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Why is glycerol the backbone of fat?
Fats are fatty acids joined onto the backbone of a glyercol (propane-1,2,3-triol).
Why was glycerol seemingly chosen by nature to be the backbone of fats? Why can't it have been a butane -1,2,3,4- tetraol or pentane with 5 alcohol groups or almost any other molecule?
So my question boils down to, is it just pure chance that glycerol is the backbone of fats or is there a deeper underlying reason?

Chance should always be high on our list of explanations of why the history of life turned out in some specific way. As James A. Coffman has described, there are a couple of different notions of chance. Evolutionary biochemistry is quite difficult because today's diversity of biochemical genotypes and phenotypes are a biased representation of the ancient past.
However, I think a case can be made that it was not 'pure' chance.
As your question itself suggests, the chemistry requires alcohols for the esterification with fatty acids to form acyl glycerols. I think that is 'sufficient' to say it is not 'pure' chance that among molecules that it was glycerol, but since you're also questioning "why glycerol?" over other alcohols, let's look at what glycerol has going for it compared to other alcohols.

Glycerol is relatively small. All else being equal, fulfilling a biological function with a smaller molecule requires less energy than larger ones. Compared to polyphenols, for example, this is a no-brainer because (1) building polyphenol would be expensive energetically, and (2) would be difficult to transport.
Glycerol is flexible. The two outer alcohols have the ability to move with respect to the central carbon so that as we go from glycerol to mono-acylglycerol, di-acylglycerol, and finally triacylglycerol, the outer groups' motion can reduce steric hinderance.
Glycerol can be converted into a lot of other things that form a part of metabolism. While it is conceivable that an extremely different metabolism without glycerol could have come to be, the fact that glycerol is directly and indirectly convertable into a large number of molecules with structural and energetic functions does give it better candidacy than molecules that are relatively unreactive or require large numbers of reactions to build anything useful biologically.
While glycerol doesn't have the greatest number of alcohol groups for its size (size in terms of carbon backbone, not necessarily molecular weight), it doesn't have the least number either. Steric hinderance or difficulty to synthesize of alcohols with the same size would make glycerol a better choice.

Hopefully that convinces you that glycerol was not completely random with respect to all other molecules or even all other alcohols. That is, not all the possibilities in those sets are equally good for the biochemical role that we now see glycerol fulfilling, and glycerol is defintely not the worst. However, there may have been other subsets of alcohols/molecules in existence at that time for which we don't have specific reasons for glycerol being better.
In conclusion, no, not 'purely' random.

UPDATE
Reading my answer above, I can see why someone reading my list of glycerol traits may think I am making a just so story on why it is specifically glycerol that we have today fulfilling a biochemical role of joining together fatty acids via acylation. To be clear, I am not addressing 'why' glycerol is the molecule fulfilling this role but rather whether it is purely random that glycerol is the molecule fulfilling this role. In my vernacular, 'purely random' implies a uniform probability distribution, which is to say that in this context each molecule was as likely as any other to fulfill the role that we see glycerol fulfilling in biochemical systems today. By citing reasons why some molecules are better suited in their properties, we show that the distribution cannot be uniform. We don't need to even place where glycerol sits on this distribution to determine that it is not purely random. We only need non-uniformity. The fact that glycerol has traits that make it more likely than others is an additional suggestion that among the molecules under consideration, glycerol was not the least likely.

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Summary
To attempt to explain why organisms evolved with a particular molecule performing a particular function it is not sufficient to consider the suitability of the molecule for that function and to compare it in abstract with other possible molecules. It is also necessary to consider the metabolism in existence at the time the function arose, and hence the molecules available as precursors. It is argued that membrane phospholipids, which use the same precursor (phosphatidate) as triglycerides, arose early in evolution, so that the ‘choice’ of phospholipid backbone probably determined that of triglyceride. One ancient pathway that is known to have existed at the time of the emergence of membrane phospholipids is anaerobic glycolysis, which includes only hexoses and trioses. It is argued that a three-carbon compound could provide a simple backbone that a six-carbon ring could not, and emphasized that the glycerol phosphate precursor is formed in a single step from the  dihydroxyacetone phosphate intermediate of glycolysis. The separate evolution of a glycerol-phosphate backbone for membrane phospholipids on two occasions in the form of the different stereo-isomers glycerol-3 phosphate and glycerol-1 phosphate in bacteria and archaea is consistent with the view that the availability of a glycolytic intermediate influenced the “choice by Nature” of the backbone of phospholipids and triglyceride fats.
Molecular Evolution: Problems and Pitfalls
Before addressing this question I would once again emphasize some of the difficulties with questions on molecular evolution, often seen on posts to this site.
   One type of question asks why something that the poster believes would be advantageous has not evolved. As I have discussed in an answer to a question of this sort, the poster often only thinks of this in abstract, rather in terms of the actual selective pressures that drive evolution.
   The second and more frequent type, typified by this question, asks “Why did such and such evolve in this way?”. The common pitfall here is to assume that because it evolution did produce this result, the molecule in question must be the best suited to this function, and hence answers tend to list the way the structure of the molecule allows it to fulfil that function. The answers tend, in fact, to be to a different question “Why is this molecule suited to this biological function?” — a perfectly good question, but one of structural chemistry rather than evolutionary biology.

To even approach an answer such questions I think one needs also to consider the evolution of metabolism, and hope Nature may have left some clues to help. I shall adopt this approach to the present question. Another example related to nucleic acid bases can be found here.
Glycolysis as the source of precursors to the backbone
My premise is that the glycerol backbone of triglycerides arose early in evolution because it was first used for the membrane phospholipids. As shown in the schema below (adapted from Berg et al.), both fatty acids and triglycerides are formed from a common precursor, phosphatidate, a  monoglyceride built upon L-glycerol 3-phosphate (G3P). (In addition, the conversion to triacylglycerol utilizes the same type of acyl-CoA derivatives used in the formation of phosphatidate.)

Even if one does not accept that argument that what holds for phospholipids holds for triglycerides, the evolution of the glycerol backbone of phospholipids illustrates the general approach that I think should be employed.

The synthesis of the phospholipid backbone requires an abundant source of a carbohydrate precursor. Clearly membrane phospholipids evolved at early stage and before oxidative metabolism that uses membranes for the chemiosmotic synthesis of ATP. Comparison of pathways in many different bacteria and archaea suggests that the enzymes for glycolysis and gluconeogenesis (which latter may have arisen first) were present in the last universal common ancestor (LUCA), so it is not unreasonable to look there for the precursor.

Examination of my schematic of glycolysis, above, reveals that the pathway includes only hexoses and trioses. These, therefore, represent the initial choice of precursors to the backbone. The particular hexose rings contain hydroxyl groups (to which a fatty acid might be attached) with different orientations, making them unsuitable for a membrane component without further metabolism. The triose, dihydroxyacetone phosphate (DHAP), can be converted to G3P in a single step, and this provides a suitable backbone for phospholipids and triglycerides. (Of course hexoses are used for carbohydrate storage, but as polymers such as glycogen and amylose.)

Perhaps, in theory, there is a better backbone than a triose, but as trioses ‘work’ (as explained in the answer from @Galen), once membranes had developed it would require a very strong selective pressure for a change to occur even if metabolism had expanded and other precursors had become available. That is my postulate.
The significance of membrane phospholipids in archaea
An interesting phenomenon that throws light — and darkness — on the forgoing postulate is the structure of the membrane phospholipids in archaea. These differ from those in bacteria and eukaryotes in being ether phospholipids, rather than ester phospholipids, as shown in the diagram below (from Coleman et al.).

The ether phospholipids are thought to be more suitable for extreme environments, but their existence raises difficult evolutionary questions regarding the relative time of appearance of the two types and how eukaryote membranes could have evolved from an archaeal cell, as is thought by many. These are discussed in several reviews listed in the bibliography, but what is more relevant to this question is the fact that the backbone differs stereochemically between the two. In the bacterial (and eukaryotic) case it is D-glycerol, derived from sn-glycerol 3-phospate, whereas in the archaeal case it is L-glycerol, derived from sn-glycerol 1-phospate. However in both cases these are derived from dihydroxyacetone phosphate in a single step, as shown in this diagram from Pereto ́ et al.:

There are two conclusions to be drawn from this. The first is that the phospholipid backbone arose on two different occasions, but in both cases from the same glycolytic/glucogenic precursor — it was not chance. However “chance” would seem to have played a part in the stereochemical conformation of the backbone glycerol, which has no influence on the structural properties of the molecule.
Bibliography
The following articles discuss the origins of membrane phospholipids:
J. Pereto ́ et al. (2004) Trends in Biochemical Sciences 29, 469–477
J. Lombard et al. (2012) Nature Reviews : Microbiology 10, 507–514
S. Jain et al. (2014) Frontiers in Microbiology 5, 1–16
G. A. Coleman et al.(2019) Genome Biol. Evol. 11 883–898


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Why there is no ELISA for SARS-CoV-2?
As far as I know, SARS-CoV-2 tests currently used worldwide are real-time RT-PCR. Why there is no ELISA for SARS-CoV-2?
Compared to PCRs, ELISA is:

Way cheaper;
Way faster;
Does not require trained technicians or complex equipment.

Because the virus is spreading for only a short time?

Yeah, @Chris has a point. While the test itself is easier to perform, the production and purification and labeling of antibodies for tests such as the ELISA does take some time.

Marion Koopmans and Florian Krammer both have preview papers describing SARS-CoV-2 ELISAs. There simply hasn't been enough time to prepare antigens, validate ELISAs, publish papers, and manufacture tests. I think this question will be out of date in a few days or weeks, so maybe isn't a good match for SE, where answers are expected to be useful to other people in the future

Another preprint (posted yesterday): Evaluation of antibody testing for SARS-Cov-2 using ELISA and lateral flow immunoassays

@iayork The fundamental question is good for future use and probably reapplicable, and it is good to have a record of why this wasn't possible at a moment in time, and indeed this is a timely question. I would say that this argument requires a bit of editing to the question semantically and a lab-techniques label.

once you are comparing ELISA with RT-PCR i will assume we are speaking about antigen tests for SARS-CoV-2. In that sense, we can note that whichever type of ELISA chosen, all of them will depend on the Ig specificity for the virus antigen.

therefore, the main reason has to do with the fact that

mutation regions in the virus appear mainly in the spike protein, we do not know whether the antibodies produced against the original spike protein can recognize the new variant spike proteins. article

I agree with @mpprogram6771 and @iayork. Development of ELISA kits consumes more time to develop and validate - the first on the market last year were not recommendable.
Now a variety of immunoglobuin SARS-CoV-2 ELISA kits are available. Mainly using IgG or IgM - IgM to detect early signs of infection, IgG for long term response.
Eg: here

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source: Stack Exchange

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Does destroying a virus envelope make the virus inactive?
Some viruses have a lipid envelope around their protein capsid. The envelope can be dissolved with soap, but does that still leave the capsid and interior genetic material intact? If so, is the virus still active?

Enveloped RNA viruses will get inactivated quickly without a membrane. RNase is a ubiquitous enzyme that would quickly digest any exposed genetic material.
Via https://www.neb.com/tools-and-resources/usage-guidelines/avoiding-ribonuclease-contamination:

RNases are found in all cell types and organisms from prokaryotes to eukaryotes. These enzymes generally have very high specific activity, meaning tiny amounts of contamination in an RNA sample is sufficient to destroy the RNA. The major sources of RNase contamination in a typical laboratory include:

Aqueous solutions, reagents used in experiments
Environmental exposure, RNases are in the air, most surfaces and dust
Human contact with hands and skin

Without a membrane (and any associated receptor-binding proteins), the genetic material of an enveloped virus would not normally have a way to get incorporated into and infect the host cell, in any case.
Your question is about enveloped viruses, specifically, but there is an interesting exception of a kind, so-called viroids that infect plant cells. These have no capsid or protein envelope, but are still infectious.

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Why do coliform bacteria smell so bad?
I have done multiple cultures of E. coli bacteria and related species over the course of my education. Almost every time, they had this revolting smell. However, other organisms used for genetics experiments (eg. Saccharomyces cerevisiae) rarely have a bad scent, if a scent whatsoever. My question is, what is it about the coliform metabolism that produces such a pungent and revolting odor? Any and all answers are appreciated.

I'll note that "revolting" is a characteristic of the owner of the nose, not the producer of the scent chemicals; perhaps the nose owning organism evolved an aversion to those chemicals for some reason.

xD Well I guess it is, isn't it?

E. coli and other bacteria metabolize tryptophan into odoriferous skatole and other indole compounds.
If you're culturing these organisms in medium that contains tryptophan, that may be what you're smelling.

Ah, Skatole! That makes sense. Thank you for your answer!


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Why/How do Cyanobacteria Produce Toxins?
I've been doing some research on the versatility of nitrogen-fixing cyanobacteria, particularly of the genus Anabaena, and I often run into safety hazards and have to add extra steps to my procedures because of the toxins produced by the genus. After doing some reading, I've found that most cyanobacteria produce toxins (collectively dubbed "cyanotoxins"). The wide variety of different structures and mechanisms of the toxins across multiple genera is astounding, especially because some of them are carcinogens, which would logically affect the host unless a mechanism to prevent this had evolved. This tells me that a lot of evolutionary "effort" must have been put into the evolution of toxin production in cyanobacteria. Originally, I just thought that the toxins were a natural part of their metabolism that evolved normally because these compounds didn't affect them in the same way as they did us. Now that I see the Huge, variable trend throughout the class, I have begun to think otherwise. My questions are as follows:

What is the evolutionary basis for the production of cyanotoxins by cyanobacteria
Are the cyanotoxins a necessary part of the bacteria's metabolism, or can they be eliminated by way of genetic engineering without directly affecting the success of the organism?
How do cyanobacteria cope with the constant exposure to native carcinogens?

These questions are only the major ones that I have, so any extra information is greatly appreciated

This available paper has some ideas,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3736421/
Search terms cyanotoxin and evolutionary give at least two more promising papers.
https://www.biorxiv.org/content/10.1101/615542v1.full
says:
i) photoprotection due to absorption of harmful ultra-violet radiation; (ii) facilitating the acquisition or more efficient use of available but limiting resources; (iii) impeding growth or resource use of competitors such as green algae or other cyanobacteria; and (iv) limiting predation by inducing toxicity in organisms predating on cyanobacteria. While the role of cyanobacterial metabolites in photoprotection, resource monopolization, and habitat dominance has been demonstrated experimentally, hypotheses regarding the anti-predation role are not entirely consistent


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Why does hexokinase bond phosphate to the hydroxyl group on carbon-6 of glucose in glycolysis?
When glucose enters the cell, it is phosphorylated by the enzyme hexokinase.
Why is this phosphorylation done at carbon-6? Why not at C-1 or C-2?
In other words, why is glucose-6-phosphate being produced rather than a different isomer of phosphorylated glucose?

To be sure: You want to know, why glucose is phosphorylated at the carbon 6? Or do you want to know, why it is called carbon 6?

I want to this question? why glucose is phosphorylated at the carbon 6?

This is biochemically an interesting question, answer soon.

Weclome to Biology.SE! While you wait for @Chris to answer, you may want to check out the proteopedia article on hexokinase and the associated links. At very least that will make sure you have the background to understand an answer. ——— You may also wish to check out the [tour] and go through the help pages starting with [Ask] questions effectively on this site. Thanks!

What do you mean by “why”? Do you mean “what purpose does this serve”, or do you mean “how is this specificity accomplished”? At present you do not make this clear. I can answer either questions, but it is your job to formulate your question clearly. Please do so.

First of all some nitpicking, but the actual phosphorylation happens not to the Carbon-6 but to the hydroxyl group bound to this carbon atom. The mechanism is a nucleophilic attack of the hydroxyl group on the terminal phosphoryl group of ATP. Schematically, this looks like this (image from here):

The main question, why the reaction happens on this carbon atom can be answered rather simple (although the explanation is a bit longer): Because only this is openly available for a chemical reaction and the others are inside the hexokinase and thus shielded.
Hexokinase exists in two forms: One relaxed, open when no substrate is bound and one closed with a changed morphology when the enzyme has bound its substrate. This mechanism is called "induced fit" and a quite common motif in enzyme catalyzed reactions and brings together the active center of the enzyme, possible co-factors and the substrate and excludes interfering other actions.
In the example of the hexokinase, glucose is brought into close proximity to the terminal phosphoryl group of enzyme-bound ATP to enable the chemical reaction. Because all other potential hydroxy groups are shielded by the enzyme, only the group at the carbon-6 can be chemically active. For more details, see the references.
Schematically, this looks like this, with the open form to the left (the arrow indicates the binding site for glucose) and the closed form right (image from here):

References

The Structure and Mechanism of Hexokinase
Mechanism of liver glucokinase.

I think this answer is much more revealing, chris. Really thank you.As far as I understand, this is related to the way glucose binds to the enzyme.In other words, other hydroxyl groups are closed by the enzyme, so only the carboxyl group is exposed.I got it right, right?

@SpartanTroy No, only the hydroxyl group on C6 is available.

but if other hydroxyl groups are protected, why is it not protected on c6. Is this related to the enzyme's association with the substrat?

https://www.youtube.com/watch?v=2gZDHMQcgtQ. If this video is as shown; So that's about the enzyme's binding site to glucose and atp. Am I wrong?

I'll look into the video later today.

I'm sorry. I think you are knowledgeable. I'm asking because I don't fully understand.

Hey, be careful. I have no time right now to watch a video to see, what is said in there. And before I watched it, I am not going to say anything about the video. Answering here is voluntary, so if you want to piss me off, you will not get any answer.

Let us continue this discussion in chat.

@SpartanTroy There is nothing to discuss here right now. I have to work and will watch the video later. And then I will answer your question about it.

@SpartanTroy I'm not familiar with the particular biochemistry here, but just take a look at the diagram in Chris's answer: see the ring? There are 6 carbons, but only 5 of them are involved in the ring (an oxygen makes up the 6th ring element). The 6th is that "-CH2-" hanging off with an "-OH" attached to it. The other -OHs are directly attached on the ring: the geometry is different, so it seems obvious that an enzyme would be specific for a particular location.

@bryanKrause yes I have it see. Actually my question is a biochemistry question. But I want to understand.I think I should learn the enzyme and substrate relationship.

In yeast, galactose is phosphorylated at the C1 position and isomerized into glucose-1-phosphate, which is then converted to glucose-6-phosphate to go into glycolysis. Given that it's possible to phosphorylate the C1 position in galactose, which has similar steric considerations, your answer doesn't really answer why it's at C6 in glycolysis. I guess it impressed the questioner at least.


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What kind of bee can dig through stone?
My house (in Israel) has a concrete structure, with a decorative veneer of Jerusalem Stone at least an inch thick. Yesterday I came out to discover a little hole in the wall - and a pair of bees coming in and out of it! (See video)

This wall is no more than 5-6 years old, and I have never drilled anything there; they're not reusing a human-made hole. I must conclude that the bees somehow dug that hole.
Is that possible? What kind of bee could do this?
Update: As interesting as these bees are I didn't want them living in my wall, so I filled up the hole with a silicone-type glue. A few hours later, they had dug through that, too.

I don't know the answer to your question, but from the video it looks possible that the bees adapted an existing hole/crevice and added mud around it, giving the appearance that they drilled a perfect hole.

Here's a paper in Current Biology1 on the discovery of a species of bee (Anthophora pueblo) in Utah (US) that burrows through sandstone. Pretty cool!
Sandstone is harder than limestone, so I suppose it could be possible for this type of bee to get through your wall material, though Utah is a long flight from Israel.
Perhaps you have discovered a related species of Anthophora local to where you live (perhaps this one?), except that it is unclear if the bee in your picture has the same large mandibles that would help it dig through stone:

As sandstone is harder than other substrates bees excavate (e.g., sand or soil), higher energy and time costs are expected. Mandible wear is consistently seen in older females, a consequence of excavation that likely limits their further use.

Unless you have a lot of similarly-sized and -shaped holes in your wall material, with large-mandible-d bees coming and going, it seems reasonable to infer that this hole came from something else and that these particular bees are just reusing it.

1. Orr, M.C., Griswold, T., Pitts, J.P. and Parker, F.D., 2016. A new bee species that excavates sandstone nests. Current Biology, 26(17), pp.R792-R793.

It's best practice to spell out references to papers in full, as links may go dead after a while.

I would not expect a DOI link to go dead.

Thanks for changing all that.

Can you explain why you would expect lots of similar holes if these were excavating bees? It's my understanding that these are solitary bees, so they wouldn't necessarily have other relatives trying to live nearby? Also see my update - these bees definitely can dig through glue, at least.

@Shaul Behr: And, moreover, given how compatible the size of the hole and size of the bee are...

My expectation was based on similarity with the linked species of bee, which appears to excavate many similarly sized and shaped holes in a concentrated area. But you have added more information to your question, and hopefully that will help others answer your question correctly. More pictures of your bees may help others, as well.


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Calculating approximate dose of UVs received by a virus
I am making a very approximate calculation to determine the dose of UVs received by a virus standing at 1.5 cm from a UV source during a certain amount of time. Please let me know if my train of thought is incorrect.
Suppose I use an LED that emits 2mW of radiant flux. Side comment: I found one that with that draws 20mA of current when a forward voltage of 6.5 V is applied, which leads to a power draw of 130 mW. Thus LED efficiency is 2mW/130mW= 1.67%. I though LEDs are very efficient...)
To avoid making complicated calculations, suppose that 80% of all the flux is concentrated in 45 degree cone. In addition, supposing that the flux per cm2 is constant (I don't know the name for that value) on a flat circle area at a 1.5cm distance from the light source and where the virus will be placed. The LED will be switched on for 5 seconds. As such, the dose received by the virus is:
$$
Dose = 80\%* \frac{2mW}{(pi*(1.5cm)^2)}*5sec
$$
Is that equation correct?
Thanks

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, this question doesn't seems like it is a good fit for this site since it isn't directly about biology. Thanks!

I'm voting to close this question as off-topic because it about estimating a physical parameter (radiation flux) rather than biology.

which SE site should I post this to?

Maybe [Physics.SE] or [Engineering.SE]? I'm not familiar with either of those sites, so please make sure you read up on the standards for each site and check them for similar questions before reposting.

To avoid making complicated calculations, suppose that 80% of all the flux is concentrated in 45 degree cone.

The actual distribution of light is probably nothing like that.  Diodes tend to put significant amounts of power at higher angles so that way less than 80% ends up in the center, and within the central spot they peak at the center and then gradually drop off:  https://photonsystems.com/wp-content/uploads/2017/03/280nm-LED-performance-informationV3.pdf
Usually beam patterns are either simulated from manufacturer ray data or measured.  Since you're looking at low power and very low efficiency diodes, and given how much UVC LEDs cost, I'm guessing these are surplus or below-spec parts being sold on ebay or similar and you don't have access to the underlying datasheets.  In that case this is a reasonable way to estimate.


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Is touching or inhaling 70% isopropyl alcohol dangerous to humans?
I bought 99% isopropyl alcohol and made 70% alcohol + 30% water in small spraying bottles as a disinfectant.
I also read that this solution is safe and recommended by Apple for cleaning iPhones.
My worry comes from reading on the 99% bottle how extremely dangerous it is to humans. Basically touching, inhaling and of course consuming it is very toxic.
On the other hand 70% alcohol solutions are found in most hand and surface sanitizers which are usable against COVID-19.
So my question is: how much should I be afraid when cleaning surfaces with my small 70% spray bottle? Since alcohol evaporates, I'd be naturally inhaling it, I mean where else could it go in the air? I'm also just spraying it on a wipe to clean my mobile, not using a rubber glove for that.
What are the health concerns when using such solution?

If you're interested in the biological or health effects of various chemicals, try to look up the Safety Data Sheet, or "SDS" or "MSDS", for that chemical compound.
Going to your favorite search engine and plugging in your chemical of interest to the search term "SDS" or "MSDS" will almost always get you to some kind of answer — either what you're looking for has a safety data sheet or it doesn't!
In the case of 70% isopropyl alcohol, there are SDSs/MSDSs out there that will tell you what potential health effects are. Here's one example for 70% isopropyl alcohol:

Potential Health Effects
Eye: Produces irritation, characterized by a burning sensation, redness, tearing, inflammation, and possible corneal injury. May cause transient corneal injury. In the eyes of a rabbit, 0.1 ml of 70% isopropyl alcohol caused conjunctivitis, iritis, and corneal opacity.
Skin: May cause irritation with pain and stinging, especially if the skin is abraded. Isopropanol has a low potential to cause allergic skin reactions; however, rare cases of allergic contact dermatitis have been reported. May be absorbed through intact skin. Dermal absorption has been considered toxicologically insignificant. The cases of deep coma associated with skin contact are thought to be a consequence of gross isopropanol vapor inhalation in rooms with inadequate ventilation, rather than being attributable to percutaneous absorption of isopropanol per se.
Ingestion: Causes gastrointestinal irritation with nausea, vomiting and diarrhea. May cause kidney damage. May cause central nervous system depression, characterized by excitement, followed by headache, dizziness, drowsiness, and nausea. Advanced stages may cause collapse, unconsciousness, coma and possible death due to respiratory failure. Aspiration of material into the lungs may cause chemical pneumonitis, which may be fatal. The probable oral lethal dose in humans is 240 ml (2696 mg/kg), but ingestion of only 20 ml (224 mg/kg) has caused poisoning.
Inhalation: Inhalation of high concentrations may cause central nervous system effects characterized by nausea, headache, dizziness, unconsciousness and coma. May cause narcotic effects in high concentration. Causes upper respiratory tract irritation. Inhalation of vapors may cause drowsiness and dizziness.
Chronic: Prolonged or repeated skin contact may cause defatting and dermatitis.

Safety data sheets sound terrible! But in reality, people use rubbing alcohol with common sense, without putting into their eyes, without drinking it, etc.
Mainly the point of this answer is to help you find the answer for yourself, if you want to find out about this or other chemicals you might be worried about.


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Is there a difference between a consensus PCR and a pan PCR?
I know that a multiplex PCR uses multiple sets of primers in one reaction to amplify multiple targets.
But what is a PCR called that uses generic primers to amplify multiple targets? Is this a consensus PCR? Or a pan PCR? Or do those two terms refer to the same thing?
What about a PCR that uses degenerate primers?
Thank you for your help.


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Can a dog run 150 km non-stop?
In Werner Herzog's 2010 documentary Happy People: A Year in the Taiga, a dog is reported to run 150 km from the Taiga back to the owner's village, without any stop and seemingly at full speed as it is running next to a snowmobile.
I am skeptical of this. I cannot find any reports of dogs running a distance even close to this. This article on super-distance dogs does not mention any distances over 40 miles (64 km), which is still less than half the distance, and together with the owner running, so at much lower speed.
Can a dog really run 150 km at full speed?

There are 100, 200 and 1000 mile races for huskies, we can check the speeds of the winners of the races: http://www.eaglecapextreme.com/index.php/the-race/race-times
97 miles run in 17.23 hours, gives 5.6 miles an hour, 10 km/h, on a cold day, 12-16 dogs towing the musher and the sledge. without a sledge, a husky can probably run 150km at 15km/h average, so that's 10 hours of running.
there have been studies about husky mitochondria and their biology.


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How much of the genotype-phenotype map do we understand in HIV?
From what I understand, viruses have very small genomes relative to those of standard model organisms used in biological research. For example, according to Wikipedia, "the HIV genome contains nine genes that encode fifteen viral proteins". This is several orders of magnitude below the complexity of the mouse genome for example, with over 20,000 genes encoding over 50,000 proteins.
As a bioinformatics student (from a non-biological background) working with mammalian genomes, I often find the link between genotype and phenotype quite abstract and I'm unable to fully get an intuition for concretely how genomes can encode the instructions (or recipe using Dawkins' analogy) for creating complex phenotypes.
With this in mind, I wondered whether viruses, in particular HIV, which I know has been well studied, provide the simplest models for understanding the principles of how genes can encode the complete phenotypes of a functioning biological entity. Having such a small number of genes, I assume it is feasible to follow the transcription, translation and interaction of all genes and proteins? If so, is it the case that we understand how all of the genes and proteins work in HIV? If not, what is the main barrier in our understanding?
Apologies for this poorly-defined question. I am having a hard time getting my head around how molecular/cellular biology fits in with the complex phenotypes I've been studying in developmental biology/physiology and hoped that a simpler species/biological system could help to illuminate how it all comes together! Any pointers to further resources would be much appreciated.

I'm sure HIV is well studied since as you know it has a small genome and is highly relevent to therapeutic research, but virus regulation can be complicated and not representative of what happens in normal cells. This is why model organisms exist. The yeast Saccharomyces cerevisiae has about 6,000 genes and researchers have systematically deleted nearly every gene and looked at what happens to the cell. This information is available on the saccharomyces genome database. For example if you search SNF1 (which has a human homolog) on SGD (https://www.yeastgenome.org/locus/S000002885). You can see the phenotypes associated with deletion, overexpression, as well as a summary of what it does and how it's regulated (with original references). I don't think it gets any better than that. A lot of what is known about genetics and molecular biology comes from studies in yeast so I think it is worthwhile learning about yeast genetics to get a better understanding of what goes on in cells.


text:
What happens to male turkeys?
My family and I have almost never seen a wild male turkey though we have seen countless female turkeys. Is the male to female sex ratio of turkeys at birth extremely low? If not, what happens to the male turkeys?

Where do you live? I assume you are talking about wild turkeys? How did you distinguish between male & females?

This is referring to wild turkeys and in the western U.S. The main way is that the male turkeys have the big tail feathers in the back. Though I admit that it is possible that I am unable to distinguish between male and female turkeys otherwise.

This article from the humane society suggests that the male-female ratio in wild turkeys is generally 1:1 1.
It's likely that nothing 'happens' to the male turkeys. Possibly you and your family may be miscounting some males as females; you mention in your comment the big tail feathers, but both sexes have fairly long tail feathers so that may not always be particularly reliable. The best way to tell the sexes apart are listed in this article 2 with pictures of both sexs and descriptions of what differences are most helpful for IDing. Younger male turkeys may also be more difficult to differentiate from females.
An additional point is that male and female turkeys often form their own flocks. These flocks interact in certain times of year, but not all the time. Depending on the consistency of the timing and location of where you're seeing the turkeys, the high degree of females might just be due to this phenomenon. The places you're frequenting might be a popular hangout for a specific hen/chick flock, or several, leading you to conclude that there are way more female turkeys than males.


text:
Has lamarckism been discredited?
Lamarckism is a pre-darwinian theory according to which an organism's traits acquired to adapt to the environment are passed onto its offspring. A couple of years ago, I attended an event with Richard Dawkins and Jerry Coyne, both preeminent evolutionary biologists, in which I remember them agreeing that it is basically B.S. and that acquired traits don't get passed but instead propagate themselves through natural selection. As a non expert in biology, it does not make sense to me that acquired traits would make their way into the genotype and then get passed on, which coincides with what Dawkins was saying. But I am a non expert.
I also have read a few things about epigenetics and it sounds strangely similar to lamarckism. Steven Pinker also discusses all these things in The Blank Slate and he gives a notion that thare is some idealistic ideology behind promoting ideas that we can radically change an organism by environmental conditioning and "save" those changes into the genotype. He says that ideology is to justify government programs aimed at rapidly enhancing mankind whereas natural selection, which proponents of such ideas may deem reactionary, simply is not so optimistic.
My questions are:

Is lamarckism, or inheritance of acquired traits, been conclusively discredited?
What does lamarckism relate to epigenetics

Can you provide any example suggesting that Larmackian inheritance is not discredited? Also perhaps search here at https://biology.stackexchange.com/search?q=lamarck and see if your question is answered by anything you find there?

I dunno if it has or not, that's why I'm asking

SE Biology is a question and answer site about biological problems that are capable of objective answers. A question on whether a theory has been discredited does not fit this bill. If I say "yes, all of my scientific colleagues agree", then I am only expressing an opinion. A better question is "is there any evidence for Lamark's claim that (e.g.) by stretching its neck a giraffe elongated its neck and this caused a change in the DNA of the gametes that was inherited by the next generation". It is up to the proponents of a theory to provide evidence. There is plenty for Mendelian genetics.

One of the crazy results of the past decade is the demonstration that conditioned fear is inherited by offspring, and even offspring' offspring. Here is a readable dispatch of the original study: Szyf, M. (2014). Lamarck revisited: epigenetic inheritance of ancestral odor fear conditioning. Nature Neuroscience, 17(1), 2.

The question is interesting at many levels. Of course, in biology and in any other science there is no absolute or 'objective' truth about some given phenomenon if we really care to look at the nuances. Lamarck seems to be vindicated mainly by a wave of empirical work on patterns of transgenerational inheritance, particularly in the field that is known as epigenetics. You can read a good intro-level review here for some recent developments, some particular examples here, or a more conceptual reading here.
As an evolutionary biologist myself, I will say that most other biologists acknowledge that epigenetics and transgenerational inheritance are important and have solid empirical support, but (for various reasons) some of them are hesitant of calling that 'Lamarckian'.
By the way, Dawkins was a very effective science popularizer, but he does not practice science nowadays, and many of his ideas lie in what is known as 'scientism', which is a blind confidence in science as an absolute truth that is inflexible. The same applies to many positions of Steven Pinker, deGrasse Tyson, etc.

Just to add that Lamarck is not given credit for epigenetics because he turned out to be somewhat right but with a wrong reasoning. In science we try to credit people who provide correct theories, anyone can be right randomly sometimes. However Lamarck contribution to the field was to popularize the idea of evolution of species. In facts, that species evolve was accepted by most biologists of the 19th century, and even the population. It became a controversial idea only after Darwin showed that humans are not any more special than macaques, frogs or goats, but just a variation of life.

The comment about Dawkins, Pinker and Tyson is unnecessary.

@baca the comment is relevant because the OP explicitly mentions them. And I'm discussing their ideas (i.e. scientism) because it is important in the context of the question (just as discussing Lamarck's ideas).

Dawkins is pretty straight forward about absolute truth not existing in science, his positions it is merely the best way of collecting and assessing knowledge we currently have, which most scientists would agree with.


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Where are there analyzable signed directed network datasets?
I'm looking for biological datasets with specific properties that are available for me to analyze. Informally put, I have a hammer and I am looking for a nail. That is to say, I have an algorithm and I am looking for suitable data to test if it can tell us anything interesting about biology. Let me start by characterizing the properties that I'd like this data to have.
Math Properties
The data must be representable as signed directed graphs, which in less formal terms means that I am looking for a network where the connections between the nodes are arrows with a +/- sign associated with them.
The signed property of the edges must represent a property of the relation between discrete objects that only takes on one of two values. One way to get signed values from quantitative data would be to use the sign function, keeping only the relations whose sign of the quantitative variable were not equal to zero. Another way is to encode Boolean values, where False is - and True is +. I'd like to further clarify that the data should not only conform to this criteria, but should have instances of both positive and negative paths within the data.
The directed property of the edges mean that we care to distinguish 'A relates to B' from 'B relates to A'; order matters. Both, one, or neither of these relations can hold in these networks between any two nodes A and B.
Data Properties
The data must be analyzable in the sense that I can obtain the data in a form where I can either (1) immediately analyze the data or (2) transform/manipulate the data into a form that I can analyze. As a computer programmer, I'm likely to be able to find packages for (or code for myself) moderately arbitrary transformations as long as they are computable and interpretable. That is to say, in your answer I would like you to not worry too much about whether you have a ready-to-use software solution for analyzing or transforming the data. What I would like considered is whether there is (1) a direct download for a/the datafile(s) or (2) an application programming interface (API) for downloading the data in either pieces or as a whole.
Preference will be given to answers that do not cost money, and do not require creating accounts (although either are acceptable).
All else being equal, I'd prefer larger datasets (n > 1000) over smaller ones.
Preference will also be given to answers where the dataset has additional variables are available on the vertices. For example, if the vertices represent genes, then additional variables on the vertices would mean more data is available that describe those genes.
Academic Properties
The dataset(s) should be citable.
Examples
While I'm open to other biological subjects, there are two biological topics that I feel should be representable in the mathematical way I've described above.
The first is gene regulation data. The vertices would be genes, and for any two genes A and B we could have any of the following relations

Gene A downregulates Gene B
Gene A upregulates Gene B
Gene B downregulates Gene A
Gene B upregulates Gene A

The second example I've thought of is in biological signaling as the signals are sometimes directional (sender to receiver) and might have some sort of sign (turn on/off, increase/decrease).
Bonus points if the data is topical (COVID-19/coronavirus-related for example).
Data Sources
I've downloaded a few datasets from BioGrid, but I didn't see the kinds of mathematical properties I was looking for in those datasets. If there are datasets here that you think meet my criterion, please mention them.

While this does look like a very nice approach, I would actually argue that there are (almost) no biological datasets, that can be directly used for your algorithm - you can only do a sort of meta analysis using results/predictions based on other datasets.
The reason for this is that the nature of a signed graph requires you to look at effects that can have opposite directions, which in biology  pretty much restricts you to regulatory functions*. The problem with that is, that is nearly impossible to directly measure regulatory effects. In all cases I am aware of, one has to measure the magnitude of an effect under different conditions and then calculate regulatory interactions based on that data.
This means any set of regulatory interactions you can put out into your network is already based on a given analysis with inherent assumptions and (potentially) biases.
This doesn't make the approach impossible, but I do think, it is something you need to be aware of, especially if you want to use multiple datasets.
As for actual datasets that would fit well:

transcription factors have already been mentioned in another answer
other regulatory effects on transcriptions (promoters / enhancers) may also work, though in this case the 'class' of the objects effected (genes/mRNA) is different than the effector
Another type of biological network that might fit are metabolic / enzymatic pathways. For these you could either also look at regulatory interactions (which again may be tricky because both proteins and metabolites can have regulatory effects) or maybe also directly at metabolic flow: in this case nodes in the graph would represent metabolites and edges reactions that produce or consume them. The KEGG database has large numbers of metabolic pathways for many different species.

*I was trying to think of other things, but presence/absence of a signal probably doesn't fit and neither does classification into strong/weak signals (i.e. interactions)

Thank you for the suggestions. I appreciate your laying out of the difficulty of getting such datasets. I didn't mention in the original post, but it was a similar line of reasoning that led me to put this question to the SE community.

@Galen I think you need a collaborator in the field. It's super dangerous (or at least embarrassing) when people with an algorithm enter a domain they don't understand without help. SE is not a replacement for collaboration.

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology. I'm glad we encourage such questions from curious people who want to learn more.

Here's some directed network graph data for regulatory networks of transcription factors (TFs), via http://www.regulatorynetworks.org/:
• Mouse TF: http://www.regulatorynetworks.org/results/networks/mm9/networks.v12032013.tgz
If you click on the site's About button, there is more information about this file. From the README, for instance:

Regulatory interactions were identified in each cell type by scanning the
  proximal DHSs (+/-5kb from the canonical transcriptional start site) of each
  transcription factor gene DNaseI footprints corresponding to the recognition
  sequences of known TFs.
The file genes-regulate-genes.txt contains two columns of gene names, at column
  4 and column 5 of the text file.
The gene in the first column is bound (i.e., contains a DNaseI footprint in
  proximal regulatory DNA) corresponding to the second column's TF gene product.
The final column (column 6) represents the number of times a motif for the
  regulating gene is found in the regulatory region (promoter) for the regulated
  gene.

The gene names are HGNC symbols and are easy to look up in resources available through UCSC, GeneCards, Ensembl, etc.
DS-numbers are internal identifiers for cell lines. However, the prefix uses that cell line's more general name and is usually easily searchable or parsable.
Disclaimer: I created the regulatorynetworks.org site and I was a contributing author on a couple papers which used the datasets rendered in it (1, 2).

Thanks for the suggestion. It looks like this data has directed edges. Can you elaborate on how the edges are also signed?

These are all positive values.

Ah, I see what you mean, you're quite right. I'll clarify in the question above that I'm looking for data that contain instances of both positive and negative paths. Sorry for the confusion.

To augment this with data that contain negative values, ChIP-seq peak overlaps may work. For TFs for which there are ChIP-seq peak datasets (on ENCODE, for instance: https://www.encodeproject.org/), you could use set operations (e.g., BEDOPS: https://bedops.readthedocs.io/en/latest/) to call overlaps of these proximal promoters with TF-specific ChIP-seq peaks as +1/-1, to specify overlap/non-overlap, true/false categories. ChIP-seq peak data would be useful, because it lends biological evidence to support that there is TF binding in the promoter (and associated regulation of the target gene).

That's just spitballing, though. The networks in my answer contain genomic intervals, and you could do set operations against any number of interval-based datasets, in order to get "signed" data. For instance: overlap/non-overlap with SNPs, overlaps with conservation values averaged over the TF binding site, etc. Conservation might be useful if you want to associate nodes with +/- values; I think either the phyloP or the phastcons conservation scores are ranged positive to negative, to specify the selection pressure over genomic regions: from highly conserved, to neutral, to highly evolving.

Enrichr has a huge (164 libraries) collection of term-to-gene relations in machine-readable format.
X2K can be more interesting for you, as it partially implements networks approach. It has a large collection of libraries as well. And two more - KEA3 (kinases to genes), and ChEA3 (transcription factors to genes).


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How did plaques form in Salvador Luria's Bacteriophage experiment (discovery of restriction enzymes)?
I was watching Eric Lander's lecture online describing Luria's experiment (see below for link), and I couldn't understand how plaques form. From my understanding,

Bacteriophage infect strain B
Viral DNA is incorporated
Restriction enzymes cut out viral DNA (mostly)
Some viral DNA is methylated before step 3 occurs.

At this point, to replicate, we would need the infected bacteria to produce more bacteriophage to infect nearby virus. However, due to step 3, the newly incorporated viral DNA will be cut out through restriction enzymes. So in my mind, we only have one bacteria with viral DNA (along with its descendants).
So how does the plaque form?
https://youtu.be/_TdJBLu6hPc?t=890

In the experiment, the genetic material of a single bacteriophage was, by chance, methylated and thus protected from restriction. In order for the phage to propagate, this DNA must be replicated within the cell. Before replication, the phage DNA is methylated on both strands of the recognition palindrome. During replication, the strands are separated and used as templates for DNA synthesis. The methylation is retained in the parent strands, leading to a condition of hemimethylation in the replicated duplex. This hemimethylated DNA is protected from restriction, allowing time for the daughter strand to be methylated (this is the same mechanism by which the bacterial DNA itself is protected after replication). In other words, once the phage DNA is methylated, the bacterial cell no longer recognizes it as foreign and continues to propagate the methylation through subsequent rounds of replication.
Jen-Jacobson L, Engler LE, Lesser DR, Kurpiewski MR, Yee C, McVerry B. 1996. Structural adaptations in the interaction of EcoRI endonuclease with methylated GAATTC sites. EMBO J 15(11):2870-2882.

...our data for the hemimethylated GAmATTC site show that [the rate of cleavage of the unmethylated strand] is reduced only -330-fold relative to an unmodified GAATTC site. ...this would seem to be an inadequate degree of protection, taken alone, during the transient existence of such hemimethylated sites in vivo after DNA replication. Even if a hemimethylated site were to suffer a single-strand nick in the unmethylated DNA strand, however, it is very unlikely that this would progress to double-strand cleavage because the [rate] for the second cut (in the methylated strand) is reduced by 4200-fold. This rate is so slow that the endonuclease would dissociate from the nicked DNA before making such a second-strand cut, and the single-strand nick would then be repaired by DNA ligase.

[image source]
Note that the lecture mentions the sequence GAATTC, which is the recognition site of the type II restriction enzyme EcoRI (discussed above). This enzyme is naturally found in E. coli RY13. In their 1952 paper, Luria and Human used E. coli B, which does not have type II restriction modification systems. Rather, the effect observed was probably due to a type I restriction modification system (EcoB in this case). In such systems, hemimethylation not only reduces nuclease activity but also increases methylase activity, thus actively protecting newly replicated DNA.
Vovis GF, Horiuchi K, Zinder ND. 1974. Kinetics of methylation of DNA by a restriction endonuclease from Escherichia coli B. Proc Natl Acad Sci USA 71(10):3810-3813.

In E. coli B, the DNA immediately after replication should possess only [hemimethylated] sites. Such sites must be modified rapidly. If not, another round of DNA replication would yield some completely unmodified [recognition] sites which would make the DNA susceptible to restriction. On the other hand, if bacterial or viral DNA synthesized in a foreign bacterium should enter E. coli B, it would do so with unmodified [recognition] sites. These sites would be expected to be poor substrates for methylation but excellent ones for eliciting restriction, the appropriate protective reaction. The in vitro action of... EcoB, i.e., rapid restriction but very slow methylation of molecules with unmodified [recognition] sites and rapid methylation but no restriction of molecules with [hemimethylated] sites, is entirely consistent with the above in vivo scenario and suggests that this enzyme is responsible for both restriction and modification in vivo.

I don't know if this increased methylase activity on hemimethylated DNA also occurs type II systems, which have separate nuclease and methylase enzymes.

This indeed a very interesting experiment. In the lecture, you can see that the obvious explanation for the initial inhability to grow in strain B indicates that the bacteria is resistant to the virus. However, ocassionally, a virus is able to form a plaque in strain B, which initially seems to indicate that it mutated. However, in a second passage from Strain A to Strain B of this initial "mutant", we observe that there are no plaques in Strain B. This indicated that something beyond the DNA (unlike a mutation) was at play, and eventually led to the discovery of these epigenetic markers (methylation) that are made by the machinery of the bacteria (thus, Strain A lacked such machinery, so it maintained the viral DNA but did not mark it as 'viral').
Because these experiments occurr in Petri dishes, where there are millions of cells (billions, in fact), there is always some probability that the restriction machinery does not work. This probability (small, but detectable) of no detection is what is observed in the "original" plaque formed in Strain B. In addtion, when the virus is just added, it is still not marked, so it needs some time to be marked (more cell replication cycles), and during this time the virus can be infective. Either of these possibilities will produce a small fraction of plaques in Strain B.


text:
Getting some concept of cancer genetics
I have two groups of patients : Responders to chemotherapy and non-responders to chemotherapy. I treat this as a dichotomous outcome we can call response to chemotherapy.
For a fixed set of cancer driver genes, I have calculated cancer cell fraction (ccf) for each group.
Does anyone know of any interaction or relation of response to chemotherapy and ccf?

Can you clarify how cancer cell fraction is derived from what you call "cancer driver genes"? I understand ccf to be the proportion of cancer cells among all cells, which is not directly related to driver genes. Are you estimating ccf somehow from driver gene copy number or allele frequency or something? That might lead to a different interpretation of ccf than other ways of estimating it. Can you link to a method or other tool? I found one possible method but I assume there are many others: https://www.nature.com/articles/s41467-020-14351-8

I have estimated ccf from variant allele frequency

Assuming that my comment is trivial, I think that there is some literature on this question. I'm assuming that the ccf in question is for the relevant tissue type for the cancer.
You might also consider cross-posting to SE Medical Sciences, where people are more familiar with these subjects.
Of course, naively one would expect that a larger ccf would yield a larger possible population of cancer cells to provide "escape" mutations or resistance to chemo, so high ccf should then be negatively predictive. As an extreme example, a highly metastatic cancer will have a high ccf over the whole body, and will be more resistant to chemo just because that's a highly advanced disease.
However, as usual things are a little more complex. The ccf itself has subpopulations. The following I got by just googling around a little bit. For some of the fundamental thinking on this, see this old paper. In this paper, the author puts emphasis for example on the fraction of cancer cells in each stage of the cell cycle; this results in what the author calls "clonogenic" and "nonclonogenic" populations that respectively yield new clones of cancer cells or do not yield new clones. Probably that terminology is somewhat outdated, but it gives a sense of the problem; related are "tumor stem cells". For a more modern treatment, you can look at this.
For a med school lecture treatment, see here to learn a little bit more. For an example of a recent prediction study which uses omic data to predict chemo response, which might be helpful in reformulating your study, see here.
In other words, not all tumor cells are created equal, some are more likely to resist chemo than others. However, overall I would expect that there is probably some kind of relationship between ccf and response to chemo, because they are both related to the mediator variable "number of clonogenic cancer cells"; it's just a somewhat oversimplified model compared to the actual biology, so it looks like the publications in question don't tend to focus on it.


text:
What is this red mushroom with the "inverted" cap?
Picture taken on 29 March 2020, Czech Republic (Middle Europe). The cap is red, and its shape is "inverted". It is quite tough, first I thought it was a piece of plastic, but apparently it is growing from the ground.
What is the mushroom - if it is a mushroom :) ?

Looks like Sarcoscypha Austriaca (scarlet elfcup). It's actually used in many textbooks as a representative species for the Ascomycetes.
Details from Wikipedia and Messiah.edu both confirm that this species is found in Europe and that it is typically found either as solitary or clustered fruiting bodies (2-5 cm wide) growing among rotting wood matter in damp wooded floors in the spring.
Photos below:

 Source: Wikimedia

 Credit: William Roody; Source: Messiah.edu
Read more at MushroomExpert.com.


text:
Making new antibodies
Is there a model of how the B-cell-antibody pool in the lymphoid organ evolves during the first two weeks of infection by a new virus ? With a model I mean something like this

At first we have $10^6$ different antibodies binding weakly to 4-5 amino acid  motives and through somatic hypermutation and selection the pool converges to a few dozen of antibodies binding strongly and specifically to some 8-10 amino acid  motives in the most numerous antigens presented by T cells (mostly motives found in the viral protein sequence since they must be in the peptide presented by antigen presenting cells).

This is what would make sense from the algorithmic point of view, which is often valid in biology, but not always. I have a few refs 1 2 3 but they stay elusive on that point.
If there is no such model then please make a few expert guesses.

There are plenty of papers with models for this. For instance, check a few hundred here.
Edit: I'm not an expert in modeling these particular processes. However, I do know about mathematical models in biology more generally. The OP asked if there is "a model" of how the B-cell antibody pool matures ('evolves'). The short answer is 'no'. There is not 'a model', because anyone can make their own model, with their own assumptions, parameters, methods, etc. The 'algorithmic point of view' is not something that is valid on itself, it is only useful (sometimes). It is the job of the modeler to navigate the nuances of her/his own model so that it ends up being useful for some particular purpose or question at hand. Thus, there is no simple answer to this question, or any other modeling question (take, for instance, all the talk about epidemic models in the COVID-19 case: even experts differ about the relevance of some particular details/assumptions). This is my long answer.

Tks, most of them are a little too specialized or hard to read, if you are an expert in this field, can you choose one and enumerate the 3 or 4 concepts you find relevant to the low affinity of the antibody pool at first and how (TCR-antigen engulf?) leads to increasing affinity and specificity, finally recognizing a few dozen of AA motives ?

@reuns check out my answer edit. In short, you are asking a hard question, because whether a model is useful or not, depends on many things, including the purpose of the model. If you want me to ennumerate '3 or 4 concepts', I could do that, but why would these be the relevant ones? No one knows but me. You need to decide by yourself, because there is no absolute truth here. You asked if there is 'a model', and I can say, in short: there are as many 'models' as you can imagine. Find one (or build one) that is useful for you. Good luck!


text:
Need either a [similar] ribosome to the following few | a heuristic for finding [similar] macromolecule given 20 others
Background :
Hi! I am running a small experiment dealing with structural heterogeneity of the ribosome, actually of ribosomes across all domains of life. It's entirely computational: I get cryoEM  samples(below) from PDB, parse the crystallographic profiles and see if I can enclose on physical clusters of proteins that persist across domains of life (i.e. uL4 reliably neighbors uL22 according to this ontology) and things like that.
So far I've been working with the following dataset of eukaryotic/eubacterial/archeal macromolecules and am feeling pretty shackled by it at this point.

Question :
I would be very happy to augment this dataset with any number of "similar" ribosomes to put through the algorithm, but I don't know much about exemplar species to draw from and decided to ask here if somebody would recommend some more or less well-studied species(or straight-up PDB IDs) that would make a good addition. If you could point a boy to where I can "just get more" that'd be even more awesome. I'm not a biologist by training so you probably know of some obvious resource I don't.
I have no other constraints on what the targets are. Thank you so much and stay safe!

 I realize that most of these listed here are like the go-to organisms in biological research.

If you have searched PDB (and that looks the case) you have what there is. I trust that you realize that a protein designated L4 in E. coli bears no relationship to the one designated L4 in eukaryotes. As far as I am aware there are very few similarities in structure between eukaryotic and prokaryotic ribosomal proteins, and in any case the nomenclature was in no way structural or functional, but based primarily on position on two-dimensonal electrophoresis. I am less familiar with the nomenclature of archaea ribosomal proteins, but these show differences from eukaryotes and eubacteria.

Thanks for the reply, @David. I should have included that, maybe, but didn't to keep it concise: I'm using the nomenclature system proposed by [Ban et al.] (https://bangroup.ethz.ch/research/nomenclature-of-ribosomal-proteins.html) which aspires to standardize on function and enables us to do actually run this study. That's the system in which I'm referring to uL22 and uL4 and all others. I figured out pretty quickly that chain ids on PDB have no particular rhyme or reason to them.

@David when you are saying that PDB is all that there is, do you have any species in mind that I can search on there to get the ribosome of or is it whatever?
My problem with the latter is most of the structures i see on there seem to be results of experimental depositions in which a ribosome just figures like Structure of a mammalian 80S ribosome in complex with the Israeli Acute Paralysis Virus IRES (Class 1), but is not the main model. I wouldn't want to dilute my sample with anything but ribosomal structures.

OK. Just thought I’d check. One way you might find ribosome structures in PDB is to search for a particular protein by number. It will also bring up that protein alone, of course. I wouldn’t have thought there was much interest in other species now, given the cost and effort involved, and the low publishability. There would have to be something special or different about the ribosomes. A recent review is the other approach, which I imagine you have tried.

@David, now we are talking. I can definitely relate to the point about the effort. It's been a pretty excruciating bead-stringing exercise wrt data-cleaning even before anything could begin to run.
What do you mean by the recent review, though? I don't think i have!

My internet connection is terrible this morning so I can do less than I intended, but I managed to find a 2019 freely-available review from Cold Spring Harbor Perspectives in Biology entitled "New Insights into Ribosome Structure and Function". I'd work back from the bibliography there (and also do the same from some of the more recent papers in your list). It would be worth your while glancing at the introductions to those papers to find out why the species were chosen. They exclude many of the usual suspects.

@David This is super generous, plenty to work with. Thank you kindly.


text:
What is the meaning of a selection regime in this context?
"Our second approach was based on modeling adaptive regimes
across a phylogeny for each of the groups in our study using an OU
model. We especially focused on the lineage leading to humans, and
tested whether a shift in the selection regime was inferred on this
branch. Under the OU model, species evolve through various selection
regimes that map to branches on the phylogeny. The goal is to characterize the regimes across the tree, and to assess whether a shift in selection regime occurred on the branch connecting Homo to the
other primates."
taken from:
Nunn, Charles L., and David R. Samson. “Sleep in a Comparative Context: Investigating How Human Sleep Differs from Sleep in Other Primates.” Wiley Online Library, John Wiley & Sons, Ltd, 14 Feb. 2018, onlinelibrary.wiley.com/doi/abs/10.1002/ajpa.23427.

I'm an evolutionary biologist. When someone says "selection regime" they simply mean the general conditions (environmental, ecological, etc.) that could have produced a particular evolutionary outcome. For instance, in the example that you mention, they seem to imply that they are interested in knowing if these condtions (i.e. the "selection regime") in the branch that lead to the evolution of humans were somehow different than these of other primates. So, it is a hypothesis, in this case. Unless they state elsewhere in the paper what exactly is this "selection regime", they are simply referring to this idea.

I haven't dug into the paper in too much depth, but I think that it is a little hard to give a precise definition of what they mean by this term in this paper, because it is used in the context of a complex phylogenetic statistical model that they analyze using MCMC simulation sampling or Ornstein-Uhlenbeck (OU) modeling.
For MCMC they appear to be estimating ancestral states (of REM sleep proportion for instance) along the nodes of the phylogeny based on the estimated values of the character for each tip (living organism) of the tree. This is probabilistic and they run the MCMC model until it converges at a reasonable set of parameter values for the overall phylogenetic model, and then they sample reconstructions of these ancestral states. You could view each of these reconstructed states as having its own "selection regime"; however they are not directly describing those regimes. Instead, they are noting only "shifts" in the selection regime, which they are defining as MCMC reconstructions that show a change on the human branch that is larger than that for the rest of the tree of primates. So, it's kind of a black box, because we only know the selection regime in terms of it being "different" between humans and the rest of the tree, as inferred by seeing a large shift in the state of the character (REM or whatever) in humans. That itself is a bit of a stretch of course, because large shifts can also happen without selection. But they're doing their best.
For the OU model, this model itself contains definitions of selection regimes, I recommend looking more into how OU models work to get more information about that. But according to my limited understanding, the OU process is trying to directly model changes in selection regime across the tree. So in looking at the black balls in Figure 2, those are direct OU estimates of the probability of such a shift. Again in this case, what exactly the selective regime is cannot be known from the paper, it is instead inferred to "shift" by the OU model based on changes in values of the character across the tree.


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How to differentiate between Bombus lapidarius and Bombus wurfleini?
I am observing frequently different bumble bees in my garden (Austria prealpine-alpine region). One of them that I frequently saw is all black with red-orange abdomen (tail). From a very simple schematic poster I found I had concluded it would be Bombus lapidarius, but now reading a bit more on bumble bees I find it could as well be B. wurfleini. My question is now what would be the most obvious/simple way to discern between the two species?


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Has there even been a clinical study where healthy volunteers consented to be infected with a pathogen?
I am curious if there has ever been a (modern) clinical study where a healthy volunteer was purposefully infected with a pathogen in order to test the effectiveness of a therapeutic or preventative measure (like a vaccine)?
If not, would the FDA allow for ethical exceptions in cases where there is an extreme case of urgency (like in a pandemic)?
Obviously these would be willing volunteers who signed waivers, etc. So Nazi experimentation, the Tuskegee trial, and other studies without total consent from the participants wouldn't qualify here.
Edit: Self-experimentation wouldn't qualify here either because the bioethics of self-experimentation are different than testing on others.

What counts as "modern"? There is a long history of self-experimentation by medical researchers many of which would seem to fit your criteria ...

Why is this question being downvoted? Is this stackexchange not appropriate for questions on medical and biological history?

@BryanKrause I was going to contribute that very example as answer, but then I realized it doesn't strictly answer the question. The victims of the Tuskegee Experiment were not deliberately infected with syphillis, rather their existing cases of syphillis were deliberately left untreated, and the diagnosis was concealed from them,  "to study the course of the disease". Appallingly unethical, but not quite relevant to this specific question.

@Charles Ah good point, I got that detail wrong. I think I'm confusing it with a separate unethical experiment.

Is 1900 considered modern? Yellow fever, in Cuba, and not just one volunteer, but a whole group.

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology. I'm glad we encourage such questions from curious people who want to learn more.

One can't easily separate ethics from how biology is done, as much as some people have tried. (Though I suppose some have made bioethics into a separate and successful media career, so it can be done in that way.)
In addition to the comment-answer about the Tuskegee Study, Nazi doctors in Germany performed experiments without consent, which included infecting concentration camp prisoners with the bacteria that cause tuberculosis.
Your question is about volunteerism, however, and the victims of the United States and Nazi Germany did not give full — or any — consent to experimentation.
In this week's issue of Nature, there is a news article which interviews bioethicist Nir Eyal about a recent preprint, of which he is a primary author.
In this interview and in the preprint, your very question about coronavirus vaccine research, specifically, is discussed, as it concerns the matters of consent, ethics, and safety of doing accelerated biological research about this virus in a time of emergency.
In answer to your first question about modern clinical studies, Dr. Eyal notes:

Are there any precedents for infecting healthy people with a pathogen?
We do human-challenge studies for less deadly diseases quite frequently. For example, for influenza, typhoid, cholera and malaria. There are some historical precedents for exposure to very deadly viruses. The thing that demarcates the design that we propose from some of these historical instances is that we feel there is a way to make these trials surprisingly safe.

As an example, there was a challenge trial for malaria performed in 2012. Healthy individuals were bitten by mosquitoes carrying the malaria parasite and then treated with antimalarial therapies.
Clinical trials are done under the aegis of government agencies with review and approval processes, some of which are described on the FDA web site. IRBs or Institutional Review Boards provide oversight:

Under FDA regulations, an IRB is an appropriately constituted group that has been formally designated to review and monitor biomedical research involving human subjects. In accordance with FDA regulations, an IRB has the authority to approve, require modifications in (to secure approval), or disapprove research. This group review serves an important role in the protection of the rights and welfare of human research subjects.

History does guide us to worry about the ethical issues surrounding medical trials, especially under exploitative regimes that leave people to fend for themselves during a time of global crisis:

Do you worry that countries with authoritarian governments could conduct such studies on vulnerable groups, such as prisoners or members of persecuted minorities?
We would only recommend conducting the studies in an ethical fashion, with fully informed consent. Vaccine makers want to sell their product to other countries. They want to publish their scientific articles in prestigious journals and there would be many obstacles if their trial doesn’t adhere to widely accepted standards.

But in the modern age, in non-corrupt regimes, science does aim, for the most part, to do the right thing, and there are methods and regulatory mechanisms in place to try to enforce societal standards that move us past the days of Tuskegee and Nazi concentration camps.

Challenge trials! Terrific answer, thank you!

This is routinely done with the common cold for all sorts of purposes, including chasing after the mythical cure.

Another example for norovirus, which I imagine was a very unpleasant study to take part in.  In this case it wasn't even to evaluate a treatment, but just to determine the infectious dose.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3952671/

As far as I remember, in the book "Microbe Hunters" by Paul de Kruif, there is a description of a vaccination trial for a deadly desease with a whole group of volunteers, not just one volunteer (done in Cuba? Early 20th century?). It was in one of the last chapters. Chapters. "...and the human cases—those brave souls in Cuba that met miserable fates in the name of science."

OK, I found it: "In May 1900, Major Reed ... The board conducted many of its dramatic series of experiments at Camp Lazear ... The risky but fruitful research work was done with human volunteers, including some of the medical personnel"

"...they learned how to stop the spread of yellow fever by finally ceasing animal experiments and testing the vaccines on humans instead."

From the preprint, it appears that the key point in whether or not such studies are ethical is if they propose an increased risk to participants. It is not yet clear if social isolation and curfew will contain SARS-CoV-2, so I am not sure if at this moment the argument can be made that most volunteers will be affected at some point in time and as such they are not facing an increased risk. Regarding the recent malaria study, this was only conducted with existing treatment of malaria. To this date, no trial of Covid-19 treatment delivered convincing evidence of effectiveness. Furthermore,

[cont’d] the Case Fatality Rate of Malaria is much lower than the apparent CFR of Covid-19, so the overall risk in the malaria setting is substantially lower than that in a proposed SARS-CoV-2 study. Even in the 20-45 year old group, case fatality rate of SARS-CoV-2 appears to be around 0.2 which means 2 of 1000 infected will die. // Dr. Eyal outlines circumstances under which a SARS-CoV-2 human challenge trial would be ethical, but I do not think we have reached these circumstances yet.

The Tuskegee Study is a bit out-of-place here, because it doesn't actually meet any of the criteria in the question: not the "purposefully infected with a pathogen" criterion, not the "in order to test the effectiveness of a therapeutic or preventative measure", etc. Rather, the subjects were already-infected men, and the study studied their untreated syphilis. (That's why it was so monstrous: the study continued for decades after syphilis was curable, but they just -- didn't. They didn't even warn the men not to infect their wives, etc.)

I discovered a book while working in a library entitled Inhumane Medicine or Inhumane Science or something, that discussed much of the Nazi efforts to produce medicine by using POWs. One passage I recall talked in great detail about the methods they used to incubate Typhus in prisoners and how to maintain the disease sustainably within that population. It was fascinating and terrifying.

Yes, Dr Barry Marshall self administered Helicobacter pylori to investigate whether it causes stomach ulcers. He won a Nobel Prize for it.
https://en.wikipedia.org/wiki/Barry_Marshall

All the time!
For example Flucamp does research on influenza, rhinovirus and (non-SARS) coronaviruses, that involves deliberate infection of paid volunteers.

When the trial starts, we only inoculate them with a weak cold or flu virus so the body can fight this off without a high level of risk, before monitoring the disease cycle as they go from healthy to sick to healthy again in our bespoke medical research facility.

Science Magazine notes that such trials are on the rise as we learn ways to weaken a pathogen before introducing it to a human subject.

Today, people are being deliberately infected with malaria, influenza, shigella, dengue, norovirus, tuberculosis, rhinovirus, Escherichia coli, typhoid, giardia, and campylobacter.

Julius Wagner-Jauregg, an Austrian psychiatrist, while investigating fever to cure forms of insanity (pyrotherapy), infected his patients with malaria. This triggered an immune response that cured neurosyphilis. He was given the Nobel Prize in Medicine in 1927.
Sources:

Tsay, Cynthia J. "Julius Wagner-Jauregg and the legacy of malarial therapy for the treatment of general paresis of the insane." The Yale journal of biology and medicine 86, no. 2 (2013): 245.
Julius Wagner Jauregg. In Wikipedia. Retrieved from https://en.wikipedia.org/wiki/Julius_Wagner-Jauregg

Welcome to Biology.SE! This looks like a reasonable answer and it's great that you provide supporting references. However, please include the complete reference information since links can break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. Thank you!

It used to be fairly common to do this with prison inmates. The inmates would be asked to volunteer, motivated by some reward such as earlier release. An example of this type of study is a 1954 experiment by Rendtorf in which prisoners were given Giardia spores in order to determine the minimum amount that could cause disease. For a description, see Rose 1991. This particular experiment was helpful to society because it clarified how minimal the danger of giardiasis is in many cases where people had previously been concerned. It also posed little serious danger to the inmates, since giardiasis is usually asymptomatic, doesn't kill you, and clears up by itself. Ethics review boards will no longer approve this type of prison study because they consider the setup to be inherently coercive. However, if I were in prison, I would have certainly been very happy to volunteer for Rendtorf's study in order to get out earlier, and I would have been angry at an ethics board that denied me that choice.
Rose 1991 - Rose, Haas, and Regli, "Risk assessment and control of waterborne Giardiasis," Am J Public Health 81 (1991) 709, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1405147/pdf/amjph00206-0039.pdf

"I would have certainly been very happy to volunteer for Rendtorf's study in order to get out earlier" -- and you'd have been a fool to do it. There is no more oversight or accountability for prisoner welfare than there was for the (pre-civil rights) blacks involved in the Tuskeegee fiasco. If it's so safe and harmless, why conduct such experiments on a demographic fundamentally incapable of seeking independent medical opinion (informed consent, ha!) and who lack the means to sue for damages in the event complications do arise?

@Ivan — Please be mindful of the code of conduct for users of this site and review the relevant [help/behavior] material. Given the context I'm not flagging your comment as abusive, but it could easily be viewed as such. Thanks!

Operation Whitecoat, a research program run by the US Army, used enlisted men who had registered as conscientious objectors and volunteered for the program. The research investigated defenses against possible biological weapons, testing vaccines and antibiotics on these volunteers.
https://en.wikipedia.org/wiki/Operation_Whitecoat

From the Wikipedia page about the British Common Cold Research Unit, which operated from 1946 to 1989:

Thirty volunteers were required every fortnight during trial periods. The unit advertised in newspapers and magazines for volunteers, who were paid a small amount. A stay at the unit was presented in these advertisements as an unusual holiday opportunity. The volunteers were infected with preparations of cold viruses and typically stayed for ten days.


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Do animals have greater tendency to care for their opposite sex siblings due to mate competition among same sex siblings?
According to the gene-centered view of evolution, siblings have p=1/2 relatedness, thus having greater altruism between them than cousins or unrelated animals.
For species with a conventional sex binary, how does sibling sex relate to altruism? My idea is that siblings of opposite sex show greater altruism than siblings of same sex, since siblings of same sex have more to compete over. Namely, same sex siblings compete for the same pool of mates. Is this something known to be true in studies of species altruism?


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Are there COVID-19 citizen science projects to compare habits and outcomes?
I've seen some "citizen science" projects for coronavirus that are not really collaborations, but simply requests for processing time.  Are there any "real" projects where people who have gotten their diagnoses could go, chat with one another, volunteer to publicly disclose their virus status, test results such as O2 perfusion, and daily self-rating of symptoms, and agree on group surveys to profile what they eat and other activities they do?
I would like to see ordinary people work together toward answers to basic questions.  For example:
a) does salt intake affect symptoms?  [re: blood pressure]
b) does drinking coffee affect symptoms? [re: type II diabetes risk]
c) does exercise affect symptoms? [re: HIFs]
d) do dietary supplements such as flax, curry, and elderberry affect symptoms?
e) does the overall intake of calories, or ratio of carbohydrates/protein/fat, affect symptoms?
Of course, trying to correlate actions by a patient with immediate self-reported changes in symptoms is fraught, as is a comparison of subsequent hospitalization or death between groups of online survey respondents.  Yet such disorder on an informal basis is where ideas often come from, and citizen science might mark out candidate factors for formal validation by professionals.  Is there anything like this going on?

I think you are looking for a very specific design of 'citizen' projects. But, if we relax a bit your criteria, there are some examples. Here, and here, for instance. One worth discussing, I think, is what Google has done for mobility tracking. Yes, the users did not 'opt-in' the study, but in essence, they provided the data!


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Unknown mite species in plant pots
Does anybody know what kind of mite this is?
It is living in my pepper plants' pots.
My region is south of Germany. (Baden-Württemberg)
I will try to take another picture including some size measurement today.

Update:
As suggested by @theforestecologist, I added pictures including a size bar.
Thanks to @tyersome, I managed to merge my two accounts now.

Hi Icke. Nice pictures! Could you please [edit] your question to include your location, what type of plants you found them associated with,  and an approximate size of the specimens. You'll get a much better answer that way. Thanks.

Since you seem to be posting using two separate accounts, you may find this information on merging accounts to be of interest ...

These look a lot like dust mites, a collective term to describe cosmopolitan house-dwelling mites in the Pyroglyphidae family.

The most common species in temperate regions belong to the Dermatophagoides genus, including D. pteronyssinus (the European house dust mite) and D. farinae (the American house dust mite).

 source: Wikipedia

See here for a closeup of D. pteronyssinus

Alternatively, they may be "storage mites" belonging to the Acaridae family, which are another group of common dwelling-inhabiting mites that are more often found in stored foods vs dust, upholstery, or carpeting.

Lepidoglyphus destructor is one such example but that is also found to be present in dust [Source: Juliá et al.(1995)]. Another common storage mite, Tyrophagus putrescentiae typically eats mold, and could be found outside a food setting if the mold density was prevalent enough.

 L destructor (according to M. Deml on biolib.cz)

I'll note that there are hundreds of mites in these two families of mites alone, so someone may be able to get to a more specific species for you. Knowing more about where you found them (species of plants, etc.) may or may not help narrow down more specifically. For example, the person in this forum post found a very similar looking mite on their pots as well (see here).

Description:

Both male and female adult house dust mites are globular in shape, creamy white and have a striated cuticle. The female measures approximately 420 microns in length and 320 microns in width. The male is approximately 420 microns long and 245 microns wide.  [Source: UFL.edu]

Human impact:
The genus name Dermatophagoides means "skin eater," but these mites are not parasitic. Their diet mainly consists of eating dead skin flakes from mammals (and some birds).  Human detritus is one of the primary food sources for these mites, and so it's no surprise that they are often associated with dust in human dwellings.
So these mites don't bite humans or burrow into their skin. However, they do tend to have a negative impact on humans. Specifically their digestive enzymes remain in their feces, and these dried fecal enzymes (along with their dried dead exoskeletons) cause allergic reactions in people. In fact, according to Raulf et al. (2015), 20 allergens are known from just the two species of hdust mites mentioned above!
From UF IAFS

Mite allergens are mainly present in feces of house dust mites and may become airborne and inhaled by patients, giving rise to asthma, rhinitis, or atopic dermatitis

In fact, the family name, Pyroglyphidae, which literally means "fire + carve", seems to be related to the "burning itchy" eczema that some people develop that results in lots of scratching (carving :p).

Multiple sources suggest that storage mites often have similar allergic impacts as dust mites. Fro example, this site suggests:

In Europe, Lepidoglyphus destructor has been reported to be a major source of mite allergy in rural and urban environments

The question is, how many people are impacted?

Well, according to studies cited again by Raulf et al. (2015) that examined 7000 Germans found that  ~16% had a sensitization to D. pteronyssinus. Other studies (discussed in Hossny et al. (2014)) seem to suggest much higher prevalence in certain populations -- with sensitivities found in up to 90% of people tested from certain populations.

What can you do??
According to UF IFAS:

To manage mite populations, reduce the humidity below 70% and thoroughly vacuum mattresses, carpets, sofas, and chairs. Very sensitive individuals should encase their mattresses in plastic. Use drapes that can be washed and change bed clothing frequently. Vacuuming does not always remove all the live mites and Korsgaard (1982) stresses reducing humidity over sanitation. No one method has been found for reducing mites and relieving allergy suffering. Immunotherapy, i.e., injections of mite extracts into the patients to increase antibody level, has had variable success (Munro-Ashman et al. 1976).

Final word(s):

I'll just mention that there is a ton of literature about these mites and their impacts on humans, so if you're interested, DIG IN!

The [Major Mite Taxa] key by D. E.  walter (find at idtools.org](http://idtools.org/) is an excellent online resource for digging into mite identification further!

Citations:
Hossny, E., El-Sayed, S. and Abdul-Rahman, N., 2014. Sensitivity to five types of house dust mite in a group of allergic Egyptian children. Pediatric allergy, immunology, and pulmonology, 27(3), pp.133-137.
Julia, J.C., Martorell, A., Ventas, P., Cerda, J.C., Torro, I., Carreira, J., Guinot, E., Sanz, J. and Alvarez, V., 1995. Lepidoglyphus destructor acarus in the urban house environment. Journal of investigational allergology & clinical immunology, 5(6), pp.318-321.
 Raulf, M., Bergmann, K.C., Kull, S., Sander, I., Hilger, C., Brüning, T., Jappe, U., Müsken, H., Sperl, A., Vrtala, S. and Zahradnik, E., 2015. Mites and other indoor allergens—from exposure to sensitization and treatment. Allergo journal international, 24(3), pp.68-80.

@Icke with more specifics (i.e., provide the details I requested in my comment above) we oculd try to make a more definitive ID.


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SARS-CoV-2 proteome: is the SPIKE protein not an issue for a hospitalized patient?
I am performing molecular docking of ligands using the modeled proteome of SARS-Cov-2. My question is, after a patient is hospitalized, is the SPIKE protein not really an issue anymore, since its role for binding with ACE2 has already been carried out?  Or, is SPIKE an ongoing issue that is not only an early event in the causal pathway?
Rationale is that SPIKE is quite large, and takes more than a minute of run-time per ligand -- thinking about excluding it to speed up runs.  NSP15 is also another "larger" protein, but I know NSPs are translated inside infected cells - so should be included in docking.

It is always a problem. "The virus" is not a single particle that only needs to enter a single cell, a single time. It is a population of millions of viral particles, that infect millions of cells. So, as long as there are more cells to infect, the viral population still needs a mechanism to enter the cell (i.e. it still needs all the proteins needed to function).

thanks for the rapid response.