text:
Is it possible to perform selection of plants without seeds?
When a plant spread using roots or branches I believe new plants keep same genome.
Many plants don't have fertile seeds. How it is possible to improve quality of genome (perform selection) for such plants?
Should we wait for natural mutation to spread across entire plant?
Strawberry is a good example of such plant and we know large verity among this species. How was it achieved?

It is not directly related to genome and selection per se, but in horticulture, viral phenotypic changes/symptoms  are often used and transmitted, especially to obtain attractive variegation of the foliage and flowers.

Most commonly by breeding with a related plant - if there is one. Mutagenesis is an old technique that technically can work.
If one part of the plant has mutated, of course you can take cuttings or plant tissue culture samples.
strawberries can be bred and characteristics selected for.
https://en.wikipedia.org/wiki/Breeding_of_strawberries
A good example of a difficultto breeed plant is bananas
See
http://www.promusa.org/blogpost363-Who-s-breeding-bananas

what technique are used for breeding if there are no pollination/seeds?

In provided article about banana researchers pollinated flowers artificially and worked with small number of survived seeds...

If you get flowers - use https://en.m.wikipedia.org/wiki/Doubled_haploidy


text:
Edema and hydrostatic pressure
I'm currently studying Robbins basic pathology, and I'm confused about a specific statement:
It states in the book that when hydrostatic pressure is low due to a lack of albumin synthesis, it leads to a net movement of fluid into the interstitial spaces.
However to me that doesn't make any sense: isn't the hydrostatic pressure the thing that facilitates the net movement of particles across the capillaries, so if there is a lack of it, shouldn't the particles not move across the membrane?
Any help appreciated

Citing the edition, chapter and page number, plus the context in which the statement is made in the book, would be helpful.

it was chapter 4, page 80-81

You might consider cross-posting this to StackExchange Medical Sciences, as human physiology is more of a focus there.

source: Stack Exchange

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

sort: votes


text:
Clarification regarding a statement in "The Selfish Gene" by Richard Dawkins
In the third chapter of The Selfish Gene: Immortal coils, Dr.Dawkins makes the following statement while arguing for the case that ultimately "the gene" as he defines it is the unit of natural selection.

Natural selection in its most general form means the differential
  survival of entities. Some entities live and others die but, in order for
  this selective death to have any impact on the world, an additional
  condition must be met. Each entity must exist in the form of lots of
  copies, and at least some of the entities must be potentially capable of
  surviving—in the form of copies—for a significant period of evolutionary time. Small genetic units have these properties: individuals,
  groups, and species do not.

I am not sure what "impact on the world" he is talking about. Could someone explain this? He then goes on to say..

An individual body seems discrete enough while it lasts, but alas,
  how long is that? Each individual is unique. You cannot get evolution
  by selecting between entities when there is only one copy of each entity!

Whereas in his other book, The Blind Watchmaker, he describes a computer drawing program EVOLUTION where he does precisely that, i.e, select between entities (here, computer drawn insect-like figures) of which there is only one copy and allows them to evolve. This seems contradictory to his above statement in The Selfish Gene. Could somebody explain?
tl,dr: Why must there be many copies of entities that are being selected for evolution to be possible?

"Impact on the world" is just his writing style.  Dawkins means "evolutionary significance".  For example, all the intermediate forms leading up to the modern horse have been evolutionarily significant because they contributed to survival of the lines of descent that are still present.  Any tiny evolutionary branch that dies out would have little significance or impact.
In the first part of your second question, the answer is again Dawkins' writing style plus the fact that he's writing for popular consumption.  And, his own thoughts have a way of evolving just as they should; so we shouldn't expect perfect consistency between what is said between sequentially written books.  The Blind Watchmaker was written to convince people that evolution can produce complex organisms without any pre-existing goal to do so, using a relatively simple process.  The Selfish Gene was written to promote his idea that the unit of evolution is the gene. (Note that his idea is not necessarily correct.)
In the second part of your second question you ask:Why must there be many copies of entities that are being selected for evolution to be possible?.  The answer to this is that it is NOT necessary.  It's simply a much more easily implemented - and generally better- evolutionary strategy.  If there is only one organism, and selection means killing it if it is unable to adapt to a given environmental change, then failure to adapt puts an end to it and all its possibilities.  If, on the other hand, that one organism produces a series of single copies (offspring) and each of them has some random genetic variation that's subjected to selection, there's a chance that some will make it past the selection process.  That's equivalent to the one organism producing a lot of offspring at the same time, each with its own genetic differences.
This is a slightly SiFi perspective on the above, but: In general, it's a lot safer to test a disposable copy of oneself against a new danger, than to test oneself directly.  If the copy passes the test, it's safe to face the danger directly.  If the copy fails, then you can test a slightly modified version of yourself against the danger.  If that modified copy passes, then if you're able to do so, you could make the same modifications to yourself and go face the danger.  However, there are now two identical new modified copies of you.  One of you is superfluous, so you flip a coin to decide which survives.
In the SiFi scenario, we have one organism evolving safely up one possible branch of an evolutionary tree.  But if that organism reaches a dead end from which there is no escape, its branch dies.  On the other hand if all the other branches are allowed to continue (that is, if you let both copies survive and evolve independently), there's a far better chance at least one branch will still be growing and branching far in the future.
I personally think Dawkins "Selfish Gene" idea fails when we try to fit it into that picture.

Your hypothetical falls apart for several reasons, not the least of which is copies take resources to make as much as the original took to make, and a copy is not superfluous, otherwise asexual reproduction would not exist, it is no safer to test on your copy as yourself, unless your copy is not a copy, which does occur , see skin cells. You are needlessly anthropomorphizing selection in your example.

It is pretty difficult to say anything about evolution in layman's language without being accused either of anthropomorphizing or of invoking a diety.  Please clarify "it is no safer to test on your copy as yourself, unless your copy is not a copy".

First that whole section is irrelevant to the the questions, but to answer you if the "copy" and the original are identical it doesn't matter which one is sacrificed, the loss is the same.

if they are not identical what you can "test" is pretty limited, the more capable the copy the closer it is to an identical copy and the more impactful the loss of time and material, and we already see such behavior, it is essentially r strategy,  make lots of low cost copies and spam the environment. similar is  multicellular life where only a few cells get to reproduce the rest only being beneficial in their ability to facilitate that. .

What you're saying is correct, but a bit beyond the scope of the question.   IMHO, only the OP knows if an answer fits the intent of the question.

Btw, take a look at my last name, blacksmithing, spokane.  We have some background in common.  Evolution is a big piece of it.

Let us continue this discussion in chat.

"impact on the world" is referring to the cumulative effects of natural selection, the progressive alteration of a lineage. If every "unit of selection" was completely unique there would be no cumulative effect of selection, individuals would die and it would have no effect on the next generation. Bodies are unique but genes are not, a body is produced by genes that are mostly conserved from generation to generation. He is drawing attention to the fact there must be something heritable that is conserved from generation to generation for section to have a lasting effect. That heritable thing is what is being acted on, for life one earth that thing is our genes.
The computer program further illustrates his point, the "genes" (code) are carried from generation to generation mostly intact, even though each body is created new and unique from those genes, just like many organisms. that is why they can evolve just like lineages of biological life.
there is a weird dichotomy in how evolution functions, it is a step removed process.  The genes are the things being altered by a process that can only interact with them through their products, bodies, but it is the genes that get altered it is the genes that are evolving.

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


text:
Vectors for genetic engineering
Well can a bacterium be used as a vector?I have learnt that Agrobacterium tumifacian can be used to deliver a gene of interest in plant cells but on a book in a multiple choice question it says that only plasmid and bacteriophage can be used and not the bacteria to deliver a gene of interest to a host cell.

It's a matter of semantics. Some would want 'vector' to be used strictly for plasmids, viruses and the like (see, for instance, the Wikipedia page). Others, like @physics12 below, would include whole bacteria since they can act as carriers of foreign DNA.

Yes, Agrobacterium is indeed a very widely used vector in plants. So it wouldn't be wrong to consider bacteria as vectors. Just to add, it's worth noting that in recent times, bacterial vector options have been explored in the case of humans also, especially in the case of gene therapy for cancer treatment, though its success hasn't been demonstrated yet. Refer https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056088/ for more information on this.
To conclude, bacteria can be considered as a vector undoubtedly.

Welcome to Biology.SE!  This is a good answer, and it would greatly benefit from inclusion of a few citations for the things you claim (i.e. bacteria as a vector in plants, bacteria as vectors for gene therapy in cancer treatment).  If you haven't yet, please check out the tour.

Well 'Twinkle sheen' if the bacterium just tranfers its plasmid into the cell and the plasmid is responsible for introducing the gene of interest and not the bacterium itself then can't we apply the same logic to bacteriophages.Bacteriophages do not act as a vector but only their genetic material does.

Thank you Dirigible. I've added a link for reference.

Agrobacterium tumefaciens and Agrobacterium rhizogenes  are soil-based plant pathogenic bacterial strains containing plasmid. This plasmid is known as Ti plasmid and is responsible for inducing tumor. Part of this plasmid called T-DNA can be integrated into the host chromosomes. So, this bacterium plasmid act as vector, but not the whole bacterial cell.
(Via: https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/agrobacterium-tumefaciens)
This is true with all the pathogenic bacterial strains, as they can transfer their DNA material to cause pathogenicity. So, these pathogenic strains can be used in genetic engineering to transfer particular gene to host/mammalian cell.
Using bacteria as a vector to treat cancer or various other pathological conditions is still at developmental stage.
(Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056088/
https://www.ncbi.nlm.nih.gov/pubmed/16362987/)

The conceptual mistake that you're making is that, Agrobacterium Tumifaciens, being a bacterium, contains additional genetic material within its cell, called the 'Ti plasmid'. Hence it is quite justified that the plasmid within the bacterium is acting as a vector, or a carrier of a foreign gene and not the whole bacterium itself.
Hence the answer provided in the book is correct.

Saying the Ti plasmid and not the Agrobacterium is the carier of DNA is like saying the passanger seat and not the airplane is the carier of humans across vast distances. Try spraying the plant with purified Ti plasmid - no transformation will happen.

Wow. That's an analogy like, Take some pasta, take some hot water, keep them side by side and voila! By magic the pasta will cook itself. You're very wrong my friend. The bacteria by itself can't cause transformation until the plasmid is activated using Calcium ions by heat shock. This means, when seen at a deeper level, it's the plasmid that's actually causing the transformation and not the bacteria by itself. Thus your comment made no sense. There may be a plane to carry humans, but the pilot, who switches on the plane is not there, so will the plane be able to fly by itself?

I’ve edited your Answer for English because the argument in your first paragraph is reasonable as an explanation of the expected answer to that educational abomination known as an MCQ. I leave you to delete the second paragraph with the reference to reverse transcriptase and bacteriophage. Quickly, before anyone else reads it.

I deleted it, but may I know the reason why you told me to do so?

I suggested you deleted it because reverse transcriptase is not found in bacteria or bacteriophages, nor is it necessary for cloning into bacteriophage vectors.


text:
Are there any small peptides with protease activity?
I'm looking for a very small protease to base an engineered protein on.  I did a search for "peptides with protease activity" but all the results seem to be as peptides to be used as protease substrates (eg in assays); I couldn't find any catalytic peptides.
What is the smallest protease or domain which has independent proteolytic activity?  (Ideally looking for something very short, a dozen aminoacids)

60 residues is the smallest I could find, ref below.
https://jbiomedsci.biomedcentral.com/articles/10.1186/1423-0127-19-54

feel free to edit answer for style


text:
Does DNA have a phosphate group or phosphoric acid?
I am confused about the structure of nucleotide of a DNA. I have seen that it has a phosphate group(PO₄³⁻) in some books but phosphoric acid(H₃PO₄) in other ones. Which one is right?

Check out this post and see if it answers your question. (https://biology.stackexchange.com/questions/3864/dna-as-an-acid). I will say, there is basically no circumstance in which the phosphate-group in a nucleic acid backbone will have a -3 charge, because two of the three available oxygens are utilized in the phosphodiester bond linking the sugar bases.

The phosphate ion has a negative formal charge and in an acidic solution its appears as a conjugate base of a phosphoric acid. That is the wey the phosphate group found in cells. The nucleotide synthesis can occur de novo or recovery ways. De novo way use phosphoribosyl pyrophosphate, which simple molecules such as amino acid, tetrahydrofolate and carbon dioxide are added.


text:
Is there a vaccine against the plague (Yersinia pestis)?
There seems to be recurrent events of infections of the plage (Yersinia pestis), from the well known Justinian plague to the Black Death and to recent years. In fact, two cases were reported in China in November 2019. However, it seems there is not an effective vaccine yet. At least until 2013 there was no vaccine approved by the US FDA. There seems to be on-going research about vaccines for the plage.
Is then no effective vaccine against the plague? If yes, does it mean humanity is still at risk of yet another pandemic of the plague?

There is little motivation right now for vaccination against plague because:

Human infections with plague are fairly rare. A vaccine administered to the general populace would have to be very cheap and extremely safe to make it cost-effective and have a net benefit given the risks of plague are so low, and because
Antibiotics are effective against plague - this makes the likelihood of a widespread outbreak fairly low. Antibiotic resistance could be a concern, but plague would not be one of the most concerning pathogens from that perspective - there isn't much exposure to antibiotics in the reservoir species that the bacterium lives in, so there is less selective pressure towards resistance compared to other bacterial pathogens.

Additionally, plague lives in reservoir species, so extensive human vaccination is not a plausible way to eradicate the bacteria entirely, unlike pathogens that have humans as a primary host.
That said, vaccines are available and can be used for certain individuals at high risk. However, they take a long time to show immune protection (>1 month) making them not that useful during outbreaks. From the same WHO report linked above:

Worldwide, live attenuated and formalin-killed Y. pestis vaccines are
  variously available for human use. The vaccines are variably immunogenic
  and moderately to highly reactogenic. They do not protect against primary
  pneumonic plague. In general, vaccinating communities against epizootic
  and enzootic exposures is not feasible; further, vaccination is of little use
  during human plague outbreaks, since a month or more is required to
  develop a protective immune response. The vaccine is indicated for
  persons whose work routinely brings them into close contact with Y. pestis,
  such as laboratory technicians in plague reference and research laboratories
  and persons studying infected rodent colonies (23).

WHO plague manual:
https://www.who.int/csr/resources/publications/plague/WHO_CDS_CSR_EDC_99_2_EN/en/

So basically, a cheap, widespread and effective antibiotic based treatment exist? I guess that is the benefit of the plague being a bacterial and not a viral disease like Covid-19.

@luchonacho Yes, exactly. Plague is still dangerous because the antibiotics need to be given quickly, but antibiotic resistance is relatively rare for plague.

It might be worth pointing out that the main reason why antibiotic resistance is of limited concern with Y. pestis is that the natural reservoir from which it sometimes jumps to humans consists of wild rodents, which (unlike humans and domesticated livestock) aren't normally treated with antibiotics. Thus, there's little to no selection pressure for Y. pestis to evolve antibiotic resistance in its natural hosts.

@IlmariKaronen Indeed, I thought I implied that but I guess I never did! I'll edit.

There is already plague vaccine in use, which is only administered to lab workers working on Y. Pestis or people residing in areas affected with plague.  (Via: https://www.cdc.gov/mmwr/preview/mmwrhtml/00041848.htm)
Plague can also be treated with antibiotics if detected at earlier stage (such as streptomycin, ciprofloxacin, gentamicin or doxycycline). Very few antibiotic resistant strains of  Yersinia  pestis have been reported till now. So, this may not become the reason for  pandemic.
As it is known, Y. pestis exhibits intrinsic genetic plasticity to transform into antibiotic resistant strain, which makes it  potent agent of bioweapon. So, Centers for Disease Control has listed Y. pestis under the category A select agent. And researchers are working for development of next generation vaccine which is more reliable by exhibiting strong cellular immune response. (Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155008/)


text:
Can untargeted metabolomics detect epigenomic changes such as methylation?
My main focus is transcriptomics analysis and very recently I have also started working on metabolomics. From my transcriptomic data it looks like there is a gene/protein that could potentially generate epigenetic modifications. I also have untargeted metabolomics data of equivalent experimental conditions that I plan to analyse soon hoping it will complete the picture. However, I have searched for publications linking specific metabolites with hyper/hypomethylation or chromatin structure and I have only been able to find a few references (see link below) and I got the feeling that untargeted metabolomics does not seem to be an obvious technique to observe epigenetic signatures.
https://www.ncbi.nlm.nih.gov/pubmed/30125527
What metabolites would be regulated under epigenetic circumstances?
Does anybody have any experience or know of any particular study that looks into this relationship between untargeted metabolomics and epigenetic modifications? Thank you very much for your help!

This is a fascinating question, and I spent a fair amount of time looking into it. From what I've been able to find regarding the relationship between metabolics and epigenetics, it seems that metabolites drive epigenetic changes, not the other way around.
This can be shown quite well by looking at cell differentiation and induced pluripotent stem cells. The epigenetic changes that happen in these processes happen due to the cell's environment.
However, epigenetic changes cause changes in transcription rates, so it can indirectly influence metabolics. The circadian clock uses this system (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3392647/).
Cell signaling appears to be the most significant cause of metabolic change, though. The aforementioned paper also says this:

As most metabolites are not diffusible between mitochondria and
  cytosol/nucleus, accurate determination of the cytoplasmic pool size
  is critical to understand their effects on epigenetic signaling.
  Although attempts have been made, so far the technology to reliably
  measure metabolite concentrations in different cellular compartments
  is lacking.

Which, I'm sorry to say, leads me to believe that there are very few metabolic pathways that have known effects on epigenetic factors.
That said, there are several references in that paper which may put you on a good path forward.

Thank you very much for your answer and the reference :) Indeed, it is very interesting. Maybe newer techniques such as super-resolution microscopy could help to define the metabolite concentrations in cellular compartments in the future.


text:
Why do E.coli form parallel clusters?
Discalimer: I am not a biologist. I am modelling E.Coli growth and in the Wikipedia gif one can see observe some groups where the bacteria are one next to each other, oriented at approximately the same angle. I did some simulations and obtained similar results. Is there any reason why this happens?

Cell division happens by division at the middle of the rod, so the result is two daughter cells that are at nearly the same angle. Over time in the absence of agitation moving cells around, this will lead to a groups of cells that have non-independent cell orientations.
For more information, including how people have induced it to do otherwise, see this paper.

Bacterial cells prefer to attach with each other in parallel orientation so that they have maximum surface of contact and could form biofilm clusters.
Both physical factors (like Brownian motion, electrostatic interactions, gravity, van der Waals forces and hydrodynamics)  and cellular function in bacterial cells (bacterial motility, production of polysaccharides, and functions of structures in outer membrane) are responsible for this orientation.
(Via: https://www.nature.com/articles/srep29516)


text:
How is cognitive ability linked to the presence of sex chromosomes?
Most cases of sex chromosomal abnormalities in humans have a case of learning disability or less developed cognitive abilities. Wikipedia says:

When additional X and/or Y chromosomes are present in 48,XXXY, 48,XXYY, or 49,XXXXY, developmental delays and cognitive difficulties can be more severe and mild intellectual disability may be present

So, the question is simply this: How is cognitive ability linked to the presence of sex chromosomes?

Cognitive impairment does not have to do anything in particular with the sex chromosomes. Downs syndrome results because of trisomy of an autosome and it also results in cognitive impairment.
So, cognitive impairment is associated with incorrect gene dosage. As mentioned in the other answer, most aneuploidies are lethal.
Persons affected by aneuploidies do not just suffer cognitive impairment but also some other physiological problems. It is just very easy for us to notice the cognitive defects. Moreover, brain is a complex organ and neuro-development has a complex regulatory network. So dysregulation of common pathways is likely to affect brain development in a noticeable manner.

There's also the family of https://en.wikipedia.org/wiki/X-linked_intellectual_disability which I think is fair to say is less about the sex chromosomes being important for cognitive ability and more that, like other X-linked genetic disorders, males with a single X chromosome are more likely to show symptoms/stronger symptoms because they have a single copy.

If you are thinking that, say, a chromosome 1 triploidy will not result in cognitive impairment... that's not quite right.  Almost all triploidies result in death.   Same with chr2, chr3, chr4...just about every chromosome is lethal if there are extras.
It's not so much that having extra sex chromosomes is bad for cognitive function, it's that having extra chromosomes is usually lethal, only a few triploidies are even survivable, and they all cause lots and lots of problems, including cognitive impairment.  Having extra sex chromosomes is the mildest one, and it results in lots of comparatively mild problems.


text:
What is this long, thin and segmented insect I found in my house in India?
Found this inside my house, along the wall, there were few going somewhere few distance from each other.
I suspect it is a centipede but didn't found similar images on Google. What is this?
Location: Mysore City, India.
Size(only which I saw): the one in the image is about half centimeter, and the smallest one was less than 1/4th of a centimeter.
Color: the one in the image is kind of brownish I guess and the smallest one's are nearly white (pigmentless?)
We assumed this thing is kind of larva of cockroach or big white ant. Is this fully grown insect or still it is a baby? These were behaving like ants do.

Please [edit] your answer to include the approximate size. thanks

 UPDATE:
Based on a comment by ArthurJFrost reminding me of the existence of a group of insects I totally forgot about, AND based on a closer examination of the cerci and what appears to be external mouthparts in the image of the OP's specimen, I think this insect might actually be a webspinner!

These insects would be also about the right size, with the described and shown body plans, but also with short (but non-pincer-like) cerci and external mouth parts as in the OP's image. Female webspinners are wingless [source], as well, as the OP's image also appears to be.

See, for example, the black webspinner (Oligotoma nigra) from New Mexico, USA from bugguide.net:

 Source: bugguide.net
See also here for additional images of Oligotomidae species. (by the way, O. saundersii is the type species of Oligotomidae within the Indian subcontinent).
@ArthurJFrost, since you are more the expert than I on hexapods, PLEASE PLEASE write up an answer detailing how we might all feel more confident knowing that the webpsinner (and not the dipluran) is the better answer. Visually it appears to be the case to me, but I think you'd be able to point out some specifics for us all to learn from!

I will certainly default to you to write up the "official" webspinner answer since my update here on my post is simply to direct away from what I now think is an incorrect answer. I would gladly link to your answer to further emphasize that you came up with this answer.

OLD ANSWER: [Informed guess, but I think it's wrong!]
Based on the thin body plan, extended, segmented abdomen, lack of wings, and pair of posterior cerci, I was immediately reminded of a dipluran (or "two-pronged bristletail").

 Sourcce: Wikimedia
It would be good to know the size of your specimen since most diplurans are smaller than 10 mm  (though some can reach 50 mm!). A better photo would also be appreciated, since diplurans typically have antennae with beadlike segments, and I cannot tell if that's the case in your photo. I will note that many diplurans have much longer and even filamentous cerci, but others (like your specimen) have shorter cerci.
I am not sure why a dipluran would be inside your house, however, since they live in soil or leaf litter. [source]
Other organisms to rule out:

Snakefly (Agulla adnixa) -- no cerci (vs. yours)
Centipede -- too many legs (vs. yours)
I can't rule out earwigs since I am unfamiliar with the species in India. However, your specimen looks longer, thinner, and possessing smaller cerci than the earwigs I am more familiar with. [A clearer image of the thorax would help to determine if wings are present or not, which (if present) would rule out diplurans altogether and suggest it might be some earwig species I don't know).

I'm always amazed when people are able to answer these ID questions from limited data, and I really appreciate your style that includes criteria for excluding alternatives - really excellent pedagogy and I hope readers pick up on those cues in addition to the specific IDs. :)

@Bryan thanks for the encouragement! I try to make all my answers thorough + informative (esp with so many inaccurate IDs across the web). I certainly am no expert in any one taxonomic group like Karl Kjer, John Robinson, Arthur J Frost, RHA, and some other of our users, but It actually gets surprisingly easy to narrow to phyla, classes, and even orders when you've ID'd enough organisms -- with most of these having tell-tale characteristics to help narrow options. Though, it's the real puzzles that have been the most fun for me to ID! (e.g., here)

Another possibility here is a wingless webspinner (order Embioptera AKA Embiidina AKA Embidiina -- at least two of these spellings have seen recent use); I base this guess on the widened front feet (where webspinners keep their silk-glands!).  If I'm not off-base, identification further will be difficult if not impossible; wingless webspinners if adult are almost always female, which sex is not usually used for identification.

WOOO! @ArthurJFrost you are the expert here, not I, and having taken a look at bugguide.net, I think you're on to something here!! The OP's specimen's cerci match the webspinner's better than any dipluran I've seen (AND, now that I look again, I think I see external mouth parts in the OP's image!). I remember learning about webspinners once, but they're not in my regular rolodex of species I think about. PLEASE write up an answer based on your comment -- preferably outlining why you think webspinner and not dipluran. I know I'd learn something! Thanks


text:
Can you vaccinate against bacterial diseases? Are there existing vaccines for such diseases?
I have the (maybe wrong?) preconception that we only vaccinate against viral diseases, and that there can only exist vaccines against viruses. I think the idea comes from the idea that only for viral diseases are you becoming immune after contracting the disease, not for bacterial. The question Is there a vaccine against the plague (Yersinia pestis)? made me think that I don't really have a justification for that, seeing that the mechanisms for combatting viral diseases and bacterial diseases should be the same (is that right?).
So, is it possible to vaccinate against bacterial diseases? Do we have existing vaccines for any bacterial disease?

Of course we can - and do - vaccinate against bacterial diseases, as these are some of the dangerous infectious diseases.
Among these are:

Tetanus (although here the vaccination is targeted against the toxin, not the bacterium itself)
Tuberculosis
Diphtheria
Pertussis
Haemophilus influenzae type B
Cholera
Typhoid
Streptococcus pneumoniae
Meningococcus: against the strains ACWY, B

A list of the vaccines against bacterial diseases can be found here.

Vaccine works by instructing our immune system to recognize and fight against infectious agent (pathogen), so it can be virus, bacteria or any other microorganism.
Particles from particular pathogen are introduced into the body which stimulates immune system and thus works to fight against it.
Bacterial vaccines can be  of different types: toxoids, subunit vaccines, killed vaccines, and live attenuated vaccines. (Via: https://www.sciencedirect.com/topics/medicine-and-dentistry/bacterial-vaccine)
List of bacterial vaccines can be checked in this wiki link


text:
Genetic mutations in plants
I am trying to plant some trees which are usually native to colder climates into Subtropical climate, is there any possibility that if i plant these 20 trees saplings in winters they will grow to be a tree, due to some random genetic mutation, given all nutrients all provided to it?
Tree in Question is Deodar

Mutations occur more-or-less at random and are only rarely beneficial, but the trivial answer to "any chance" is yes. ———  To improve your question I suggest you think about what you really want to know. If you are interested in whether you can get that species to grow where you live ask that on [Gardening.SE]. If you want to know about genetic adaptation in trees, then you could try to reformulate your question for this site. However, I think you would benefit from reading some introductory material on evolution first.

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

I think that the potential survival of your seedlings could more likely be credited to your care and management than random genetic mutations. While, of course, DNA mutations happen during cell replication, evolution at the whole-plant scale primarily occurs over the course of generations, not the lifespan of a single plant. You may well be able to get these trees to thrive in your environment with some care and love, although they may not grow as vigorously. Here is a link to a gardening website with tips on growing ceaders in a home garden, although I agree with the commenter that you'll get much better help at the Gardening and Landscaping Exchange!
Best of luck with your horticultural endeavors!


text:
ABO allele frequencies: Why use the EM algorithm?
In textbooks and lecture notes and slides posted online, determining allele frequencies using blood type information (ABO), under the assumption of Hardy-Weinberg equilibrium, is accomplished using the EM algorithm. It seems to me, though, that this problem can be solved using basic algebra: If $a$, $b$, $o$ are the frequencies of the $A$, $B$, and $O$ alleles, respectively, and $p_A$, $p_B$, and $p_O$ are the proportions of the population in question displaying blood types $A$, $B$, and $O$, then
$$
p_A = a^2 + 2ao,\quad p_B = b^2 + 2bo,\quad\text{and}\quad p_O = o^2.
$$
Inverting the third equation gives $o$ in terms of $p_O$:
$$
o = \sqrt{p_O}.
$$
Plugging that into the first equation and rearranging, we get the quadratic equation.
$$
a^2 + 2\sqrt{p_O}a - p_A = 0
$$
Solving using the quadratic formula and throwing away the negative solution, we get
$$
a = \sqrt{p_O + p_A} - \sqrt{p_O}.
$$
Symmetrically,
$$
b = \sqrt{p_O + p_B} - \sqrt{p_O}.
$$
Thus, we've solved for the allele frequencies $a$, $b$, and $o$ with only basic algebra.
In the standard textbook case in which $p_A = fa = 186/521$, $p_B = 38/521$, and $p_O = 284/521$, this gives
$$
a \approx 0.21,\quad  b\approx0.05, \quad\text{and}\quad o\approx0.74,
$$
which is close to what you get after a few iterations of the EM algorithm.
Question (finally): If the above calculation is correct (if not, please let me know!), what is a "simplest" non-synthetic (real data, from the literature) example of an allele frequency computation from phenotype data that actually requires a sophisticated technique like the EM algorithm?


text:
How can paternal chromosomes be present in an egg cell during meiosis I or crossing over, if fertilisation has not yet occurred?
I am very confused about crossing over. It is said that crossing over increases genetic variation as it is a combination of paternal and maternal chromosomes. However, crossing over occurs in meiosis 1 but meiosis 1 occurs before fertilisation, so my question is how are there paternal chromosomes in an egg cell prior to fertilisation.

Maternal and paternal here are referring to the mother's parents, not the father that is fertilizing the egg.

when they say paternal chromosome, they mean chromosome of the father of the organism. Not the father of the offspring of the specific organism. During meiosis ,in order to form the gametes, the chromosomes of the mother and the father of a specific organism interact, because homologous chromosome pairs consists of a pair of the organism's fathers chromosomes, and the mother's.
please tell if you still don't get it.


text:
What is the name of this part in plants, fruits, vegetables?
What is the name of this part of the plant, fruit, vegetable? The thing that the plant is connected with the tree and gets nutrients with? The part we usually cut out when eat fruit.
Examples below
Papaya

Banana

Mango

google the word stem.

@John that's not a stem. What is the name of the plant part that stem gets into in the plant. This part of the fruit is not a stem.

@John I googled, it shows science, technology, engineering and mathematics

'Stalk' or 'pedicel' would be an appropriate term (see, for example, this paper or this one). Specifically, you could say 'terminal part of the stalk/pedicel', though I don't know if there is a word for that.
Note that the term pedicel is commonly used for the stalk of a flower; it makes sense to use it for fruits too as they are derived from flowers.


text:
Why's there no vaccine against Respiratory Syncytial Virus (RSV)?
RSV was discovered in 1956. Here’s why we can’t rush a COVID-19 vaccine | AAMC

Respiratory syncytial virus (RSV): This pervasive respiratory virus has proven resistant to vaccination. Children treated with one vaccine in the 1960s developed an  enhanced form of the disease, suffering high fever, bronchopneumonia, and wheezing. Many were hospitalized and two died.
“That set the field back years,” Poland said, as researchers and manufacturers “were afraid” to try again.
Researchers have since tried but still not developed an RSV vaccine for public use, according to the CDC. Babies at particularly high risk for RSV are sometimes injected with an antibody to help fight off infection.

I don't grasp the Canadian government's Overview of the respiratory syncytial virus vaccine candidate pipeline in Canada, CCDR 46(4). E.g. so what if "amino acids do vary in prefusion specific epitopes"?

Challenges to RSV vaccine development
Antigen diversity
A successful vaccine candidate will account for the diversity of antigens presented by RSV in the form of the structural variability of the proteins on the surface of the virus. The protective, neutralizing antibody response to RSV is dominated by antibodies targeting the prefusion F protein on the surface of RSVFootnote 17Footnote 18. Although the genetic sequence of F does not vary substantially between strains of RSV [89% of its sequence is identical in both A and B strainsFootnote 19], amino acids do vary in prefusion specific epitopes [bolding mine]. As new products are authorized and make it into broad usage, it will be critical to understand the sero-epidemiological responses at a population level to understand whether prefusion or postfusion antibodies are dominant responses, and whether these demonstrate equivalent protection against both RSV type A and B.
RSV infection dampens the immune response
[...]
There are no clear correlates of protection
[...]

See also https://medicalsciences.stackexchange.com/questions/23174/why-is-the-immune-response-to-rsv-so-short-lived-and-what-else-makes-a-vaccine (Your title and sub-question are actually pretty different.)

Why is there ommission in your question: "RSV infection dampens the immune response"?S in RSV is for "Syncytial". My idea is  that reason for non-success is mutability which is enhanced by syncitialization brought about by vaccination. Have you heard of anything similar in concept?

Refering to "E.g. so what if "amino acids do vary in prefusion specific epitopes"?" Is it understood that "prefusion" does not refer to fusion of viral and host membrane but to syncitialization of host cells?

RSV has been a difficult virus to create a vaccine against, though an experimental vaccine has finally been developed and is being tested by the University of Texas at Austin. Your article with Canada is probably talking about how certain amino acids and antibodies seem to be effective against the virus. However, this virus is a strange beast that is hard to treat. A potential vaccine was tested in the 1960s, but all it did was increase the rate of infection for the RSV, leading to some scientists classifying RSV as "immunopotentiation" or vaccine-enhanced. Normally, a vaccine contains a dead version of the virus or weakened byproducts of the virus to create a strong immune response to defeat a virus. However, with RSV, this process tends to make the viral infection worse. Hopefully, this new vaccine will yield results (and even if it doesn't, a medication called palivizumab can be given to babies and children to protect against the virus).

In answer to the specific question,
This paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741363/ is the one the review was talking about.
The epitope that is targeted (the F protein) varies between strains, so a produced vaccine would only work on that strain. The protein (an obvious vaccine target) was selected because it exists on all strains, and is needed for the virion to fuse with the human cell.
In the vaccine The F protein epitope is fused with an immunostimulatory particle to get a good immune response. That's why they mention "prefusion" and "postfusion". There is confusion in the terminology because the F protein is so-named because of its role in fusing the virion to the cell.

Feel free to edit my answer to format the ref, I only have a tablet so editing is difficult.


text:
Barring Antibody-dependent enhancement (ADE), how else can vaccines enhance the infection?
The link to the 2007 article below was broken for me. I Googled and read it on NCBI.

Decades ago, vaccines developed against another coronavirus, feline infectious peritonitis virus, increased cats’ risk of developing the disease caused by the virus (T. Takano et al. J. Vet. Med. Sci. 81, 911–915; 2019). Similar phenomena have been seen in animal studies for other viruses, including the coronavirus that causes SARS (Y. W. Kam et al. Vaccine 25, 729–740; 2007).

At p 737 on the right column, the authors "could exclude this mechanism of enhancement as
sera from triSpike vaccinated mice did neutralize, rather
than enhance, virus infection on VeroE6 cells." So I similarly exclude ADE for this question. But in the last para. they wrote

Interestingly, we observed the
  enhancement phenotype only in human B cell lines but not in
  mouse macrophages despite the presence of FcγRII. Reasons
  for this are unclear, but the respective role of activating and
  inhibiting human FcγRII which have identical extracellular

p. 738

but heterologous intracellular domains and signaling capacities
  might play a role [63].

So, what is your question? It would be great if you could not only post it in the title but also in the question box.

@Chris Sorry! To paraphrase my title: how else can vaccines enhance the infection, if the cause isn't Antibody-dependent enhancement (ADE)?

Vaccines are now well-tested to make sure that they don't do make infection worse, but there are many ways they COULD.
Two early formalin-inactivated vaccines (RSV and measles) both had this effect. See this Reddit post  to understand the mechanisms.
Theoretically, a poorly-designed vaccine could worsen viral infections  in three ways:

by biasing the adaptive immune response in the wrong direction that makes it harder to effectively respond to the actual virus.  This might be by priming the wrong type of response, e.g. producing a strongly biased Th2 response when a Th1 is required); creating the right response but to the wrong epitopes, in a way that subsequent exposures can't overcome - "original antigenic sin"; or by inducing T/B cell anergy or tolerance to the virus in question.
immunopathology.  For many viruses, the immune system's attempts to kill the virus, not the virus itself's direct cytolytic effects, damage the host.  E,g, Hepatitis C has 3 broad outcomes to a natural infection:  about 20% of people create an early, strong, multi-specific CD4/8 response that clears the virus.  The rest develop chronic infection.  In most people with chronic infection, the immune response damages little - viral loads can be extremely high but liver fibrosis is minimal.  But in \~10-20%, there is a strong immune response: chronic inflammation, infiltration of lymphocytes, and constant direct killing of virally-infected hepatocytes by CTLs leads to deposition of scar tissue and, eventually, cirrhosis.  So if you created a vaccine that failed to clear the virus and instead generated a pro-inflammatory, pro-fibrotic immune response, it would be a disaster.
Increased target cells.  This was a concern with one of the experimental HIV vaccines.  It increased the number of CD4+ cells permissive to HIV infection in the female genital tract (and the rectum, but I don't remember), thus giving the virus more target cells to infect (there was also an experimental HPV vaccine that was feared to do the same).  Those vaccinated thus had increased risk of infection.

Hmmm... I wonder how does a vaccine increase the production of the target cells. Do you know the mechanism by which that takes place?


text:
Why do human vaccines affect different animals differently?
Doubtless the simple answer is that these animals differ, and that the amino acids of their ACE2 receptors differ. Are there other reasons?

Chan, working with his HKU colleague, microbiologist Kwok-Yung Yuen, and others, pinpointed the problem by doing a cross-species comparison of the segment of ACE2 to which SARS-CoV-2 first attaches. In the mouse, 11 of 29 amino acids of this critical domain differed from the human version. (Rats had 13 differences, but hamsters only had four.)

I quote p 738 of Y. W. Kam et al. Vaccine 25, 729–740; 2007.

      Vaccine-mediated protection against SARS-CoV infection
  in mice has been demonstrated using different vaccine
  approaches [19,20,65]. However, mice do not replicate
  SARS-CoV to high titers and do not showpronounced pathology
  in lungs [15]. On the contrary, ferrets [28], cynomolgus
  macaques [29] and hamsters [30] have been shown to support
  high titer replication of SARS-CoV in the respiratory tract
  associated with pneumonitis. In order to assess the respective
  role of neutralization or ADE in vivo we performed SARSCoVchallenge
  experiments in hamsters vaccinated with three
  doses of 2, 10 or 50 g of protein in alum adjuvant. All vaccinated
  groups showed a significant decrease of viral load at
  3 days post challenge by at least four orders of magnitude
  without signs of enhanced lung pathology. The rare foci of
  hepatocyte necrosis that we observed in these hamsters did
  not correlate with pre-challenge neutralizing antibody titers,
  liver enzyme levels (pre- or post-challenge), or immunohistochemical
  detection of SARS-CoV antigen suggesting that
  hepatic cellular necrosis is unrelated to SARS-CoV immunization
  or infection in Syrian golden hamsters. This contrasts
  with a report of hepatitis 28 days following challenge with
  SARS-CoV in ferrets vaccinated with a poorly immunogenic
  recombinantMVAvaccine expressing SARS-CoV spike protein
  [24].

Why will it take so long to develop a COVID-19 vaccine? - The Globe and Mail

Another study revealed that some investigational SARS vaccines produced negative side effects in some types of animals (such as ferrets) but not in others (such as mice). For that reason, many researchers are convinced that a vaccine should be tested in two different types of animals, Kozak says.

What makes you think effects should be the same (principally)?

One big reason for the difference is how close the vaccine's epitopes match the natural epitopes in the animals. When they are similar an attempted immune response to the vaccine will either tend to give an autoimmune response; or no response as the relevant immune cells were destroyed during maturation (to prevent autoimmune diseases).
The reports of autoimmune disease from SARS-Cov-2 (kawasaki disease) would seem to reduce the targets for a successful vaccine.
Sorry no refs on this.

Can you add some ref on  "When they are similar an attempted immune response to the vaccine will either tend to give an autoimmune response..." (basic textbook would suffice)


text:
Why bother studying SARS-CoV-2 in mice? Why not start with rats?
Mice, hamsters, ferrets, monkeys. Which lab animals can help defeat the new coronavirus? | Science | AAAS

Other SARS-CoV-2 researchers are turning to rats. They are no more susceptible to COVID-19 than mice, but their larger size is an advantage. “You often want to do repetitive bleeding in an experiment, and you can’t do that with mice,” says Prem Premsrirut of Mirimus, whose company is collaborating with an academic group that’s using CRISPR to create a rat model with a human ACE2 receptor. Vaccine studies, for example, often assess how different doses affect antibody responses over several days. Premsrirut notes that “most toxicology studies” of drugs also start in rat. “If you can study a drug directly in rats, you’re a step ahead.”

I'm assuming that you can repetitively bleed rats, but not mice, because rats'  "larger size is an advantage", because

"A rat weighing 400 g would therefore have a total blood volume (TBV) of approximately 64 ml/kg x 0.4 kg = 25.6 ml." But a mouse weighing 25 g would therefore have a total blood volume (TBV) of approximately 58.5 ml/kg x 0.025 kg = 1.46 ml.
the same percentage of TBV yields more blood in rats than mice.

Have you ever worked with either mice or rats?

Perhaps because (to borrow a phrase from NASA) mice are "smaller, faster, cheaper" than rats?

Because the knowledge base about mice is larger that that of rats.
Knockout mice were produced in 1989, knockout rats in 2003 (https://en.wikipedia.org/wiki/Knockout_mouse)
The immunology of mice has been studied more than any other animal except humans. Correlations have been made between many components of immunology between mice and humans.


text:
Is the receptor of SARS-CoV-like viruses in bats still unknown?
A fairly detailed 2012 review (Whittaker et al.) on the Mechanisms of Coronavirus Cell Entry Mediated by the Viral Spike Protein noted that

SARS-CoV-like viruses have been isolated in bats. In this case, entry does not occur via ACE2 and their receptor(s) is/are unknown; however, replacement of the amino acid sequence found between residues 323 and 505 with the corresponding sequence of the SARS-CoV RBD is sufficient to allow human ACE2 receptor usage [46].

Is the actual (bat) receptor that allows SARS-CoV-like viruses to replicate in bats still unknown?


text:
how does acetic acid induce pain?
how does acetic acid induce pain? I am finding the whole mechanism of it but cannot find any papers or writings. please help.
If you have links that would be nice too.


text:
What’s the Difference Between Grass and Sedge?
What’s the difference between grasses and sedges? in terms of anatomy and classification.

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

 Short answer
Sedges have edges, and they're in different families.
See Minnesota Wildflowers for a great summary with images.
 Long answer
Both are in the order Poales, but they are in different families:

Grasses = Poaceae (of the graminid clade)

Sedges = Cyperaceae (of the [non-monophyletic]1 cypirid lineage)

Some anatomical differences:

 Compiled using info from here and here

 Source: New York Botanical Garden

 Citations
 1. Bouchenak-Khelladi, Y., Muasya, A.M. and Linder, H.P., 2014. A revised evolutionary history of Poales: origins and diversification. Botanical Journal of the Linnean Society, 175(1):4-16.

What is an "edge" in this context?

@Terdon see the stem shape. Sedges have triangular stems instead of round. Each face of the triangle is an "edge"


text:
Questions regarding serial passage of virus through animals arising from the paper The proximal origin of SARS-CoV-2
In this answer on bioinformatics.stackexchange.com to the question inquiring about the validity of the paper Kristian G. Andersen et al, The proximal origin of SARS-CoV-2, the author asserts the following two points, which I do not understand.

Serial passage of a virus through either animals will always attenuate the virulence, say the affinity to the ACE2 receptor, of the virus. My question: Could people artificially select for thus increase the virulence of the virus?
We can always tell whether a virus is artificially serially passed because we know the mutational patterns of other serially passed viruses. My question: How does this distinguish artificial from natural passage?

No. Serial passage through animals attenuate the virulence of a virus In It's ORIGINAL Host. it can cause and will cause an increased virulence in the animals that were used in serial passage, and, if the animals have similar receptors as humans, increase the virulence in humans as well. like the two experiments that passed bird flu across ferrets until they become virulent and airborne across them.
https://www.cidrap.umn.edu/news-perspective/2014/04/experiments-render-h7n1-virus-more-contagious-ferrets
https://www.scientificamerican.com/article/pandemic-bird-flu-studies-public/
https://science.sciencemag.org/content/336/6088/1534.full
https://jvi.asm.org/content/88/12/6623

+1. Any comments on the second question?

It is hard to visualize but according to virologists passage into (mice) cells is very different to passage into (mice) lungs. The later greatly increases virulence (when the virus comes from another species) while the former is more likely to produce an attenuated vaccine strain. My opinion is that a last possibility, passage into cells then  once adapted passage into lungs may produce a more virulent variant. @Hans

@reuns: By "cells" do you mean in vitro, or tissue samples in a petri dish, and by "lungs" do you mean, in vivo, or lungs in a living animal? In the papers cited, the virus is first modified then serially passed in vivo amongst ferrets.  ferrets have the human-like ACE2 receptor.
By the way, do you know the reason for the large difference between passing in vitro and in vivo? I understand they are generally not equivalent. I am asking the reason about the large difference in this particular case

In-vitro : immortalized cell lines. The exact process of SARS-CoV-2 passage into mice lungs is described in there.
The 1st Wuhan institute of virology paper was showing that hela cells stopped to be susceptible when replacing human-ACE2 by mouse-ACE2, so the overall mechanism is quite complex. @Hans

@reuns: Nice reference. This supports the answer negating the assertion of attenuating virulence.


text:
Is the colour of a chrysalis predetermined?
Usually, chrysalis of butterflies camouflages with the surface it is attached to, for protection, as I understand it. There are exceptions, though; For example, the golden chrysalis of Euploea core is reflective and literally pops out of its background. My point is, what is the evolutionary advantage of that?

Edit: user -personjerry pointed out that shiny colours indicate poison.
So the main question now is,  if the aim was to scare off predators, why aren't they red/black in colour (as red means impending danger in the animal world)? Also, wouldn't developing a red pigment be much easier?  In these cases, is the colour predetermined?

Flashy colours are often an indicator of poison

Hi. Thanks for the information. I edited my answer to include your comment. I hope you are fine with that. :)

Generally, in biology nothing is designed but if something is working it is saved for the future generations. Chemistry of colors is a complicated field, you can't just slightly modify single "color" molecule to get any color you want. Maybe in chemical sense the material of this shell can be easily modified to get shiny. Suppose it happened occasionally once due to sporadic mutation and no one dared to eat this chrysalis, which gave abundant progeny.


text:
How is the carrying capacity of a logistic growth model calculated?
I am reading a book in epidemiology where the carrying capacity for a standard logistic growth rate is given by
K = (b - delta) / gamma

where:
K is the carrying capacity
b is the birth rate
delta is the death rate

but what is gamma?
Thank you

Your equation is not a difference equation (discrete time) nor a differential equation (continuous time). It therefore cannot describe a population growth. I don't know what the authors may have intended with this equation but we would need more information to address that question (book reference, page number, full description of the equation, etc...)

@Remi.b is correct that you haven't given us very much information, but I think we can reconstruct what's going on. Suppose the population growth rate is written out as
$$
\frac{dN}{dt} = N ( b - \delta - \gamma N)
$$
then the equilibrium (carrying capacity) occurs when $N>0$ and $dN/dt=0$, i.e. $b - \delta - \gamma K = 0$.  Solving this for $K$ gives $(b-\delta)/\gamma$ (as you stated).
So what is $\gamma$?  It is the decrease in the per capita growth rate per unit of increase in population density, or more biologically speaking it's the decrease in the birth rate or the increase in the death rate per unit of increase in population density. This could be due to increased competition for resources, or decreased environmental quality, or attraction of predators, or ...
Another, vaguer way to say this would be to call it the "effect of density-dependence".
Given the equations you list in the comments, with a $-\gamma N$ term included in the per capita growth rate for each compartment ($S$, $E$, $I$), we can say more specifically that $\gamma$ determines the rate of density-dependent increase in the ("natural" or disease-independent) death rate per unit population density. This parameter would not typically be broken down into lower-level processes.

sorry, I thought it was a standard measure, thus no information needed -- and in fact, you reverse-engineered. K was mentioned in a SEIRD model. Is gamma a constant or is it derived itself from more basic data? Thank you

Can't really answer that question without more context.  Can you give a link to the source, or post a screenshot of the relevant part of the text, as part of your question?

the context is a SEIR model with:

the context is a SEIR model with: dS/dt = (b-delta-gamma * N)*S - beta * S * I; dE/dt = beta * S * I - (sigma + delta + gamma * N) * E; dI/dt = sigma * E - (delta + deltaI + gamma * N) * I; with b = birth rate, delta = death rate, 1/sigma = latency, gamma as you said, N = total population.

I'm curious: can you say what book you're using?

It's actually a kind of pre-print/internal manual from the ETH Zurich. I could not add yesterday this: "this model assumes that the population dynamics of the host in absence of infection are governed by the standard logistic growth model... in absence of infection it equilibrates to a carrying capacity given by K = (b - delta) / gamma".

It's actually a kind of pre-print/internal manual from the ETH Zurich. I could not add yesterday this: "this model assumes that the population dynamics of the host in absence of infection are governed by the standard logistic growth model... in absence of infection it equilibrates to a carrying capacity given by K = (b - delta) / gamma".

I think it's also important to note two things. 1.  as a "capacity" is not very useful concept. Although the disease-free equilibrium can be calculated as (−)/, that's not interesting or useful because you are trying to model disease. 2. It's important to note, as was pointed out in this answer, that the units for  and  are different:  has in units of individuals and  has units of per-capita.  is used in the SEIR model to include a negative effect of crowding/density-dependent effects, and 's "relevance" is vestigal.


text:
Because we don't live as closely to livestock, are we at a greater or lesser risk of plagues?
Give recent events, some people have called for the 'wet markets' in China to be shut down, (for many reasons) but largely because it is likely the source of the recent plague outbreak, due to the close human-animal contact there.
(I am not here to debate if the markets should or should not be closed down. That is something for another question.)
However looking at the (very short and incomplete) history of the smallpox vaccine: Someone noticed that milk maids didn't have the ugly smallpox scars those who had survived a smallpox infection had. They conjectured the maids had caught the mild cow pox off their cows, and had gained an immunity to smallpox as a bonus. Cowpox was then developed in to a vaccine, fast-forward a few years and now smallpox has been eradicated. The 'natural' cow pox was basically an attenuated live vaccine for smallpox.
Now today we have supermarkets and mechanized agriculture and so have far less contact with animals (e.g. back in the day many households would have their own cow and chickens, we rode horses for transport, etc.) Therefore we have less of a chance to develop immunity to 'naturally attenuated' diseases, which they can immediately fend off if the disease does mutate/break the species barrier into a plague worthy foe.
I am not suggesting we should go back to milking our own cow before breakfast, however:
Does our lack of contact with domesticated animals mean we have less 'naturally attenuated' disease exposure and therefore we are at a higher risk of plagues?

Cleared out the comments because they were turning into an argument and drifting away from being nice. For OP: I think it's an interesting question but one that's difficult to answer in the SE format. You've identified what are probably the two key factors: immunity due to 'natural immunization' and exposure to zoonotic diseases. Someone might be able to make an answer by compiling some expert speculation on either side, but I don't think it is likely that a comparison has been/can be made.

The question is based on a false premise.  Although a smaller percentage of the population has contact with domesticated (or indeed, wild) animals than in previous centuries, population growth means that there are more individual humans who have such contact.


text:
Reasons why this protein is not suitable as an immunogen?
In a paper entitled "Progress and Prospects on Vaccine Development against SARS-CoV-2", the authors write the following in section 2.5:
"Compared with S, N, and M protein, E protein is not suitable for use as an immunogen. For one reason, it consists of 76–109 amino acids in different coronaviruses with channel activity, thus the immunogenicity is limited. Studies have shown that SARS-CoV E protein is an important virulence factor, and the secretion of inflammatory factors IL-1β, TNF, and IL-6 are significantly reduced after
knocking out E protein"
Question
Why does the fact it consists of 76–109 amino acids in different coronaviruses with channel activity imply its immunogenicity would be limited?

https://www.sciencedirect.com/science/article/pii/S0168170215001136 in 2015 thought the E protein would be a good target. I dont understand.

@PolypipeWrangler Thanks for your comment. Doesn't that paper comment on how removing the E protein weakens the virus and therefore SARS-CoV with the E protein removed might be a candidate for an attenuated vaccine? It doesn't discuss whether the immune system can be trained to go after the E protein itself.

You are right, viroids without E protein were weakly infectious. I will try to follow the citation chain forward to see if anything interesting turns up.

@PolypipeWrangler I actually think it's useful to keep your comments because that is how we all learn.

https://virologyj.biomedcentral.com/articles/10.1186/s12985-019-1182-0 is a 2019 article on c-virus proteins. out a year ago.

i find the article in google scholar, then use the "cited by" button to see who cites the article. then order by date.

@PolypipeWrangler Are you able to answer the specific query I had in my question? If so, you should post an answer.

The article implies E proteins are quite different between the previous known strains - so a vaccine targeted against E protein may only affect a limited range of strains.
But when I do a BLAST search on CS079032.1 I find nearly all the protein sequences are identical (results below).

Thanks for posting an answer. Maybe I have misunderstood, but I don't see how this answers the specific question I asked though?

Thats OK. The line from the article about 76-109 amino acids implies that the E proteins are too diverse for a useful vaccine - but that is not what I am finding.

I could be wrong but aren't the authors of the paper in my question implying the E protein won't provoke a strong immune response (not that it's not useful as an immunogen due to variation between strains)? I'm trying to understand the reasoning underlying their claim the immunogenicity would be limited.

I hadn't found evidence that the E protein has reduced immunogenicity. I dont know why they say so.

Firstly, for better immunogenicity, we should select short peptide of approximately 20 amino acids.  Longer peptide will definitely increase the immunogenicity, but that also increase the possibility of cross-reactivity. So, shorter peptide is more specific.
And secondly channel activity means, it contains more hydrophobic amino acids, so that it can form the transmembrane domain. But hydrophobic residues will decrease the solubility of a immunogenic peptide in the aqueous solution.
Reference: https://www.proimmune.com/custom-peptides/


text:
Definition of "genomic adaptation"
I have encountered the term genomic adaptation in some literature (for example Sikkink et al. 2017). I am struggling to parse the term, and I have not been able to find a definition for it.
Is genomic/genome adaptation the changes accrued by the genome as a result of evolution?
Or does it refer to some sort of active response by the genome to a particular environment upon introduction (of the organism) to said environment?

From glancing at the introduction it seems like a pretentious way of saying genetic. They are talking about mutations in genes. Genes are in genomes. Hence, make it sound complicated and different to disguise the fact that it is not. But the genome is in the organism and the organism is in the ecosystem, so why stop there. (But please don't.)

@David seems like you're right. So much for rigor and precise terminology.


text:
What is the principle behind Microagglutination test (MAT)?
Could some one please help me understand the principle behind the MAT. Also, is it only used to detect leptospira or can it be used to detect other pathogens as well? Kindly share links to papers if possible. Thanks!

Microagglutination tests for the presence of antibodies, which declare themselves by sticking their antigens together into clumps.
Leptospirosis serodiagnosis by the microscopic agglutination test.

The microscopic agglutination test (MAT) is the gold standard for
  sero‐diagnosis of leptospirosis because of its unsurpassed diagnostic
  specificity. It uses panels of live leptospires, ideally recent
  isolates, representing the circulating serovars from the area where
  the patient became infected. A dilution series of the patient's serum
  is mixed with a suspension of live leptospires in microtiter plates.
  After incubating for about 2 hr at 30°C, results are read under the
  dark‐field microscope. The titer is the last dilution in which ≥50% of
  the leptospires have remained agglutinated

You know antibodies work by sticking to things.  If I have antibodies to a thing it is because I have been exposed to that thing, here leptospirosis.  This version of the test uses live leptospires.  If the antibodies stick to them and they clump up, the plate gets clearer.
The good thing about this is that you don't need to know anything about the antigen except it is on the germs, or anything about the antibody except it sticks to the antigen.  Also the germs are big enough to make clumps.  If you have antigens for something small that won't make noticeable clumps (for example a virus, or an individual antigen of interest) you can stick it to microscopic latex beads.  Then just as the leptospires clump up when the antibody sticks to them, the beads will clump up if there is antibody specific to the antigen you have stuck onto them.
Historically the clumping was interpreted by a human with a microscope.  You can do it with an optical density meter too.
This approach is used for lots of different diagnostic tests.  You can find them with google and "agglutination" but those links do not all explain how the test works.

Thank you Willk for explaining it so well..


text:
Help identify this insect with a fan tail
I am trying to identify this creature... I took the shot in Medellín, Colombia. It is about 1cm in size.

This is the nymph stage of a planthopper, an insect in a suborder of the hemipterans.
The "fiber-optic-like" tail is actually made out of wax! From Wikipedia

Nymphs of many [planthoppers] produce wax from special glands on the abdominal terga and other parts of the body. These are hydrophobic and help conceal the insects. Adult females of many families also produce wax which may be used to protect eggs.

The fact that there are about 12,5000 species of planthoppers and I am fully unfamiliar with the fauna of Colombia, I can only provide a quick image confirming that it is a planthopper. (Perhaps you have a field guide or key available to you to help ID to genus or species)

 Credit: Malcolm Burrows, source
You can find an aditional image of a species more similar to yours here.

thanks so much! I was able to find this other video
https://www.youtube.com/watch?v=jPCRwuPpf9M


text:
Difference between viral and native RNA
I am a data scientist with really next to no training in microbiology.  I hope you'll all forgive my ignorance to entertain these questions.  The attention COVID-19 has gotten recently got me thinking:  What is the fundamental difference between viral RNA and the RNA native to a particular cell?
What I mean is, we are often told in school that viruses hijack the cell's protein manufacturing facilities to express their own genetic material.  The cell produces so much of the viral protein that it eventually lyses (for example).  But what is it that makes the cell produce so much of the viral proteins?  How does the cell not produce too many proteins from the cell's own DNA?
I suspect the answer comes down to the lack of gene regulation for the viral RNA.  But is every gene that is native to the cell really subject to some sort of regulation?  If so, is the real danger of viruses that they lack any kind of regulation?  Then that seems to be a fairly easy thing to detect- at least theoretically.  In other words, a cell, or a scientist could label a sequence of RNA as dangerous simply because it is unregulated, regardless of whether it came from a virus.
A second question is, we are told that the viral proteins self-assemble and encapsulate copies of the viral RNA just by chance.  Doesn't this seem unlikely?  Are the virus's components really so ubiquitous in the cell that the virus will self-assemble including all its necessary components a significant portion of the time?  I suspect for this to happen, the virus's RNA would need to be copied many times so that it would be plentifully available.  Then it comes back to the same question as above.  Is viral RNA unique in that it gets copied indefinitely?

There is no fundamental difference between viral RNA and and native cellular RNA other than the sequence of RNA bases in them.  The sequence differences are not biochemically apparent in the RNA, only in the protein products produced from the RNAs.
Regulation of native RNA is done in a huge variety of ways (nothing in the cell is designed; everything is ad hoc, so any random happenstance can become established).  Native regulation is essential, otherwise runaway production will happen leading to cell death or to cancer.
Much, if not most, of the native regulation is done by regulating transcription of DNA into RNA. Once the RNA is in the cytosol, little further regulation is done, so viral RNA in the cytosol has the run of the cellular protein factory.  But at least some viruses have acquired further advantages which help their RNA out-compete the native mRNAs for use of the protein machinery (see, e.g., Hijacking the translation apparatus by RNA viruses)
So it is not really an easy thing to "label a sequence of RNA as dangerous simply because it is unregulated" as the wide range of normal RNAs in the cytosol does not provide a basis for determining if any are "unregulated" and the cell cannot be protected in that manner.
Self-assembly is widespread in normal cellular functions as well as in viral production.  The molecules involved have long-honed attractive points for their mate molecules, and in the jiggling molecular soup of the cell the molecules can soon bump into each other and join up.  Thanks to the virus's uncontrolled production, new viral particles have plenty of component molecules available for this assembly.

(If you wonder I'm posting two answers, it's because this q-post asked two questions in one.)
Regarding the issue of virus self-assembly... studying it has indeed been a challenging issue. There's a recent (2019) PNAS paper on that:

Despite decades of study, how capsids self-assemble has remained a mystery, because there were no methods to measure the assembly kinetics of individual capsids. We surmount this obstacle using a sensitive microscopy technique based on laser interferometry. The measurements show that a small nucleus of proteins must form on the viral RNA before the capsid assembles.

Overview of the measurement. (A) A structural model of the MS2 capsid (PDB ID: 2ms2) shows its small size and T=3 structure. The 2 coat-protein dimer configurations are shown in gray and purple. (B) We inject a solution of unassembled dimers over a coverslip on which MS2 RNA strands are tethered by DNA linkages. As dimers bind to the RNA, the resulting particles scatter light. The particles appear as dark, diffraction-limited spots because of destructive interference between the scattered light and a reference beam. (C) We monitor many such spots in parallel. Shown is a typical image of the field of view, taken 126 s after adding 2-μM dimers and representing an average of 1,000 frames taken at 1,000 frames per second. (D) The intensity of each spot is proportional to the number of bound proteins within each particle and changes in the intensity as a function of time reveal the assembly kinetics of each particle. The darker the spot is, the larger its intensity. (D, Top) Time series of images for the boxed spot in C. (D, Bottom) Intensity trace for the same spot using a 1,000-frame average. We discuss the relationship between intensity and number of bound proteins, as well as how we calculate the spot intensity, in Materials and Methods and SI Appendix.

Some videos posted as well in the Supplemental.
And a bit more on the observed dynamics:

We find that the “growth time,” the time required for a particle to reach the size of a complete capsid after it nucleates, varies from particle to particle, ranging from 30 to over 200 s (Fig. 2A and SI Appendix, Fig. S1). Of the particles that grow into a complete capsid, some grow at a constant rate, others slow as they approach completion, and still others contain intermediate pauses lasting up to 25 s (Fig. 2A and SI Appendix, Fig. S1). Despite these differences, essentially all of the traces are monotonic, with little or no observable disassembly steps.

So yeah, quite interestingly, the virus capsid just build and builds itself; even if it takes "lunch break" it's not a problem reversing the build progress in a significant manner.
The failure mode(s) of this self-assembly process are actually related to building/attracting "too much stuff", or two (or more) viral RNAs getting entangled by common protein shards they both (all) attract. Basically too much density of building materials can lead to problems...

The growth times also decrease with increasing protein concentration, but less rapidly than do the nucleation times (Fig. 4A) [below]. Thus, we conclude that the RNA, which promotes nucleation at low protein concentration, creates a competition between nucleation and growth that can lead to overgrown structures at higher concentration, as sketched in Fig. 4B. This pathway provides a possible explanation for the “monster” (5) and “multiplet” (19) structures observed with other RNA viruses.

I mostly agree with mgkrebbs (+1), but note that while viruses generally have some kind of RNA replicase subunit (RdRP) to help them out, viroids completely lack those, yet manage to reproduce:

While RNA viruses encode subunits of the enzymatic complex (RNA replicase) that catalyzes initiation and elongation of viral RNA strands, viroids must rely for this replication step on pre-existing host RNA polymerases.  In principle, the best candidates would be RNA-dependent RNA polymerases, whose existence in plants has been known for a long time. However, viroids do not use these enzymes for their replication, but DNA-dependent RNA polymerases redirected to accept RNA templates.

The closest thing to a viroid in humans is Hepatitis D. Until last year, it was thought that it was mostly a human disease, but a 2019 survey found that HepD analogs are quite widespread in invertebrates, fish, snakes etc.
Viruses are "much more nasty" than viroids in that replication regard because

Positive-strand RNA viruses replicate by using virally encoded RNA-dependent RNA polymerases (RdRPs) that provide a direct RNA-to-RNA replication function not found in host cells.

Some recent research suggests that RdRPs have been independently lost in many animal clades. Ironically, the roles of these (former) host RdRPs was [most likely] to provide an anti-viral mechanism via RNA silencing (see [section] below for details), but evolution has provided with alternative host mechanisms for producing the same.
While it's possible to recognize the [core of the] viral RdRPs in software, it's not clear/known how to translate this into a general anti-viral strategy, as far as I know, due to their fairly substantial variation. (In general it's not enough to know the genetic sequence encoding the RdRP of some virus to even screen inhibitor drugs for it; additionally one must know the crystal structure of the RdRP complex for that virus.)

If you're curious about "intra-cell" (i.e. RNA-based) anti-viral defense... there exist mechanisms like that, but are substantially more complicated (that what you suggest), being based instead on RNA silencing:

In eukaryotic RNA-based antiviral immunity, viral double-stranded RNA is recognized as a pathogen-associated molecular pattern and processed into small interfering RNAs (siRNAs) by the host ribonuclease Dicer. After amplification by host RNA-dependent RNA polymerases in some cases, these virus-derived siRNAs guide specific antiviral immunity through RNA interference and related RNA silencing effector mechanisms.

Key steps in RNA-based antiviral immunity induced in Drosophila
melanogaster by infection of positive-strand RNA viruses such as flock house virus.
Following entry and uncoating of flock house virus (FHV) virions, the genomic
positive-strand RNA ((+)RNA) serves as both mRNA for the translation of viral
RNA-dependent RNA polymerase (RdRP) and as a template for the synthesis of
antigenomic negative-strand RNA ((–)RNA). Preferential production of (+)RNA by viral RdRP
is achieved by multiple rounds of initiation of RNA synthesis from the 3ʹ end of the low
abundant (–)RNA. The resulting double-stranded RNA (dsRNA) formed between the
5ʹ-terminal nascent progeny (+)RNA and the (–)RNA template is recognized by Dicer 2
(DCR2) and cleaved into small interfering RNAs (siRNAs), thereby triggering RNA-based
antiviral immunity. The viral siRNAs are assembled with Argonaute 2 (AGO2) into the
RNA-induced silencing complex (RISC), methylated at the 3ʹ end (depicted by a black
circle) by HEN1 and used to guide specific clearance of FHV RNAs. As a counter-defence,
FHV encodes a viral suppressor of RNA silencing, the B2 protein, which targets two
steps in this immune pathway: inhibition of viral siRNA production by binding to viral RdRP
and the viral dsRNA precursor, and sequestration of viral siRNAs by binding duplex siRNAs.
Loqs-PD, loquacious-isoform PD.

And yes, the RdRP of viruses (the most significant part of the self-copier machine they come with) is an important drug target, e.g.

CoVs employ a multi-subunit replication/transcription machinery. A set of non-structural proteins (nsp) produced as cleavage products of the ORF1a and ORF1ab viral polyproteins (5) assemble to facilitate viral replication and transcription. A key component, the RNA-dependent RNA polymerase (RdRp, also known as nsp12), catalyzes the synthesis of viral RNA and thus plays a central role in the replication and transcription cycle of COVID-19 virus, possibly with the assistance of nsp7 and nsp8 as co-factors (6). Nsp12 is therefore considered a primary target for nucleotide analog antiviral inhibitors such as remdesivir, which shows potential for the treatment of COVID-19 viral infections (7, 8). [...]
The efficacy of chain-terminating nucleotide analogs requires viral RdRps to recognize and successfully incorporate the active form of the inhibitors into the growing RNA strand.

So while it's not so simple to detect/fight viruses' as you suggested, some replication-targeting strategies involve either "jamming their own (RdRP) copier with fake parts" (as e.g. remdesivir does) or producing [hopefully] as many "copy cancelers" as possible, for which the RNA silencing machinery actually uses parts from the virus copies themselves.


text:
Possibility a child could genetically be also the child of its grandparent
When two people have sex, it is my understanding their diploid set of chromosomes is randomly split in half to create two haploid sets which unify into the diploid chromosome set of the child. For each parent, there are $2^{23}$ possible permutations or a chance of about 1 in 8 million. Let these two be the grandparents A and B, having a child C
When that child C has a new sex partner D and they make their own child E, in any case E shares half of its genetic makeup with both C and D (i.e., E is the child of C and D). However, with a probability of roughly 1:8000000, when halving C's diploid choromosome set, it always chose the A parts.
This means that E would then have a diploid set A+D, which would make E appear to be both the child of C but genetically could also be the child of A.
Is this understanding (discounting for crossing over and other genetics) generally correct? With a probability that high, if it is possible there should be recorded cases of this (although for all intents and purposes you would never know without sequencing DNA). Are there such cases?

But can we ever discount crossing over? Crossing over is a very consistent feature of meiosis. Perhaps what you say is possible for certain closely linked loci (e.g. HLA haplotypes). But it is hard to imagine for the entire chromosome complement of a sexually reproducing organism.

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Since this question "addresses a basic biology concept that may seem trivial to biology professionals", it qualifies as  "homework". In particular, you can't discount crossovers since they are essential. ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

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

One of the hallmark features of meiosis is the formation of chiasmata, that is the crossing over and exchange of genetic information.
These structures are generally necesssary for a normal meiosis to happen and you should never get a cygote without any crossing over. Therefore, taking this into account, the probability of your scenario is 0.

I've been thinking some more about crossing over, and think it might not be an issue at all. In the 1:2^23 case, even with crossing over, the DNA would be mixed with some other, but would generally still appear to have both the actual parent and the grandparent as possible parents. Or would the crossing over make this always distinctively clear?

The crossig over in meiosis in the child (C) of the grandparents (A and B) means that all of the chromosomes will be a mixture of A and B. Therefore, the information to the subsequent child E cannot be purely A or B. There may be instances that on a particular chromosome where crossing occurs in a perfectly homologous region making it invisible. But for this to happen on every chromosome A and B would have to be perfect clones.

I think this 1:8000000 should be further diminished twice by the chances to get "intact"(no cross-over) chromosome from A to C and from C to E. So the final probability is far less.


text:
Is it still true that C. elegans has no known natural viruses?
I read in a 2009 review that

While mammals and C. elegans each have a single Dicer that makes both miRNAs and siRNAs, Drosophila has two Dicers: Dcr-1 makes miRNAs, whereas Dcr-2 is specialized for siRNA production. The fly RNAi pathway defends against viral infection, and Dicer specialization may reduce competition between pre-miRNAs and viral dsRNAs for Dicer. Alternatively, Dcr-2 and Ago2 specialization might reflect the evolutionary pressure on the siRNA pathway to counter rapidly evolving viral strategies to escape RNAi. In fact, dcr-2 and ago2 are among the most rapidly evolving Drosophila genes. C. elegans may achieve similar specialization with a single Dicer by using the double-stranded RNA-binding protein, RDE-4, as the gatekeeper for entry into the RNAi pathway. However, no natural virus infection has been documented in C. elegans. In contrast, mammals may not use the RNAi pathway to respond to viral infection, having evolved an elaborate, protein-based immune system.

Is it still true that no know natural virus infects C. elegans? And is this [thought to be] due to the effectiveness of its viRNA (virus-derived small interfering RNAs) immunity/defense mechanism?

It has a natural virus, an Orsay virus.
https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1000586
is the paper of the discovery. found by searching "virus infecting C elegans"

Indeed even has wiki page https://en.wikipedia.org/wiki/Orsay_virus

Also the RNAi suppressors of the Orsay virus have been studied already. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648182/ And it seems to have a novel fusion protein https://www.sciencedirect.com/science/article/pii/S004268221300679X

And it seems to have an egress protein https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6026750/


text:
Analysing bird diversity data across 2 sites and 2 time periods - Ordinal data. Shannon's and Jaccard?
I am looking for the best way to analyse the data below to measure and compare the bird diversity between 3 sites and across 2 time periods - basically are they different from each other and have they changed over time.
I don't have count data from 1992 so have applied the categories used in a historical publication to my own data. I was planning to use Shannon's on the table below and Jaccard's using presence/absence data. Is that the most appropriate, and will these give me p values? If not what further tests would be needed?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, since this question appears to be entirely statistical in nature, it would be a better fit for [CrossValidated.SE]. Thanks!

I’m voting to close this because it is a purely statistical question and so belongs on [statistics.se].

Update: see also answers here.
I would strongly recommend reading more about species co-occurrence analysis, e.g. here and here. This is a big field where a lot of work has been done on its statistical analysis and interpretation.
You can apply any metric that you want for a a basic idea of correlations in the data, and for that the simple distances are a reasonable place to start (I would probably just look at a correlation matrix or do principal component analysis to start, but it's a matter of taste). But you will likely want to use something more sophisticated to account for multivariate structure in the data.
In terms of statistical inference, e.g. p-values, you will need to do something more than those metrics. Distance measures are just metrics, they don't apply tests and they don't have a null hypothesis per se. The easiest thing to do would be to apply an empirical null distribution by generating a large set of permuted datasets (where you shuffle the labels of the rows and columns), compute the metric for each permuted dataset, and then use that distribution of metrics as a null distribution. That's still a fairly naive analysis, but it is at least accounting for some of the structure of the data.
I think that your best bet is to go read some more about how people have analyzed this kind of data in the past, and use some of those tools. If you are comfortable with R, the vegan library is a good place to start, it has already implemented a lot of the basic analyses you might use.
Update on ordinal data:
For helpful background on ordinal data analysis, I would suggest reading this paper. As for transforming ordinal data to ranks, that is fairly simple as long as it's ok for the method for you to have ties in rank.
I am also assuming that you have data that look like this, in addition to the table that you screenshotted:
Site |  Species  |  Amount   |
A    |     X     |  common   |
A    |     Y     |very common|
A    |     Z     |    rare   |
B    |     X     |    rare   |
B    |     Y     |   common  |
B    |     Z     |very common|

You can turn this into ranks:
Site |  Species  |  Amount   |
A    |     X     |  2        |
A    |     Y     |  1        |
A    |     Z     |  3        |
B    |     X     |  3        |
B    |     Y     |  2        |
B    |     Z     |  1        |

Thanks for your comment. I have read the links that you supplied and would like to produce rank abundance graphs as shown in the paper. As I mentioned I only have ordinal frequency data (very common, common etc), so how do I transform this so that I can attribute a numerical frequency to each species?

Ah, just from looking at the table I guess I didn't understand very well what you meant. See update.


text:
Why such diversity in sexual dimorphism in passerines?
In searching for info to answer my question, I’ve found a fascinating 1998 article  by Owens and Hartley from Proc. R. Soc. Lond. B. It reports such cool findings as that

When we break up plumage-colour dimorphism according to whether it is due to melanins, carotenoids or structural colours, we find that each category of plumage-colour dimorphism shows a different pattern of covariation. The correlation between overall plumage-colour dimorphism and the rate of extra-bond paternity is due to structural colours, whereas melanin-based dimorphism is associated with sex differences in parental care.

Intriguing, but not on point for my question; so I turn to StackExchange.
Is it known why, for example, northern cardinals (Cardinalis cardinalis) are essentially monomorphic in size but dimorphic in plumage color, American robins (Turdus migratorius) and blue jays (Cyanocitta cristata) are pretty much monomorphic for both traits, and the sexes in the brown-headed cowbirds (Molothrus ater) vary so in size and coloration that they could easily be mistaken for separate species?
Whether it involves caring for young or pair monogamy or whatever, how does one species arrive at a particular morphological-behavioral complex while another ends up someplace entirely different? Is that entirely a matter of evolutionary contingency?


text:
What is the lipid membrane of SARS-CoV-2 made of?
SARS-CoV-2 is an enveloped virus: in structural diagrams it is drawn with membrane glycoprotein (M), envelope protein (E) and spike protein (S) embedded in a lipid membrane.
What specifically is the lipid membrane made of?
I assume it is derived (somehow) from the host cell membrane, and would have a similar composition.  It doesn't necessarily have the same composition.  If it just host membrane from a typical mammalian cell, it may be mostly phosphatidylcholine (PC) and cholesterol on the outside, and phosphatidylethanolamine (PE), PC and cholesterol on the inside.  It should equilibrate over time, since the virus does not contain a flippase to keep an asymmetrical distribution.
Related questions: Does the composition depend on the cell that the virus was assembled in?  Does it have any selectivity, or does it simply pick a random piece of the host membrane?  How exactly is the viral membrane detached from the host?
Probably most important question: Does the infectivity of the virus depend on the composition of the membrane?

Structural protein (M, also S,E) have transmembrane domains anchored inside cell's Ergic ER and Golgi infection-modified vesicles, they'd take some lipids with them during the assembly of the virions (expression of M plus low amounts of others produces self-assemblying viral like particles), origin of those virion factories vesicles is unclear.

The last reference says it is the virion factory vesicle (1 2 3) which is exocytosed all at once.

I don't know if this questions has been studied in detail even for SARS, let alone SARS-CoV-2. As noted in a comment by reuns, the virus lipid envelope is most likely derived from that of the endoplasmic reticulum.
What we know however from from some studies on influenza viruses, that's hardly the end of the story though:

Using rigorous virus purification, marked differences between virions and host were observed. Over 125 phospholipid species have been quantitated for three strains of influenza (HKx31- H3N2, PR8- H1N1, and VN1203- H5N1) grown in eggs. The glycerophospholipid composition of purified virions differs from that of the host or that of typical mammalian cells. Phosphatidylcholine is the major component in most mammalian cell membranes, while in purified virions phosphatidylethanolamine dominates. Due to its effects on membrane curvature, it is likely that the variations in its content are important to viral processing during infection.

And this part is a bit of a "reverse answer", but lipid rafts on the membrane of the target cells are thought to be important for the entry of coronaviruses, including SARS. One experiment found that depleting cholesterol from the cell membranes dramatically slowed SARS virus' ability to enter them.
(Regarding how SARS-CoV-2 might come out [with different envelopes] from different cells: we only had confirmation very recently that it substantially infects intestinal enterocytes. So expecting a lot of extra details on that is a bit premature right now.)