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CO2 availability to phytoplankton in oceans and climate change impacts
I learned through research that increasing levels of atmospheric CO2 was increasing the acidity level of ocean waters. I then was looking into how this was affecting the phytoplankton and read that warmer water was actually decreasing the amount of CO2 in the water for the phytoplankton to use.
I am now confused as to why many sources claim that greater atmospheric CO2 is making ocean waters more acidic but at the same time CO2 is decreasing in availability to phytoplankton. How does all of this relate to climate change? Would you be able to explain to me what is happening or direct me to sources that explain it?

One of my students in my Environmental Science class asked me this question, and it seemed very much worthwhile to post the Q&A to Bio.SE!  [Note: the student never got back to me with her sources of information, so unfortunately I cannot include them here].

Is all the ocean water becoming more acidic or is it only in certain areas and how are those areas moved by currents? Same question as regards temperature. The use of averages often hides important detail...

@SolarMike yup, of course there must be huge variability in both space and time. However, the student originally asked the question in a broad, global perspective (as do many individuals when asking about global change), and so I have copied their question and responded to it from this fairly global viewpoint. Notice in my answer that I hint toward more localized impacts, but I did not go into much detail given the already global scope of my biogeochemical answer (and its formidable length!!)

https://earthscience.stackexchange.com/search?tab=relevance&q=acidification

 Short Answer
I do not believe that CO2 will become less available to phytoplankton on a global scale in the foreseeable future. Instead, I believe that rates of increasing concentrations of CO2 (and resulting chemical products) will not remain sustained at their current levels.
There are two global change phenomenon occurring that are relevant:

increasing concentrations of atmospheric CO2 and
increasing global temperature.

As CO2 concentration increases in the atmosphere, diffusion will lead to higher concentrations in ocean waters as well. The rate of diffusion is related to the relative concentrations of CO2 in both air and water.
Increasing temperatures can impact this diffusion rate as well in two ways:

Increased atmospheric temperatures result in higher surface water temperatures, which leads to less mixing of water (i.e., ocean stratification). This functionally reduces the volume into which CO2 can diffuse and therefore will slow the diffusion rate. (but not decrease the amount of dissolved CO2).

Increased temperatures often decrease solubility of gasses in water, and this decreased solubility may result in offgassing of CO2. However, decreased mixing of strata may result in less upwelling and therefore less offgassing.

As long as global ocean temperatures don't get too warm and atmospheric CO2 doesn't get too low, it seems that the above will result in a net global slowing down of CO2 absorption into oceans but not a reversal (i.e., loss of CO2). In other words, I do not believe absolute CO2 availability to phytoplankton will decrease, but that only the rate of further increased availability will decrease.

Though perhaps such decreases could be experienced as local phenomena?

 Long Answer
It's not immediately clear to me what you're referring to. I'll try to react with some things that come to mind. My response is mostly biogeochemical in nature, so I invite others to address this physiologically if appropriate.
Are you sure you didn't misread something and it's really the declining CO32- that you read about?  (see here). Assuming that's not the case, read on...
Raising Temperatures may decrease the absorption rate of CO2
Alternately, maybe you read that as oceans warm, the water can absorb less CO2 (as in the rate of absorption will decline).
This is due to warm water not mixing as well with cooler lower water, so you end up with unmixing layers (called stratification). Eventually, the surface layer saturates with CO2 and can't absorb more from the atmosphere. It's not that this top layer of water has less CO2, but rather that it gets so saturated that it can't absorb any more (causing the rate of absorption to decline).

Under less warm conditions, the "layers" of water aren't so different in temperature, and so more mixing of layers can happen. As a result, all that CO2 that is being absorbed at the surface level can be exchanged to lower layers of water where it will be stored longer. In other words, with cooler surface temperatures (and therefore greater mixing of layers), the volume of water that can hold CO2 is no longer just the surface, but a much "thicker" layer of water. Result: more CO2 absorbed.

So... raising temps can cause less mixing of water due to more stratification (layering), which results in less water in the ocean available to absorb and hold the CO2. This means that as atmospheric CO2 continues to increase, the non-mixing surface layer of ocean water (which will become saturated with CO2 at some point) won't be able to keep up with more and more and more CO2 in the air. As a result, the ocean will decline (and eventually potentially fail) in its ability  to "buffer" the ever increasing CO2 in the air. This would mean that the rate of CO2 in the air will start increasing more rapidly (since less and less of it is being absorbed by the oceans).
As for the phytoplankton (which are in this top layer of water), this stratification will not directly result in less CO2 availability to them. As atmospheric CO2 increases, so will the amount in this top layer of water. The rate of increase in CO2 concentration will just slow until a saturation point is reached, but absolute levels will not decline.

Though, note, however, that phytoplankton tend to thrive in areas of high nutrients (i.e., upwelling zones). Less mixing of waters will decrease the upwelling of nutrient-rich, cooler subsurface water. So less mixing (i.e., more stratification) likely would lead to declines in phytoplankton abundance due to decreased nutrients availability. (See here). Perhaps this decreased nutrient availability (which would include loss of carbon sources) is related to what you're referring to?

Read here for some more thoughts: https://earthobservatory.nasa.gov/features/OceanCarbon
Raising Temperatures may decrease CO2 solubility
However, given all this, the solubility of CO2 in water does decline with increasing temperature (see here for raw data). This suggests that some rise in global temps may impact CO2 concentration in ocean waters.

The cause for this decreased solubility with increased temperature is due to the imbalance of an equilibrium state of free energy required for dissolving/off-gassing gasses in/out of water. Since the dissolution of CO2 into water is an exothermic reaction (i.e., one that releases heat), any addition of heat will lead to a greater favoring of the opposite endothermic reaction (release of dissolved gasses in this case). In more chemical terms, added heat to the solution provides energy to overcome attractive forces between the CO2 and the solvent (i.e., water) molecules. The result is decreased solubility. See here and here for further explanation.
(The partial pressure of gasses are also impacted with increased temperatures, so investigating Henry's Law might also be pertinent to your research. (This link I found quickly explains a bit of the phys/chem).)

However, to further complicate all of this, not all of the CO2 absorbed by ocean water remains as carbon dioxide. Much of it undergoes reactions to become carbonic acid, carbonate, etc. (see here). This means that the equilibrium state is more complex to model or understand vs simply examining these effects on CO2 in water in a controlled lab setting.

This solubility fact, in combination with the mixing of layers above, are why polar waters tend to absorb more CO2 and equatorial waters tend to give off more CO2.
From http://www.carboeurope.org/education/CS_Materials/CO2solubility.pdf:

In the world oceans, the northern Atlantic and the southern Oceans act as major sinks of CO2 because they are colder. Adding to this, cold water is denser than warm water, causing it to sink. The carbon dioxide taken up in the surface can be effectively transported to the deeper waters by convection hence the CO2 is stored in the bottom layers of the ocean.

On the other hand, warm equatorial waters tend to release CO2 into the atmosphere. In these regions upwelling of CO2-rich deep waters occurs. When the water reaches the surface, it is warmed decreasing gas solubility leading to the degassing of CO2 .

However, note that if there is greater stratification of water (i.e., less mixing) as described above, such upwelling could actually decline. This would result in trapping more CO2 in cooler waters instead of warming those waters as they rise to the surface and offgassing that CO2 back into the atmosphere. (We won't even begin to discuss how ocean currents in general will be impacted by changes in temperature...).

To add even more complication, as waters warm, ice will melt leading to (at least temporary) increased mixing of ocean waters!! (see here). If temperature decline from ice melt is great enough to combat the increased surface temperature, then perhaps for some period greater mixing and offgassing could occur.

End results
What does this all mean for climate change?
Well, as atmospheric CO2 increases, it's going to make the oceans more acidic (due to carbonic acid). In other words, if we kept temperature constant, more atmospheric CO2 means more ocean CO2. (You can see that from my previous two links -- again, here (showing ocean CO2 concentration on Y axis) and here).
However, as the earth warms up, water temps will warm up. This means less mixing and therefore less net CO2 absorption. It also means that the warmest surface waters will not hold as much CO2 due to its reduced solubility, which will result in greater "off gassing" of some CO2. The combination of these two things means essentially that the rate of CO2 increase in the atmosphere will likely accelerate.
But what is the net impact on oceans? (and therefore on plankton)
Well, in regards to the oceans themselves, there is probably some calculable "tipping point"  in which the higher concentration of CO2 in the atmosphere (and therefore greater diffusion pressure) doesn't outweigh the reduced solubility of CO2 (due to higher temps and less mixing). At whatever temperature that tipping point occurs, then I assume that the CO2 in the oceans can/will decline instead of increase. In reality, though, gasses are constantly moving back and forth between atmosphere and ocean, so it's unlikely the ocean water will get so warm that there is a net movement out of the water, but probably just a decrease in the rate of further absorption.
On a more local level, if the phytoplankton are living in an especially warm region of ocean, it is possible that off-gassing of CO2 increases in those regions due to the decreased solubility as described before. However, again, if the concentration of CO2 in the atmosphere and the temperature of the atmosphere both keep increasing, then these effects would (at least partially) negate the increased offgassing from reduced CO2 solubility. Again, modelling when this would occur is much too complicated for me to figure out for this post, but I'm sure we have experts working on calculating this "tipping point" as we speak.

Again, the bigger issue for the phytoplankton is probably the reduced upwelling of nutrient-rich water due to greater climate-mediated stratification of the ocean column.

Final Thoughts
Given all of this explanation, ice-core research by Pedro, Rasmussen and van Ommen (2012)  (summarized here) suggests that after only a few hundred years of warming, CO2 concentrations seem to decline in ice cores. This may suggest that perhaps a net release of CO2 is possible within a hundred years or so. Again, this "tipping point" is likely calculable, but it's too complicated for me to figure out for a stackexchange post ;p.
Further readings:
Basu, S. and Mackey, K.R., 2018. Phytoplankton as key mediators of the biological carbon pump: Their responses to a changing climate. Sustainability, 10(3), p.869.
Hülse et al. (2017) Understanding the causes and consequences of past marine carbon cycling variability through models. Earth-science reviews, 171, pp.349-382.


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A question about entropy and Thermodynamics
According to the Second Law of Thermodynamics (also known as the laws of conversation of energy and mass), anything is an isolated system cannot increase in complexity. For example, a wearing suit will eventually decompose.
Now we know the sun (and Earth mantle) is pumping energy into the system so the earth is not a closed system. However, the sun sends dangerous radiation that harms and even kills bacteria.
I am an advocate of evolution, but how can entropy begin when raw energy, unshielded from the sun, is ultraviolet light. As biological molecules require amino acids, proteins, DNA, and RNA is untenable when radioactive UV light kills simple bacteria.
I am well aware that the human body is a very complex machine. That is not the issue. My question concerns the first cell (inorganic material) from which life would sprout, as we know it. This inorganic material (soup that came alive) would not have been very complex at all. How did it survive the various heat of the sun in which all primitive life forms decay?
Source, please.

There are some  misconceptions here. The second law of thermodynamics is not known as the "law of conservation of mass and energy". And the second law of thermodynamics makes no mention of the word "complexity".

@Cell I heard that according to the 2nd law of thermodynamics progression is always downward, a law.

The second law of thermodynamics states that the change of entropy of an isolated system, under a physical or chemical process, is never a negative quantity. It is not an equivalent formulation for the energy and mass conservation laws.

In my opinion, the question should be rephrased, since what @Turk Hill wants to know is how did early life cope with UV radiation. There is not an special connection to entropy and thermodynamics.

@LuisSierra Do you think it is a natural law that everything progresses downwards or progresses upwards, but gradually.

If by everything you mean entropy, in regard to an isolated system, it increases with respect to time.

@LuisSierra I agree since the earth is not an isolated system (ie the sun is pumping energy).

What is "up" or "down"? Define complexity in mathematical terms for clarity, please.

Perhaps research "probabalistic density" and "disorder" on the topic of entropy and use that info to redefine complexity.

https://www.youtube.com/watch?v=Tr_gv5CKB1Y

The blanket statement that UV kills bacteria is wrong, the huge number of earth bacteria that thrive in sunlight would be evidence of this. UV mostly just causes mutations, this could actually accelerate the evolution of early life.

@AlexReynolds I meant "up" and "down" in complexity in an isolated system. But of course, this 2nd law cannot be applied to everything since the earth, for example, is not an isolated system, since the sun (as well as its mantle) is constantly pumping energy into the system.

@com.prehensible Yes, that is correct. Thank you for the link.

@John Yes, I agree with you. The answer below explains that life likely formed in the deep ocean, which would be further from the sun but not far enough to receive its energy.

@John I would have to disagree, a mutation in an essential gene could easily converge into cellular death. One can presume that early bacteria did not have DNA damage associated mechanisms (e.g. SOS response), so they were indeed vulnerable to UV-light induced mutations. Eventually, they had to develop such mechanisms, which is bacteria can thrive in sunlight exposed habitats.

@LuisSierra vunerable to mutations is not the same thing as killed by, especially at early stages when the genome would be very small. As I said that could actually lead to more rapid evolution. would it kill some of course would it kill all of them no not in the least.

It's unclear how the laws of thermodynamics relate to the dangers of UV light in your question, but if I understand correctly your reasoning is the following:
1) The laws of thermodynamics say that order cannot increase in an isolated system, precluding life.
2) Life exists anyway because the Earth is not an isolated system: it receives energy from the Sun
3) Therefore, the energy received from the Sun is necessary for life
4) However, the Sun's rays also contain UV light, which would be fatal to primitive life forms
5) This leads to a contradiction, how do we resolve it?
The answer to the question as posed this way is that there is a flaw in items 2 and 3. It is true life needs inputs of energy to exist. It is also true the Earth receives energy from the Sun, and that this is the main source of energy that powers the modern biosphere. However it is not the only source of energy life can use to function; some organisms generate energy from chemical reactions such as the oxidation of hydrogen sulfide into sulfur. You yourself bring up "the Earth's mantle" as a possible source of energy, which is... The answer to your question :)
https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Book%3A_Introductory_Biology_(CK-12)/02%3A_Cell_Biology/2.24%3A_Chemosynthesis
I believe it is generally agreed upon that however the first organisms got their energy they would not have used photosynthesis, and thus could perfectly well have developed away from sunlight and damaging UV radiation. See for example this article on the evolution of photosynthesis, which describes the consensus that it is a very ancient process that evolved not long after the origin of life:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2949000/
Here is a hypothesis of the origin of life that suggests the first life used chemosynthesis, and in fact would have occurred in hydrothermal vents - about as far from sunlight as you can get:
https://m.youtube.com/watch?v=3jW9dH6NOQ0

I agree with what you stated, and it seems that early life developed far from the archean ocean surface, where UV radiation would be several magnitudes of order above the radiation you would get now. Early life must have survived in certain depths such that the radiation dose would be very low, atleast until DNA damage response mechanisms were developed.

Thank you for your answer. @LuisSierra I agree with what you wrote about the ocean. Oosaka, thank you again for sending the links.

source: Stack Exchange

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

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Frogs stop croaking at same time
I know frogs start croaking at the same time to attract a female.
Why do they all stop at the same time?

Calling is a risky activity because it makes the frog conspicuous to predators. When calling in a group, the risk to any given individual is minimized to the point that the minimal risk is outweighed by the advantage of attracting a mate. However, a single frog calling on his own is assuming all of the predation risk. So, the frogs are playing a bit of game theory and when too few are calling simultaneously to make the risk worthwhile, they will all tend to stop.

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


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How can I obtain a uniform bacterial sample?
I'm currently doing a research project wherein I will be testing the antibiotic resistance of a bacterial sample. Due to a risk of contamination during transport, I'm not allowed to request a uniform bacterial sample form a clinical laboratory. So, I have to produce my own sample. Then, I'm planning to identify the morphology of the bacteria to confirm the species or type.
The ideal scenario is obtaining a sample which is entirely one species of bacteria. However, taking a swab, either from somewhere in the lab or from the body will produce a sample with multiple bacterial species. What source of bacteria can provide the most uniform sample, i.e. a sample with a majority of one species of bacteria? Or, is there another way to obtain a uniform sample? Also, note: I will be conducting the experiment in a school laboratory, so I must be able to safely contain the pathogen.
Edit: I have recently updated my project to be specified towards testing on bacteria present in the throat. So, a bacteria present in this area or similar areas would be preferable.

Do you have a particular bacteria in mind? For safety, I have a link. Especially culture well below body temperature, and use common media e.g nutrient agar. https://www.riskassess.com.au/info/micro_issues

I have no specific species/strain in mind. However, I have recently updated my project to be specified towards bacteria in the throat. So, a bacteria which is present there or in similar areas would be preferable (I'll also update the question).

This is what streak plating is for.

You could inoculate your sample in a selective medium or an enrichment medium to kill off the unwanted species. Of course, you will need to do a literature search to find the optimum medium for the species of your interest.
Another option is to streak plates like so. With successive 'generations' of streaks, the inoculum gets diluted, so that you ultimately get separate colonies. Each colony is founded by a single bacterial cell: by picking up one such colony, you get a pure sample.
For even better results, combine both the methods described above by first growing in a selective medium and then streaking on a solid medium to get individual colonies.


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What's this parasite?
Any microbiologists or parasitologists recognize this? It's from my pet bearded dragon in the eastern US and the vet's never seen it before.

Welcome to Biology.SE! Identifications questions should include: 1) the location (e.g. country and region — the more specific the better) where you observed this organism; 2) habitat information — e.g. from what type of lizard and from where in/on the organism it was isolated; and 3) an estimate of the size of the organism. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

It could be a whipworm, a common parasite in dogs with a flagellum.
Check the image here:
Image at:
https://www.texaswestveterinarian.com/whipworms/

Thanks. Afraid it's probably not that. What my lizard has is microscopic, whipworms are 3-5 cm.


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What is the meaning of the word "Ligandable" in "ligandable proteome"?
I see "ligandable proteome", "ligandable proteins" and "ligandable targets" an awful lot.
But really I don't know what exactly the word "ligandable" means?
Is that it means, for example, "ligandable proteins" means proteins have ligands?
Thank for your help.

Can you please add some references that use the terms "ligandable proteome", "ligandable proteins" and "ligandable targets"?  Context helps elucidate meaning.

In biochemistry, ligand is usually taken to mean a substance which binds to a larger molecule such as an enzyme or other protein, thereby forming a larger complex.  The study of ligand binding has been important for pharmaceuticals, particularly in ligand-based drug design.
The term ligandability (and hence ligandable) seems to have come into significant use with a paper by Edfeldt, Folmer, and Breeze in which they say:

In recent years, the term druggability has increasingly been adopted to describe the ability of a protein target to bind small molecules with high affinity; however, we believe the term ‘ligandability’ is more appropriate for this purpose. Although ligandability is a requirement for finding drugs for a particular target, it is not a guarantee that such ligands will make good drugs.

So, ligandable usually refers to the capability of a molecular target of drug design to bind small molecules.  A ligandable proteome would then be a set of proteins capable of binding small molecules.

Thank you for identifying the culprits. I believe there is a special place in hell reserved for such as they.

Woah, I couldn't thank you enough. It really helps me a lot. Now, I get exactly what it means.

Ligand is borrowed from Latin ligandus, imperative verb tense of ligo (“bind, bandage, unite”), From Proto-Indo-European *leyǵ- (“to bind”).
You can find it in many words in English, French, Spanish, i.e. Liaison which means "to link, to associate"
In chemistry, it means: An ion, molecule, or functional group that binds to another chemical entity to form a larger complex.
Ligand is a latin scientific word which means "to link, to associate, to bind together" so you can just substitute the text books for one of those words. European scientists often know 500 or 1000 latin and greek word constructions like that. Words like Astro, Geo, Bio, logos, Con, anti, which are used commonly in science.
https://www.google.com/search?q=rely+etymology&oq=rely+etymology&aqs=chrome..69i57j0.4031j0j9&sourceid=chrome&ie=UTF-8

So, in conclusion, "ligandable proteins" means that proteins have an ability to link, right?

yes that's correct


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If black absorbs light, then why did Africans evolve black skin? Wouldn't that make the heat worse?
Wouldn't it have been more adaptive to develop light skin and so reflect incoming light?

First, I think you have things backwards.  Africans came first: lighter skin is an evolutionary adaption to living in more northerly climates.
Second, evolution works with what it has, not necessarily what's best.  Mammals had the genes for melanin production long, long before hominids came on the scene, so it's fairly easy to apply selection to increase or decrease melanin production in a population.  The classic example is the British peppered moth: https://en.wikipedia.org/wiki/Peppered_moth_evolution  (Note: I'm not clear whether the moth pigment is melanin or something else, but the principle holds.)
For a white blocking pigment (or transparent to visible light - think sunscreen) or a reflective skin to be evolved, we'd have to wait around until some mutation happened that would allow the body to produce the right sort of chemical.  AFAIK, mammals don't actually produce white pigments: white fur is due to the scattering of light in the absence of pigment.  (Just as snow is white.)  So animals in sunny climes might evolve white fur, but that makes the animal conspicuous.

Check out this page on skin color adaptation —

Nature has selected for people with darker skin in tropical latitudes, especially in nonforested regions, where ultraviolet radiation from the sun is usually the most intense.  Melanin acts as a protective biological shield against ultraviolet radiation.  By doing this, it helps to prevent sunburn damage that could result in DNA changes and, subsequently, several kinds of malignant skin cancers.


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How do beavers learn how to build dams?
I was wondering whether all beavers, from all around the world, know how to build dams and lodges? Do they need to learn it from their parents? If you release a group of beavers in the wild that haven't been in contact with their parents, would they start to build stuff? or just hopelessly die/starve to death?

Question summary: is dam building learned or instinctive in beavers?
A blog post from 2011 references an article in the Juneau Empire titled Running water is sound of spring for beavers.  This article is no longer hosted on the Juneau Empire website, but archived versions are available.
Here's an excerpt (emphasis mine) --

Swedish biologist Lars Wilsson spent years studying captive and wild beavers, and he gained remarkable insights into their behavior. He raised beavers in an outdoor enclosure and in a large indoor terrarium ...
Wilsson initially captured four adult beavers and later he raised a number of beavers from infancy, some in small colonies with their parents and some completely isolated from adult beavers. He isolated the young beavers to see what beavers learn from their parents and what behaviors are instinctive.
He found that young beavers - who had never even seen a beaver dam - were able to build almost-perfect dams at the first opportunity.
The foundation of sticks and logs anchored to the stream bottom, the interwoven lattice of trimmed branches, the mud chinking, every aspect of dam building was hard-wired. Beavers do get more skilled at dam building as they gain experience, but the building behavior is instinctive.
Wilsson learned that the sound of running water is the cue for dam building and dam repair. In one experiment, he played a recording of running water, and the young beavers built a dam in a tank of still water in the terrarium. In another peculiar experiment, his captive beavers built a "dam" on a concrete floor against a loudspeaker that played the sound of running water.


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Range for which the Verhulst-Pearl model is a good approximate
The Verhulst-Pearl model describes the growth of a population using the differential equation,
$$\frac{dN}{dt}=rN \left(\frac{K-N}{K} \right)$$
where N is the population (no. of organisms), r, the intrinsic growth factor and K the carrying capacity of Nature for that species.
Solving the differential equation, we can obtain a relation between time and instantaneous population, given as,
$$\frac{N}{K-N}=\frac{N_o}{K-N_o}e^{\frac{rt}{K}}$$
Where $N_o$ is the initial population.

For a general value of $N_o$, the logistic growth model can predict the the population fairly accurately. But I don't think the graph would be entirely correct if we have very low or very high values of initial population (nearing saturation).
So, What is the range of initial population where the logistic model works as a good approximate?

"I don't think the graph would be entirely correct if we have very low or very high values of initial population." Why?

@AdhishSethi For very low populations, I guess external factors play a much pronounced role, and fluctuations are fairly high. For the very high values (still less than K), I think the graph would exceed the carrying capacity and later come down to the value of K (not in the way the graph shows).


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Why does the structure of RNA change?
RNA only has one strand, but like DNA, is made up of nucleotides. RNA strands are shorter than DNA strands. RNA sometimes forms a secondary double helix structure, but only intermittently. Why does RNA change structure? We see that DNA has a well-defined structure of a double helix. Why does RNA have to change it's own?
EDIT - My main focus is on this line "RNA sometimes forms a secondary double helix structure, but only intermittently."

Please clarify. 1. Are you talking about a particular type of RNA — ribosomal RNA, mRNA, virus genomic RNA? 2. What do you mean by “change structure”? Form secondary structure, suffer mutation? Or are you asking why RNA is usually single stranded, or what advantages RNA genomes have for viruses? At the moment your question is unclear to me.

...or perhaps you are asking why different RNAs have different structures rather than a single structure like DNA, or why mRNA doesn't have a distinct structure but can adopt different structures? If you can clarify we can help you. It's what you mean by "change" that seems to be the root of the problem.

@David My main focus is on this line "RNA sometimes forms a secondary double helix structure, but only intermittently." Why does this double helix structure form intermittently?

Intermittently conveys to my the sense of change in so far as sometimes it’s one structure, sometimes another. This would be true for mRNA. For rRNA and tRNA the situation is that some parts of the RNA are double-stranded, others not. I can answer regarding either or both, as you wish.

@David it would be great if you would answer for both. Thanks!

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, quotes must be referenced — this is considered good practice in scientific communication and will help other users understand the context for the quote. Thanks!

I have now provided an answer, which really is to the question "Why do different nucleic acid species have different structures". If my answer addresses your problem, I think this would be a better title for your question in which I think the word "change" is misleading, and their is an implication that all DNA is double-helical and all RNA is not, which is incorrect.

Summary
Most nucleic acid species have specific structures (or a limited number of alternative structures) which may involve a greater or lesser amount of double helix through complementary base pairing. The extent of such helical components depends primarily on the availability of sequences of complementary bases, which is obviously greatest for the two distinct strands of a double-stranded DNA or RNA genome, but also occurs in a specific manner within RNA species where base-pairing has been evolutionarily conserved in particular regions.
Two ways of interpreting “why?”
When responding to questions about biomolecular processes and structure, I think it important to differentiate between two meanings of “why”, and I shall distinguish these by appropriate numbering in my answer.
1. The mechanistic “why”
This is generally easier to answer objectively, as it is request for a physico-chemical explanation for the formation of a structure (RNA or RNA in this case) or operation of a process.
    It is worth emphasizing that just as different macromolecules of the class “protein” can adopt different particular structures — globular or fibrous with many variants on each — so can different RNA, and even DNA, species, as described below.
2. The functional “why”
By this I mean “what function(s) can a particular structure serve?”.
    This is more difficult and beset with dangers. Whereas, we can say that the structure of myoglobin allows it to bind oxygen and release it as the partial pressure in tissues falls, with some macromolecules the function of their structural features may be less clear. The dangers here are in thinking that suggestions of function are facts, and that a particular function can only be accomplished or is best accomplished by a particular structure or structural feature.
The physico-chemical principles governing structure of macromolecules
Put simply, the structure adopted by a macromolecule in a particular environment is that in which it has the lowest thermodynamic energy (Gibbs Free Energy) in that environment. This is the structure in which the sum of the individual interaction energies (generally hydrogen bonds and Van der Walls interactions) is greatest.
    Thus, a macromolecule is able to adopt alternative structures when these structures have similar energies, and the equilibrium between such structures can be changed by action of or interaction with other molecules.
Genomic DNA Structure(s)
Double-stranded DNA (dsDNA) genomes
1. Double-stranded genomic DNAs form an anti-parallel helical duplex structure (double-helix) primarily because they consist of two perfect complementary sequences that allow maximum hydrogen bonding of A–T and G–C base-pairs. The helical structure of the duplex allows the maximize the energetic π– π interactions of the stacked bases.
2. The function of genomic DNA is to maintain the genetic information of an organism and allow it to be transmitted to daughter cells. The double-stranded structure protects the bases from external modifying influences, to some extent, and allows the semi-conservative replication of the strands when a cell divides.
Single-stranded DNA (ssDNA) genomes
Some small viruses of bacteria and eukaryotes have single-stranded DNA genomes, illustrating that this particular function can be served by different structures.
1. Although the replication of ssDNA viruses involves production of a strand complementary to that of the genome, the genome is not double-helical — negating the generalization in the question. The simple reason for this is that the replication mechanism generates many more copies of the genomic DNA strand than the other: complementary nucleic acid sequences are required  to form a double-helix! One could imagine a ssDNA having local regions that could base pair to one another, but this is prevented by the compact supercoiled structure that they adopt, which is a consequence of their closed-circular nature.
2. The compact super-coiled structure of such ss genomic DNAs (e.g. φX174) is suitable for encasing in a viral capsid (although ds circular viral genomes also supercoil).
    The question of why some viruses have ssDNA genomes whereas most have ssDNA genomes is neither a mechanistic nor a functional  “why”. It may be worth discussing, but falls into the realm of hypothesis.
Genomic RNA structures
1. To a large extent, the remarks above about the structure of genomic DNA apply to the genomic RNA of viruses. Genomes of dsRNA viruses have an anti-parallel helical duplex structure because two perfect complementary sequences are available in equal proportions from replication. Genomes of ssRNA viruses do not have this structure because replication generates primarily one type of strand. The ssRNA viruses, unlike the ssDNA viruses, have linear, rather than circular genomes.
2. I have nothing to say about the relation of these structures to function. Both are packaged into viral particles. Both can be replicated.
Transfer RNA (tRNA)
1. The single-strand of tRNA has a clover-leaf stem-loop structure with three short double-helical stems formed by Watson–Crick base pairing, folded into a three-dimensional L-shape by other hydrogen bonds. The sequence of bases in tRNA determines that this self hydrogen bonding can only occur in a manner to produce the particular structure.
2. The purpose of tRNA is to bring an amino acid onto the ribosome in response to a particular mRNA codon. The non-hydrogen bonded loop at one end of the folded molecule contains the anti-codon, allowing it to interact with a complementary mRNA codon; the free 3′-end at the other extremity is covalently attached to an appropriate amino acid. The compact hydrogen-bonded ‘L’ is of a shape that can be accommodated in the A or P site of the ribosome.
Ribosomal RNA (rRNA)
1. The single strands of the two major rRNAs are folded into a complex of stem-loops formed by short stretches of internal double helices involving either Watson–Crick (A–U, G–C) or single hydrogen-bond G–U base pairs. There is conservation of base pairs in the helical regions, without necessary conservation of particular bases. This determines that a specific structure is formed.
2. The double-helical stems are thought to play a structural role in the ribosome. The unpaired regions are free to interact with the various substrates of protein synthesis on the ribosome, and the catalytic centre is constituted of such unpaired bases. In this respect the ribosome represents catalytic RNA in which double-stranded regions have a functional role but the catalytic bases need to be unpaired.
Messenger RNA (mRNA)
1. mRNA is generally thought to lack hydrogen bonded secondary structure or have a limited amount of such structure, depending on the particular mRNA. This presumably reflects a general lack of complementary stretches of nucleotides in mRNAs. In eukaryotic mRNAs there is significant secondary structure at the 5′ end in the untranslated region. Phage RNAs (and perhaps other mRNAs) do have significant double-stranded regions.
2. This can be rationalized as arising from the fact that the primary role of the bases in mRNA is to specify the sequence of a protein, and the mRNA must be capable of being translated by the ribosome. The secondary structure regions that do occur limit this, and may allow the control of translation. This latter point illustrates RNA flexibility — the potential for a switch from one structure to an alternative. This can only occur if the alternative becomes more energetically favourable, e.g. by unwinding of the helical region at the 5′ end of eukaryotic mRNAs.′


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First neurotransmitter?
Cnidaria are considered to be the first phyla to develop a nervous system. Nervous systems having 1, 2 and three neurons are considered to have appeared first in Cnidaria, with 2-neuron nervous systems having already specialized neurons for sensory and motor functions.
This takes us to the first synapse, which is thought to be of chemical nature, as the sensory and motor neurons in early Cnidaria utilized a chemical to communicate. This would be the first chemical to be used as a neurotransmitter, but which was it?

the difference between neurotransmitter and any other cell to cell signalling molecule is largely semantic, multicellular organisms are full of signalling molecules, which one you co-opt for nerves may well have multiple origins.

I cannot give a thorough answer right now (if I even find one) because I'm on my phone, but here are some papers that could inform the question in the meantime (or their abstracts at least!)
One element I have gathered so far is that the evolution of nervous systems likely involved not the evolution of wholly new molecules and structures, but the cooptation of existing structures for new purposes. Meaning the first neurotransmitters would have been pre-existing with some other purpose in early proto-neurons, not new molecules evolved expressly for the first synapses. One paper talks about neurotransmitters like dopamine being common across all life, including plants (no nervous systems there!). This does not answer which of these molecules would have been the first neurotransmitters however.
The abstract of this paper doesn't say much but the title is tantalizing:
https://link.springer.com/chapter/10.1007/978-3-319-20215-0_2
"New Trends and Perspectives in the Evolution of Neurotransmitters in Microbial, Plant, and Animal Cells"
This paper shows a unicellular eukaryote reacting to various neurotransmitters. If the full paper goes into the phylogeny some more it might be interesting:
https://sciprofiles.com/publication/view/0cc41fa28399e0e366d3199c3bcc48eb
"The Phylogenetic Background of Neurotransmitters in the Unicellular Organism Tetrahymena Pyriformis"
This paper's abstract says all I was saying about the development of neurons and synapses relying on pre-existing molecules and structures:
https://pubmed.ncbi.nlm.nih.gov/2830635/
"Evolution of Neurotransmitter Receptor Systems"
What I'm looking for to find how close science is to answering your question (or if it already has) is papers looking at the phylogenetic relationships of different neurotransmitters and related molecules. That might say a lot about which ones have been used as neurotransmitters the longest. I haven't found this yet but I'll try more tomorrow when I'm not on mobile.
ETA: will re-edit this comment later, but this paper answers your question I believe, or as well as any could at present at least:
https://cichlid.biosci.utexas.edu/sites/default/files/evoneuro/files/liebeskind_et_al_2017.pdf?m=1511200627
"Evolution of Animal Neural Systems"
This paper, which is available in full and is a review paper from 2017, looks at the evolution of every aspect of animal neural systems (i.e. nervous systems mediated by neurons, a concept the paper also defines because the line is apparently blurry). One interesting aspect of it is that while you point to Cnidarians as the most "primitive" nervous systems, the paper points out the latest evidence suggests Ctenophores are the earliest branch off the animal tree, meaning nervous systems either evolved convergently, or sponges lost their nervous systems secondarily, in which case Cnidarians would lose this special status.
The paper has a section about neurotransmitters, which says the following:

Several types of molecules are used as neurotransmitters; their evolutionary deployment in different synapse types across animals is fascinating and still poorly understood. Many are used widely in eukaryotes for intercellular communication, but some of the biogenic amines may be present in animals as a result of the late horizontal transfer of synthesis enzymes from bacteria(Iyer et al. 2004). For instance, epinephrine and norepinephrine are important neurotransmitters in vertebrates but not in protostomes (but see Bauknecht & Jekely 2017), whereas the opposite is true of octopamine and tyramine (Figure 4). Cnidarians make a set of neurotransmitters similar to those in vertebrates (Kass-Simon & Pierobon 2007), but Nematostella expresses most nonpeptide types in the endoderm near the pharynx and testes—only peptide transmitters are found in neurons(Oren et al. 2014)
Intriguingly, ctenophores seem to use a much more restricted set, as glutamate is the only well-validated neurotransmitter (Moroz et al. 2014). This is consistent with the theory that neurons arose independently in ctenophores and planulozoans because vertebrates and most protostomes use acetylcholine at the NMJ [neuromuscular junction I assume -my edit]. However, arthropods use glutamate at the NMJ, just as ctenophores do ( Jan & Jan 1976), and cnidarians probably use neuropeptides (Oren et al. 2014). Although sponges do not have true synapses, they use γ-aminobutyric acid (GABA), glutamate, and nitric oxide to coordinate contractions (Elliott & Leys 2010). Trichoplax individuals also lack synapses,but their secretory flask cells label for FMRFamide, suggesting a conserved role in transmission for this peptide class (Smith et al. 2014).

This gives at least a few names of neurotransmitters that are particularly conserved and candidates for neurotransmitters the common ancestor of neurons used (glutamate, acetylcholine; they may have been peptides, whatever that covers), and I think makes it clear that it is very much not known what those first neurotransmitters were.

This is an amazing answer. Thank you.


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Does the cell release the empty capsids?
The virus via the spike of the capsid connects to a receptor in a cell, then the DNA enters the cell wall.
My question is what happens to the capsid - does it stay connected to the receptor or is getting loose.
(e.g disconnected from the cell).

Which virus, and where did you read this? Please provide details — preferably with a link — to your source so that we can try to help you.

I mean any virus. Does it connect to a receptor? After the DNA gets in, what happens to the capsid?

But only certain viruses have spikes, and different viruses use different strategies to enter cells, and those surrounded by a membrane will behave differently to those that don’t, and how long is a piece of string. I suggest you read a little about viruses in general (try Wikipedia), and then about coronaviruses, if that is your interest (try the links on Meta). However it is my understanding that decapsidation generally occurs within the cell, and the capsid proteins are left as litter.

I understood that this is true only for a certain type of viruses namely the bacteriophages. In that case can their capsids gained from a culture be used to induce antibodies?

If your real concern is raising antibodies to capsid proteins, that is a different question. If your interest in antibodies is for detection of viruses or as antiviral agents I suggest you might like to look at some of the links on the Meta page devoted to reputable sources of information about coronavirus.


text:
Does rotten food produce methane gas?
If we put a meal into the food storage container, does it produce methane gas while it is getting rotten or what else types of gases it produce?

Food hardly rots  by itself but is decomposed by organisms, such as bacteria and others. What gases will be produced depends on what food it is, what "microbes" digest it and, at what temperature and if there is oxygen present.  I guess your question is not specific enough to get a satisfying answer.


text:
How it will taste if one puts two substances on tongue simultaneously?
If we put two substances having different taste on tongue simultaneously how it will taste? Does specific part of tongue is sensitive to specific taste?

The popular "tongue map," which depicts the tongue having distinct regions where you can only taste certain tastes, is completely inaccurate and was debunked quite a while ago. There are regions of the tongue that are slightly more sensitive to tastes, however. A google search of "taste map" or "tongue map" will yield links on the origins of the myth.

This would perhaps be more suited for the Cooking site :-)  Though most taste is actually smell.


text:
How to determine which allele GRCh37 has?
is there a website where I can search GRCh37 by location or rs IDs, to determine which allele it has at a specific location?
I think http://grch37.ensembl.org/ might be the answer to my question, but I'm not sure if when it says the "ancestral" allele on the results page, if that allele is the one in GRCh37. Or if it'll tell me which one GRCh37 has somewhere else on the page.
Also as a side note: I assume GRCh37 only has one copy of each chromosome (i.e. it can't be heterozygous for something?).

Why are you using GRCh37/hg19? It's pretty out of date. If GRCh38 is ok, you might consider poking around the UCSC browser with the SNP track turned on: https://genome.ucsc.edu/cgi-bin/hgTracks?db=hg38&lastVirtModeType=default&lastVirtModeExtraState=&virtModeType=default&virtMode=0&nonVirtPosition=&position=chrX%3A15560138%2D15602945&hgsid=850023477_A5lwHGMEgIZ6APPQrAAOmPBJcTzT

(it does have GRCh37 data but it may not be convenient to access what you need)

I have data in terms of GRCh37, and haven't looked into translating it, but maybe I should. And thank you for the link! I will take a look.

Ok- UCSC browser has a tool to do the liftover from hg19 to hg38 if that is helpful: https://genome.ucsc.edu/cgi-bin/hgLiftOver

Oh that's great, thank you!


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Do humans emit more carbon through respiration or defecation?
Where does most of the carbon we ingest go? I understand that a large amount is exhaled as carbon dioxide, but what percent is defecated (and theoretically deposited in the ground)?

not sure why the question got downvotes, but realised 'excretion' probably wasn't the right word, so changed it to 'defecation' to be more clear - pooping or breathing, where does most of the carbon we ingest go?

You should use the term "bodily waste" or something else. The answer depends on the icountry, chaing the ratio by 100%, individual's diet and exercise habits in the sense of calories, and if you mean carbon which is converted to CO2 and methane after digestion. you can rephrase it as "do humans use more calories than they waste after digestion" .... rich countries eat nearly twice as many calories as they use, and other countries use 1 to 1.5 times as many... consider that average daily calories breathed out is about 2000:  https://en.wikipedia.org/wiki/List_of_countries_by_food_energy_intake

note that hot countries also have different characteristics.

The short answer
In a comparison between exhaled and faecal carbon, exhaled carbon wins.

The long answer
Warning: Assumptions, approximations and averages ahead.
Calculating faecal carbon excretion
The average human being produces about $29 \text{ g}$ faeces (dry weight) per day, the major component of which is bacteria [1]. For now, neglect variations with fibre and other dietary components. Also, assume that all of it is bacteria.
Now, carbon makes up about $50 \%$ of bacterial dry weight [2]. Thus daily carbon excretion in faeces is about $15 \text{ g}$.
Calculating carbon exhalation
An adult human being breathes about $20$ times a minute [3]. Each breath has a volume of about $500 \text{ mL}$ [4]. Thus the exhaled volume per day is $20 \times 60 \times 24 \times 500 \text{ mL} = 1.44 \times 10^7 \text{ mL}$.
Exhaled air is about $4 \%$ carbon dioxide [5]. The density of carbon dioxide at $37 \  ^{\circ} \text{C}$ and $1  \text{ bar}$ is $1.713 \text{ kg m}^{-3} = 1.713 \times 10 ^{-3} \text { g mL}^{-1}$ [6].
Hence, the mass of carbon dioxide exhaled per day is $0.04 \times \left(1.44 \times 10^7 \right) \times \left(1.713 \times 10^{-3} \right) \text{ g} \approx 987 \text{ g}$.
And since $\text{CO}_2$ is $\frac{12}{44}$ carbon, the mass of carbon exhaled per day comes out to be $\frac{12}{44} \times 987 \text{ g} = 269 \text{ g}$, which is at least an order of magnitude greater than the figure we got for faecal carbon.
References

Rose C, Parker A, Jefferson B, Cartmell E. The characterization of feces and urine: a review of the literature to inform advanced treatment technology. Crit Rev Environ Sci Technol. 2015 Sep 2;45(17):1827-1879. https://doi.org/10.1080/10643389.2014.1000761.

Lawford H, Rousseau J. Studies on nutrient requirements and cost-effective supplements for ethanol production by recombinant E. coli. Appl. Biochem. Biotechnol. 1996 Mar 1;57-58(1):307-326. https://doi.org/10.1007/BF02941710.

Hooker EA, O'Brien DJ, Danzl DF, Barefoot JA, Brown JE. Respiratory rates in emergency department patients. J Emerg Med. 1989;7(2):129‐132. https://doi.org/10.1016/0736-4679(89)90257-6.

https://en.m.wikipedia.org/wiki/Tidal_volume

https://www.bbc.co.uk/bitesize/guides/z9hycdm/revision/3

https://www.engineeringtoolbox.com/carbon-dioxide-density-specific-weight-temperature-pressure-d_2018.html

I didn’t like the question — who cares? But the answer is exemplary.

Sorry you didn't like the question, David. However, Adhish gave a very clear and simple answer, so the question can't have been that bad! Thankyou Adhish, that was great.

I also had no idea that bacteria make up the majority of faecal dry weight, that is fascinating


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What do repopulation and expansion mean in stem cell biology?
I was studying a lecture on the effects of cytokines on hematopoiesis, and it uses these two terms often in the context of the effects of regulators on hematopoietic stem cells:

All repopulating bone marrow HSCs express a fibroblast growth factor (FGF) receptor that supports HSC expansion
TPO may has a role in promoting the survival of repopulating HSCs, however, it contributes to both generation and expansion of HSCs during definitive hematopoiesis.
Etc.

I looked online and honestly struggled to find any form of a definition on these two terms. They are used awfully alot though which makes it kinda weird too frankly.


text:
Why do viruses cause different symptoms?
If the sole purpose of a virus is to hijack the nucleus of a cell to replicate, why do we have different symptoms for different viruses?
I can think of the following coming into play:

immune response of the body
destroying tissue of type A is different than destroying tissue of type B
the rate of the destruction --- some (virus, cell) combination are causing more harm than others

Reference:

Why Do Viruses Cause Different Symptoms In Different People? --- talks about how we can have different symptoms for the same virus.

Welcome to SE Biology. Although we accept medically-related questions, you will see from the Tour that we prefer them to be about "the biological mechanisms behind medical conditions". As your question concerns the whole organism, I feel that it would be a better fit for Medical Sciences Stack Exchange.

every virus having differ differ spike proteins so they make infection  a particular type of cell ( just like HIV that only bind with CD4 type of receptor) and make effect. another fact is that every virus have different genomic marital so that have different codon and these different codon make different protein and that different proteins make different effect on host cell metabolism that's why different virus having different symptoms.

Welcome. This doesn't seem to target the question. Rather, your answer looks like a textbook description of the general makeup of a virus.


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Ants and their love for sweet and sugar
I have observed many times that ants are able to reach the box where sweet items are kept even if the box is kept in secret.
How do they identify it??

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). At very least please search on this site for before posting — there are several related questions with decent answers present.——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and either delete or [edit] your question accordingly. Thanks!


text:
How are Moluccan cockatoos so loud?
They say a Moluccan cockatoo's screech has a decibel level of around 129 or even more (e.g., 135). That is almost as loud as a jet engine (140 dB at 100 feet).
How are they able to emit a screech that loud? Don't they hurt themselves?

Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In general, we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, your question should have at least one reference that supports your assertion about the loudness of this bird's call and should also include other evidence that you have attempted to find an answer yourself. Thanks!

I was able to find a reference to the book Good Parrotkeeping by Robin Deutsch (©2009) from a forum post which purports to list several species' call loudness level (sorted by dB):

Nanday conure, 155 dB
Moluccan cockatoo, 135 dB
Mealy amazon, 124 dB
Quaker parrot, 113 dB
Mustached parakeet, 111 dB
Macaw, 105 dB
Mitred conure, 100 dB

I don't have a copy of the book so was not able to check the author's sources. However, I can answer a more general question about how birds are able to make loud noises in general.
Birds have a syrinx instead of a larynx as in mammals. This is situated at the bottom of the trachea, instead of at the top. Given this, birds can take advantage of acoustic resonance, which can allow for some extremely loud calls.
In a 21 Oct 2019 article in the New York Times titled "The Loudest Bird in the World Has a Song Like a Pile Driver" (paywall), the South American white bellbird is said to be the loudest bird in the world at 125 dB. (With the screaming piha now in second place). The study, "Extremely loud mating songs at close range in white bellbirds" was conducted by Dr. Jeffrey Podos and Dr. Mario Cohn-Haft in 2018. Unfortunately, it does not seem to cover the biological mechanics that produce such loud calls, but rather focuses on the evolutionary and sexual pressures that have led to such outliers in avian acoustics.
Edit:
Note that decibels are a measure of acoustic sound pressure, and vary greatly depending on the distance from the source they are measured. In order to be scientifically sound, the loudness of something should be measured from a fixed distance under controlled conditions. Note that the table of examples of sound pressure levels contains a "distance" column, which is extremely important for comparison purposes between sounds. I have no idea whether the parrot measurements were conducted using the same criteria as the white bellbird study (very likely not). Therefore, the higher dB values listed there may be due to measurements with much smaller distances.

It seems like you might be a valuable member of a proposed Bioacoustics Stack Exchange. Please consider committing to the page so we can get closer to making it to the Beta stage. Cheers!
https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680


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Why are men more susceptible to severe COVID-19?
It seems that globally, men are more susceptible to severe COVID-19 than women:
https://www.theguardian.com/world/2020/mar/26/men-are-much-more-likely-to-die-from-coronavirus-but-why
This is seen in other coronavirus diseases (SARS, MERS) but not respiratory diseases generally. Do we know the reasons for this?

Why the downvotes? :(

Update -- In the time since this question was asked, two relevant articles have been published, one in Nature Reviews Immunology and one in medRxiv (note: medRxiv is a preprint server and is therefore not peer reiewed).
Scully, E.P., Haverfield, J., Ursin, R.L. et al. Considering how biological sex impacts immune responses and COVID-19 outcomes. Nat Rev Immunol (2020).
Takahashi, T., Wong, P., Ellingson, M., et al. Sex differences in immune responses to SARS-CoV-2 that underlie disease outcomes. medRxiv (2020).
Besides the genetic factors related to viral entry that I've explained below, these papers explain the immunological factors that may determine the higher susceptibility of males to severe SARS-CoV-2 infection, including sex-specific differences in early antiviral response, innate immune repsonse, and adaptive immune response.  Figure 2 of Scully et al. provides a graphic summary.

Genetic factors
SARS-CoV-2 entry into human cells is thought to depend on two human proteins:

ACE2 -- a transmembrane protein important for blood pressure control.1  The viral spike protein binds the enzymatic domain of ACE2, facilitating translocation of the virus into the cell.2
TMPRSS2 -- a serine protease with a transmembrane domain.  The proteolytic activity of this enzyme is thought to play a role in "priming" the viral spike protein.3

So, a place to start would be to ask if there are sex-specific differences in the expression or localization of these proteins.
ACE2
No significant differences in lung ACE2 activity have been found between male and female mice.4  In rats, however, lung ACE2 levels are reduced with aging in both males and females, with significantly higher ACE2 expression in old female rats compared to old males.5 Assuming that rats are a good model for sex-specific human lung protein expression, this observation counters the simple explanation that men are more likely to have severe COVID-19 due to higher ACE2 expression.
A recent preprint 6 presents an interesting hypothesis -- that ACE2 mosaicism due to X inactivation may be protective against SARS-CoV-2 in women.
From the abstract:

The fact that the human ACE2 protein is encoded on the X chromosome means that males who carry rare ACE2 coding variants will express those variants in all ACE2-expressing cells, whereas females will typically express those variants in a mosaic distribution determined by early X-inactivation events.

So, since males are hemizygous for the X-chromosome, males that have an ACE2 variant that binds strongly to the SARS-CoV-2 spike protein will only express that variant in their lungs.  Females have two X-chromosomes, though only one is expressed in any given cell due to X-inactivation.  If a female is heterozygous at the ACE2 locus, with one allele that encodes a protein that strongly binds SARS-CoV-2 spike protein and one allele that encodes a protein that weakly binds SARS-CoV-2 spike protein, mosaic expression of the maternal and paternal alleles may give partial protection from infection.
The authors found that ACE2 is generally intolerant of loss-of-function variants, though many missense variants occur at and near residues predicted to bind SARS-CoV-2.  Such variants were detected at a rate of 3.9 males per 1000 and 8.5 females per 1000.  However, the most popular missense variant, rs41303171, does not lie in a domain of ACE2 that is predicted to interact with SARS-CoV-2.  Additionally, this SNP is only observed in 1.7% of male and 3.1% of female samples, so it is not obvious that this explanation can account for the sex-specific discrepancy in severe COVID-19 at the population level.
TMPRSS2
Currently, evidence suggests that there are no sex-specific differences in TMPRSS2 expression in the lungs of humans or mice.7  Note, however, that only transcript levels have been evaluated in this context, and that TMPRSS2 activity would need to be evaluated to determine that proteolytic action is not different between sexes.

Non-genetic factors
Worldwide, men smoke five times as much as women.8
Smoking is co-morbid with severe COVID-19 9, likely due to decreased lung capacity, though possibly through a mechanism involving increased TMPRSS2 expression.7  From the same TMPRSS2 paper cited above:

regardless of sex, smoking significantly increases the expression of TMPRSS2, which reverts back to never-smoker levels in former smokers

Indeed, one recent study of more than 1,000 COVID-19 patients reported greater than two-fold increased risk for intensive care unit admission and death in smokers as compared with non-smokers.10
There may be cultural factors affecting disease progression, as well.  If men are less likely to wear masks or follow other guidelines to reduce the risk of infection, then infected men may be exposed to a higher infectious dose than women. Initial infectious dose may be positively correlated with viral load 11, and higher viral load is associated with a more severe prognosis for SARS infections.12
It could simply be the case that symptomatic men are less likely to be tested (a "tough it out" mentality), and therefore would be less likely to receive treatment that prevents a mild infection from becoming severe.

Citations

A Novel Angiotensin-Converting Enzyme–Related Carboxypeptidase (ACE2) Converts Angiotensin I to Angiotensin 1-9
SARS coronavirus entry into host cells through a novel clathrin- and caveolae-independent endocytic pathway
Activation of the SARS coronavirus spike protein via sequential proteolytic cleavage at two distinct sites
Sex differences in renal angiotensin converting enzyme 2 (ACE2) activity are 17β-oestradiol-dependent and sex chromosome-independent
Age- and gender-related difference of ACE2 expression in rat lung
ACE 2 Coding Variants: A Potential X-linked Risk Factor for COVID-19 Disease
No evidence that androgen regulation of pulmonary TMPRSS2 explains sex-discordant COVID-19 outcomes
Gender empowerment and female-to-male smoking prevalence ratios
COVID-19 and smoking: A systematic review of the evidence
Clinical Characteristics of Coronavirus Disease 2019 in China
SARS-CoV-2 viral load and the severity of COVID-19
Initial viral load and the outcomes of SARS

The following GWAS finds another ACE2 related X-chromosome allele correlated with COVID-19: https://news.bugbank.uk/2020/05/xpnpep2-is-genome-wide-significant-in.html

Besides biological reasons, men are often more risk-prone and take less precautions, which certainly has some impact. Here in South Korea, the share of men that wear masks is definitely lower than the share of women that wear it (based on anecdotal observations at least).

@Olorun, that would explain a greater rate of infection among men, which seems to be the case. Though I'm not sure how that would cause a greater rate of severe COVID-19 cases in men, unless (1) men are being exposed to a greater viral load, if greater viral loads are correlated with adverse outcomes, or (2) men are less likely to seek treatment at the onset of symptoms, leading to a worse prognosis.  I'll edit my answer to reflect those possibilities.

Both seem like very real possiblities, especially the "tough it out" mentality - if the men with lesser symptoms are less likely to be tested, then the overall share of infected men with severe symptoms will be higher.

What does "priming" mean in simple terms, presumably it alters the folding of the spike protein in some way? Is priming common among viruses in general?

@SingleMalt, TMPRSS2 is a transmembrane protease, which means it sits on the outside of the cell membrane and cuts other proteins. Studies in SARS-CoV have shown that cutting of the viral spike protein by TMPRSS2 increases the likelihood of viral entry into the cell. Similar activation by human protease is observed for influenza A and metapneumovirus.


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Can we graft a tree with cells from the seed directly?
Are there any limitation to the grafting so we could only graft a branch to another tree? Could we just use cell from the seed, or just a sprout, to graft onto the tree of the same species?

If you could do this, the process wouldn't be grafting, as that's defined as attaching a branch or twig.  Tissue culture is used to raise plants from cells.

Tree grafting involves a rootstalk and a scion (part to be grafted onto the rootstalk). Here is a reference on the basics of grafting. Usually, this is done to combine the advantage of a strong or mature root system (from the rootstalk) with desired fruits or buds (produced by the scion). In this case, the roots of the scion plant might be sensitive, disease-prone, or just take a long time to develop (read more here). It is also possible to graft a scion onto the same variety of cultivar. Grafting refers to the joining of vascular cambium of a scion and a rootstock in such a way that they can share resources and continue to grow together (see previous links). As such, adding cells from a seed to a larger plant would not be grafting, because there wouldn't be that pre-established vascular tissue to connect with the vascular cambium of the rootstock. Additionally, a single sprout would not have a good chance of binding well to the vascular system of the rootstock (see link 2).
If you are interested in reading more about different forms of (non-seed) propagation, this resource describes the why/when/and how of grafting and layering (another technique that might help you, if you're trying to propagate only one tree variety as indicated in your question), and there are many great resources on youtube about the basics.

Thank you very much. What I am after is, I was known that growing a fruit tree from seed take so much times and effort for them to establish into a tree that can bear fruit. So I just think how could we speed up this process. One way I see is, (some?) tree can sprout a young bud from the branch that look very much the same as sprout from the seed, so shouldn't it possible to graft just that and it would become just another branch but contain new DNA, that's what I thought

Yes! Grafting budwood from younger trees to more established rootstalk is a fundamental practice in many orchard crops! If you are interested in learning more about budwood I would recommend this video (citrus) https://www.youtube.com/watch?v=l1HSOy-3JGU&feature=youtu.be

I see, so are there any problem for doing the same thing on apple and some other families except citrus? Because I have learn that the practice of grafting of some other plant family, such as apple, need 6-10 years to grow from seed and bear fruit before they graft it's branch to other tree. I just think if we graft the seedling and force it to be a branch it should speed up this process, or is it not?

The citrus video was just an example. If you google "bud grafting apples" you will get a plethora of resources. For example: https://ptes.org/campaigns/traditional-orchard-project/orchard-practical-guides/grafting/bud-grafting-2/ and https://extension.psu.edu/bud-grafting-apple-trees

What I have seen is just grafting a bud of branch, which is common, not a grafting from seed sprout


text:
Why is an intron (or exon) still called intron (exon) if retained in (excluded from) mRNA?
In most explanations, the sections of RNA removed during splicing are called introns, and the remaining segments that are stitched together are called exons.  That is, introns and exons are defined in terms of the splicing process.
But I've come across several counter-examples.  For instance:
From A simple answer for a splicing conundrum:

Exons without these elements [exonic splicing enhancers (ESEs)] are
generally not recognized and tend to be excluded from the mature
mRNA.

And from Wikipedia on alternative splicing:

Intron retention: A sequence may be spliced out as an intron or
simply retained...

In what sense is an exon still an exon (and not an intron) if it tends to be excluded from the mRNA?  In what sense is an intron an intron if it included in an alternatively spliced mRNA?

Try searching for “alternative splicing”. It’s not a question of nomenclature.

You must know that:

Introns are non-coding regions of an RNA transcript, or the DNA encoding it, that are eliminated by splicing before translation.
An exon is any part of a gene that will encode a part of the final mature RNA produced by that gene after introns have been removed by RNA splicing.

Now, about the exceptions, alternative splicing: Here,

particular exons of a gene may be included within or excluded from
  the final, processed messenger RNA (mRNA) produced from that gene. There are numerous modes of alternative splicing observed, of which the most common is exon skipping. In this mode, a particular exon may be included in mRNAs under some conditions or in particular tissues, and omitted from the mRNA in others.

Apparently, this greatly increases the biodiversity of proteins (since there are differences in their amino acid sequence and, often, in their biological functions) which might explain why it is so common.
So in this case, it becomes easier to understand if you use 'coding' and non-coding' as the difference instead of 'spliced' and 'not-spliced'.

EDIT- The coding region of a gene:

In DNA, the coding region is flanked by the promoter sequence on the 5' end of the template strand and the termination sequence on the 3' end. Although this term is also sometimes used interchangeably with exon, it is not the exact same thing: the exon is composed of the coding region as well as the 3' and 5' untranslated regions of the RNA, and so therefore, an exon would be partially made up of coding regions. The 3' and 5' untranslated regions of the RNA, which do not code for protein, are termed non-coding regions.

I had previously forgotten about the UTR's, so I have included that. Now, if there is a definite sequence where coding regions are found, it points out to the fact that coding regions must be intrinsic. Another point in favour:

The evidence suggests that there is a general interdependence between
  base composition patterns and coding region availability.The coding
  region is thought to contain a higher GC-content than non-coding
  regions. There is further research that discovered that the longer the
  coding strand, the higher the GC-content. Short coding strands are
  comparatively still GC-poor, similar to the low GC-content of the base
  composition translational stop codons like TAG, TAA, and TGA.

Thanks.  I am still not 100% clear.  Given your comment, I think it boils down to this:
Is whether a region is coding or non-coding, a property that exists regardless of whether it is included or not in the mRNA?
In other words:
Are regions inherently coding or non-coding, and the splicing process selects for that?  Or, does the result of the splicing process itself determine whether a region is encoding or non-encoding?
If it is the former, then what exactly is it that gives a region its coding property?  If it is the latter then the questions I asked above remain.

A biologist (but not geneticist) friend suggested that:
"An exon is any region that is included in at least one of the alternative splices, and an intron is a region that is included in none of them."
Regarding intron retention, he hadn't heard of it, but on further inspection said:
"It's looks looks like an aberrant case and shouldn't detract from the main definition"
Would you agree with this?

RNA splicing ultimately determines what part of the sequence becomes translated and expressed.  So, exons (since they code) should, usually, be included in mRNA. Your friend's statement seems alright to me, though I still suggest exons to be defined on the basis of coding regions.


text:
How much fat can the body absorb? Implications for daily fat distribution
This question is named analogous to this research: How much protein can the body use in a single meal for muscle-building? Implications for daily protein distribution http://ncbi.nlm.nih.gov/pmc/articles/PMC5828430
How many grams of lipids can the body absorb in one sitting? (I ask because a strict vegetarian or vegan diet is characteristically low in fat. Therefore, I consume extra virgin olive oil and nuts.)

Most of the research on pubmed.gov is about oral lipid drug administration/absorption. This work that seemed to come close is over my head and just doesn't seem to specify:
Intestinal Lipid Absorption and Transport by C T Phan 1 and P Tso
PMID: 11229876 DOI: 10.2741/phan
https://www.bioscience.org/2001/v6/af/A612/fulltext.htm

Image sources: Cronometer.com and Jackedonplants.co.uk

just a piece of advice, "nuts" covers a lot of things many common nuts are very low in saturated fat, and so its olive oil.

Indeed, lipid fecal loss remains below 5% (w/w) even in situation of
  high fat supply in healthy humans, [30].

All about those guts and bowls folks!

Niot, I., Poirier, H., Tran, T. T. T., & Besnard, P. (2009). Intestinal absorption of long-chain fatty acids: Evidence and uncertainties. Progress in Lipid Research, 48(2), 101–115. doi:10.1016/j.plipres.2009.01.001
https://sci-hub.tw/10.1016/j.plipres.2009.01.001
[30] Ross AC. Overview of retinoid metabolism. J Nutr 1993;123:346–50

The issue remaining is how Ross' work doesn't seem to say anything about lipids. Yet, it appears from the mice studies nearly all fat is absorbed (except for ones with special conditions).
Ross, A. C. (1993). Overview of Retinoid Metabolism. The Journal of Nutrition, 123(suppl_2), 346–350. doi:10.1093/jn/123.suppl_2.346
https://sci-hub.tw/https://doi.org/10.1093/jn/123.suppl_2.346

Your first sentence answers the question. Or practically: If the amount of fat you consume does not make your stools fatty (steathorrhea), it means you are absorbing most of it.

Maybe the amount of bile liver is able to produce and gall to secrete is some super natural limit.

@Jan or gut bacteria is breaking it all down inot something else.


text:
Why do arteries have a small lumen?
My biology textbook says that arteries have a small lumen relative to the thickness of their walls. I understand why they need thick walls, to withstand high pressure and stretch etc. But when explaining the reason for the "small" lumen, it says that it is to "maintain the high pressure". I'm not quite sure what this means.
What would happen if the lumen was larger? Wouldn't a small lumen create resistance to blood flow? And what exactly is blood pressure? Also, it says that veins have a "large" lumen. Why is this so? I think my confusion is a lack of understanding of what blood pressure really means. Why does velocity not seem to make a difference?

Physics. Given the same volume that must pass through a tube per minute, do you think the pressure would be as high in a 3 inch pipe or a steel straw?


text:
Why do the calicheamicins bind to DNA at the minor, rather than the major, groove?
I am trying to understand why some drugs bind only to the minor groove and not to the major groove. More specifically, I am interested in calicheamicins.

They target DNA and cause strand scission. Calicheamicins bind with
  DNA in the minor groove, wherein they then undergo a reaction
  analogous to the Bergman cyclization to generate a diradical species.
  This diradical, 1,4-didehydrobenzene, then abstracts hydrogen atoms
  from the deoxyribose (sugar) backbone of DNA, which ultimately leads
  to strand scission.[7] The specificity of binding of calicheamicin to
  the minor groove of DNA has been demonstrated.

It would be helpful if you could provide a source for the extract you quote, preferably with a link.

this particular quote is from wikipedia, https://en.wikipedia.org/wiki/Calicheamicin

Accommodation in the major or minor groove
I am not in a position to generalize about all drugs that bind to the major groove of DNA, but at least one well-known example, actinomycin D, does so because it intercalates between the base-pairs in the double helix. Although other weak chemical interactions stabilize this binding, much of it is through base stacking with base-pairs. Hence binding requires it be inserted into the major groove in which the base pairs lie (see e.g. PDB 101 Molecule of the Month article).
Binding of calicheamicins, in contrast, involves interaction with two parts of the molecule. The ‘head’ of the molecule makes specific interactions with a TCCT sequence in the DNA (in the case of calicheamicin γ1), which is achieved from the minor groove (intercalation is not necessary) allowing the saccharide ‘tail’ to fit into the minor groove. (Ikemoto et al. 1995).

(Constructed from 3D Structure images on the Protein Data Bank website)
Sequence specificity
A concern of the poster is the fact that the interaction of calicheamicin is sequence specific (there is apparently a preference for d(T-C-C-T).d(A-G-G-A)) whereas access to the bases is restricted in the minor groove. This is addressed in the paper by Ikemoto et al., but without illustration, assuming you are able to visualize the chemical interactions in your mind. I have used Jmol to view the structure 2PIK, have prepared a couple of screen shots to help illustrate the details I shall quote from the text of the paper.

Cleavage of the DNA is performed by the enediyne aglycone (R), which does not make contact with the bases. Two of the regions that do interact with bases are the thio-sugar ring (B) and the aromatic ring (C). These are shown below in the complex of  calicheamicin (coloured yellow) with a deoxy-oligonucleotide duplex, together with a close-up of the interactions of these rings.

In the left-hand frame the DNA has standard cpk colouring, and the phosphates (orange–red) lining the minor groove are evident. The base-pairs are perpendicular to the plane of the image. In the second frame I have tilted the image slightly to allow the rings of the bases to be seen, and coloured the bases (actually the whole nucleoside) red/white/green/blue for A/T/G/C. Quoting from the Ikemoto paper:

The thio sugar B is positioned edgewise in the minor groove and contacts the A20 residue through van der Waals and hydrogen bonding (B ring hydroxyl to N3 of the base) interactions. The aromatic ring C is positioned between the walls of the minor groove with its iodine and CH3 groups directed toward the floor of the minor groove.… The S-carbonyl linker, which adopts an orthogonal alignment relative to the plane of ring C (favored by the steric demands of the ortho aromatic ring substituents), bridges the minor groove and makes van der Waals contacts with the opposing walls of the groove.

This may not have the clarity of, say, Watson and Crick base-pairing, but neither does the interaction of proteins with particular DNA sequences — one needs to examine the multiple interactions that occur. What I think it does show is that this drug can make specific contact to bases, even though it binds in the minor groove.

thank you a lot for your reply. however still I cannot fully understand..I thought that binding with minor groove is non-specific, in contrast with binding with major groove that is specific. So that's why I wondered since the binding is not specific and major groove is wider than minor, why calicheamicins act only in minor groove. thank you in advance!

@marilu — Generalizations have their uses, but biology is full of exceptions, and if you are talking about interactions you are talking about individual chemistry. One needs a representation with drug and DNA in stick representation to see the interaction, although then the grooves are not obvious. Unfortunately the original paper does not have a suitable picture. I'll see what I can find and then flesh out my answer. May take a few days.

thank you a lot!

@marilu — That's the best I can do. If you need more detail you'll have to grapple with the paper yourself and get to grips with a molecular graphics program like Jmol. (It can be fun, but there is a learning curve.)

I am so grateful!THANK you so much for your time and help!!!I get it now!:)

@marilu — You are welcome. I learned something from your question.


text:
Why is ACE2 not used as drug against covid?
Can ACE2 be produced and used as drug against covid? I read it is the receptor molecule. If it is in the organism the virus should bind to it and could not attack cells anymore? Is that right?

There's a Cell pre-print by Monteil et al. (DOI: 10.1016/j.cell.2020.04.004) which argues that human recombinant soluble ACE2 protein can competitively bind to SARS-CoV-2 virus and reduce its ability to infect and replicate:

Here, we report that clinical-grade human recombinant soluble ACE2 (hrsACE2), which has already been tested in phase 1 and phase 2 clinical trials (Haschke et al., 2013, Khan et al., 2017), can reduce viral growth in Vero E6 cells by a factor of 1,000-5,000. Moreover, we show that human blood vessel organoids and kidney organoids can be readily infected, which can be significantly inhibited by hrsACE2 at the early stage of infection.

Though it is not perfect, in that other factors and receptors may be implicated in infectivity:

Our data now show that this clinical-grade human ACE2 molecule - but not mouse soluble ACE2 - can significantly inhibit SARS-CoV-2 infections and reduce viral load by a factor of 1,000-5,000. However, as observed in antibody neutralizing experiments of many viruses, the inhibition is not complete, though clearly dose-dependent. This may be due to the fact that there might be other co-receptors/auxiliary proteins or even other mechanisms by which viruses can enter cells, as had been initially proposed for SARS (Jeffers et al., 2004; Qi et al., 2020).

One person is right to comment that these are in vitro studies. In other words, they treat cell cultures on the functional equivalent of a Petri dish: Vero cell lines or simulations of human tissues (organoids), and they see what happens.
The in vitro studies are useful and important but it is a big step from those to 1) treating people in vivo — designing a drug that can actually and safely target the virus where it infects respiratory and renal tissues — and, 2) making and distributing that drug in quantity, cheaply, safely, etc.
But the larger point of these studies is to show that scientists are definitely thinking about the mechanisms by which the virus infects cells, and to see if there are ways to interfere with and limit the virus, by doing so.
Like your thought to use ACE2, some researchers have looked at other viruses, like poliovirus and HIV, to see if there are similar soluble ligands that they can bond to antibodies and deliver safely to humans, as a general therapeutic idea.
They found that HIV-1, which uses binding to the CD4 receptor as a means to infect T cells, could develop mutational resistance to soluble CD4 and use other mechanisms to cause infection. But by adding a second receptor CCR5 to the immunoglobulin, other researchers were able to limit the ability of HIV-1 virus to evolve resistance to both receptors, which provides some possibility of this approach as a vaccine, down the road.
These issues all complicate use of receptors as a way to "fake out" the virus. But it is an avenue being explored, especially for this virus during a time of emergency.

It should be noted that the study referenced is in vitro and no efficacy has been demonstrated in actual infected individuals, though there are earlier trials (I assume these are the citations in the quote) showing clinical efficacy in ARDS - I believe that relates to the enzymatic activity of ACE2, though, not anything to do with binding to viral particles, and I don't know of any proof-of-concept that would suggest the receptors make it into the lungs where the virus is.

Good points, definitely. Read the preprint in depth.

@AlexReynolds thank you. In that regard I have a question. Has someone tried to use human cells with artificially damaged cell interior that will accept the virus by its ACE2 and other receptors (but not reproduced it and finally destroy it)?

I don't know if such a therapy exists. Maybe others would know. Usually these are immunoglobulins, immune system proteins with unique bits attached that a virus would bind to, instead of the receptors on a lung or other cell that it would normally try to infect.

What about any side-effect of "taking away", i.e. scavenging, the natural ligand of ACE2 (which is physiologically expressed on membranes of epithelia and neurons too(?), thus especially  leading to a lack of counterbalancing of high blood pressurem as ACE2-axis is considering beneficially downregulating the AngioensinII-AT2-axis?


text:
In north America is their mammals that can survive from falling from hundreds of feet?
Like animals have great attributes but is their any mammals that have unique attributes to survive such fate of death?

There are quite a few, including Corynorhinus townsendii virginianus, Eptesicus fuscus, and many others.

No I’m asking about resilience animals to surrive such fate

Like surviving falls. That can kill people but mammals are munch stronger then human so they have more of chance of survival


text:
DNA from sweat on the hat band?
My father died in 1987.  I have an old cowboy hat of his.  Can I use a FamilyTreeDNA test kit to recover any DNA?

Related: Does sweat contain DNA information?


text:
What coronaviruses have been identified in racoon dogs?
Christian Dorsten says in an (Apr 26) interview in the Guardian that racoon dogs as [intermediate] source of coronavirues have been overlooked (in China):

Q: What do we know about that intermediate host – is it the “poor pangolin”, as it’s come to be known?
A: I don’t see any reason to assume that the virus passed through pangolins on its way to humans. There is an interesting piece of information from the old Sars literature. That virus was found in civet cats, but also in raccoon dogs – something the media overlooked. Raccoon dogs are a massive industry in China, where they are bred on farms and caught in the wild for their fur. If somebody gave me a few hundred thousand bucks and free access to China to find the source of the virus, I would look in places where raccoon dogs are bred.

So what studies are there on coronavirues in racoon dogs up to now? (A quick search found a 1992 US paper that some coronavirus [unsurprisingly] infects racoons too. But I can't find much else. Is there more up-to-date survey? Also, duh, racoon dogs aren't even the same family [Canidae vs Procyonidae].)

Here's an abstract for a paper from 2006: https://www.ncbi.nlm.nih.gov/pubmed/16450706

An RT-nPCR assay was used for testing fecal samples of dogs, foxes, raccoon dogs and minks for the presence of canine coronavirus (CCV). The animals were raised in homes, dog schools or farms... Among 24 raccoon dogs samples, 22 were CCV type II-positive, and from those 16 were additionally type I positive.

Here's another paper from 2003: https://www.ncbi.nlm.nih.gov/pubmed/12958366

A novel coronavirus (SCoV) is the etiological agent of severe acute respiratory syndrome (SARS)... Evidence of virus infection was also detected in other animals (including a raccoon dog, Nyctereutes procyonoides) and in humans working at the same market.

So at least a couple types of canine coronavirus and other strains closely related (but not identical) to the coronavirus that causes SARS.

Racoon dog is almost like dog (only 10 million years, human and chimpanzee is 6)

So it seems obvious the canine betacoronavirus_1 (OC43 & BCoV related) CRCoV infects racoon dogs


text:
What is this insect? And does it eat aphids on plants?
I found this insect that looks like a praying mantis on my plant which was infested with aphids. I sprayed neem oil and most aphids died, even one of these praying mantises did. But here in this picture is one and I want to know if it is going to eat the aphids so I can stop spraying neem and killing every bug in the process.
The insect is around 2 centimeters long.
This is in a hot and humid area in the middle east. The plant, I guess, is from the jasmime family. It produces small scented roses (hasn't flowered yet due to the aphids problem).

Based on the head morphology and the upper limb visible on the first picture, I would say it looks like a mantis. The length of the abdomen also confirms the same.

The internet is also full of several non-scientific sources that seem to confirm they eat aphids. Animals will normally learn to avoid bitterness in food as it's a sign of toxicity. I haven't found a lot of information about how bitter are aphids, however mantis are sit-and-wait predators, so they will try most things that crawl their way. Judging by the following pictures (and the article linked at the end), I would say it's very likely:

Indeed, catching every prey would be a beneficial strategy because of uncertainty in encountering another prey due to a sit-and-wait strategy. By holding prey with its forelegs and gradually eating the prey by chipping away at it, the mantis has enough time to find edible parts of prey and reject unpalatable parts/prey (Reitze and Nentwig 1991).

Sources:

https://en.wikipedia.org/wiki/Mantis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5882761/
https://praying-mantis.org/what-do-praying-mantis-eat/


text:
What is this bug found in a garden in Utah?

Apologies for the poor quality of the photo.
I found this bug in a garden in Utah.  The body was flattish, with teal markings (lighter than it looks in the photo) with an interesting pattern of three dots along the back, and a pink cone projecting down to the rear.  It was about the size of my smallest fingernail.
From the searching I've done, the shape and the light "rim" on the outside of the shell look like a June Bug or a Stink Bug, but this one was not as green and the markings seem a lot more pronounced.
Is it a pest to be concerned about?

Based on the pattern of yellow spots it might be a Say Stink Bug.
Check out this list of common Utah stinkbugs

The 12 - 17 mm size is consistent with OP's description and the fact that this insect is often found on ornamental shrubbery is consistent with finding it in a garden.

The picture on Wikimedia is an even closer match.  So much easier to find when you know what you are looking for.  Thanks.


text:
Are changes in flexibility from stretching due to changes in the nerves or the muscles?
For many people, stretching repeatedly over a period of time improves their flexibility. I want to know whether this improvement commonly seen is due to a change in the nerves or the muscle’s material properties.
Are the changes in flexibility seen on the order of minutes/hours to weeks/months due to changes in the nervous system's reaction (e.g. reflex habituation) or changes in the viscoelasticy properties of the muscles (e.g. muscle length via serial sarcomere number)?

Excerpts:
To help answerers, I want to provide a few excerpts from two sources. The first source is from 1998.

"This article reviews recent findings regarding passive properties of
the hamstring muscle group during stretch based on a model that was
developed which could synchronously and continuously measure passive
hamstring resistance and electromyographic activity, while the
velocity and angle of a stretch was controlled. Resistance to stretch
was defined as passive torque (Nm) offered by the hamstring muscle
group during passive knee extension using an isokinetic dynamometer
with a modified thigh pad. To simulate a clinical static stretch, the
knee was passively extended to a pre-determined final position (0.0875
rad/s, dynamic phase) where it remained stationary for 90s (static
phase)."
“A significant decrease was observed for energy (30%) and
stiffness (13%) in the dynamic phase, and passive torque in the static
phase. However, the observed decline in the variables measured was
transient and they returned to baseline within 1h.”
“Long-term stretching (3 weeks) increased joint range of motion as a result of a
change in stretch tolerance rather than in passive properties.”

Source: Magnusson, Stig Peter. "Passive properties of human skeletal muscle during stretch maneuvers." Scandinavian journal of medicine & science in sports 8.2 (1998): 65-77.
The second source I want to cite is The Complete Guide to Stretching by Christopher Norris. Paraphrasing pages 56-58, he says stretching can affect the following:

Habituation – when the stretch reflex becomes desensitized and the
reflex doesn’t activate as easily when stretched
Muscle stiffness – a muscle has an elastic recoil when stretched. The degree of this
recoil is the “muscle stiffness”
Stretch tolerance – the amount of discomfort induced by a stretch that a person can endure
Serial Sarcomere Number (SSN) – a muscle can lengthen or shorten in length
when the number of sarcomeres change

Norris also notes that the first 3 criteria usually change on the order of months (called “acute” or short-term) while the SSN tends to change on the order of years (called “chronic” or long-term).