an extract of a gallery of nymph-stage Planuncus cockroaches:

To view the full gallery: https://www.inaturalist.org/taxa/732965-Planuncus/browse_photos?term_id=1&term_value_id=5
You can change the "Life stage" attribute from 'nymph' to 'adult' to see what the fully-grown versions look like and see whether they look more familiar to you in that form.


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Bootstrap values
What do the bootstrap values indicate about the relationship between the species? I'm working on Mega program but I don;t understand what bootstrap value means in simple terms and also what does it indicate about the relationship between species

Welcome to Biology.SE! What research have you done before asking it here?

The bootstrap values belong to a wide category of values called support values. Support values in general are used to give some indication of the degree to which one can be confident that the branch represents some "signal" present in the data.
In particular, bootstrap values indicate how robust the branches in the tree are, that is, how resistant they are to perturbation in the data. They are obtained by re-sampling columns in the data matrix, building trees from such re-sampled matrices, and looking at the proportion of the obtained trees that contain a given branch.
In the case of bootstrap, the re-sampling step is done the following way: Suppose that the original data matrix has N columns (i.e. N encoded characters, that can be nucleotides or amino-acids in an sequence alignment, morphological characters, presence-absence of genomic features, etc.). A new matrix will be obtained by randomly drawing one of these columns, N times. The new matrix will therefore have the same number of characters, but some from the original matrix will be present multiple times and some will be absent. This will influence the topology of the tree. For instance, if a branch was supported by characters that now are absent, this branch may not appear any more with this particular re-sampling. The re-sampling is usually done around 100 or 1000 times.
A low bootstrap value means that if the tree is built using a subset of the data, it is likely that this branch will not appear.
A high bootstrap value means that the branch will likely appear on a tree built from such a re-sampled matrix. This does not necessarily mean that the branch is more likely to represent the true historical relationships, though: sometimes, reconstruction artifacts can be robust. For instance, with some molecular phylogeny reconstruction methods, taxa may end up being grouped based on similarities in genome composition. High bootstrap values indicate that there is a strong signal in the data supporting the branch, be it historical signal or other.

Nice answer +1. Would you mind clarifying how we resample. Just explaining how are the data organized in the matrix might help to clarify what re-sampling columns in the data matrix really mean. Does it mean subsetting the SNPs sequenced, or the individuals available, or some other pre-processed statistics, etc...?

@Remi.b I tried to expand a little my answer. This is re-sampling of characters (conventionally encoded as columns), not individuals (conventionally encoded as lines). Note that re-sampling of individuals would lead to trees on different sets of taxa, and it would therefore be impossible to simply compare branches between trees and compute branch support values.

@Remi.b If you can read French and are interested in these support values thing, you may have a look at the introduction of my thesis (pages 9 and 10 of https://tel.archives-ouvertes.fr/tel-00331825/). I see that I mentioned "perturbations de l’échantillonnage taxinomique" in ways of measuring robustness, but I can't remember what I had in mind...

Wow I did not know people are still writing PhD thesis in french! It feels like a pain having to translate your publications from english to french just for the thesis. Yes, I can read french. Thanks for the link.

In France, I think it is still pretty common to write theses in French (especially in humanities, but not only). The main text of the thesis was written in French, but the articles were included as is, in English. I'm happy I could write in my mother tongue: it made the experience much more enjoyable.

Good. While french is my mother tongue, I personally always have a hard time to talk science in other language in english (which can arguably be a bit of a handicap for me). Where I am currently doing my PhD (at UBC, Vancouver, BC, Canada) the thesis is basically the publications copy-pasted together replacing in this article by in this chapter and writing a few words to make everything fit together so there is not much rewriting to do, that's why it feels like much work having to write the thesis in another language to me. Anyway... Cheers!


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ant ID montreal, qc canada
I'd like to know what type of ants this is. These appeared in my basement recently.
I am thinking those are called "pavement ants" after comparing online. Please help me identify them.
( Sorry for the blurry image quality, these are quite small and are scared of my camera )


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Explanation for lack of wing-leg-fin transformations in arthropod evolution?
I don't know much about evolutionary biology so I may be missing something obvious.
It seems that vertebrate evolution somewhat frequently re-invents the fin out of the leg or wing and the wing out of the leg or fin.
If this pattern was extended, one would expect to see gliding spiders with leg-wings (dear God); insects whose ancestors had wings that now use their wings as a 4th pair of limbs for grabbing, sensing, or fighting; crustaceans or sea-spiders that swim with fin-like legs, etc. But as far as I know, for all their incredible number of species, we never see leg-fins, leg-wings, wing-legs, or wing-fins in arthropods. The occasional swimming bug (shrimp, etc) just uses its body segments and tail, and if it uses its legs at all it's just for stabilization or steering. Insects may or may not have wings, but they never have back-mounted limbs for grabbing, sensing, or fighting.
Is there a straightforward reason for this?

Life emerged in the water. Ancestors of insects, spiders, myriapods and crustaceans were probably terrestrial but then, crustaceans evolved to living in the water again. Finally, woodlice went back onto land!

Ancestral structure of wings in insects is somewhat unknown but it started out with 3 pairs of wings (could come from gills, could come from the exoskeleton). One pair was then lost in all living insects today. Drosophila lost a second pair afterward. Some lost both remaining pairs. In Membracidae, the first pair of wings became a whole bunch of crazy structure.

paddle crabs? e.g. Charybdis japonica


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Hybrid corn yield vs mass-selected corn
I am a social scientist and I was reading "The political economy of hybrid corn" by Jean-Pierre Berlan and Richard Lewontin.
https://go.gale.com/ps/i.do?id=GALE%7CA4325182&sid=googleScholar&v=2.1&it=r&linkaccess=abs&issn=00270520&p=AONE&sw=w&userGroupName=anon%7E8cf008c1
They claim that the R&D cost for inventing hybrid corn was much higher than the mass selection of corn varieties (Mendelian selection scheme). One reason hybrid corn was adopted was that farmers had to revisit the seed seller every year to maintain their corn yield because the second generation hybrid corn is much less productive, while the selection of a new productive corn variety will make the seed company obsolete once the productive crops are distributed. It was claimed that Henry A. Wallace, the founder of hybrid  seed selling company and the son of Secretary of Agriculture Henry C. Wallace, pushed for hybrid corn at the expense of using Mendelian scheme.
I was wondering if there is any academic article or experiment result that compare the productivity hybrid corn versus corns that were developed by "Mendelian selection scheme."

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Hybrid corn IS a "Mendelian selection scheme". The issue here is more predictability and uniformity of crop growth and yield.
Normally, plants are genetically varied and having different versions of each gene from mother and father usually increases the fitness of the plant (this is sometimes called "hybrid vigor"). When farmers replant with seeds from only their "best" plants, over the generations the plants become more uniform and predictable in that (good) aspect, but also become more and more inbred (having both copies of a gene be exactly the same instead of slightly different). This inbreeding reduces plant fitness (e.g. yield or disease resistance).
With the discovery of genetics in the early 20th century, farmers realized they could get the benefits of hybrid vigor without the drawback of inbreeding. It's a two step process: separately breed two different varieties of a plant, each highly inbred, then produce seeds in a "seed factory" that have one variety as the "mother" and one variety as the "father". Each inbred parent passes on only the one version it has of each gene, but each (offspring) seed ends up with both different versions of each gene, one from each parent.
The resulting hybrid seeds called "F1" are both genetically uniform AND show "hybrid vigor" because each has two different versions of every gene. They just don't breed true, as the different versions of each gene get mixed up again ("reassorted") in further generations.
However, as long as the two original inbred parent varieties are propagated (remember, they remain genetically identical as they are inbred), the F1 hybrid offspring seeds can be recreated whenever desired. This naturally leads to a larger organization (like a company) maintaining the two parent varieties and continually producing reproducibly uniform F1 hybrid seeds for farmers to actually use.

Thanks for the detailed explanation. My understanding of Lewontin's article was that non-hybrid seeds that were properly developed would have been better than hybrid corn. Does that sound outrageous? Thanks

It seems quite unlikely. After all, nothing is stopping farmers from using non-hybrid seeds; if they didn't see an advantage to buying the hybrids, they wouldn't do so. The complexity comes in when you deal with multiple features of the plant. For example, maybe a given "heirloom" (inbred) variety has a special taste that nobody has been able to incorporate into a hybrid, so a farmer is willing to accept a lower yield or less hardy plant because they can get a significantly higher price for the product at market. In home tomato growing both hybrids and heirlooms seem to hold their own.

"Hybrid corn IS a 'Mendelian selection scheme'."

You've missed the point: that true-breeding (and predictable and uniform) vigor might also have been possible to select for, but seed companies didn't bother trying, since it would have let farmers replant seed—unlike the hybrid-corn business model of making farmers buy new seed each year.
(Tl;dr if hybrid vigor is because of heterozygote advantage at various loci, you couldn't select for true-breeding vigor. If it's because of dominant good genes in each parental strain covering up recessive bad genes in the other strain, you could.)

@DavidBahry We've learned a lot in the past 15 or so years of the genome era. One of those lessons is that in real life different alleles of a gene are not all good or all bad; in fact, many genes have multiple functions as part of the same gene! This has supported the assertion that hybrid vigor is due in large part to heterozygote advantage rather than just increasing the proportion of loci with "dominant good genes".  In this case, it seems the business model is indeed supported by the science.


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Is Hydrogen rich water safe and beneficial for health
Is Hydrogen rich water safe and beneficial for health ? I just bought a Hydrogen water machine to try and relieve muscle inflammation.

What (the heck) is a "Hydrogen water machine"?

You should use Magnesium... 60 percent of humans are deficient in magnesium but it is used in hospitals to treat inflammation, they inject it in asthma patients who are having an acute attack into their bloodstream. it helps with cramps, stiffness, bad sleep and other stuff. nerves have massive amounts of magnesium and calcium in them.

Results
The consumption of hydrogen-rich water for 6 weeks reduced reactive oxygen metabolites in the blood and maintained blood oxidation potential. QOL scores during radiotherapy were significantly improved in patients treated with hydrogen-rich water compared to patients receiving placebo water.
Conclusions
Daily consumption of hydrogen-rich water is a potentially novel, therapeutic strategy for improving QOL after radiation exposure. Consumption of hydrogen-rich water reduces the biological reaction to radiation-induced oxidative stress without compromising anti-tumor effects.


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What is the ratio of head to waist and waist to floor of the human anatomy?
I'm trying to find the ratio of upper body to lower body. That is, the ratio of the length of the waist to the head over the length of the waist to the floor.
It's been harder to track down a readable outline of the ratios of the human body than I expected.

Since I can't comment, I'll answer using the answer above - given the image shown, the 0.52/0.485 ratio is comparing the top of the head to the inseam relative to the inseam to the floor. Notice that the image given shows the waist at between 0.53 (the practical waist that most of us use when we wear clothing) to 0.630 (the anatomical waist, the narrowest point on the torso above the hips). That's actually the only number you need - subtract that from 1 and you have the other number. In short: above waist ~= 0.37 of total height, 0.63 below waist. The previous answer gave a reasonable image, b

@TPStacker: Simple observation would suggest that there is no such ratio.  Some people have long legs compared to their torso, other people have short legs.  That would seem to be true of other body proportions as well.

The study of those measures is called anthropometry. Typing anthropometry on google image returned this

This is definitely not a peer-review source and might eventually be a good approximation only for white males (or whoever they considered to take these measurements on) but if we believe this image, then the ratio head-to-waist over waist-to-floor is $\frac{0.52}{0.485} = 1.072$.

Perfect! And thanks for the additional comments on likely assumptions and approximations. And for the help with the correct term to look for.


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If the effect of increase CO2 in the air has a negative effect, why doesn't decreased CO2 have a positive effect?
I recently asked a question about whether there were studies on the effects of reduced CO2 level air and got what sounds like a good answer:
Are there studies on the effect of reduced CO2 levels on human cognition?
The answer posted to the above question states that there is no reason to expect low inhaled CO2 levels to even make a difference in the relative levels of CO2 in the lungs, with are ~100x higher than in the ambiant air. This seems like a rational argument.
But with further thought that argument seems inconsistent. If average CO2 levels in the air are around ~400ppm, just 3x that number, ~1200ppm, is known to be associated with drowsiness and complaints of poor air quality (if my research is correct).
If the argument above holds, that reducing CO2 levels in the air from ~400ppm to ~0ppm, isn't going to significantly affect the ratio of CO2 in the lungs, then why doesn't that argument hold also with a seemingly small increase of 3x CO2 levels in the air (as compared to the 100x levels in the lung already)?

The US Navy has tried to replicate the (highly dubious) results claimed by some recent "Green" buildings research (which is the stuff you're referring to, even if you don't say it explicitly). The Navy replication study failed to find any differences whatsoever in their replication. Non-replicable research gets published in psychology all the time, alas. Also the "Green" building research contradicted decades of prior research on the matter.

Thanks, that's a really good reference, that's the kind of stuff I was hoping to find with this question, you should post that as an answer. I am interested in the references to the decades of prior research. I'm not an expert in this field, so I look to places like wikipedia and stack exchange to cue into it, and I've been seeing contradictory publications.

3X atmospheric CO2 does not have appreciable cognitive impact.
Indoor air typically is already much higher in CO2, especially in a room full of people, because they are all breathing out CO2. It would not be unusual to find 2-3X atmospheric CO2 inside.
In the answer to your previous question, I referred to much higher concentrations that do have appreciable impact. For example, at 100X normal atmospheric concentration, the concentration in the air is similar to the normal concentration in the lungs, such that CO2 builds in the lungs and dissolved levels increase in the bloodstream.

So is a site like this is publishing incorrect information? https://www.dhs.wisconsin.gov/chemical/carbondioxide.htm, they state that: "1,000 - 2,000 ppm: level associated with complaints of drowsiness and poor air."

@davidparks21 They're being super safe for safety's sake. They aren't publishing incorrect information, they are publishing guidelines for keeping building air overturned. If CO2 levels inside are rising to 1000-2000 ppm, probably the building air isn't turning over much. There could be lots of other things in the air, and particular individuals who already have breathing problems (i.e., the CO2 in their blood is already high) could have symptoms.

I see a variety of numbers published that are hard to disentangle here. On this wikipedia page: https://en.wikipedia.org/wiki/Carbon_dioxide#Toxicity, I note two quotes, (1) "In concentrations up to 1% (10,000 ppm), it will make some people feel drowsy and give the lungs a stuffy feeling.[115]", which seems to support this line of reasoning, and (2) "A study of humans exposed in 2.5 hour sessions demonstrated significant effects on cognitive abilities at concentrations as low as 0.1% (1000ppm) CO2 likely due to CO2 induced increases in cerebral blood flow.[121]", which seems to question it.

Bryan is right, I think. The level of CO2 is used as a measure of indoor air quality because it is convenient, not because CO2 is toxic at these concentrations. There are probably confounding factors in studies which find a correlation between CO2 level and effects on cognitive function at 1000ppm. Studies controlling the level of O2 and other confounding factors have found have found no dose-response for CO2 under 2000ppm.


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Are there studies on the effect of reduced CO2 levels on human cognition?
I see studies that indicate elevated CO2 levels (>>400ppm) can cause cognitive impairment.
Are there also studies that investigate the effects of cognition under low CO2 levels (<<400ppm)?

I can't think of any biological basis for such a study.
CO2 is produced as a waste product of metabolism and exists in the blood and lungs at levels far higher than atmospheric levels (~100X). Relative to the air in the lungs, the atmospheric concentration of CO2 might as well be zero.
Very high atmospheric CO2 (relative to normal atmospheric levels) can have cognitive effects (among others) because it prevents CO2 clearance from the lungs and therefore increases blood CO2 (hypercapnia) and can cause respiratory acidosis.

Here's another good reference that supports what Bryan says here: https://en.wikipedia.org/wiki/Breathing

I guess impaired gas exchange makes sense for very high concentrations. Also in some studies high CO2 might correlate with cognitive effects due to confounders.


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What do white blood cells do with FOREIGN white blood cells?
White blood cells or leukocytes are known to fight invaders, infections or basically anything foreign. They also contain DNA (while red blood cells don't). But what about foreign "white blood cells" received in a transfusion or sexual intercourse (as semen, not sperm, holds "lymphocytes" which are a type of white blood cells, they can "possibly" enter the blood circulation, not quite sure).
Anyways, my question is:
1) Do white blood cells "fight" the foreign white blood cells and kill them off? OR is that something cleaned by the spleen itself? (considering WBC lifespan is 13-20 days so they die off their own). So do they "get" attacked by the host's WBC or do they naturally die off their own?
2) Does the body detect them as "foreign"?
3) I've also heard about the "extracellular DNA" phenomenon. Which is, the ability of DNA to exit a cell (while it's dying) and float in the extracellular (non-cellular) environment. The DNA is degraded during a cell death but it can definitely exit a cell and float non-cellular in the environment. This is also true for the cell's RNA. This is labelled as an "extraceullar DNA/RNA" or a DNA/RNA without a cell. So that being said, can the DNA of foreign leukocytes or white blood cells that do not belong to the host (having a completely different DNA, of course) exit it's cell during it's death and become extracellular DNA? Is that even remotely possible? Also, can that extracellular DNA (keep in mind, the DNA is a fairly stable molecule) ever remain in the circulation or the human body for life? Perhaps in the bloodstream? or in one of the organs? or in a biofilm? (considering exDNA is a component of a biofilm) Does that even have the "slightest" possibiliy of happening? For it to remain there for life?
1) If it is, wouldn't the body (the immune system or WBC) ever "react" or "act" on eliminating the "foreign DNA" of another person that's floating around? Or is that something which will remain for life OR be eventually faded away? I'm well aware of enzymes such as DNAses/RNAses (enzymes responsible for DNA and RNA degradation) but do they do that in the blood? And that being said, "sometimes" in a biolfilm they don't.
2) And even if it gets stuck in a "biofilm" (assuming it's possible?), would it "EVER" degrade eventually or remain there for life? OR CAN/WILL the "biofilm" holding such extracellular components degrade eventually or will it remain for life as well? (can they remain there forever?).
3) A simple way to explain this would be if I insert hundreds of "foreign DNA" (strands, not cells) into your blood stream, what would happen to them?
4) Can it get "stuck" or get glued to an organ or it's cells and remain there for life somewhere out in the deep where they won't be found? Since I'm not an expert in molecular biology I don't understand. In other words, can it EVER remain there for life with "ANY" slightest 1% possibility with all the possibilities I've explained or any other possibility of it remaining there for life? And same goes for the RNA. Having someone else's DNA and RNA scares the shit outta me. And having that for the rest of my life, makes me really uncomfortable.
My question is for both the DNA and the RNA.
I don't want "assumptions" or hypothesis please. Please answer if you're an expert in microbiology/molecular biology, others, etc. And are well aware of what I'm talking about. I will greatly appreciate it.
Also, this is a tricky one! (I completely don't understand this)
The molecules secreted by these "foreign" white blood cells after their death would provide structural and biochemical support to other cells so wouldn't a part of his trace (his molecules) would remain in other cells forever once they consume it? Or the molecules get replaced on a cellular level itself if I'm not mistaken? Wouldn't his molecules be a part of my body forever?
Please answer if you're an expert in microbiology/molecular biology, others, etc. And are well aware of what I'm talking about. I will greatly appreciate it. I don't want assumptions or hypothesis only whatever is known, proven, researched & concluded as a fact. :)
Thanks guys,
Marry

Please shorten your question body. Your question body has some unnecessary sentences.

It might be good for getting answer of your question that you don't restrict the job to specialist in molecular biology. Most of the people are here not specialist, but they are enthusiast and can provide good answers.

Okay, you have a lot of questions there. I'll try to give some answers, but if you want more details or background knowledge I'd recommend you to read /study more about immunology (none of your questions are actually about molecular biology or cell biology).
2) Foreign cells are generally recognised by the immune system, based on the HLA molecules on the cells: all cells that do not have the exact same HLA molcules are recognised as forgein and attack by the immune system (cells without HLA are not human and by 'default' foreign). Since there are many different variants of the HLA class I gene and humans have usually 6 different ones, its very unlikely that a cell from someone else would not be attacked (that's why it's so hard to find matching organ donors).
1) Foreign cells are attacked by the immune system, the spleen's purpose is to remove/recycle old blood cells from the body itself. Depending on how the immune system recognises a cell (e.g. by antibodies or diretcly by immune cells) different strategies to fight the foreign cell are activated.
3) There are certain receptors on some immune cells that can recognise extra-cellular DNA or RNA. This recognition is not sequence specific und usually causes an inflammatory reaction, because extra cellular DNA is a sign of either cell damage (by necrosis) or invading pathogens. After the immune system recognised such 'invading' factors they are usually taken up and removed by macrophages.
Generally speaking all of this only happens if foreign cells or DNA manages to get into your body (e.g. if you would inject it). It's very unlikely that DNA or cells can pass into your body unless you have open wounds. (White blood cells usually only are able to pass the endothelium of blood vessels, not other kind of barriers)


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Clinical Microbiology Books
I am looking for a good book about Clinical Microbiology, particularly good in Bacteriology and Bacteria Diagnosis (medium, plates, type of colonies...). With good photos. What are the bests in your opinion?
Thank you.

Manual of Clinical Microbiology.
My version is old, but it is an excellent reference considered gold standard in the clinical science industry and by educators.   It has been used by clinical microbiologists for many years and is still coming out with updated revisions. It comes as a two volume set due to comprehensive content. Published by the American Society for Microbiology.
http://www.asmscience.org/content/book/10.1128/9781555817381


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Wasn't extinction of dinosaurs necessary?
Beginning from the triassic era, dinosaurs crawled for millions of years. So my basic idea is, that had the dinosaurs not been wiped out, they would have eaten all the flora on the planet then. Because :
1)They (herbivore giants like brachiosaurus, triceratops etc) didn't have any predator. So population growth.
2)they must have had a great requirement of food for one day. (think of an elephant who has to eat a tenth of its way)
Doesn't All of this sum up to speak that nature found a way to save the biosphere (then) by extincting them?

That's not really how anything works in nature.

Speaking in the language of nature, if dinosaurs are fit enough for their environment, they deserve to live as long as they get sufficient food. And if plants and trees can't protect themselves from dinosaurs, they deserve to be eaten up.

Basic misunderstand about how one can make sense of nature
Nature is not a conscient being (or at least not falsifiable conscient being) trying to optimize the amount of flora or whatever you would like to optimize. There is no conscious will in the processes of evolution, in the course of a meteorite or in the decay rate of some radioactive material. Things just happen through causality (and eventually pure randomness when you go to quantum physics), not because there is a wish for this thing to happen.
So, in short no, dinosaurs did not get extinct because someone thought it would be better this way.
This discussion is not a matter of science but of philosophy of science and philosophy of knowledge. You can further this discussion on Philosophy.SE, they will be much better than me at addressing this misunderstanding.
Dinosaurs did not really get extinct
By the way, dinosaurs did not really get extinct as birds are dinosaurs. The number of dinosaurs lineages just suddenly (sudden in terms of geological time at least) decreased.
Loosely related to that, you might want to have a look at the post If dinosaurs could have feathers, would they still be reptiles?
For how long were dinosaurs there?
Dinosaurs (excluding aves, that is the lineage giving rise to modern birds) have roamed the earth from 226 millions years ago to 65 millions years ago (period called the Mesozoic). There is much more time separating the Plateosaurus (late Triassic; ~210 millions years ago) to the Triceratops (late Creaticious; ~68 millions years ago) than between the Triceratops and the first Homo sapiens (~250 thousands years ago). Dinosaurs have been around for long enough so that we can consider that they were not just eating all the plants!
As you assumed that predator population would just grow indefinitely in absence of preys, you might want to have a look at What prevents predator overpopulation?.

@SiddhantShekhar I just want to bring your attention to an edit in the section For how long were dinosaurs there? to try to help you getting a sense of how long was the so-called "age of dinosaurs".


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How does fish breath under water?
How we will describe the whole mechanism of fish breathing under water? How they absorb oxygen and and then remove oxygen through a process known as gas exchange?

Did you read articles like this about respiration in fish already? If so, could you please edit your post and add, what exactly remained unclear?

Fish are able to obtain oxygen that is dissolved within the water, and exchange it along with Carbon Dioxide through their gill structure, called filaments.  The gills are located adjacent to the mouth and filaments include a large amount of blood vessels.  Those blood vessels (capillaries) are close to the gill filament surface and move in the opposite direction to the water flow, which they are exposed to by means of the fish drawing in water through it's mouth.  The tissue that comprises the filament is porous and allows for diffusion of these small molecules (oxygen and carbon dioxide) across this tissue and into the blood vessels.  Each red blood vessel consists of four "Heme groups," which are designed exclusively to bind to oxygen and transport it through the body. A process called the Root effect (Bohr effect in other vertebrates) in hemoglobin regulates the "drop-off" of oxygen by recognition of low pH values.
Hughes, G. M., & Morgan, M. (1973). The structure of fish gills in relation to their respiratory function. Biological reviews, 48(3), 419-475.
Bonaventura, C. E. L. I. A., Sullivan, B., & Bonaventura, J. (1976). Spot hemoglobin. Studies on the Root effect hemoglobin of a marine teleost. Journal of Biological Chemistry, 251(7), 1871-1876.


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What is this very tiny insect that was in my bedsheets?

I found it in my bedsheets. I'm in Bordeaux, France. It is 3mm long and is the only one that I found.
Should I be worried that there might be others? If so, what should I do?

Related: Can anyone help confirm this tiny insect larvae?, Bug Identification: Is this small tubular, black bug..., How to protect my mounted insect specimens..., Varied Carpet Beetle Larvae, What is the name of the critter depicted..., What small insect is this?, What bug is this...

That is almost certainly the larva of a carpet beetle, likely the Furniture Carpet Beetle (Anthrenus flavipes). They are distinctively hairy and striped.

(image from wikimedia)
Carpet beetles are found world-wide and are a pest of homes, workplaces, museums, basically anywhere that textiles, paper, or foods are contained. They will happily eat wool, silk, fur, hair, bone and shell (e.g. tortoise shell, not sea-shell).
Getting rid of them is difficult - you need to clean out any areas where they can live, this includes all your clothes (hot tumble-dry for 1 h, or keep in sealed bags for 2+ months), any natural-fiber carpets, cupboards, furniture - literally anywhere dust can accumulate. Often easiest to get a pest-control expert in to deal with them.

Although for items that are small enough, keeping in the freezer overnight would be more than enough, no need to ruin your clothes. They do not cause as much damage (relative to their population density) as clothes moths in my experience.

@CaroZ True, freezer should work, but the internets are telling me at least 48h, and that dry-cleaning and ironing should also work.


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Difference between heritability on the scale of liability versus the scale of observation
I was reading a paper on disease heritability ("Estimating Missing Heritability for Disease from Genome-wide Association Studies") and it struck me that I don't have a great understanding of the differences between heritability on the liability scale and the observed scale. The main thing that I've read about is how the liability scale operates on an assumption of normality (since traits are treated as being continuous) making it unimodal and only appropriate for multifactorial disease. However, I'm not sure if I've caught on to the full extent of the difference.
Any input would be appreciated, even if it's just pushing me in the direction of a useful resource :)

Welcome to Biology.SE. Does this page from our sister Bioinformatics site help? OR maybe this page?


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What are the oldest living plants in the world today? What can you know about them? Why can some plants live so long?
What are the oldest living plants in the world today? What can you know about them? Why can some plants live so long?

please ask only one question and try to be spesific,what type of research has you done so far.you have multiple questions here.

Arguably Pando, an aspen grove that is a single connected organism: https://en.wikipedia.org/wiki/Pando_(tree)  But for the many plants that spread by vegetative methods such as root suckers, the question of what exactly an individual plant is becomes rather difficult to answer.  For instance, I have many varieties of roses in my garden, all propagated (for instance, by rooting cuttings) from plants that were in some cases bred a century or two ago.  Are they still the same plant?

Just to be clear; you are asking for oldest individuals of plants, right? Not the oldest still living species (~living fossil)?

Great Basin bristlecone pines (Pinus longaeva) have been known to live to be thousands of years old.
The oldest known living individual is named Methuselah and is estimated to be more than 4,800 years old. It's been credited as the oldest living non-clonal organism on Earth.
There are multiple other trees over 1000s years old.


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What does "the scaffolding of biology" mean here?
In Zoltan Torey's The Conscious Mind, the author discusses the emerge of self-awareness:

Turning to the changes that the acquisition of language instantiated, Damasio reflects on these changes in some detail:
To hold extensive memory records not only of motor-skills but also of the facts and events, in particular of personal facts and events, those that make up the scaffolding of biology, of personhood and the individual’s identity, these depending on the ability to reconstruct and manipulate memory records in a working brain-space, parallel to the perceptual space, an off-line holding area where time can be suspended during a delay and decisions freed from the tyranny of immediate responses.

What does this mean?

It's just a metaphor. Look up scaffolding in a dictionary.

This sort of question actually has nothing to do with biology, and would be more appropriate on SE English Language Learners. However, in addition to it being pretentious twaddle, I don’t find it a very good metaphor, given that scaffolding only supports something (and not necessarily even that) until it is built or repaired. “Framework” strikes me as better. But, again we are in a realm other than biology — perhaps philosophy.

I agree with David that the specific meaning here is not really worth dissecting or understanding from the perspective of biology; it won't bring you any closer to any knowledge or understanding of biology.


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How can we explain that glucose at its concentration less than a Km for the transporter enters the peripheral circulation?
I'm studying biochemistry from Kaplan's book. In it, I found the following paragraph in the topic on glucose metabolism:
"GLUT 2, a low-affinity transporter, is in hepatocytes. After a meal,
portal blood from the intestine is rich in glucose. GLUT 2 captures the
excess glucose primarily for storage. When the glucose concentration
drops below the Km for the transporter, much of the remainder leaves
the liver and enters the peripheral circulation."
A similar question has already been here, but it didn't help me find an understanding of this. How can we explain that glucose at its concentration less than a Km for the transporter enters the peripheral circulation? Why is this related to Km? I understand, that at glucose concentration equal to a Km, V will be equal to half V max. But even at a low concentration, glucose will still bind to the transporter, although not so actively. Correct me if I'm wrong, but I think that transporting glucose into the hepatocytes at a low speed will be energetically unprofitable or because of the speed of blood flow, it will no longer have time to get into the hepatocytes. Please, give your opinion

I correct you as invited because you are wrong. Please read the sections about enzyme kinetics in your text very carefully. You will find nothing about energetically or “speed” and certainly blood flow is irrelevant as the next unit of blood has the same concentration as the preceding one.

@David Ok, thank you very much


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What does the concept of information mean in biology?
We use a lot of borrowed analogies from other sciences; linguistics, computational sciences but what do we really mean, mean with information in living systems?

bioinformatics can be a research topic.

The word "information" is not borrowed from any other science, it is borrowed from the English language. The genetic code, for example, was deciphered before most University Computing Science departments were established. This question is both basic and wide. I would start by reading about the genetic code, which is used to encode a certain subset of genetic information. If your background is such that you can't understand the Wikipedia entry or other web accounts, you need to buy and read a molecular biology text.


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Blood transfusion
Can we exchange the antigen present on membrane of RBC's so that it can be transfused from one person to other ?
As we face problem to find  required bloodgroup at the time of emergency especially O negative. So can we have some other technique to simplify our problem ?

In theory it's possible to change the blood types A & B into O, since the antigens for them have longer sugar chains than the O antigen (as seen on this picture from wikipedia). The problem is finding a  way of actually removing this extra sugar molecule(s) without destroying the viability of the blood cells.
An attempt was once made by a student team in the iGEM competition, but they were not successful - I don't know if anyone else ever tried it.

To be clear the iGEM team was partially successful they did remove most of the antigens,  but removing all the antigens present in the blood required an impractical amount of the enzyme being used.


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Estimation of species range fragmentation
While discussing species distribution patterns along spatial, temporal or functional gradients one often finds a hump shaped species richness pattern.
This is well documented in many taxa and spatial scales and known as the   mid-domain-effect (e.g. Colwell & Lees 2000 ).
These patterns also arise stochastically (depending on the species range frequency distribution). So random distribution of species ranges midpoints are used as null models to test for these mid-domain-effects.
However, these models assume unfragmented species ranges. With a highly fragmented species range the pattern would look quite dissimilar.
So I don't want to start a discussion on the validity of this concept but rather ask:
Given a gradient and known species occurences on that gradient.
Has anyone read an article about (or has an idea) what would be a good/unbiased* estimator for species range fragmentation?
Thanks
*e.g: One that doesn't over- or underestimate fragmentation for rare or abundant species

Good equestion. However, I think this might be hard to answer since fragmentation is used in a number of quite different ways (so methods to estimate them may differ). For instance, are you referring to fragmentation at the landscape scale (e.g. as a result of logging previously continuous forest), or to "fragmented" species distributions at the country level (e.g. a species that is found in five areas/regions of a country with large gaps in between)?

I didn't think that the premise of the question was black and white kind of clear, In fact It seems that you wish to have a clear answer to a difficult to measure and define topic. Species range fragmentation is ephemeral and a . quote. hump in species richness pattern is difficult to associate with fragmentation measures.

Very interesting question +1. I don't know the literature on the subject very well but I did not find much by looking for it. I know that a number of methods exist when you have genetic data (STRUCTURE or some of the work of J. Novembre probably).
Here are two possible solutions
Fitting $x$ distributions
You could be fitting 1, 2, 3, ...., n normal (or uniform) distributions to the observed data. Each time, compare their maximum likelihood (for which you might need a MCMC with 2⋅x parameters, where $0≤x≤n$ is the number of distributions you're fitting) and select the "best" model with some information criterion such as AIC or BIC.
The number of fragments is just the $x$ value associated with the lowest AIC.
Logistic regression
Another (faster and simpler) solution would be to fit a logistic regression to your data.
Iteratively fit a logistic regression of degree 1,2,3,...n and then again use some information criteria to select the 'best'.
To find the number of fragments, you can then either use the number of degrees in the model or even better use some threshold on the the probability of getting a zero (which you could compute with the package effects in R).
Notes
It will probably takes you a day or so if you're at ease with these methods and have intro knowledge in programming.
You might want to get opinions from stats.SE as well.

Very interesting answer as well! I will have a look into both approaches. About the Opinions from stats.SE: Is it possible to link this question in crossvalidated or do i have to post a new thread over there?

Many people don't like cross posting. I would advice to accept the current answer here before and then ask your question on stats.SE while making sure to add a link to the current post on stats.SE. You can also link the stats.SE post here.


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insect paralysis in response to predator echolocation frequency
I remember a case in which some insect had evolved an adaptation in response to a predator's (bat's?) echolocation frequency. In mid-flight, it's wing muscles would become paralyzed and it would suddenly drop like a stone directly towards the ground. Does anybody know what this insect is? I thought it was a moth or a mantid.

Many different species react to bat echolocation sounds by altering their flight path or diving. This includes moths and mantids, but also other insects such as crickets, flying beetles, and likely many others as the following list (taken from this review by Miller and Surlykke (2001): How Some Insects Detect and Avoid Being Eaten by Bats: Tactics and Countertactics of Prey and Predator) is in no way exhaustive:
Crickets
"Many bush crickets can hear bats, but few seem to react to bat echolocation. However, the bush cricket, Neoconocephalus ensiger, shows an acoustic startle response during tethered flight in the laboratory (Faure and Hoy 2000). When the insects hear intense batlike sounds with frequencies from 15 kHz to at least 60 kHz, they dive."
Mantids
"Flying mantids (Parasphendale agrionina) react at distances as great as 10 m from a loudspeaker emitting batlike signals at natural intensities. They react by turning or with dives and spiral flight. The responses are all nondirectional, as would be expected from a functionally monaural system."
Flying scarab beetles
"In response to pulsed ultrasound, flying scarab beetles, Eutheola humilis, dropped or flew toward the ground, and walking beetles stopped."
Moths
"Freely flying, unidentified moths exhibit a variety of behavioral responses to bats and to synthetic batlike signals (Roeder 1967a; for recent results, refer to Acharya and Fenton 1992). Moths far from the source often turn and fly away, whereas those close to the source show zigzag and looping flight, power dives, or passive falls."
For a more recent review of the literature for the specific example of moths, I suggest reading Evolutionary escalation: the bat–moth arms race by Hofstede and Ratcliffe (2016).


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Could one hear without his ear?
Might be a stupid question, but I'm quite curious about finding out ^^
If someone looses his ear, or for example cuts it of, just as Van Gogh did. Would he still be able to hear, since the actual organs that are responsible for hearing are on the inside of your ear canal? The ear itself more or less is just flesh, right?

Short Answer
Yes, you could hear, but it would be harder to localize sounds.
Longer Answer
The "ear" from a biological perspective includes the inner ear which is all of course necessary for hearing.
The external part of the ear is called the pinna/pinnae (plural), and yes, you can hear without pinnae; that's essentially what you do when you use in-ear headphones since they project right into the auditory canal and don't use the pinnae at all.
However, the pinnae are important both for collecting sound (therefore increasing the amplitude) and for sound localization, because they both shape the volume of sounds depending on direction (you can localize continuous sound by turning your head back and forth) and have a vital contribution to the head related transfer function that is crucial for localizing sound in elevation.
Sound localization experiments that use in-ear headphones sometimes first record the head-related transfer function with a microphone in the ear to then apply this filter to sounds that are played. This varies somewhat from individual to individual and captures the unique shape and position of the pinnae.
Note that sound localization is not only important for knowing where sounds are coming from, it can also be important to identify and pay attention to auditory objects, especially in noise, like one person talking in a cocktail party.

Algazi, V. R., Duda, R. O., Duraiswami, R., Gumerov, N. A., & Tang, Z. (2002). Approximating the head-related transfer function using simple geometric models of the head and torso. The Journal of the Acoustical Society of America, 112(5), 2053-2064.
Batteau, D. W. (1967). The role of the pinna in human localization. Proc. R. Soc. Lond. B, 168(1011), 158-180.
Brungart, D. S., & Rabinowitz, W. M. (1999). Auditory localization of nearby sources. Head-related transfer functions. The Journal of the Acoustical Society of America, 106(3), 1465-1479.
Hofman, P. M., Van Riswick, J. G., & Van Opstal, A. J. (1998). Relearning sound localization with new ears. Nature neuroscience, 1(5), 417.
Wenzel, E. M., Arruda, M., Kistler, D. J., & Wightman, F. L. (1993). Localization using nonindividualized head‐related transfer functions. The Journal of the Acoustical Society of America, 94(1), 111-123.


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too low extention time for Taq polymerase PCR
I am currently working on my masters degree and have recieved the following question:

"you want to amplify by PCR a gene 1kb long. The Taq Polymerase you have in the lab is able to synthesize 1kb/minute. You make a mistake in programming the PCR machine and set the extension time to 30 seconds instead of 1 minute. what will happen? what do you expect to see on a gel?"

The answer I came up with was that there would be insufficient time for complete replication of the target and therefore only incomplete copies would be made. These strands would show up in a band below 1 kb because the are shorter.
This answer however, was incorrect. I browsed the web but could not find any clear answers on what would happen. anyone knows what happens?

To get amplification of a DNA fragment you need primers to anneal first so that you can extend from. The extension time is designed so that DNA is synthesized from one priming site to the other. Therefore if you have a lower extension time you will make a product that is missing the other priming site. This means that all new template strands can be amplified from one end only and you get linear amplification, not exponential. Therefore there will be too little DNA to visualize on a gel.


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Is this a tick?
My dog has been vomiting today and I recently found this insect/arachnid near his dog bowl. Since vomiting is one of the symptoms of a tick bite, I am concerned that this insect/arachnid is a tick. Unfortunately, since I've crushed it partially, it's hard to tell how many legs it has and what it actually is. Additionally, I'm aware that tick larvae can have 6 legs and the older ticks have 8. Below are some photos next to an Australian $2 coin, which has a 2cm diameter. P.S. This tick should be "native" to Australia.
Do you guys think this is a Tick? Could it be a flea?

This insect is squished beyond recognition for me.

No beetles are of any know threat to dogs. They eat plants and detritus.

No, neither a tick nor a flea. That is a little beetle, and would have nothing to do with your dog's symptoms.


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How did the orchids evolve to support pseudocopulation when they do not have any organ for vision to see how insects look like?
How could they guess so perfectly how a moth or whatever the pseudocopulating organism looks like. They do not have eyes to see the shape or structure. What could possibly be the reason they evolved with such accuracy to deceive an animal?

plants don't consciously control their shape why would they need eyes?

Evolution does not work based on an organism (or designer) "seeing" a problem and seeking a solution. Evolution via natural selection works when members of a population that have a certain heritable trait are better at reproducing than other members of that population. Because they are better at reproducing, subsequent generations of the population have a greater percentage of individuals that have that heritable trait, and the process continues, sometimes to the extent that all the individuals of that species have that trait (this is called "fixation").
The way something like this would evolve is that some predecessor to modern orchids has some morphology or chemical secretion that was particularly attractive to insects. This increased the ability of that predecessor to reproduce. Over generations, any other random mutations that further promoted attraction of insects also were selected for, until they accumulated all of the adaptations we see in a modern orchid.
Today, we can study that process and realize post facto that "Oh, these adaptations worked because they tricked the insects into thinking they were copulating, when really they were just dispersing pollen."
However, the flower never needed any knowledge of insect copulation, it just happened that flowers that had those traits did better at propagating their genes to the next generation.
These types of questions are more easily understood with a broad understanding of evolution. One great resource is Understanding Evolution from Berkeley.


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Male and female seahorses: which is which
Seahorses have two sexes. One has mobile gametes, the other gives live birth. I imagine that a biologist who discovered the seahorse would initially call the first "male" and the second "female".
That is not the case: for some reason (why?), the ones with the mobile gametes are called "female", and the ones that give live birth from a pouch are called "male". I would like to know why.

I don't think the eggs transferred are mobile by themselves...

Is that what happened? They looked at the gametes that are transferred from one sex to the other under a microscope, and noticed "these are not mobile, therefore they are eggs, and the sex that emits them is female"?

I would imagine they compared the male and female ones, perhaps morphologically but more likely by chromosome spreads and determined that way. Male has the heterogenous chromosome (XY in our case, other species have other genetics), but I don't know what that might be for seahorses.

Of course its arguable that our sperm need some transfer too, but they are mobile once ejaculated.

One has mobile gametes, the other gives live birth - this is not true. In reality it is one has mobile gametes and gives live birth while the other does not have mobile gametes but does not give birth (they lay eggs instead - inside the males - inside the ones with mobile gametes)

I'm no expert at all but my first thought was: In any species the sex that produces egg cells is considered the female. Is this not the case here too?

@Ivo - Yes. That's the case here. The confusion comes from thinking that the eggs are mobile - they're not. Like any other species it is the sperm that's mobile. The eggs happen to be ejaculated/laid and the sperm is not ejaculated.

@bob1 Many species use the "ZW" sex-determination system, where the female has the heterogenous chromosome. But that really just begs the question: chromosomes are named Z and W rather than X and Y because they occur heterogenously in females, not because of any feature of the chromosomes themselves, so you need a prior definition of "female" to make that determination.

Please provide links to papers describing these different gametes, otherwise it is not possible for me (and others) to analyse the situation. 2. The general assumption in the question and comments is that the designation of gametes as male or female is made on the basis of “mobility”. However a recent(ish) question about giant sperm in Drosophila professed that the “generally accepted view” is that “size” is the determinant (the bigger is the female). I got severely squashed when I expressed surprise at this, but nobody could provide an  original reference to this idea.  And mobility?

Seahorses are fish. Most fishes use external fertilization to reproduce (there are certainly exceptions, though), so there's not really any aspect of "giving birth" to sex definitions (that's a mammalian bias perhaps): both sexes release gametes externally. One or both or neither fish may guard the fertilized eggs; if one is on guard, it's usually the male that does so, which isn't too different than the male seahorse's behavior, which is just more extreme.
Usually it's gamete size that is used to identify male versus female sex; female seahorses have larger gametes they include the yolk that will feed the developing embryo. Male gametes are also typically mobile. Both of these fit with seahorses: even though the female deposits her eggs in a male pouch, the eggs don't themselves move, any more than eggs move when a female fish simply releases gametes for external fertilization.
Wilson, A. B., Ahnesjo, I., Vincent, A. C., & Meyer, A. (2003). The dynamics of male brooding, mating patterns, and sex roles in pipefishes and seahorses (family Syngnathidae). Evolution, 57(6), 1374-1386.


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Law of Segregation (Genetics)
What if the two factors/different factors of a character did not segregate during gametogenesis and blended together?

Welcome to iology.SE. What do you call a "factor of a character"? If you have a hard time to explain what you have in mind, you may want to try with a (eventually made-up) example.

When you say "did not segregate", you are thinking of a single event of reproduction where the two loci have not been separated by a recombination event or are you thinking about a case where two loci are perfectly linked?

According to the law of segregation:- Pair of contrasting factors or genes for a given character, never blend but segregate during gametogenesis. My question is what if the opposite of the above said law happened

The factors that segregate according segregation law are the two alleles of any gene (https://en.wikipedia.org/wiki/Mendelian_inheritance). The only way to avoid that two alleles segregate at meiosis is to have them inherited in the same gamete, as shown in the picture below . Thus, if the two alleles would not segregate you will double you number of alleles (and chromosomes) at each generation. The effect on any given allele would depend on the level of dominance (dominant, recessive, additive), but that would be the least, since at each meiosis the offspring would have twice the number of chromosomes compared to the parents.

Not all genes are bi-allelic unlike implicitly suggested in your first sentence. 2. The law of segregation does not only apply to genes but to any loci 3. Your diagram shows a case of selfing with whole genome duplicate which may be a little confusing.

if the two alleles would not segregate you will double you number of alleles this is simply wrong. You misunderstand the definition of segregation (at least as used in the Law of Segregation). 5. Your comment on dominance is misleading as well.


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Human can't digest cellulose.....but the length of small intestine is approximately same in humans and herbivores
My question is why herbivores are able to digest cellulose and why can't we??

Depends on what you mean by "digest". Herbivores aren't able to digest grass on their own, they keep bacteria in their guts to do that. Grass-eating herbivores also tend to have long digestive cycles and some have several stomach chambers.
In short, cellulose is a pain to digest.