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How do antibiotics create drug-resistant strains
I've heard for years that low-level use of antibiotics causes the spread of drug-resistant strains of bacteria, but the explanations always fall short.  I understand mutations and natural selection, and that a bacterium can randomly mutate into one that is more resistant to the antibiotic than the wild-type.  I understand that the antibiotics kill off the less resistant strains and leave the more resistant ones, but those more resistant strains would be there even without the antibiotic use, right?
Do the more resistant bacteria compete somehow with the less resistant ones and the antibiotics kill off the competition?
(Edited: previously used the terms "strong" and "weak" which apparently have unintended connotations, and was unclear about the role of mutation).

The last part of your question is confusing. Can you reword your question and talk about mutants and wild-type instead of "strong" and "weak"? Those are value-laden words, and may not even apply to the populations you're talking about.

Resistance to an antibiotic doesn't make it "strong"; it makes it resistant to an antibiotic. If it happens to take hold in a wound, it will flourish no better than a wild-type bacteria, but it will survive exposure to the antibiotic, that's all.

Resistant strains might have been there but they would not have been in a position to outcompete the nonresistants without selection, for the reasons I gave in my answer. If you properly treat bacterial infections long enough and at a high enough dose with a combination of drugs, and have a patient with a functioning immune system, then the adaptive immune response should be able to clear the infection. When we didn't allow that to happen, or we gave antibiotics for viruses, we selected for the resistant mutants, and the adaptive response wasn't able to target and clear them.

There is no such thing as a "stronger" or "weaker" strain until the bacteria are treated with antibiotics.
It is true that potentially antibiotic-resistant mutants will still occur whether or not treated with antibiotics.
However, the mutants would not be "stronger" without the antibiotic use, so there is no selective pressure for them to survive to any greater degree than the wild-type. Without the antibiotic, something else will kill that mutant bacteria, meaning that the mutation ultimately did not make it any stronger.

All things being equal, in an environment without the selective pressure of the antibiotic, then the non-resistant wild-type will have a growth advantage.
EDIT

The events of random mutation and the attendant natural selection in the presence of a given antibiotic provide ample opportunity for the advent of the resistance phenotype. It is interesting to note that the survival cost to the microorganism in the evolution of drug resistance is high as it is highly dependent on the environment in which it happens to exist momentarily. One could envision that in the case of a plasmid-borne resistance factor, the organism must synthesise the additional genetic material and the protein that it encodes. However, this energy cost factor may be affected by the nutritional limits of the environment in which the organism finds itself. Furthermore, alterations of chromosomal genes encoding the targets for antibacterials may present the opportunity for the selection of resistance to antibiotics. However, such modifications may jeopardise the normal function of the gene products and make the organism that carries them less fit in the wild, or diminish or lose the capacity to survive in the absence of the antibiotic. Numerous studies indicate that genetic adaptation by secondary mutations elsewhere in the genome and natural selection reduces this ‘cost’ to the organism in several generations of growth, such that the cost is either reduced or eliminated entirely. Indeed, recent studies suggest that a progression of bacterial resistance to given noxious agents involves a sequence mechanism that renders the organism increasingly resistant to the agent, but nevertheless at a cost to its survival fitness

-Martins, A., Spengler, G., Molnár, J. and Amaral, L. 2014. Bacterial Antibiotic Resistance. eLS.
In order to truly grant resistance to an antibiotic, the bacterium needs to be expressing the enzyme the confers resistance constitutively so that it can react to the antibiotic when the cell comes in contact with the antibiotic. If the bacterium has to wait until it encounters the antibiotic to start expressing the resistance gene, then the bacterium will likely be killed before it has a chance to produce the protein that will protect it. This is especially true for antibiotics that target the bacterial ribosomes to prevent protein synthesis.
The result is that the bacterium has to use energy to produce the enzyme. It also has to maintain that gene either on a plasmid or incorporated in a very small genome. That again means the resistant cell needs more energy for replication, and likely a bit more time to divide. That may seem trivial, but if the nonresistants can divide every 20 minutes while it might take the resistants 25 or 30 minutes, the resistant bacteria will be out competed by the nonresistant bacteria, for the simple fact that the nonresistants are using less energy to survive and replicate and they are doing it faster, so the will have more descendants.
Another thing that you need to realize is that a lot of times the use of antibiotics only holds a bacterial infection in check until our adaptive immune system can be raised and respond to the infection. So not completing a course of antibiotics means that during the period of time that the antibiotic was used the resistant bacteria had a growth advantage over the nonresistant bacteria.
If you stop taking the antibiotic before the immune system can clear the infection completely, then both types of bacteria will begin to divide again, and there will be more of the resistant bacteria than there will be nonresistant, so they will contribute more descendants to the reemerging infection.
Another problem is that the more resistant bacteria there are the more of a chance there is that they can pass on that resistance gene to bacteria that didn't have it before. Now when you go back on the antibiotic, less and less of the bacteria in the infection will be affected, and you will get uncontrolled growth of the infection. There is a point where your immune system either is overwhelmed and cannot respond, the toxicity level from endo and exo toxins produced by the bacteria makes you very sick, or your immune response responds too strongly and does significant damage to your own tissue trying to fight off the bacteria.

"All things being equal, in an environment without the selective pressure of the antibiotic, then the non-resistant wild-type will have a growth advantage." Do you have a source for this? CA (community associated)-MRSA has mostly replaced HA (hospital associated)-MSRA because their doubling time is much less, giving them a competitive advantage over even "feral" SA unrelated to their methicillin resistance.

@anongoodnurse Your example is of an already resistant, already highly virulent strain of bacteria, and that is not what I am describing. I am describing how you go from a situation where the majority of the organisms are non-resistant and then through the incorrect use of antibiotics, you give rise to strains that have resistance.

Must it be incorrect use? What about correct use? All I'm asking for is a source to back up your claims. If you don't have one (or more), it's just opinion.

@anongoodnurse I also looked at several papers on CA-MRSA, and non them mentioned anything about a growth rate advantage due to replication speed. They have different virulence factors, and are more adept at causing infections in otherwise health people, and the prevalence of these infections has increased dramatically in comparison to HA, but non mentioned the rate at which they replicate.

@anongoodnurse Incorrect usage was the bases of the OPs question.

@anongoodnurse Edit to show source that supports my experimental observations.

How does low-level translate to incorrect usage? (I assumed lower dose, not incorrect.) Note the great difference in the possibilities they state and the certainties with which you frame your answer. I can easily accept the paper's hypotheses. You state it as if it's a known fact. The fact that you restricted antibiotic use to incorrect use shows a certain frame of reference which is restrictive, not open. "... my experimental observations." Are you doing microbiological research?

@anongoodnurse Yes.

@anongoodnurse I translated low-level use to be at amounts below minimum inhibitory concentration or incomplete treatment, and much of the first part of my answer, while factually accurate, was geared more towards correcting the OP's misconception that nonresistant = weaker. The advantage that resistants enjoy goes away when there is no selective pressure, because better breeders win out. Once established, as with MRSA and the other superbugs, they will be the predominant strain, because they have survived countless generations of selection that WTs did not. Their competition was wiped out.

I see a lot of explanation of how low-level use of antibiotics makes the ratio of resistant to non-resistant climb, but I don't see anything that would explain the absolute population of resistant going up or, more to the point, more people being infected with the resistant strain, because of the antibiotic use.

@user170733 Vertical Gene transfer. If, in a selective environment, the resistant strain is able to pass on its genes through replication, the larger the population gets in relation to non-resistants. Horizontal Gene Transfer. Resistant Bacteria, either the same species or entirely different ones are able to transfer the resistance gene, either by Transformation, Transduction, or Conjugation. Without antibiotics, there is no selective pressure, so the energy cost outweighs the benefit of resistance. With selection, the resistance gene(s) can be maintained...

@user170733 So now, because of decades of antibiotic use that was insufficient to kill off resistant strains, either below MIC, incomplete treatment, or from immunocompromised people that did not have an immune cyst that could fight the resistant bacteria, we have more resistant strains, and the rest is down to probability. More resistant strains = a higher probability that that is what will infect you.

@user170733 The issue isn't so much that antibiotics were used, it is that they were not used in high enough doses, for long enough periods of time and were often used as mono-therapies, instead of combination therapies that attack the bacteria multiple ways, making it less likely, at least initially, that you will have any bacterium will be resistant to all of the drugs, which is what we see now, because one drug didn't kill them, so the survivors are mostly killed by the second, but there are some that survive because they develop resistance to the second drug as well, and on and on.

@AMR - "I also looked at several papers on CA-MRSA, and non them mentioned anything about a growth rate advantage due to replication speed." Seriously? It's everywhere (it's a very hot topic.) Makes it difficult to comprehend your statements...

@anongoodnurse The paper only has a comparison between CA and HA. I tried to find the reference, but it was from a book (peer-review?) that I wasn't able to track down. You are giving one example, and when it comes to bacteria, I have learned never say never, but that doesn't change the fact that sub minimum inhibitory concentrations that reduce the competition for resistant strains is one of the driving forces in their emergence and prevalence. I provided you with a peer-reviewed link that backs that up, which you are not satisfied with. You got your downvote, let it go at that.

@anongoodnurse If that isn't enough, then please feel free to raise an edit to suggest the changes you would like to see, or submit your own answer to the question.


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What kind of tortoise is this?
Can you help me to ID this tortoise? It was walking around near to my house and then my mom found it, so we'd like to know more info. Its Straight Carapace Length is about 5+ inches. Found it in mid-Mexico (Guanajuato state). Most part of the year we have a warm weather.

Where do you live?

@canadianer just edited the question.

Could you please post the number of toes on the hind legs when you have a chance? Thanks.

The front end of the plastron (the flat 'ventral' part of the shell) is hinged, so that the turtle can enclose itself almost completely, a characteristic of box turtles.

Box turtles are turtles of the genus Terrapene native to North America (United States and Mexico). They are also known as box tortoises, although box turtles are terrestrial members of the American pond turtle family (Emydidae), and not members of the tortoise family (Testudinidae). The twelve taxa which are distinguished in the genus are distributed over four species. They are largely characterized by having a domed shell, which is hinged at the bottom, allowing the animal to close its shell tightly to escape predators.

Your turtle certainly has a domed shell. There is a lot of wear and tear on the shell, but not so much on the plastron. Box turtles can live 100 years.
From the lack of coloration on the top part of the shell and the paucity of markings on the plastron, I think it is either a Three-toed Box Turtle (Terrapene carolina triunguis), or a Mexican Box Turtle. The Mexican box turtle can grow slightly larger than the Three-toed box turtle. I can't really tell them apart. Boxturtles.com might help.

Their appearance is similar to that of the Three-toed Box Turtle.

The three-toes refers to the hind feet (which can also have four toes, to make matters worse.)

Three-toed box turtles have a domed shell which grows to an average 4.5 to 5 inches in length. The record shell length for this subspecies is 7 inches. The highest part of its carapace or upper shell is more posteriorly positioned than in the other subspecies. The dorsal and limb coloration is commonly completely absent, although some dark blotches are common in adult turtles. These areas more often being a uniform olive green or tan color.

From another site:

Shy and quiet are the traits of a Three-toed Box Turtle, both in its personality and in its coloring. Unlike the bold patterning and color seen on other eastern box turtles, the color of this species is quite subdued. Occasionally there will be a Three-toed that is more brightly colored, but for the most part they are a fairly uniform olive-brown to brown or horn color.

See also Reptiles & Amphibians

Thanks for your response, will update with the number of toes as currently  later as I'm out of town but this was a really good first approach to know it.

source: Stack Exchange

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sort: votes


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Can body temperature affect the quality of sleep?
If so, how does it influence our sleep? And what can we do to improve the quality of sleep by adjesting our body tempurature?

This question is way too broad. If your question is on the last three examples, and on those examples only, it is quite answerable, but rather poorly researched. They look like assumptions - where did you read it?

@AliceD Our tutor asked us to make a presentation on it. Having searched on the internet, we think these factors may have influence on people's quality of sleep, but we are not sure.

Try sleeping in a noisy floodlit insecure environment, with people stumbling upon you all the time.

If you can make your question more specific, please do. As of now it would need a uni library to answer. Then a better question would likely be "What does not affect sleep?" :)

@AliceD Like this?

Awesome. Much better +1

Might be more on-topic on health.SE.

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Do animals' facial expressions have similar meanings to humans'?
In the following pictures, the dog seems to be smiling to the camera. People staring at these picture also tend to feel comfortable and relaxed, presumably because they think it's very happy playing with the swing.
However, my question is, is the dog really happy, or we are just (incorrectly) interpreting the dog's facial expression according to our experience used to read humans' facial expression?

Not a scientific article but a pretty good answer: http://www.smbc-comics.com/?id=3172

I have no reference, so this is not an answer, but when I was a veterinary student I was told that the dog smile as illustrated above is seen only in dogs, and is only used to humans.  It is apparently true that dogs can discriminate smiling humans from a blank face, so the leap is not completely ridiculous.

I would say no, facial expressions in humans do not generally relate to facial expressions in other animals. Even though there are some cases (as described in the comments an previous answers) that refer to domesticated animals, I do not know of any convincing evidence that the facial expressions of humans are faithfully interpreted, or even mimicked, by other animals - at least outside the group of great apes. Further, the cases arguing that (domesticated) animals can do it are often anecdotal (I am not saying wrong!). Taking an evolutionary perspective, I would not even expect it to be happening (or rather by very close relatives only, i.e. other great apes) because facial expressions as behavioural signals are part of communication and therefore often rather species-specific.
But not only that ... there is emerging evidence that facial expressions are not even interpreted uniformly in all human populations: in this article by Crivelli et al. (2016) in Front. Psychol. the authors argue to include anthropological data to cognitive studies. According to their findings, not including a human evolutionary perspective might result in strong biases. They strengthen their point by giving an example of differential interpretation of facial expressions in a Melanesian society which is described in more biological terms in PNAS [Crivelli et al. (2016)]. What they found is that adolescents of this society interpret a facial expression (gasping face) that in other societies conveys fear as a threatening and angry expression.
Generalising this means that if there is divergence in signaling by facial expressions even among human populations, I would consider it unlikely that there is a general homologous system of facial expressions among mammals. There might, however, be a trend in domesticated animals to understand human expressions and adapt behaviour according to them. It still is an extraordinary claim to infer from this that they can actually mimic these expressions, and I have not yet seen convincing evidence for that.

Get to know dogs' facial expressions and you will find that there are comparable facial expressions of a canine with that of humans.

Our cousins in the primate world share the same base facial expressions as we do, happy, sad, disgust, etc; it would make sense that other mammals are capable of facially displaying emotional registers.
However, canines can't pass the mirror test for self awareness, but chimps can. However however, it is known that dogs' oxytocin level rises when they stare into our eyes (similar for female human into her baby's eyes). Thus, if the dog is experiencing elevated feel good neurotransmitters, then a smiling face would appear to make sense.
The question is, have you seen dogs smiling in abused situations?
My other thought on this is that the smile could just be a pavlovian manifestation: you become happy shen the dog smiles, so the dog smiles more--the dog has an association of you being happy to something good happening to it, so it wants to make you happy more.
Sorry I don't have a definite answer for you, but afaik the neuroscience / psychology of dogs keeps expanding in complexity, so I would say that yes, the dog is happy.

Beautifully written answer. Please do add some links and/or sources to back up what you wrote.

This post requires references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted. Please see this meta discussion for more.

Thanks for the kind words :) most of my post came from stuff I remembered from my psychology classes at university. I would have to hunt down my old textbooks, but to anyone interested you can pick up an introductory / survey psych textbook for a penny on Amazon; check out the chapters on neurotransmitters and emotion. The dog and primate example are pretty common.
I'll have to keep in mind to get sources prior before answering further. It was kind of a spur of the moment thing ^-^ glad that it was intriguing to you!


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Did cyanobacteria commit evolutionary suicide by producing oxygen?
I heard this story from one of my friends:

Cyanobacteria can convert carbon dioxide into oxygen through
  photosynthesis, so the concentration of oxygen in the atmosphere kept
  going up over a long period after their appearance. Finally, those
  oxygen poisoned cyanobacteria through some mechanism, which
  effectively killed many of them. As a side effect, the oxygen produced
  lead to the evolution of fishes and other fantastic creatures,
  including human beings.

I wonder whether it is true. After some searching, I found that cyanobacteria can perform photosynthesis. However, I can't tell whether oxygen is poisonous to them.

By the term "suicide", one generally refers to the decision of a single individual to self-detrsuct (which you realized I suppose as you put the term in quotation marks). The kind of process you are referring to (where a population pollutes its environment to the point of threatening the persistence of the clade) is called an evolutionary suicide.

@Remi.b Thank you! I've edited the title to make it more scientific.

Oxygen is inherently a toxic substance as it is the second most reactive non-metal. However, most organisms have evolved mechanisms to counter the toxicity caused by oxygen.

@WYSIWYG Since cyanobacteria is such a primitive creature, I guess they don't know how to protect themselves from oxygen. Also, there wasn't much oxygen in the atmosphere before their existence, so I think the resistance to oxygen hasn't been vital by the time they evolved.

@SunQingyao Organisms don't think and implement strategies. They evolve to acquire traits that allow them to survive. Please read more about evolution. Understanding evolution is a good place to start.

@WYSIWYG In fact, I meant an individual cyanobacteria could still survive that environment even if it isn't equipped with resistance to oxygen, so those born with oxygen resistance (by accident) didn't have advantage over those who haven't. As a result, oxygen resistance failed to be passed to the next generation. When the oxygen in the atmosphere became poisonous/fatal, everything was too late (There wasn't enough time for another useful mutation to occur). Anyway, I'll read the materials in the link you provided :)


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Why aren't the twin organs like both the eyes, ears, hands and legs lying both sides of a human body identical?
Both the eyes are not identical in geometrical shape and size i.e. physical appearances of both the eyes of a person are different from each other. The same difference is observable in both the hands, ears.
I don't know which causes the difference in geometrical shape and size of the twin organs in the human body.
Any explanation will be greatly appreciated.

Does it help to think about it the other direction - why would they be the same?

Well, both the eyes belong to the same person and develop under apparently similar conditions but they are geometrically different. I really don't know where this geometrical difference in twin organs comes from.

"Similar", not identical.

Well, which conditions must be identical so as the twin organs become geometrically identical? Doesn't DNA or other biological change influence geometry of twin organs?

"which conditions must be identical" - All of them. Which is pretty much physically impossible. If DNA influences geometry, you'd expect less variance within an individual than between individuals. I'd be pretty confident that if you go looking for this, you'll find it for the cases you describe.

Maybe a nitpick, but the paired limbs/organs generally aren't identical, they're mirror images.  Which might have some influence on development: perhaps the most obvious is human handedness, with the preferred hand being used more.

The topic you're looking into is fluctuating asymmetry, a broad field of study.  Among the free reviews this one is a bit old but well on topic.  The general idea is that there is "developmental noise", which is opposed by mechanisms for developmental stability.  The review covers a variety of conclusions people try to read in to these studies, often about the stresses on the organism or the mechanisms by which development is "canalized" to reach a specific goal.
The nature of the noise is usually presumed rather than proven, since many different factors are presumably adding up to make small differences.  We may assume (though I'm not always sure it is true) that mRNA, protein, and signalling molecules diffuse to reach their targets, which is to say they are subject to Brownian motion with random variations in timing.  The need for multiple factors to get together for a complex process like transcription or translation means that the number of copies of a protein produced under a given circumstance will vary.  An example of this in hypertrophic cardiomyopathy has been proposed to contribute to disease progression, due to random bursts of transcription in individual heart cells affected by the disease.

Body development is a complex process in which the interaction of a huge amount of molecules and the environment give rise to the final product.
In such a complex system is not surprising that some chaotic dynamics exists, and if so, small perturbations during the process give rise to not so small difference in the final product.
What is surprising is that, even with such a big complexity, the final product (like the two eyes) is a stable state.
So I think the main question is not what make them different, but how the development process achieves to generate symmetry.

The other answers talked about how asymmetry happens. Here I say my idea on why asymmetry could be beneficial. Focusing on left and right brain lobes, you see that the difference between these lobes give new functionalities to brain and these new abilities could be beneficial during evolution of the taxa. I think asymmetry which looks like stochastic, maybe in thousands and millions of years, little by little (and some times suddenly) make new (useful and harmful) inheritable functions.

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What is the difference between Amino acids from blood and urine?
I would like to understand the difference between different tests for Amino Acids. Any blood laboratory offers amino acids tests using 3-4 methods

Blood serum
Urine Random
Urine 24 hour (all the urine samples collected in the last 24 hours)

After having tried Google and coming up empty, I have the following questions that I would like answered.

What would be the difference between testing it via each of the above methods?
What's the purpose of each of these different test methods?
Is one method better than the other? If so why?

Thank you.
Disclaimer: This question is for general knowledge purposes only. Please don't use the question or answers given as personal health advice.

Detecting protein and elevated levels of amino acids in the urine is generally a bad thing and is usually indicative of an underlying disease.
Kidneys are supposed to filter out waste products and retain metabolites that your body needs. There are many possible diseases that can cause amino acids to be detected in the urine, some as innocuous as overexertion or exposure to temperature extremes, and some as serious as Hodgkin's lymphoma, Amyloidosis, Malaria, Lupus, etc. For a more complete list see this Mayo Clinic page.
As for the blood, there are certain normal levels of amino acids found naturally in the blood. The reason for testing these levels is that certain imbalances can be indicative of different medical conditions. A doctor can use these levels to help to identify a problem that may not be noticed or may use it to diagnose a disease that you are seeking treatment for. This MedlinePlus page, has information.
Testing of Blood and Urine amino acids can and will be done in conjunction with one another in order to help narrow down the possible diagnoses that are likely.
Disclaimer: Personal medical questions and health advice are off-topic on Biology SE. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice.

Edit to address comments
"Also, based on your answer and the Mayo Clinic link, what I understand is in a healthy individual - testing amino acids from urine might give false positives?"
I think that your concept of false positive here is incorrect. A false positive for this test would be indicating higher levels of amino acid in a sample than the sensitivity and standard error for the test would allow for.
That there is a laundry list of reasons why one might find abnormal levels of amino acids only goes to the fact that the kidneys "see" the results of several metabolic processes (normal or abnormal) and urinalysis is only a single datapoint from a spectrum of data for a clinician to begin to recognize a pattern and formulate a diagnosis.
As for greater accuracy, when comparing "Urine Random" to "Urine 24 hour" I would say that the "Urine 24 hour" test is more accurate strictly from a perspective of statistics. The larger the sample size for any test, the greater the level of confidence that the results observed are not due to random chance, error, or outliers in the data.
But this is the same concept for a political poll, marketing research analysis, or medicine; larger sample size gives you a clearer picture, but it does so at an increased cost. So the single screen is there just to look for issues, possibly based on a complaint that brought you into the doctor's office, or a way of monitoring a previously diagnosed condition and/or treatment, while the time courses are done to provide a clearer understanding of what is representative for the levels in that individual.
The single test has a number of reasons why it might be anomalous. Maybe the elevator from the underground parking garage was out of order and you had to walk up several flights of stairs to the office where they were collecting the sample, so it would show an elevated result due to exertion. Or maybe your drank a liter of water before the exam and your urine is dilute, causing a false negative. So to mitigate those anomalies, you run the time course, but usually only if there is a problem suspected because of the fact that it is an increased and unnecessary cost if all other indications are that the person is healthy or the result is easily explainable due to other data collected.

"I also understand that at times they would be used in conjunction - which seems logical. What I am trying to understand is which would give more accurate 'picture'. If one is not more accurate than the other, then what would be the difference between the 'picture' acquired from a blood test and the urine test."
Each test has its own parameters and give you an independent picture, that can be used to put together a more complete whole. Their accuracy will be based on their own sensitivities and built in standard errors and one will not be more accurate than the other because comparing free amino acids in the blood versus in the urine are two different pictures with different normal outcomes.
More samples, i.e. "Urine 24 Hours" or multiple blood draws over a time course is really the only way that you will improve on the accuracy of the individual tests, for the reasons I gave above.
They also have different baselines. Blood you expect to find free amino acids and there are ranges of normal results that you would expect to find in the blood. Here, too much or too little amino acid would be an indicator of a possible problem. For urine on the other hand, one would not expect to see elevated levels of amino acids, so here, a test that indicates elevated levels of amino acids indicates that more follow up is needed.
Think of it in terms of an analogy about astronomical observation. The electromagnetic spectrum is far broader than any one instrument can detect, so astronomers/astrophysicists use different sensors; visible light, radio waves, infrared, x-ray, etc. telescopes to detect many of these different pieces of data coming from the same object to gain a better understanding of what they are studying as a whole. Each gives slightly (or very) different views of the object, all of which contribute to a more complete picture of the object as a whole.

The first sentence is incorrect. Normal urine contains a small amount of protein. Of course an excess of protein in the urine (proteinuria) could have a number of underlying causes, some of which are "bad". Though I wouldn't necessarily call a transient proteinuria from strenuous exercise a "bad thing".

@AMR - Thanks for the answer, this is not a personal health advice question. I just want to understand as a clinician (I am not a clinician) which would be more helpful. I also understand that at times they would be used in conjunction - which seems logical. What I am trying to understand is which would give more accurate 'picture'. If one is not more accurate than the other, then what would be the difference between the 'picture' acquired from a blood test and the urine test.

@AMR - Also, based on your answer and the Mayo Clinic link, what I understand is in a healthy individual - testing amino acids from urine might give false positives?

@AMR - Finally, if my question is off-topic on Biology SE, please advise where to post the question for it to be safely answered. As I mentioned this is not for 'my specific condition'. It's a general question to understand why do different tests exist to test for a the same amino acids. I have the same question for glucose (which can be tested via blood AND urine). I would like to understand the difference.

@andthereitgoes I didn't necessarily think that your question was related to a personal medical question per se, however as this question / answer may be referenced by someone trying to understand their own medical condition, I think it is better to consult with their physician than use my answer as a basis to calm their fears or fuel their concerns.

@AMR Yes, makes perfect sense. I have edited my question to display a disclaimer for the same. Thanks.


text:
Is there a plant particularly suitable for absorbing Hydrogen Sulfide
I live in an area with some open sewers and in the morning I can usually can smell the gas inside my house.
There are many plants like snake plant which improve indoor air quality but I was wondering if there are any that are particularly useful for absorbing sewer gas (hydrogen sulfide)


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How does the modern synthesis theory explain the evolution of birds from dinosaurs?
The theory of evolution claims that birds evolved from dinosaurs only by mutation, genetic drift, migration and natural selection.
However, it seems to me that wings were not selectively advantageous for dinosaurs.
Would you show me a book or a paper which explains this point in detail with academic accuracy?
Level of the book or the paper should have detailed information for an advanced reader.

An introductory course to evolutionary biology such as Understanding Evolution for example might help you.

@Remi.b I'm looking for a book or a paper (or an internet site) that explains the evolution of dinosaurs to birds in detail with accademic accuracy. Does that site you mentioned have such an account?
If yes, would you please show us a link to it?
I checked the site, but I was unable to find the one.

No the site I linked is not specific to your question. But having a better understanding of evolutionary processes in general will help you to answer the specific questions you may have (such as the one you are asking in this post).

You might want to have a look at this post to avoid potential semantic issues about what a dinosaur is.

The question is unfortunately too broad. There have been many changes from the ancestors of modern day birds and modern day birds. You should reduce your question to one specific trait and also probably precise whether you are interested in knowing the phenotypic intermediate stages or the specific genes involved in the evolution of this specific trait.

@Remi.b "The question is unfortunately too broad." Why on earth do you think a question is too broad that asks for a book or a paper on a specific subject?

@MakotoKato this is broad because one would have to explain you about phylogenetic and palaeontological methods. These are not really laboratory simulations of macroevolution but inferences drawn from what is observed from the remains of these organisms.

@MakotoKato You will hopefully find this popular article interesting and useful: How Dinosaurs Shrank and Became Birds (it has also been reprinted in Scientific American)

@WYSIWYG You talk as if you know the answer.
In any case, I'm asking for a book or paper that answers my question.
What's wrong with it?

Try asking about a particular aspect such what you seem to be interested in,  the early evolution of wings and flight in maniraptorans. the entire process of birds evolving from dinosaurs would fill several large books, hence too broad.

First of all, dinosaurs did not evolve to birds. A better way of saying it is that modern birds evolved from a particular type of dinosaur. That, however, is not the same as the blanket statement "dinosaurs evolved to birds". The latter implies that dinosaurs somehow morphed into birds and stopped being dinosaurs. What actually happens is that a species starts changing and, eventually, a sub-population of that species has changed so much that we call it a new species. It is a subtle distinction but important.
As for a specific paper, no we don't have anything like that for any specific examples. What we have is a huge collection of observations all of which point to the process of speciation occurring via the processes of mutation and natural selection. It's impossible to know the precise series of mutations that led to the creation of a new species for a variety of reasons.
All we have is the current species. If we know an ancestor, we can deduce a possible path that leads from the genome of the ancestor to the genome of the target species but we have no way of knowing whether that specific path was followed. For an analogy, consider computers. If I were to give you a modern desktop PC and one of the first computers:

You might be able to guess certain changes that were made to the old ones in order to build something like the new ones but would you be able to figure out every single step along the way? How would you detect all the attempts that failed? The ideas that didn't pan out? Would you be able to infer the existence of floppy disks, for example?
The same problem applies to species. It is essentially impossible to infer the precise series of mutations that led species B to split from species A. Especially since, usually, this happens through species A.1, A.2, A.2.1, A.3 etc, and all we have is species B.
Add to that the fact that evolution is not a linear process, there are many dead ends (way more than in computers), and the story gets even harder to understand. This graphic illustrates it quite well:

Obviously, if you have the first red dot on the far left and the last blue on on the far right, it will be impossible to infer the entire evolutionary history linking these species.
So, with this in mind, given that dinosaurs and birds share a common ancestor, it is essentially impossible to get the full, true, path that led from that ancestor to either dinosaurs or birds. More importantly, as shown in the image above, dinosaurs did not evolve into birds in the first place so the question is moot.

If the "common ancestor" was a dinosaur, then it would not be incorrect to suggest that birds evolved from dinosaurs.

Could you give me a clue how reptilians(I hope the nomenclature is more accurate than dinosaurs),
for example, grew wings and lost most of bone marrows?
It seems to me that those features are not advantageous for them to survive unless they were able to fly.

@vervet as far as I know, that's not the case. I may be wrong though.

@MakotoKato well, for a clue, have a look at this answer about bats. Look at the gliding mice. You can imagine similar intermediate steps.

@terdon "First of all, dinosaurs did not evolve to birds. That is a common misconception. You might want to have a look at the answers here. What you're probably thinking of is that modern birds and dinosaurs share a common ancestor."
I beg to disagree.
http://evolution.berkeley.edu/evolibrary/article/evograms_06
"The discovery that birds evolved from small carnivorous dinosaurs of the Late Jurassic"

@MakotoKato thanks for the link. I hadn't expressed myself clearly. My main point was that while modern birds may well be descendants of certain dinosaurs, you can't say that dinosaurs evolved to birds. Only that birds evolved from dinosaurs. The first statement implies that dinosaurs were replaced by birds rather than simply that they gave rise to them.

@MakotoKato you greatly misunderstand evolution when you presuppose that all the traits that exist have to be selectively beneficial. We know that the vast majority of new mutations are near-neutral and selection can be quite weak. Also, a trait may simply piggyback on other beneficial traits - take a gene for resistance to a pathogen, for instance and a gene for fur colour in a predator free environment where the disease is selective; if the two traits emerge in the same lineage fur colour will be selected for just because disease resistance is selected for.

@AnkurChakravarthy "We know that the vast majority of new mutations are near-neutral and selection can be quite weak." Suppose wings were selectively neutral for dinosaurs. Then the probability of the evolution of birds from dinosaurs would be very very very small. It would be like a monky typing entire Shakespeare's Hamlet.

@MakotoKato perhaps, but that wouldn't mean it couldn't happen. More importantly, wings would never be selectively neutral. They immediately open up an entire new ecological niche and all sorts of new defensive options. They would most certainly not be neutral.

@terdon "but that wouldn't mean it couldn't happen."
In realty, no, it could never happen.
"wings would never be selectively neutral."
If they were selectively negative, birds would not exist.
The only option is that they were selectively positive.
But this argument is flawed because it assumes that the theory is correct.

Um no,  firstly , depending on population size even deleterious alleles can be fixed by drift.
The other thing is neutral traits can be fixed as if under selection due to chromosomal linkage with another trait that is subject to selection ; this effect is called genetic hitchhiking.
There is no evidence that wings at all stages had to be of adaptive benefit for the evolution of birds to be possible. The notion that birds couldn't have evolved if wings weren't selected for is wrong.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1459830/

That wings could be selected for, on the other hand, also enjoys support; one only needs to look at the rapid diversification of Pterosaur lineages for  a period of nearly 75 million years, and even after that Pterosaur diversity did not drop off a cliff until near the end of the cretaceous.

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


text:
Saturation vapor pressure effect on human body
I found this calculator:
http://www.decatur.de/javascript/dew/
It calculates the dew point based on temperature and humidity.
In the result it is mentioned the saturation vapor pressure.
I barely understand the notions of vapor pressure, but I read somewhere that divers are rising back to water surface slowly, because the vapor pressure has negative effects on blood vessels, which can pop.
My goal is to find if a similar situation  (like divers' one) can be encountered by runners who are exercising when the vapor pressure is very high.
Thoughts?
Edit:
Is it possible to experience the effects of diving 10 meters in water, at surface with the contribution of climate factors (humidity, temperature and atmospheric pressure)?

Welcome to Biology and thanks for your question. Divers encounter problems with gas bubbles, known as 'the bends', divers' disease, or Caisson disease. It has to do with gas pressures under a column of water versus those at the surface. Nitrogen accumulates at low depths, oxygen starts to accumulate at ~30 m etc etc. It has little, if anything to do with cells popping afaik. Further and quite frankly, I don't understand your question... Could you add references or sources to your claims?

If the divers then rise up back to the surface too quickly, these gases will be forced out of their dissolved form and form bubbles in the blood vessels. These gas bubbles can then cause the blood vessels to pop, causing much physical pain and serious medical issues.  << An excerpt from http://chemwiki.ucdavis.edu/Physical_Chemistry/Physical_Properties_of_Matter/Phases_of_Matter/Liquids/Vapor_Pressure .My question is, is it possible to replicate the situation of divers by a person who is running in certain weather conditions?

Your question said "blood cells." The reference you give says "blood vessels." Blood vessels are made of endothelial cells, and the gas bubbles don't rupture the cells, it breaks the junctions between the cells causing blood to leak into the surrounding tissue. If the blood vessel that bursts happens to be in the brain, then that is a stroke and there is a good chance the person will die unless the rupture can be repaired. While it is possible that a person's own (high) blood pressure could cause a small capillary to rupture, variations in normal atmospheric pressure will not do it.

Thanks @AMR So, if I understand correctly, if the atmospheric pressure is very high, maybe above 800 mmHg, the humidity is 100%, temperature above 35 degrees Celsius and a person is exercising at lactate threshold, the diver's conditions are almost similar. Is that correct?

The problem is not the pressure itself, it is a rapid change in pressure.


text:
electrotonic spread and screening
(In physics.stack I have been suggested to post my question also here.)
In the classical theory of passive neurons (where the action potential is not yet excited), the voltage is successfully described by cable theory. The (unmyelinated) axon is modeled as a series of cylindrical sections in series. Each section is described by an electric circuit (in 1D) with an axial resistance, and the membrane is modeled as a capacitor.
If charges are injected at one end of the cylinder, the "cable equation" gives the transmembrane voltage at steady-state in the shape of an exponentially decreasing function of space. Here the characteristic 1/e decay length of the voltage can be long in large axons, of the order of mm.
Question
My question is about the apparent lack of charge screening in this picture. At physiological conditions (where ions and counter-ions are present), I'd expect that an excess of charge, like the one injected by a micro-pipette, or generated by the opening of channels, is screened very quickly (microseconds), so a few Debye-lengths (nm) apart, the voltage should not be seen.
How can the theory and experiments show a voltage that persists at millimeter distances at physiological conditions where screening should be present?
EDIT from a comment:
The electrotonic transmembrane potential is exponentially decreasing along the membrane. If we assume one side isopotential (say the interior), the other side should then have a voltage that decreases along the membrane. So measuring the voltage on two points along the membrane, one should see a drop in voltage, if the points are distant enough. Therefore on that side there is a current, and the charges on that side are not screened.
Is this description correct?

In biological membranes, the primary physics principle resisting change in voltage is described by capacitance of the membrane, which is a key aspect of the cable equations. If you model some instantaneous change in charge (not particularly biological, but something like it is possible using an amplifier in patch-clamp electrophysiology), the change in membrane potential will be smoothed by the membrane capacitance.
When people talk about voltages in biological systems, they're talking about an electrical potential difference across the membrane, not measuring within nanometers inside the cell. Yes, if you somehow placed two sensors nanometers apart in the cell you'd have some difficulty measuring a voltage between them - for practical intents you can consider the intracellular space to be isopotential over the distances relevant to molecules.
Thinking about other ways to phrase this: maybe it will make sense to you to think about a distinction between charge of a solution and a particle (e.g., a single ion in that solution). When you have more positive than negative ions on one side of a membrane compared to the other, you're going to have a voltage where it's more energetically favorable for positive charge to move on the negative side than vice-versa. Charge-screening refers to how the total charge of the extra positive ions (or lack of negative ions) distributes in solution, such that it's not like you have "islands" of positivity on the positive side around each positive ion (as long as you're viewing from outside Debye lengths), but rather the charge is still somewhere in the solution when you measure compared to the other side - that's the membrane voltage. Note that when you look at the equation for voltage over a capacitor:
V = Q/C
the equation just involves the charge and the capacitance, not the specific locations of the charges.

thank you for your answer. The electrotonic (transmembrane) potential is exponentially decreasing along the membrane. If we assume one side isopotential (you suggest the inside one), the other side should have a voltage that decreases along the membrane. So your two point measurement should see a drop in voltage, if the points are distant enough. Therefore on that side there is a current, and the charges on that side are not screened? Does this sound correct?

@scrx2 No, it doesn't sound correct, when I'm talking about being isopotential I mean over the short distances where charge screening is relevant. You're not appreciating that charges can't move across the membrane freely, where the actual membrane potential is realized.

Maybe here's a different way to think about it: you have net 10 charges on one side of the membrane, and net 10 on the other. Now you move one across so you have 9 charges on 1 side and 11 on the other. If charges now cannot move across the membrane, how would you arrange those charges in space on each side such that there is no voltage across the membrane?

yes, there will be a voltage difference across the membrane, following an exponential profile along the membrane (say X). But, because of this exponential profile in X, there should be a potential difference also along X. Along X, as an electrical resistance is present, there will be a current. Do you agree?

Are you saying that the extra charge brought, by say one ion pump, from one side to the other cannot be screened? I'd agree

So measuring the voltage on two points along the membrane, one should see a drop in voltage, if the points are distant enough. Therefore on that side, there is a current, and the charges on that side are not screened.

You are correct that in theory along an axon membrane for example, the decrease in voltage is exponential in space. However, you need to consider saltatory conduction. There, the action potential propagation occurs from one node of Ranvier to the next. This mechanism increases the conduction velocity of action potentials and also decreases the exponential voltage drop.

How can the theory and experiments show a voltage that persists at millimeter distances at physiological conditions where screening should be present?

The uninsulated nodes of Ranvier are the only places along the axon where ions are exchanged across the axon membrane, regenerating the action potential between regions of the axon that are insulated by myelin, unlike electrical conduction in a simple circuit. That's where cable theory falls short.
The saltatory process also allows for maintaining voltages along a vast distance of biomolecular membranes. In addition to increasing the speed of the nerve impulse, the myelin sheath helps in reducing energy expenditure over the axon membrane as a whole, because the amount of sodium and potassium ions that need to be pumped to bring the concentrations back to the resting state following each action potential is decreased. Also, keep in mind that the axon potential propagation is unidirectional because the absolute refractory period (of the channels) prevents the initiation of an action potential in a region of the membrane that has just produced an action potential.
This literature might touch on the physics in more detail: The Membrane Potential and its Representation by a Constant Electric Field in Computer Simulations

thank you for your answer. I'm specifically interested in passive conditions, under the firing threshold, to forget the voltage-dependent channels. And as you correctly mention it, I'd add that I'd like to consider unmyelinated axons. Thank you for the ref too, seems interesting!

Under the firing threshold, the ion exchange over the membrane is in a steady-state model. In such physiological conditions, a couple of important physical principles need to be considered: The electrochemical potential is NOT in equilibrium. Meaning that Nernst-potentials and cable equations fall short! Meaning a steady-state model is more accurate. In this case, the Goldman-potential or Goldman equation is used to describe the state of no net flow of ions.

But even with this model a couple of assumptions are made:

Steady-stateI: on-concentration are in
steady-state dc/dt=0. The membrane
potential Vm is constant (dV/dt=0) and there
is no net current across the membrane (I=0).
The membrane has a thickness d and is physically homogeneous
The different ion fluxes are uncoupled.
We have a distribution equilibrium for an ion i between the solution and membrane interface.
Simplification: Only monovalent ions.
Flux in the membrane is conservative, nothing gets lost.

I feel like you might want more sophisticated mathematical models so check out Goldman–Hodgkin–Katz flux equation, Hindmarsh–Rose model, Hodgkin–Huxley model, Morris–Lecar model


text:
Unknown animal - What could it be?
It's the first time I use this website and I really need help
because I'm totally stuck
Now I'm in school, but I'm trying to prepare for the Olympics
During the preparation, I found the issue on the anatomy of the animals, but it's something new for me - I can't even determine what it is!

What kind of animal is it? Could you determine some, the most vital and major of highlighted points? If you can help me to determine the kind of it, i will be able to use more specific books to find out.
I will be very grateful for any help!

Click on edit and insert in your edit all the terms for the numbers.

@SANBIsamples - that's part of the question, it's homework

okay @AliceD what's unhappy with homework?

@SANBIsamples, there's nothing that's unhappy, but by the looks of it you asked for clarification, but OP asks to have the numbers explained. In other words, you re-asked the question.

@AliceD I consider your homework question closed.

I have no idea what animal this is, perhaps a mussel?

Assuming you mean the Biology Olympiad, I would hazard a guess that this is a deshelled snail, judging from the visible helix in the middle and right images.

This looks like a very specific picture taken from a lab or lecture notes. Unless you were in the lab or lecture, or have access to the notes, it will be tough. Comments above suggested snail and mussel, which were also my first two ideas but it's really too tough to tell.

or a turtle fetus?

The animal is very suggestive for Dog whelk-like mollusc removed from its shell.
I try to mark the organs, do not rely on these marks as an absolut.

Testis
Renal vein
Gill
Mantle
Prostate
Osphradium

10 and others - digestive and reproductive systems, cannot mark precisely.

Digestive gland

source for comparing etc


text:
Can galls be formed from mutualistic relationships?
According to Wikipedia, galls (cecidia) are formed by parasitic insects and mites like gall wasps (Neuroterus albipes). At some metamorphic stage, these organisms alter cell division processes in meristematic tissues of their host plants, which creates a tumour on (typically) the surface of leaves, branches or roots. These organisms use the galls as their habitat and/or food source (exploiting the sugars present).
However, I also know that bullhorn acacia and ants form an interspecific mutualistic relationship (with galls), so apparently galls don't need to be parasitic. Are there any other specific plant-insect pairs that have the same type of mutualistic gall relationship as the acacia-ant system?

Pardon the initial link and thank you for clarifying the question

Thanks for fixing it. I'll remove the now obsolete comment.

From what I know of ant-Acacia mutualisms, I've never heard of an ant gall in an Acacia. The link in your question also never mentions a gall. You've likely confused either domatia or Beltian bodies as a gall. Both differ greatly from galls in that domatia or Beltian bodies are created by the plant and not by the insect.
Domatia are small plant-made chambers that house mutualistic insects (though are often invaded by non-mutualists).
Beltian bodies are a type of food body (or plant-made structures containing nutritional substances (often high in protein) that attract a mutualist species of ants in Acacia).
See here or here for more info about galls.
To answer your overarching question of whether there are mutualistic galls, I would have to say no. I do not know of any instances of which this is the case. Further, galls are inherently parasitic (not mutualistic). Even if the swollen cells do not interfere with normal plant function (e.g., as is common in Solidago spp.)1, the parasitic insect (or other arthropod) is still required to chew its way out of the gall. Last I checked, chewing on your host's tissues is never very mutualistic.

 1: Crutsinger, G.M., Habenicht, M.N., Classen, A.T., Schweitzer, J.A. and Sanders, N.J., 2008. Galling by Rhopalomyia solidaginis alters Solidago altissima architecture and litter nutrient dynamics in an old-field ecosystem. Plant and soil, 303(1-2), pp.95-103.

Yes, pollinating fig wasps are gall inducing and mutualistic at the same time, and actually essential for the pollination of figs (see e.g Martinson et al., 2015). During the very intricate mutualism, fig wasps deposit eggs in some of the flowers and leave others. The flowers with eggs and later larvae will develop into galls that will produce new wasps but no seeds, while the flowers that lack wasp larvae will produce seeds. However, the hatched females that leave the figs will pick up pollen before leaving, and are essentially the only vector for cross pollinations between fig plants.
(with the aim of expanding the answer later...)

I do not believe that galls are categorically non-mutualistic. However, as noted above, ant domatia (of acacia at least) are not galls, the trees produce them in the absence of ants. However, the size and number of domatia seems to be mildly inducible by the presence of their symbiotic ants.
But back to galls as mutualistic, my argument is that seemingly purely parasitic/herbivorous galls may also provide indirect fitness benefits to their host through their affect on the endophytic community. There is a vastly underappreciated universe of endyphytes, many are commensal and benign, but there undoubtedly parasites among them, and perhaps their predators as well, qualifying those endophytes as 'mutualists', and thus there are nested ecological interactions in many wild plants which are not apparent when we zoom in on two characters in the whole scene. Insects introduce certain hormonal factors, antimicrobials, and other chemicals which directly affect the dynamics of these endophyte communities. Basically the parasite benefits from keeping its host alive, and may provide immune function to its host in order to keep its food source alive longer, increasing the fitness of both the gall-maker and the host plant. Thus, from a somewhat game theory, lesser-of-two-evils kind of argument, this would qualify an apparent herbivore (a gall-making insect) as a mutualist under certain conditions.

Welcome to Biology.SE! Your answer is much more likely to receive a favorable response if you [edit] it to be based on published research rather than personal speculation and included supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and is thus off-topic for this site. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!


text:
Found this bug in my apartment in New York. Does anyone know what it is?

It was around 2-4 mm in length.


text:
Why do we urinate more often in winter compaired to summer?
I have been thinking of this question for a long time, but I do not seem to find an answer yet. Is there a hormonal change in our body during winter due to which we have to run to toilet often?

Is this really the case and not just observation bias? It is possibly that it is connected to more sweating in the summer - the body produces higher concentrated urine then to save water.

Is this a well-known phenomenon that and general to others? As in, is there evidence for this pattern?

I posted my answer @user28194. Hope you find it useful :)

Who exactly is 'we' here?  I don't, at least to any noticable degree, though I admit to not keeping detailed records of frequency/volume.

Istead of counting your volume why dont you answer the Q. I had asked the Q.because it is generally seen in many people. You may be an exception case but a lot of people are having this probem.

It's a problem? Seems like a solution.

@user28194 If "a lot of people are having this probem [sic]", then surely you can find a scientific citation for this phenomenon? Saying that "it is generally seen in many people" is not proof, it is anecdotal evidence at best. Also, you would do well to stop insulting people and demanding answers. You don't have a right to have your question answered. We are all volunteers here, and answer if and when we feel like it.

There is no 100 % sure answer for this as, obviously, nobody is that much interested in studying about urination. But there are some theories, of which the most popular and accepted one is cold diuresis.

Cold-induced diuresis, or cold diuresis, is a phenomenon that occurs in humans after exposure to a hypothermic environment, usually during mild to moderate hypothermia.

According to this theory, what exactly happens is this (I'll explain in steps for better understanding):

When your body senses cold or low temperature of environment, it constricts the blood vessels near your skin and external organs and restricts your blood to the inner core of your body to maintain its temperature.
Thus, it causes the blood pressure to increase as there is same amount of blood in lesser volume.
This induces negative feedback on ADH (a vasoconstrictor) i.e. its secretion is reduced.
Now when blood vessels in kidney get proper amount of blood (as blood vessels aren't constricted now), they sense high blood pressure and try to reduce it as soon as possible.
So they transfer more amount of water from blood to bladder which fills the bladder more quickly and causes an urge to urinate.
Thus, we urinate more in colder climate.

There are some more theories related to it too, but they aren't as popular. According to another theory, when we are exposed to cold weather, aquaporins are inhibited around the body, making it impossible for water to be taken in by cells, leaving a lot more of it in the blood. Again, the body will try to balance that pressure, pulling water from the blood and storing it in the bladder. You can get a more frank and interactive explanation here.

So i am not wrong completely...ADH is responsible.

Yeah it is responsible, but not how you thought it to be ;)

@GerardoFurtado yeah right, but I said so as its secretion is induced from kidneys. I'll correct that, thx.

I think that due to cold temperature the hormone ADH cannot function well. As in low temperature the enzymes becomes less active. So as the ADH hormone is not working well the suger concentration will increase in our blood due to which more amount of water will transfer from our cell to the blood stream. And this excess water will be removed by the kidney and result in polyurea.

First: What is ADH? Then: Although enzymes do have a lower productivity when it is colder, this plays no role here. The outside temperature does not influence your body temperature (at least mostly) so this does not play a role.

ADH is the antideuratichormone or anti diabetic hormone.

It would be good to edit your answer, so people who are not familiar with the topic can understand this.

Well its anti-diuretic hormone (i.e. unrelated to sugar control) if that wasn't a typo error. The reason is actually different, I'll post an answer soon.

Ok..i am looking forword to you answer.@another'Homo sapien'


text:
I know why phototaxis happens but why did those bees die?
There is a tube light in front of my veranda. This is just spring. So at night when I turn on the tube light many bees gather around the tube for phototaxis. But in the morning I see many of them are lying dead on the floor.
Why does this happen?

Are you sure they are bees? You should post a picture of the insect that you are talking about. Some insects actually have a short adult lifespan.


text:
At what temperature do human bones disintegrate?
I know, the human skin can get damaged as quickly as 2 seconds, when exposed to temperature above 80 Celsius.
However, what about human bones, say the skull?
For example, when you cook a meal, at great temperature, the chicken bones, still stay hard and intact, that's why I am asking.

Boiling point of hydroxyapatite is around 1500°C so you will need this temperature to make bone literally evaporate.
Prolonged exposure to lower temperature (like reference in other answer 220°C) will break collagen and make bones weak and extremely fragile.

While this answer shows that collagen denatures at 220°C under dry heat, it is possible to break down the collagen in bones at much lower temperatures by means of hot hydrolysis.
This hydrolysis can be accelerated by use of either strong bases or acids (as shown in this paper), which help to break down the peptide bonds between the collagen and release the calcium phosphate deposits. Once the matrix is destroyed, the bone quickly loses its strength.

The mechanical properties of bone (like Elastic modulus) are generally dependent on a protein called collagen and its cross links. According to this paper, collagen denatures at temperatures around 220 degrees Celsius in a dehydrated environment after gradual heating at transitional temperature intervals.

When you cook a meal, at great temperature, the chicken bones, still stay hard and intact.

The typical (and of course recommended) temperatures for cooking poultry (like chicken) are below 100 degrees Celsius. I think this is why chicken bones are usually still hard after cooking as they normally become fragile after collagen denatures.


text:
How to keep activated sludge viable for a week?
I am working in biological waste water treatment and I need to collect some activated sludge samples and have them characterized through different methods. The characterization will take from a few days to a week. How do I keep the sludge viable in this time? How do I make sure the bacteria do not die?

What about cooling these samples to 4°C?

I though about that as well, but ... I do not know if it is enough. I was thinking about aerating them and feeding some... yeast extract now and then? I don't know. That;s why I am asking the experts. :D

@Pompilia activated sludge would have different kinds of microbes and the general yeast-extract based media may not be suitable for all the microbes. Therefore, I think 4°C cooling may be a better option.

@WYSIWYG It is also the simplest method, so I'm fine with that.
Let's see if someone suggests something else.
Thanks!

Have a look at this review: http://www.sciencedirect.com/science/book/9780123914538, it discusses the issue of mass-producing organisms in a more general sense (i.e. not just bacteria)


text:
Why do cats meow but lions and tigers roar?
So as far as I know the cat animals are related to each other by evolution. (Please correct me on this if I am wrong?)
How come the big cats; lions, tigers et.c. roar but smaller cats like house cats meow?
Has the evolution of meowing contra roaring been backtracked?
Is it possible to tell from the anatomy of a cat and a lion what differences cause the meowing and the roaring? Is there some peculiarities in the design of their voice boxes which cause the differences in sounds?

They have different vocal cords, differently-shaped pharynx. I would imagine that is all that explains the difference in sound. As to mewing versus roaring, the vocalizations you reference are not applied to similar sithations.  I wonder if there are videos of baby lions mewing or making similar sounds to get their monther's attention?

OMG you are right. I could youtube it. meowing lion cubs.

tiger kittens seem to meow. source: https://www.youtube.com/watch?v=nX6XnIxPqO0

Also, cats will yowl, which (to my ear, anyway) isn't that much different from a roar, given the smaller size/higher pitch of the cat/.


text:
Discrepancy in time for genetic differences between human and chimpanzee to accumulate
Genetic differences between human and chimpanzee include ~50,000 amino acid changes, ~30,000,000 point mutations in non-coding sequences, and millions of insertions, deletions, inversions, genomic rearrangements, and transposable element movements [1]. The vast majority of these genetic changes are neutral [2] [3]. For neutral mutations, the expected number of generations required to reach fixation in the population is the reciprocal of the mutation rate per site per generation [4]. This holds irrespective of selection at other linked loci, changes in population size, or almost any other conceivable complication [4]. The human mutation rate, μ, is ~10-8 per site per generation [5]. Although μ can be orders of magnitude greater at certain sites, the fact that, as cited above, millions of neutral mutations occurred in the human line since its divergence from the chimpanzee line indicates that at least thousands of mutations occurred at the average rate of 10-8 per site per generation. Since the expected number of generations required for any one of these mutations to reach fixation in the population is the reciprocal of μ, this number equals ~108 generations. Since a generation is ~20 years for humans [5], the time required for any one of these thousands of neutral mutations to reach fixation is ~109 years.
According to the currently-known fossil record, the human line diverged from the chimpanzee line between 6 and 8 million years ago [7].
How is this major discrepancy between population genetics and the fossil record to be reconciled?
References
[1] Chimpanzee Sequencing and Analysis Consortium. Initial sequence of the chimpanzee genome and comparison with the human genome. Nature 437, 69–87 (2005)
[2] Harris, E. E. Non-adaptive processes in primate and human evolution. Am. J. Phys. Anthropol. 143 (Suppl. 51), 13–45 (2010)
[3] Vallender, E. J., Mekel-Bobrov, N. & Lahn, B. T. Genetic basis of human brain evolution. Trends Neurosci. 31, 637–644 (2008)
[4] Lanfear et al, Population size and the rate of evolution.  Trends in Ecology & Evolution, January 2014, Vol. 29, No. 1, Pages 33-42
[5] Kong, A. et al. Rate of de novo mutations and the importance of father’s age to disease risk. Nature 488, 471–475 (2012)
[6] Walker, R. et al. Growth rates and life histories in twenty-two small-scale societies. Am. J. Hum. Biol. 18, 295–311 (2006)
[7] Levin, N. Annual Review of Earth and Planetary Sciences, 43: 405-429 (2015)

I mean 10 raised to the 8th power.

Oh ok.... you can replace 108 by $10^8$ and 10-8 by $10^{-8}$ for a much better formatting (don't forget the dollar signs). Just use the edit button to edit that.

HTML markup is much easier to remember — 108 for 10 to the power 8 (won't show in a comment). Use  for subscripts. And that's what is being rendered by your browser.

Good literature work here and good question +1! In short, your main mistake was that you based your calculations on a single site and not on the whole genome. More info below.
Genome-wide vs sites specific mutation rate
The statistic of $10^8$ generations that you computed is the average rate of fixation of new neutral mutations per site. As considered the genome-wide statistic between humans and chimpanzee, you have to scale your predictions up to the entire genome. There are about $3 \cdot 10^{9}$ nucleotides in either the human of the chimp genome. That would result in a genome-wide mutation rate of $U ≈ 2 * 10^9 \cdot 10^{-8} = 20$  (the two is because mammals are diploids). Hence, the rate of fixation of 0.05 generation.
So, the expected time it would take for $30 \cdot 10^6$ new mutations to fix would be $30 \cdot 10^6 \cdot 0.05 = 15 \cdot 10^5$ generations. Because, such mutation can happen in either lineage (humans or chimps), we have to divide this number of 2 leading to $7.5 \cdot 10^5$. With a generation time of 20 years, that would take $1.5 \cdot 10^7$ years or 15 million years.
15 million years? Why not 6-8 million years as expected from fossil records?
Most of the discrepancy is probably due to vague approximation made in the computation. For example, you assumed a mutation rate of $10^{-8}$ while in reality, the average mutation rate is rather twice as large (Nachman et al., 2000, Kong et al., 2012, Wang et al., 2012, Rahbari et al. 2016).
Doubling this mutation rate would divide by 2 our expectation of 15 million years leading to an expectation of 7.5 million years that perfectly match the fossil records!
There is however another source that may cause an overestimation of the time needed... You assumed the absence of incomplete lineage sorting or in similar words, you assumed that the standing genetic variance in the ancestral population negligibly affected divergence among the two lineages. However, these discussions are for another time!

And you are assuming that the mutation rates stay stable over that many generations, which they probably don't.

@Nicolai I am not sure how fast the mutation rate evolves but to the level of approximation used here and given that we're dealing with genome-wide averages only, my intuition is that such an assumption is rather negligible.

You  have to half your estimated time because chimps have been evolving for that same amount of time not just humans. You are measuring two separate descendant lineages ,not comparing humans to their ancestor. Generations are also shorter for chimps, and presumably our distant ancestors.

@John I already did. Check out the sentence Because, such mutation can happen in either lineage, we have to divide this number of 2 leading to [..] I have now clarified what I meant by "either lineage".

@Remi.b, I see, I assumed you were referring to the incorrect mutation rate, Thanks for the clarification.

The correction for the OP's biased estimate of the mutation rate is in the last section (15 million years? Why not 6-8 million years as expected from fossil records?)

@lenantak Did the answer answered your question? Please let us know if not. If you think it did, you can click on the checkmark next to the answer.

20 years seems rather too long a generation time for both humans and chimps.

@jamesqf From OECD.org, In most OECD countries, the average age at which women give birth now stands at 30 or above [..]. I don't mean to claim that OECD countries are representative of all countries, and certainly not representative of our ancestors. Chimps only mature at about 15 years of age and then have only one child every 5 or 6 years. So, using 20 years felt like not too an awful choice but please, if you can come up with some references, I'd happily change this 20 to someone more accurate.


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Is it possible to breed neanderthals through selective breeding?
I've heard most non-subsaharan africans have neanderthal DNA with it being more prevalent in northern regions, that sometimes 1-4% of the DNA has neanderthal origins.
Speaking strictly scientifically, would it be possible through selective breeding to breed an individual where the majority of the DNA is neanderthal?

No, it is not. As you said only 1-4% of non-subsaharan africans' genome is from Neanderthal and it is more or less the same sequences. The entire Neanderthal genome is not present in modern day humans, it is only a small set of sequences.

only 1-4% of non-subsaharan africans' genome is from Neanderthal and it is more or less the same sequences More "more" than "less". A 2014 study Resurrecting Surviving Neandertal Lineages from Modern Human Genomes identified around 20% of the Neandertal genome out of just 665 modern humans; presumably a larger and more varied population would pull out more than 20%. Probably somewhat less than half the original genome, though.

I'm more than a little puzzled here, since numerous sources state that humans share about 96% of their genome with chimpanzees.  (Or 99% per this: https://www.sciencemag.org/news/2012/06/bonobos-join-chimps-closest-human-relatives )  It would seem that Neanderthals ought to share at least that much with modern humans, no?

Do apes and humans share 99% of DNA or 99% of genes? What is the difference? (particularly the answer by @rg255).  Summary, the Neanderthal genome in humans is alleles while the >99% similarity is in terms of DNA.

Selective breeding will select for genetics that are already present in your population, but won't introduce new DNA sequences that aren't carried by any of the population members. It would technically be possible if everyone carried a different 1-4% of the Neanderthal genome, since it would be possible to reconstruct the full Neanderthal genome by creative combinations of DNA that exists in the population. That's not the case, though, it will be a fairly consistent set of regions for which you can substitute Neanderthal DNA for homo sapien DNA and still have a functional human.
So no, this isn't possible - the complete genome of Neanderthals doesn't exist split among the human population, so it can't be refined to be complete through selective breeding.

I agree with the two previous posts, but they are a bit light on references / evidence, so I thought I'd throw my two cents in.
The answer it seems is most likely no. As others have alluded to, in order to 'breed' a Neanderthal selectively from modern humans, it would need to be the cases that the entire ~3.1Gb of the Neanderthal genome would need to be represented in modern humans.
Methods exist which are able to identify the specific segments in modern individuals which are derived from the Neanderthal admixture event. One recent example is IBDmix [1] from Josh Akey's group in Princeton. They inferred 110.98Gb in total across 2504 worldwide individuals from the 1000 genomes reference panel, which works out as an average at about 0.04 Gb per individual, or 1.3% on average across all individuals. There is a substantial amount of variation between population, with Africans having less Neanderthal ancestry than non-Africans.
However, when you collapse down the Neanderthal segments into non-overlapping regions, it turns out we can only identify 1.29 Gb of unique segments. This means that we have 1.29Gb / 3.1Gb = ~40% of the entire Neanderthal genome present in modern day humans. A similar, older study inferred a slightly smaller amount of 1.1Gb [2]. It is very unlikely this figure will change a large amount in the future.
This is why 'breeding' such an individual with 100% Neanderthal  DNA would be impossible; around 60% of that ancestry has been totally lost from modern humans, either through genetic drift or purifying selection.
References
[1]: Chen, Lu, et al. "Identifying and interpreting apparent Neanderthal ancestry in African individuals." Cell 180.4 (2020): 677-687.
[2]: Sankararaman, Sriram, et al. "The genomic landscape of Neanderthal ancestry in present-day humans." Nature 507.7492 (2014): 354-357.


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Bit by unidentifiable spider
Live in South Florida and was outside cleaning and believe I got bit by this spider.
It is painful and need help identifying.

You need to provide a photo and an approximate size

The only North American spider species of concern are the black widow (Latrodectus mactans) and brown recluse (Loxosceles reclusa). Unfortunately, these both occur in south Florida - but so do many other spiders.
I'm guessing the spider that bit you wasn't one of these two, for the following reasons:

Black widows are widely identifiable by the general public, and you'd likely have recognized that by the highly characteristic red hourglass on black.
Black widow bites hurt a lot. It takes an hour or so for the pain to really set in, but you'd know it was a serious problem.
Brown recluse bites are rare, despite their wide range, and tend to happen indoors.

If you were bitten by anything else, the odds are incredibly high that the worst you'll deal with is a little red bump of irritation that goes away shortly.


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Can HIV be transmitted via mosquitos?
It is known that HIV is usually transmitted by direct blood or body fluid contact between an infected individual and a healthy person (like blood transfusion or needle sharing):
Suppose a mosquito bites an individual suffering from AIDS and in the process sucks up some T cells infected with HIV along with RBCs. Then it bites another person not suffering from the disease, and transfers these infected T cells. Isn't there a high probability of the second individual contracting HIV?

Well.. that would probably be a much more important vector of transmission than sex or blood transfer, especially in the right parts of Africa. The number of infected there is rather big, so if mosquitoes were able to routinely transmit the virus, almost everyone would be infected by now. Of course, this is just a relatively weak conjencture, but it's a decent first guess.

@Luaan: And yet, not everyone in Africa has Malaria...

@eggyal That's not a bad argument. I suppose it's a combination of natural resistance, improved artificial defenses and perhaps the past mass deployments of insecticides. And of course, not all of Africa has massive mosquito trouble that's why I said "especially in the right parts of Africa". More importantly, malaria isn't necessarily terminal, and the people who survive are immune to further infection - and when it is terminal, it kills quite quickly. On the other hand, AIDS is a very prolonged infection. If you're dead, you're no longer part of the statistic :) http://tinyurl.com/yolhob

No, this is not possible. There are a few reasons for that, but most important are that the only thing a mosquito injects is its own saliva, while the blood is sucked into the stomach where it is digested.
To be able to infect other people HIV would need to be able to leave the gut intact and then also be able to replicate in the mosquitos which it cannot do, due to the missing of the CD4 antigen on the surface of the insect cells. These are needed as a surface receptor for the virus to bind and enter the cells. This is also true for other blood sucking insects like bed bugs or fleas.
Other pathogens can do this, examples would be Yellow fever or Malaria. In Yellow fever the virus first infects epithelial cells of the gut, then enters the blood system of the insect to finally end up in the salivary glands, where the virus is injected together with the saliva into the biten person. In Malaria the pathogen is also able to leave the gut region and mature in the salivary glands.
HIV can only be transmitted through blood (either through direct transmission, operations etc.), through semen (cum), pre-seminal fluid (pre-cum), rectal fluids, vaginal fluids, and breast milk. See reference 3.
References:

Why Mosquitoes cannot transmit AIDS
Can we get AIDS from mosquito bites?
HIV Transmission Risk:  A Summary of Evidence

Is there a zero probability that tiny droplets of blood remain on the proboscis of the mosquito long enough for said mosquito to inject its proboscis into the bloodstream of another person? In particular, in what physical aspects is the proboscis different than a needle or razor? I am not talking about blood sucked into the gut of the mosquito, I am talking about blood remaining on the proboscis.

@MarcusJuniusBrutus Very interesting question - I've asked it as a follow up question Why doesn't blood remain on a mosquito's proboscis in quantities that could spread blood-borne diseases?

What if you swatted the mosquito while it was attached? Leeches, for example, will vomit previously ingested blood into you if stressed.

@OrangeDog Good point, I have read something about this somewhere, I have to only find it back.

"Would it be posssible for a swatted mosquito that previously fed off a HIV carrier to infect your blood through the hole it made, or a nearby cut?" (copied from comment directed at Chris by @user2104648, posted as a now deleted answer)

@OrangeDog I don't find my reference back, so I only write this as a comment at the moment, but it was classified as highly unlikely but not impossible. First: HIV needs relatively high viral loads for a sure infection. Then mosquitoes usually only feed off one victim per time (given they are not disturbed), so they will not need another victim until this blood is digested. If they are disturbed the amount of blood is even smaller (we are talking about the range of 3µl and less) so an infection gets less likely. It would be really bad luck.

I am not a medical doctor but in my view this is within the realms of possibility. The probability has been estimated by Princeton at 1 in 10 million. This is per bite, assuming - I presume - that the mosquito that bit you was just feeding on an HIV-infected person of sufficiently high viral load. It is not against the laws of Physics that blood cells can remain for some time on the proboscis or other mouth-parts of a mosquito.
Whether this is probable is a matter of interpretation depending on your definition of 'probable'. But your question is about possibility, not probability. Personally, given that this is comparable, if not lower, to the probability of being struck by lightning I wouldn't give it a second thought.


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Why are fruits so large compared to their seeds?
Why do many plants produce such large fruits(apples and strawberries,for example) if those contain only relatively small seeds?

Although I'm not an expert, after a bit searching, I've found this article : link , even if it does not mention about the seed-size relationship, it gives some information about the points that affect size of fruit

Much of the size of commercial fruits is due to selective breeding by humans.  Compare the size of a store-bought strawberry to a wild one, or an apple to a wild crabapple.  For wild fruit, the standard explanation is that the fruit serves as a lure: some critter eats the fruit, the seeds pass through its digestive system and are deposited (along with a nice bit of fertilizer) some distance away from the parent.

The short answer: Fruits are large compared to seeds because humans have made them large.
In the natural environment, there is a different set of evolutionary pressures. A fruit has to be able to successfully propagate itself using its seeds, while commercially farmed fruit is usually cloned via vegetative propagation. Therefore, the commercial farmed fruits do not need large seeds to propagate, since they are cloned by the farmers. In many cases, their seeds are actually nonviable (i.e. they will not grow when planted).
For example, this is a wild banana, before being selectively bred by humans. As you can see here, the seeds are enormous compared to those in commercial Cavendish bananas.

Similarly, this is a wild strawberry compared to its commercial farmed variant.

Fruits with large seeds don't appeal to consumers, and therefore farmers who sell fruits with large seeds will get a poorer return on investment.
Therefore, farmers who plant the fruits which appeal the best to consumers by being the easiest to eat (small seeds) will reap the greatest profits.

Not true about taste.  Farmers tend to plant what grows & ships well, and has eye appeal in the store.  Taste is way down the list of desirable factors, if it's considered at all.  Compare the taste of 'heirloom' varieties vs common commercial ones: for apples, a Cox's Orange Pippin vs Red Delicious or Honeycrisp.  Another factor is that commercial fruit is often treated with growth-enhancers such as gibberellins (or was, back when I was a farm worker), which adds watery size at the expense of flavor.

@jamesqf Fair point, updated.

@jamesqf Can confirm this, working with watermelons. Usually wilder varieties are smaller and more concentrated in flavor, but harder to eat due to seeds, etc.

Just to note, the Cavendish banana, like all other edible bananas doesn't just have small seeds, it is seedless. In fact, all banana plants (of the same variety of banana) are genetic clones of one another produced by vegetative reproduction rather than sexual reproduction.

@JackAidley "Seedless" in most cases just means their seeds are non-viable and reduced, not that they do not exist. New Scientist article

@MarchHo: Okay, fair point. What I mean is that it's not just that they have smaller seeds it's that these seeds are, as you say, totally non-viable.

Just for reference: The 'wild strawberry' is not a true strawberry, but a related plant called Potentilla repens. True strawberries have white to pink flowers, and conical fruit with seeds that reside in sunken pits, while Potentilla has bright yellow flowers with spherical red fruit with seeds that stand erect on top of the skin.

Because seeds are not appealing to animals and they can only be carried by animals if they are made appealing - there are exceptions of course such as this one -. Seeds are covered with juicy layers that can be nutrient to animals in order to be made appealing and to be dispersed. Animals eat those juicy layers along with seeds, seeds resist digestion and fall on the ground where animals defecate. If the layer was thin and provided only protection to seeds, animals would not eat them and the seeds would have to be dispersed by other means. Therefore we would not call them fruits. The reason why seeds are not as large as their fruits is:

They have to be dry to resist climate changes while staying dormant below ground. And dry is generally small.
Seeds' task is to be dispersed, not to be nutritious to animals. And they usually do not taste very  well compared to fruits - some do taste well as we know but I do not know why -. So why make them large and irritate the animal? Make them small so they will be overlooked by the animal and be dispersed happily

Most fruit/seed evolution is probably a reflection of the plants propagation strategy and any existing symbiotic forager relationship.
The strawberry expands its range by creeping with feeder shoots. It is also heavily foraged by small birds , thus the exterior small seeds.
Nut trees i.e. walnuts , are on the other end of the spectrum. The seed is nearly the size of the "fruit". All they want is some little squirrel to shake them loose and fall to the ground, then try to outgrow everything else.
cherries....
Just making all this up.

If you are "just making all this up", do you mean it is nonsense? If yes, please remove the answer. It sounds OK though. If you support your answer, could you edit it to be a bit more professional? i.e. the "cherries..." doesn't make sense.

@AliceD: To a certain extent any answer that involves the 'why' of evolution has to be made up, because we're taking a situation that exists as a result of a multitude of factors acting over millions of years, and using reason to try to figure out the 'why'.  Since we weren't there watching every step, there has to be a lot of guesswork involved.

@jamesqf,  obviously, but while educated guesses are appreciable, nonsense, unfounded and  fabricated answers should be discouraged


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Is COVID-19 claimed to get less deadly over time? If so, why?
From a TV news report of a press conference from (I think) the German Robert Koch Institute, I remember hearing an expert declare that he was expecting COVID-19 to get less deadly over time.  Unfortunately, I don't know what press conference it was (I'm not sure if it was the Robert Koch Institute — it might also have been the Charité university hospital) and cannot find such a stated expectation on the internet.
Why would an expert express this expectation?
Is it because we're heading toward summer (at least where most COVID-19 cases have been reported), or is it a standard pattern, perhaps either due to people's immune systems or due to the virus evolving and becoming weaker?

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

While the data are much too sparse and noisy to give an answer about what is happening to COVID-19's virulence (the technical term for the "deadliness" of an infectious disease), or to forecast what will happen to its virulence in the future, there are indeed theoretical reasons that one might expect the virulence to decline in the future.
There is an entire theoretical literature on the evolution of virulence (e.g. see Read 1994, or see Wikipedia); Robert May and Paul Ewald are two researchers who contributed seminal ideas. The basic idea is that infectious 'organisms' (including viruses) may face a tradeoff between their ability to produce lots of infectious particles (e.g. by replicating faster within the host) and the length of time that they can stay in the host before it dies or activates immune defenses sufficiently to end the infection. In this case, some intermediate level of virulence may evolve.
Evolution of virulence in ways predicted by the theory has been observed in the real world in such diseases as myxomatosis (a viral disease of rabbits). The theory has also been suggested to apply in HIV and syphilis.
The actual forecast can depend on many details of the biology and epidemiology of a particular organism. If COVID-19 happened to have a higher-than-optimal virulence in humans at the time of emergence, we could expect its virulence to decline over time. It could also decline if epidemic control was applied in such as way as to differentially affect more-virulent strains; this has been suggested by Tang et al. on the basis of the pattern of mutations in different strains, although their logic has also been criticized on Twitter by an expert in genetic epidemiology, and now by a more official rebuttal by McLean et al. (with some back-and-forth discussion between the authors and critics).
This explanation doesn't include the possibility of host evolution, which is theoretically important but not really relevant to COVID-19 — it would only happen over many generations, and only if the epidemic was so severe that it was a significant overall cause of death or failure to reproduce ...

Tang et al. "On the origin and continuing evolution of SARS-CoV-2", National Science Review, nwaa036, https://doi.org/10.1093/nsr/nwaa036 .
Read, Andrew F. "The evolution of virulence." Trends in microbiology 2.3 (1994): 73-76.

To summarize, the most performant virus is the one that keeps the hosts well enough and socializing for the most time with the highest output of virus to others in their vicinity.

There's a theory that a highly deadly virus kills its hosts and therefore replicates less. With Covid killing somewhere between 0.1% and 1% of infected people, that seems to be completely irrelevant.
There's a better theory that when a virus is very deadly then people will do whatever they can to stay away. Boris Johnson wouldn't have shaken hands with Ebola patients. A virus same as Covid but 50% lethal would have massive voluntary lockdown and fights for vaccines. For those reasons, it would spread less than Covid. With 50% lethality you could expect 99% of people to lock themselves up out of fear, and the 1% in the streets shot on sight.
I am told that the current Omicron variant has changes which body parts it affects (throat instead of lungs). And these changes make it at the same time less lethal and more infectious. This sounds reasonable, but not necessarily true. So you may try to think of something that makes the virus both more lethal and more infectious at the same time.
But fact is that the virus has no advantage from killing people. No evolutionary gain. However, it has an advantage from being more infectious. On the other hand, Covid is very infectious already, so a random change is very unlikely to make it more infectious. The "better" it is at infecting people, the harder it is to improve.