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Why isn't hearing the same as tasting? How do we feel and differentiate external stimuli?
When I was at school, I learned that:

Skin, tongue, ears, and other sensory organs have sensors/convertors that turn external environment stimuli into "electric" signals.
Neurons send information as electric propagation of K+ / Na+ along their axon. Hence, the real nature of the stimuli is definitely lost in translation.
Each region of the brain is a cortex specialized for vision, sound, smell, and other sensations yet they all are made of the same neurons.

So:

Then how do we feel? How are "electric" signals turned into taste or smell?
Why does the brain not feel the same way about these different stimuli, rather than only differentiating amplitude and frequency of the signal?
Why do we even feel pleasure or pain at all? A machine would just transfer the information.

That part was never explained to me. Is it quantum (entanglement?) physics-related? Or even metaphysical? Does anyone really know?
Philosophically speaking, I am not even sure I taste things or feel music the same way other people do.

Ordinarily, it's not good to ask so many different questions in one question on Stack Exchange. However, in my view these questions all actually boil down to one central question, so I've provided an answer in that regard.

Why does your computer's keyboard do different things than the mouse or a attached camera?  (Or any of the multitude of other sensors you can buy?)  They're just electrons moving through identical gates etched in chunks of silicon, aren't they?

@jamesqf so you don't get it...drivers and hardware only process information, they don't feel it, the question is more complex than that

@fdsfdsfdsfds: No, YOU don't get it.  Just as those drivers all run on essentially identical hardware (after the actual sensor), so the different areas of the cortex are "drivers" made of neurons.  Then you consider that the types of information are fundamentally different: it would be fairly useless to display an audio file all at once, or play an image file as a stream of bits.

@jamesqf If you want to post another answer, great, but...I think there is a lot of uncertainty in something you seem to be certain about. Even as an extreme materialist I agree that there is a difficult understanding here that isn't the same as one applied to computers. OP has a pretty common question and I was kind of surprised to not find a canonical answer here yet - maybe I missed one.

@jamesqf  you're confusing processing (how data is pre-chewed by the brain) and the feeling produced by that perception; try "building a machine" that mimics brain, and tell me how you made it actually taste food and feel pain or pleasure, while it is built from good old hardware/software, and the only thing the it receives are electrical data.. I am talking about the taste/smell itself, and it's profound subjective nature... there must be something deeper and out of human reach, Bryan is right, read his answer, he, at least, gives different tracks to follow to learn about the subject

@Bryan Krause: I don't want to post an answer because I am trying to point out (politely!) that "answers" are pretty well meaningless, because the question is nonsense.

@jamesqf  just read me instead of deliberately ignoring something you refuse to understand...information will never be converted into a taste (a QUALIA)

The problem you are seeking an answer to is referred to as the hard problem of consciousness, the term originally coined by David Chalmers, or more generally the mind-body problem.
Just how "hard" this problem is seems a bit unclear; some people argue it isn't truly "hard" at all, but they make these claims in support of their own particular views of the nature of consciousness. Since not everyone agrees with them, it seems like to at least some extent the "hard problem" description is appropriate.
There certainly are quantum explanations, and you will find proponents like Stuart Hameroff, but most neuroscientists consider his theories to be crank science since he hasn't provided any evidence of his theories, only hand-waving explanations of how they could be plausible.
There are also metaphysical explanations, going back to the dualism of Rene Descartes. The problem with these metaphysical theories is that they aren't scientifically disprovable, and the more we learn about the brain the more of its functions can be explained physically. Dualism is ultimately a religious or philosophical stance rather than a scientific one.
There are several neuroscientific theories of consciousness, including integrated information theory(IIT) and global workspace theory(GWT). For IIT, consciousness occurs through the integration of information in a causal structure like the structure of a brain. GWT proposes that consciousness occurs through the transmission of information through particular central brain structures. In both, the qualia that are experienced occur through the neural substrates of either the processing or the information carried. Hearing and tasting are different because they involve different groups of neurons and synapses; you don't typically taste a sound because the parts of the brain that process taste are not getting direct auditory information.
However, that doesn't mean that senses are completely disconnected: it is possible to form relationships between senses by association, like how both written and spoken language evoke the same meanings, or how certain colors seem to be associated with "hot" versus "cold" temperature.
As far as what it means to experience things how others do, I'd recommend Nagel's What Is It Like To Be a Bat? which argues that subjective aspects of consciousness cannot be completely understood, but that there are objective features that can be understood. So, although you cannot know that others taste or feel music in subjectively the same way as you, you can objectively understand that other people can taste sweet and sour, can hear music in a similar frequency range, etc.

thanks I'll dig these for sure..I am glad I was going the right direction, and you gave me so much material to read...I have seen many Roger Penrose videos recently on youtube, I guess he must have been digging a lot around that subject (and others apparently)

"involve different groups of neurons" I guess you're right, I heard that some people had a brain issue making them ear food and smell sound or something, but even if the brain is wiring things in a deviated way, in the end smell is smell, sound is sound, taste is taste; I build robots and I always wondered "how would I make it feel pain or pleasure"; not sure it would be a good idea ethically speaking


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Why do some mammals have incomplete orbits?
I've noticed that a lot of carnivorous/omnivorous mammals (most, if not all the members of carnivora and some ancestral cetaceans), as well as some herbivores (marsupials), have incomplete orbits that merge into the temple near the zygomatic arch. I'm wondering what the evolutionary purpose of this is, as well as why we would lack them.

not some, most mammals have incomplete orbits. only a few groups have closed it. It seems to be related to the position of the temporal fossa. https://www.ncbi.nlm.nih.gov/pubmed/15844100 the whole region varies quite a lot in mammals https://www.ncbi.nlm.nih.gov/pubmed/18211281

Some things to think about are the size of the field of view, the protection of the eye, and the normal orientation of the head.

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What does it mean to say that the sympathetic nervous system is organized for diffuse activity?
"Sympathetic activities generally serve to mobilize the energy stores of the body, to increase the blood flow through certain regions (e.g., the heart) at the expense of other areas (e.g., the abdominal viscerae), and to exhibit the outward signs of alarm and excitement.
Because the sympathetically innervated effectors generally have a wide distribution, even when the sympathetic supply to only one type of effector (e.g., the vasomotor fibers to the cutaneous blood vessels) is stimulated, the bodily response is diffuse."
1-By 'mobilize the energy stores' they mean metabolize or use up ?
2-'The bodily response is diffuse' - does that mean several parts of the body participate in the response but with no major effect individually ?

"Mobilize" in this context means to:

to release (something stored in the organism) for bodily use

Merriam-Webster
"Diffuse" means "spread out": it doesn't say anything about whether the effect is "major" or "minor" and I don't think it's useful to think in those terms. Instead you should just appreciate that there is no specific target affected by sympathetic activation, rather it is a whole body response: almost every organ system is involved.
Sympathetic nervous system activation occurs when an organism needs to be ready to act immediately (such as in a 'flight or fight' response), which includes more metabolism in the muscles and increased sensory sensitivity. It also includes compensating by reducing metabolism in the gut: even though digestion is a source of energy, it is slow rather than immediate and costs a lot of energy in the short term through the processes of digestion.

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Are there people blind to touch?
There are people who completely blind or deaf. Are there people who are completely blind to touch in a particular area or in the entirety of their body? If not, are there people in whom the temperature modality of touch or the pressure modality of touch is completely absent? It seems that this might be related to congenital insensitivity to pain, but it is not quite the same thing.

USH2A mutations can cause degrees of deafness and partial touch insensitivity in humans. Do those count or is full loss of function a requirement?

@AlexReynolds I thought Usher's syndrome affected sight and hearing only?

There is a paper from 2012 that suggests a mutation in that gene can cause partial loss of touch sensitivity (ref. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341339/)

Short answer
In a way, yes.
Background
One prime example where the sense of touch is diminished is when peripheral sensory neurons degenerate, which is called sensory neuropathy. Diabetes is currently a common cause of this disorder, resulting from the high blood glucose levels that damages the small blood vessels which supply the nerves. This prevents nutrients reaching the nerves, eventually damaging nerve fibres, which may end up in a disappearance of the nerve altogether (source: diabetes.org).
Sensory neuroptahy can lead to a multitude of complaints, including weakness, numbness and pain, usually in the hands and feet (source: Mayo clinic).It can also lead to the loss of ability to feel pain, changes in temperature and coordination when you lose proprioception is affected. The loss of the sense of pain is dangerous. An often heard complaint is that wounds to the feet are not noticed. If ignored, even minor injuries can develop into infections or ulcers (source: diabetes.org). I fact, my grandmother-in-law recently underwent an amputation of the lower leg, because of a diabetes-related, neglected injury to her toe. It lead to an ulcerating wound and eventually necrosis. At a certain point it caused terrible pain, but the initial wound had gone unnoticed.
A related condition is Carpal Tunnel Syndrome, also called median nerve compression. It is a condition that causes numbness, tingling, or weakness in your hand. It is caused by pressure on the median nerve that traverses a passage in the wrist called the carpal tunnel.
This may not be exactly the answer you are after, as sensory neuropathy mainy causes numbness of the extremities, rather than a complete loss of sense of touch. Remember, however, that blindness rarely results in a complete blackness. Beside the fact that the great majority of blind people are 'only' functionally blind, as they still have rudimentary visual function left, perceptions of phosphenes are in fact really common, and some people even start seeing complete visual scenes with people and objects included (Charles Bonnet syndrome). This is not unlike deafness, where many people still have residual hearing, yet too little to be of any functional use. For instance, people that are eligible for a cochlear implant often still have substantial residual hearing left. Like phosphenes in the blind, tinnitus in the 'deaf' emerges akin to 'phantom' sounds. These 'hallucinatory' sounds are actually generated more centrally by the brain after prolonged deafness. In short, blindness and deafness are relative, the great majority of folks don't lose their senses, they have reduced functionality of them.


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Are these structures real petals?
I don't know the name of the plant. It's a common house plant in Bangladesh. What interests me about its flower is the colorful leaflike structure that probably functions as a petal. What is this structure homologous to? Petal, sepal, bract or leaf?

The plant looks like something in the genus Bougainvillea. These plants are native to South America, but found as introduced ornamentals in many places.
The colored petal-like organs are bracts (see the Wikipedia link above). The entire structure is an inflorescence with the flower buds growing out from the surface of the colored bracts — you should eventually see those flowers open and you could then dissect them confirm that the usual flower structures are present.
This is a well labeled diagram:


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Technologies that rely on evolution
It's possible that this is offtopic here; if so, please let me know.
I'm wondering what technologies exist that rely on evolution being a correct model; I'd like to be able to offer examples of that to people who find it to be "just a theory". As an example, I can point out lots of technologies for which our models of electromagnetism have to be correct to an immense accuracy for them to work - computers, any electrical wiring, electrical motors, light bulbs, electrical ovens, etc. etc.
The best I could find as examples of technologies that require our models of evolution to be fundamentally correct are things like pharmaceutics that work against germs that have developed a resistance against other pharmaceutics.
What are some good examples of technologies that require our models of evolution to be fundamentally correct for those technologies to work?

I think this is probably too open-ended and discussion-based to make a good SE Q&A, but I'll reserve my close hammer for now. "All of molecular and cellular biology and almost all modern medicine" would be a start of an answer. Ultimately, though, I think this is probably a poor strategy for argument: people who have decided to believe evolution is false have not done so based on fact, so additional facts are unlikely to persuade them.

@BryanKrause I realize that it's probably a bit wide of a question, thought I'd give it a shot anyway; maybe "all of molecular and cellular biology" could be narrowed done to a handful of striking examples? As for whether it's a good strategy for argument, I'm optimistic it helps. Many people have been argued out of all kinds of denialisms and cherished irrationalities, and even people who don't rule out creationism come in flavors of being less convinced than card-carrying religious fundamentalists. I've found it's relatively effective to have something concrete, specific to talk about.

Not a technology, but a biotechnological product. The enzymes required to fermentate milk and make yoghurt will ( and gonna ) mutate. So, you can genetically modify and setup bacterial lines with a fixed sequence that ensure the production of enough and functional enzymes. Also, the creation of clonning vectors is a technique developed with evolution in mind. Sometimes you want evolution, and sometimes you dont need it.

Vaccines, and nearly anything else based on epidemiology. Most of modern agriculture is based on artificially selected organisms. If evolution did not work, hens would only lay a few eggs a year and an ear of corn would still be as small as a head of wheat, and tomatoes would still be the size of grapes.  basically all forms of animal testing, including much of genetics, rely on common ancestry.

This site does not exist to supply people with debating material on evolution. If you cannot marshal the arguments yourself you are never going to convince anyone else. Certainly not in this case where you are using a false premise because you don't understand that evolution is an explanation of something that happened with no predictive power, unlike the laws of physics, for example. In any case you are reckoning with people who will not be convinced by rational argument because their position is based on irrational religious beliefs. Don't waste your time.

Evolution is not the type of theory that is mainly directed towards technological applications, as opposed to many physical theories. It is a principle to understand living systems, from the simplest to the most complex. So it mainly gives understanding, not 'solutions' to particular problems.
That being said, evolutionary principles can be applied to many 'practical' problems.
For one, all of the technologies that rely on sequence alignment and phylogenetic inference use models of substitution based on evolutionary principles, in which you have hypotheses based on the probability that some evolutionary changes occur (these changes can be at the nucleotide level or at the organismal level), and then you infer which hypotheses are the most plausible given the evolutionary and ecological context of the problem. A 'practical' side of this, for instance, would be to infer the evolutionary trajectory of the COVID-19 epidemic, or the study of the geographic spread of the virus given the sequences of the virus at different locations/time. A lot of modern molecular biology is based on a comparison of sequences.
Another 'application' is that of designing enzymes or other molecules, that have a desired function or feature. In fact, a recent Nobel prize was awarded to Frances Arnold for harnessing the power of evolution in her research on molecular design.
Some other applications besides the ones people have mentioned in the comments above are medical applications. It is well known that cancer lineages evolve, so the principles from evolution can be used to better treat cancer progression, for instance by adjusting the evolutionary outcomes of a particular treatment (you can read a fascinating example here). In fact, the understanding of cancer itself, besides therapeutic interventions, has used evolutionary principles for some years now (see a nice example of evolutionary dynamics in metastases here).
I also want to mention an important example from microbiology. It is a pressing issue of public health the fact that no novel antibiotics have been developed in the last few years, and that the existing ones are less and less effective given to the evolution of antibiotic resistance. What if we could make "evolution-proof" antibiotics? That's a fascinating question that some people are starting to explore, for instance by combining classical antibiotic treatments with phage therapy or molecules different than the traditional antibiotics (a cool paper here).
Finally, I want to mention that these applications of evolutionary principles do not "rely" on evolution being "fundamentally correct". Evolution is a process for which we have a lot of evidence, so at this point (and for a long time) evolution is an uncontroversial fact to the scientific community. This is similar, for instance, to the fact that we have lots of evidence for the phenomenon of gravity; so what scientists are doing at the moment is figuring out the mechanisms by which evolutionary processes occur (just as physicists are looking for gravitons). Another addendum is that evolution seems to be an open-ended process. This means that many of the mechanisms we can find in evolution will be, to a high degree, statistical in nature, because there are just so many possibilities that we cannot account for all possible outcomes. This is a fundamental difference to many theories in, say, physics, where there are clear "solutions" to a problem (in the form of an equation, for instance). I say this because people keep coming up with examples that "disprove" evolution, but they just don't consider that evolution is a statistical process, which allows for "outliers". In fact, the outliers are quite informative for evolutionary theory, not at all undesirable (consider for instance the origins of life, or the emergence of consciousness, these are unique 'events' for which we have no mechanism to explain why did they emerge).

These are all interesting examples, thank you for that. While I don't think they fit what I'm looking for, your last paragraph does a great job at explaining why what I'm looking for might not be easy to come by, or exist at all; especially the statistical nature of evolution probably prevents this.

This is an excellent Idea which is actually a tool used in everyday Molecular biology if you look at it with the right perspective.
Evolution, if broken down into its basic components has been with us and created many technologies to date.  This is probably not all encompassing, but lets look at diversity and selection which are principal components of Darwin's fundamental theory.  Darwin distinguished between 'Natural Selection' and 'artificial selection'. That's a great place to start.  Artificial selection is a means people have used for millenia to get desirable traits for products.  Beef (well all of our meat), wheat, textiles from wool and cotton, pets, fruit and vegetables are all the product of selection where the farmer/flock owner will save individuals with desirable traits and breed them for the next crop.  This is one of the principle evidence for Darwin's work: He extended the case of Artificial Selection to understand how it works in the natural world.
In more more recent decades we have come to use Artificial selection with genes and pieces of DNA, changing them, adding them.  Molecular biology uses a selection technique where genetic changes of interest are accompanied by a resistance to an antibiotic.  Now we are changing how well the genes work and using them to say make better insulin for diabetics.
Artificial Selection can look very much like Natural Selection since the definition of 'Artificial' is simply that people did it; by definition there never will be a technology that comes completely from Natural Selection.
There have been more sophisticated versions of Artificial selection where artificial selection have used diverse genetic backgrounds to find individuals with amazing abilities.  One of my favorites is an experiment where they simply were looking for yeast cells that floated.  They created an environment where the floaters were carried on for further experiments for i think it was about a month.  In the end they found some yeast that tend to stick together and form colonies - a trait that was on the edge of multicellular life.

Two types of technologies come to mind. The first involves techniques that improve the traits of strains used in biotechnology. For example if you are using genetically modified yeast in wine making or for making a commodity chemical and want to improve quality or production rate of that compound you can generate yeast mutants that meet your goals. One easy way to do this is to subject the yeast to UV radiation and look for good mutants. Someone who has no understanding of genetics and molecular biology would not understand why subjecting yeast to harmful radiation will help make them better. The reason is that UV radiation creates DNA damage and innacurate repair of that damage leads to diversity in traits, which may enhance or worsen the trait you are after.
One could say "you don't really depend on evolution for that to work because if you try it once and it works then it will work for another trait". But why should we believe that because mutagenizing yeast with UV radiation helped make wine better it will help make more acetic acid? The reason is because the mechanism is the same. And how do we know that we aren't just wasting our time and some traits can't be improved. The reason is because all the diverse life around us developed from a common ancestor through the same principles.
The other technology is ancestry analysis through genome sequencing. We know that we don't need to look at all the billions of DNA bases that make up our DNA to see if we are related to someone or some group. We only need to look at a smaller subset like single nucleotide polymorphisms (SNPs). And using this information we can track the migration of human populations over long periods of time. Again looking at DNA sequencing data could be doubted as just a coincidence or that other explanations or possible. Maybe contrary what the genomics data tells us, population A didn't migrate from population B, but it arose at the same time? But the theory of evolution assures us that our conclusions are the most reasonable.
I should also add that if evolution wasn't true then both of these technologies would be nonexistent and we might not even have any alternatives to answer the questions that these technologies are employed for. If organisms don't adapt how can we make yeast produce more ethanol without dying to it? If humans don't have common ancestors why does random variation exist even among our progeny and how do we explain archaeological data?


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Can there be significant new changes in physical features of Humans due to evolution in 10000 years of span?
Humans migrated from Africa about 60000 years. And in these years humans physical features undergone significantly in terms of skin color, hair, eye color and facial features.
So, with this we can say that given 10000 years of span we can see a significant noticeable new changes in physical features of humans? like some humans with new skin color (apart from today's white, black and brown), new color eye balls, big heads etc.?

@tyersome Below answer gave me appropriate answer. Thanks

@tyersome : The link you provided was more specific to evolution of human in future whereas mine was more specific to evolution changes in terms of a window/range of 10000 years. So, below answer is more appropriate.

Yes & perhaps (or probably?) no, depending on what you define as significant changes.
Less than 10,000 years ago everyone in the british isles & the rest of europe were dark skinned so the answer if (unlike me) you consider the change in skin color a significant change is obviously a resounding yes.
Here's what English people looked like 10,000 years ago

Darker skinned than you were expecting perhaps.
If as suggested in this article white skin arrived in Europe around 5,000 years ago that only leaves 2,000 years before early Greek & Roman art we have available which shows it as ubiquitous, so it perhaps took only 2,000 years or so (maybe less) to become dominant in europe, that's fast.
Using 20 years as the measure of a generation that's only 100 generations, so, very fast.
Timeline of human prehistory
The first reconstruction in the link below is a reconstruction of a Neanderthal woman found in a cave in Gibraltar. She died at least 30,000 years ago.
Here she is, the skin tone may not be accurate but we do know from gene's recovered from Neanderthal remains that they were relatively light skinned.

Personally I don't consider her appearance to be significantly different from modern humans.
29 Reconstructed Faces Of Ancient People
So my answer based on what I consider significant changes would be no.
But for you or others the answer may well be yes.
And of course a mutation for a new eye colour could appear at any time in one individual & spread like wildfire practically overnight just because we think it's unusual & 'cool' (aka sexual selection) so if eye color ticks your boxes it's a very definite yes.

Your first link - https://curiosity.com/topics/the-earliest-humans-in-england-didnt-look-the-way-youd-imagine-curiosity/ gives me the answer. 10000 years before there were no light skinned in Europe and it took less than 10000 years for homosepiens to get the lighter skin? I presumed it would take about 100000 years for such big change like skin color.

I thought it might :)

"about 10,000 years", nope, a mutation can spread pretty fast if it's beneficial or selected for by sexual selection, once it appears, blue eyes spread fast too when they turned up, what takes a long time is the mutation, it's a lottery & useful (or just non-damaging ones) aren't that likely so 'on average' are often a long time apart, reduce it to only ones that provide a noticeable phenotype change & rarer still.

@barath : Which all means a single change of some sort can just happen, & pretty quickly, but multiple changes to a phenotype such as you need to go from something chimp like to something man like will take a really long time & for that 10,000 years isn't even remotely long enough.

@barath : "such big change like skin color" : Skin, eye or hair colour may be noticeable & obvious but they aren't 'big' changes, not really in any qualitative sense, they can occur with just a single mutation to a single gene so they're really pretty small changes genetically speaking.

@barath : "what takes a long time is the mutation" : Ooops, edit required > what takes a long time is waiting for the mutation to turn up : mutations themselves are of course pretty instantaneous, caused as they are by DNA copying errors or random background radiation jiggling with a single strand of DNA, they (or at least noticeable non damaging ones) are just few & far between, useful  or desirable ones more so.

Yes, I didn't consider mutation into account. Probably there was a mutation for light skin among very a few human beings and other human species might have attracted/preferred to those lighter skin and produced more offsprings with them and eventually lighter skin spread significantly across Europe as a natural selection of humans.

@barath : It's pretty much all mutation somewhere up the line. Light skin may have arrived in europe as little as 5,000 years ago, lactose tolerance in adults as little as 4,000 years ago, so yes, the spread can be fast if the mutation is beneficial or desirable to the opposite sex.

@barath : Light skin is an advantage for vitamin D production in a 'less sunny' climate (europe, compared to africa) so it had a definite advantage for health & survival to offer & doesn't need the sexual selection angle to explain it's rapid spread.

Yes, agree. Thanks.


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Overcoming palmitic acid intolerance
What can stop the body from being able to process or break down palmitic acid?  The acid stays in the stomach and burns causing a similar reaction as heart burn when the volume is high.  Heart burn medication makes the issue worse. In smaller doses it causes the esophagus to swell causing a asthma type reaction and wheezing when breathing through the mouth but leaves the nasal passages unaffected.  The symptoms appear several hours after consumption.  The reactions have been noted in any food containing the acid natural or additive usually in the form of palm or peanut oil.  Once such natural example is a Pizza with Mushrooms, several hours after eating nausea will occur along with the burning sensation.  Expelling of the contents reveals acidic liquid and the mushrooms only.
Is there any recourse for neutralizing the acid safely or supplementing the body with the missing function to process the acid.

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Does opponent process happen in the retina or in the brain?
I understand that both the Trichromatic Process and the Opponent Process take place in human vision.
Trichromatic Process is widely accepted to happen in the retina,
however I heard differing accounts of where Opponent Process happens - in the retina or in the LGN.

Opponent process happens BOTH in the retina, and in the brain (Lateral Geniculate Nucleus).
Here is the excerpt from Vision Science: Photons to Phenomenology by Stephen E. Palmer:
In the brain (LGN):

Physiological psychologist Russell De Valois (1965) and his colleagues (De Valois, Abramov, &
  Jacobs, 1966) measured responses in the LGN of macaque monkeys and
  discovered color-selective cells whose responses to wavelengths of
  light were incompatible with trichromatic theory but conformed roughly
  to the pattern predicted by Hering's opponent process theory. Some
  were excited by red light and inhibited by green (R+G- cells). Others responded in the opposite way,
  exciting to green and inhibiting to red (G+R- cells). In addition,
  they found cells that were excited by yellow and inhibited by blue
  (Y+B- cells) as well as ones showing the reverse pattern of responses
  (B+Y- cells). Together, these LGN cells can reasonably be interpreted
  as a neural implementation of Hering's opponent process theory.

In the retina:

Further research has shown that these patterns of response are also
  present in the bipolar and ganglion cells of the retina. Output of R+G- opponent cells can be derived by combining excitatory
  input from the L cones and the inhibitory input from M cones,
  essentially computing the difference between the output of these two
  cone systems (L - M).


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How do tree gnarls develop?
What causes the trees to develop gnarls? I can't find anything on internet other than dictionary definitions.
Are they caused by a mold, like the burls?

If I understand what you're talking about by "gnarl", they are usually caused by a bacterium like Agrobacterium tumescens infecting and creating a gall.
Update: Forgot, also in some cases caused by insects.

Thanks, that means that "gnarl" is the same thing with "crown gall" ? By gnarl I meant the most common dictionary definition of it - a rough, knotty protuberance, especially on a tree.

@Ark25 I guess it depends what you mean by "gnarl"- it doesn't appear to be a very specific technical term. Looking at what shows up when you google image search, it shows both extreme twistedness and protuberances. If protuberances are what you mean, they indeed mostly seem to be caused by pathogens such as insects or microbes.


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Base-stacking interactions versus hydrogen bonds
Is it correct that the hyperchromic shift in DNA is a result of the disruption of the base-pairing hydrogen bonds, but the actual denaturation of dsDNA has more to do with the base-stacking interactions? Why does separating the strands have any effect on the stacking of the bases? Why wouldn't the bases in ssDNA still experience stacking interactions?
I really appreciate any help with this. Thanks!

Related: https://biology.stackexchange.com/questions/89614/why-does-absorption-at-260nm-of-ssdna-increase-with-temperature

For a direct reference on the contribution of these two forces see here.
If it helps, think of the double helix of dsDNA as a more rigid structure than ssDNA, which flops around and generally is capable of a lot of steric freedom that dsDNA doesn't have. This freedom means that the bases of the ssDNA backbone may not always be in the correct orientation for stacking, because the two strands of the helix aren't forcing the bases together into that orientation. "Usually the DNA double helix is considered to be a relatively rigid structure. Certainly it is much more rigid than its component single strands." (see the review for a much more detailed discussion of this issue)
It's true that base stacking still occurs in ssDNA, it's just not enforced in the same way. It also appears to be somewhat sequence-specific, occurring more in polypurines than polypyrimidines, possibly because purines are bulkier molecules with more steric hindrance.
For a related conversation see here.


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which specific field to study to know more about genes and genomes
I recently got interested in specific subjects :
1.Evolution
2. DNA, genomes etc and its structure
3. Abiogenesis
I am a software engineer with good fundamental understanding in math & physics and I was thinking to read some biology to get knowledge on it in my free time.
An associate free course or a book which can build my broader understanding in fields of biology would definitely help.
Regards

People who downvoted are seriously useless if they do not consider leaving a comment.

I believe that you're looking for fields with names like "genomics" "genome evolution", "population genetics", "molecular evolution", and possibly "computational biology"/"bioinformatics".
Each of these is a huge field with a large literature. I'll try to recommend some resources but they're not exhaustive.
For a simple mathematical introduction to population genetics and microevolution, I like Joe Felsenstein's book (free online).
Joe furthermore has a lot of slides up along with audio tracks for courses he's taught covering several of these areas. He is coming at it from the perspective of a mathematically-sophisticated computational biologist with an interest in designing software for phylogenetic inference, so it might be a point of view that works for you. I'm sure that there are lots of other similar resources but I'll admit that I'm personally fond of Joe's style.
It does look like there are online courses for genomics intros, I don't know how good they are. The field changes so quickly that it may be hard for them to keep up.
MIT has a computational biology course up- I imagine it's probably pretty good.
Abiogenesis is a bit harder, but you might look into the field of exobiology/astrobiology- here is a list of online courses.

Thanks for replying back with an answer which definitely helps. Can you also point me out some good computational biology courses. Also, books take a lot of time. I may be silly but as a hobby getting a high level knowledge on this will help than to get deeper knowledge.

updated with computational biology info. Understand about high level knowledge. .

This should be good for a start. Will come back again if need be. Thanks :)

My standard recommendation for this is The Cartoon Guide to Genetics. It may sound overly cute, but it's actually reasonably information dense, and pitched at intelligent readers with no background in biology. I covers the basics of both classical genetics and molecular biology.


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Are stroma lamellum and grannum lamellum the same?
I have a picture in my textbook that is confusing me as to how they are different.I tried looking for some info on the internet, but could'nt get it clear.Please help me.

Could  anyone please help with this homework issue,now that schools are closed?

I will try to help. But, in the future, please post a picture of the confusing diagram to help us help you.
edit: now that I see your diagram, I'm not sure if this answer is helpful. Will re-consider and possibly edit this response. Thanks for including it!
Grana lamellae refer to the lamellae (membranes) in direct contact with photosynthetic stacks (grana), where the stroma lamellae are the ones that are connecting between individual stacks (see here). My understanding is that they are functionally and compositionally very similar, the only difference being the region of the lamellae in question (link to paper, sorry for JSTOR paywall). Check out the Wikipedia page for Chloroplasts for some more diagrams. Maybe one here will help this make more sense to you!

Is thylakoid membrane continuous with inner membrane ?


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Parietal and Visceral epithelia
If you google visceral and parietal you get: The parietal layers of the membranes line the walls of the body cavity (pariet- refers to a cavity wall). The visceral layer of the membrane covers the organs (the viscera).
but
the first image that pops up is this :

I don't understand how the inner layer is covering and the outer is lining ?

Yes, the parietal pleura is on the wall of the thorax. That picture isn't great.  Each lung has its own pleural cavity, ie its own visceral+parietal.  Another important thing is the folding over.  Imagine the parietal pleura running along the inside of the ribcage...when it gets to the middle of the chest (the mediastinum), it folds over, or "turns the corner", and is now the visceral pleural running along the surface of the lungs.  The pericardium functions similarly, and so does the peritoneum/mesentery.  Here's another diagram that could help:


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what is “a group of living things that can interbreed and produce full interfertile offspring”?
lets call this term "collection" Example: group of humans.
what is not a "collection" horses and donkey: can't produce full interfertile offspring, lions and tigers: can't produce full interfertile offspring, Camels and Lama: can't produce full interfertile offspring.
And no this is not "species". Polar bear is a species grizzly bear is a species they can produce interfertile offspring, they are of the same "collection"
Two species can belong to the same "collection". Two different "collections" can't be of the same species.
And no this is not a homework question.
Why is this not defined in biology?
Why is this down-voted? I know what ring species is. First and last generation do not interbreed naturally. But it does not say they can not interbreed at all or can not produce full interfertile offspring.
The question is about having the ability of intebreeding and producing full interfertile offspring.
I will add more details:
The term species is a fuzzy term and makes a lot of confusion. I'm not asking about it.
There is a clean cut for all living things that intebreed and produce. For a given group of living things they either can intebreed and produce full interfertile offspring or not. There are many example.
Why is this clean cut not have a term in biology?
Again. This is not a "species" and from my point of view the term species should not be used in biology. Anything is a species... Homo sapiens, Neanderthals two different species although they had interbred and produced full interfertile offspring.....
Different dogs "races" are sometimes called different speices although they can intebreed and produce full interfertile offspring.
I already know about the fly experiment where the author claims that he got two different "species" of flies after some year of combination of sexual isolation and interbreeding. But no, all flies during the whole experiment of the same "collection" even if the author says they are different "species". The author did not make sure that they intebreed, he let them naturally decided whether they want to interbreed or not. They did not because they are not attacted to each other, but this does not mean they can not interbreed and produce full interfertile offspring.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and then edit your original question rather than posting a new version. Also, note that "homework"(https://biology.stackexchange.com/help/homework) can apply to questions even if they are not assigned as homework. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

This version of your question is clearer, but part of the reason that previous version was closed was because you don't demonstrate that you have done enough background research. ——— I recommend that you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley. You should also do reading on "species concepts", which I think may ultimately be what you are trying to understand ...

I am going to upvote this back.  The species question is not trivial - the above link to species concepts illustrates this in quotations, but this is not truly a matter of species.  The questioner's example of U. arctos and U. maritimus is a good one.  Typically we apply the species concept to what does interbreed, not what can interbreed.  There is no a priori limit to how far interbreeding could take place, and some genera such as Aquilegia are known for looser limitations.  Well researched answers here should make interesting reading.

Part of the problem here is you are using an overly narrow definition of species, by many schools of thought neanderthals are not a separate species nor are brown bears and polar bears. It all depends on whether you are a splitter or lumper.

Based on the biological species concept, you're referring to two different species that experience ecological isolation (also called "habitat isolation") as a prezygotic reproductive isolating mechanism.
See here for a simple explanation of various concepts regarding species.
This, of course, is just one of the many reasons (see here for more) why we have multiple species concepts. Some might argue that these organisms are the same species based on their ability to produce interfertile offspring. If said researcher wanted to do so, they would define these organisms using a different concept.
Recognize that “species” is an artificial construct to allow conceptualization and organization of an incredibly complex, dynamic, and otherwise continuously variable genetic world.
We have not found a perfect way to "cut up" the world neatly/consistently into describable and functionally useful units, and --in fact -- we likely never will. Why? Because the lives of these organisms do not care about our cataloging and description systems -- these concepts are strictly for humankind to functionally relate to and react to their presence. The concept chosen almost inherently relies on the underlying motivation of the describer for naming the organism in the first place.

And remember the problem with defining species when you include fossil specimens, where you cannot test for inter-fertility. As I point out to my students if allow a single species to be distributed in time, (Aka a fossilized horse and a living horse are the same species), all of life can be one gigantic complex ring species.


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Could some identify this bird call? (from the hu - wolf totem)
What species is making this sound?
You can hear the sound it makes at the end of the music video: The HU - Wolf Totem

Before the wolves howling yes?

yes. it starts at 06:16 at the video

You could try the forum at xeno-canto.org, if you don't know about that site yet.

Same bird from Spirited away. There's a part when they get off the train when you can hear it. If you figure that out, you'll find the bird

I believe the bird sound belongs to a member of Gaviidae, specifically Gavia arctica, which has a common name of the Arctic Loon or Black-throated Loon in North America and Black-throated Diver in Eurasia.
The first impression when I heard this was a loon/ diver. Since The HU are Mongolian throat singers, I assumed that they likely used a loon/ diver from Mongolia of which there is one breeding species of the five members of Gaviidae. You can listen to calls and sounds of Arctic Loons here: Macaulay Library
The Arctic Loon sounds much higher pitched than other species of Gaviidae, which is similar the call in the song at 6:16.

Yep, Loon was my thought too. Amazingly eerie calls.


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What are the obstacles to a quick survey of statin usage in COVID-19 patients?
A recent preprint paints a grim picture of the effect of role of obesity in COVID-19 infection.  A high role of C-reactive protein (CRP) is specifically indicated as a risk for critical illness.
It is possible to reduce the level of CRP by statin administration, but statin administration raises the level of ACE2.  It is not known whether that increases or decreases the risk from the virus.  The use of statins for coronavirus patients has been suggested - so has the possibility of the discontinuation of statin use by infected patients.
Obviously I would hope to see a study of statin use in COVID-infected patients, and one does begin recruiting this month.  The entry, however, says that it will be completed in August 2021.  My thought is that surely somebody could run around the New York COVID wards with a clipboard, though I'd hope for a wiser way to do this, asking patients whether they use statins versus whether they have ever turned down the suggestion of taking statins when their doctor mooted the issue, and seeing how many of which group ended up in the ICU.  What are the factors preventing data like this, which could have such influence on the way people respond to the outbreak, from being collected and published within a couple of weeks?

Because this is not the way a clinical trial is done. If you are not blinding the patients/doctors you at least want to randomize the patients into treatment groups, otherwise you will possible severely skew the data you get out. Or select already much sicker patients for your "study" in one of the arms which will either affect the outcome or mask small effects of a drug.

I’m voting to close this question because this is a suggestion for a clinical trial of a drug, not a question about biology in the terms of SE Biology.

The problem with your setup is that by targeting an ICU ward you are already narrowing your study to those who developed severe COVID-19. A more robust design would be a retrospective cohort study, where the exposure of interest has already been recorded.
E.g. the UK Biobank (~500,000 participants) has recently incorporated SARS-CoV-2 test results into its dataset, so you could use this to:

create a case/control split based on exposure (i.e. patients' historic use of statins)*
study the effect this has on outcome (i.e. development of severe COVID-19)

In  this  study,  we implemented rapid dynamic linkage, which allows us to provide a regular feed of new COVID-19 (SARS-CoV-2) test results to UK Biobank to facilitate rapid and urgent research into the epidemiological and human genetic risk factors for severe infection in the cohort.

Dynamic linkage of COVID-19 test results between Public Health England’s Second Generation Surveillance System and UK Biobank, Microbial Genomics (2020) **

* Or any of the other thousands of variables recorded in UKB.
** Disclaimer: I have worked on this project.


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Is there any current knowledge of how DNA polymerase is "motivated" to perform error corrections during transcription?
I was trying to understand the process of how polymerase performs error corrections on DNA. Every paper on this topic mentions what happens during the process, but there's no mention of how it happens. I even looked up the page on enzymes and it only explains enzyme binding sites, enzymes acting as catalysts and the types of reactions the enzymes perform.
It'd be reasonable to theorize that codons on DNA would have chemical properties that can attract certain enzymes to them to start the transcription process. But during transcription when the enzyme makes an error, what incentive does the enzyme have, to move backward to correct the error? I know that sometimes the error correction is performed only after the transcription, but the question is the same: How does the enzyme know what to do? Moreover, if enzymes were mere catalysts, does this mean that even without an enzyme, the DNA would get transcribed at an extremely slow rate? Could this mean that the "software code" that contains instructions of what to do during a transcription, is in the DNA itself?

Biologists look for mechanisms, not "motivations". No enzyme has "incentives" to do anything. Enzymes perform their functions because they have a chemical propensity to do it (encoded in their primary, secondary, tertiary or quaternary structure). Not because they feel any "obligation" to do so. Error-correcting mechanisms are just a type of propensity encoded in the enzyme's structure. It is a probabilistic event, whether they do or not, favored thermodynamically. Transcription involves many enzymes & proteins, not just polymerases; transcription would certainly not occur without enzymes.

Language and personification of enzymes aside, would you be satisfied with an answer to how does polymerase recognise it has made error as oposed to situation when it has integrated correct nucleotide? In other words what is the pysical stimul which triggers exonuclease activity of DNA polymerase? That would be answerable scientific question.

By motivation/incentive what I meant was the mechanism which makes it perform such a specific action. Codons showed us there was some kind of programming, so perhaps the way enzymes and proteins are folded are a kind of a programming that makes cellular bonds behave in a certain way. Anyway, from your replies it looks like we haven't figured this out yet. @ BagiM: I'd definitely like to know how the polymerase recognizes an error, but the answer would need to explain both the how and why of what happens. I reckon science doesn't yet have that answer.

There are no codons on DNA, only deoxribonucleosides.


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What defines a single organism?
I suppose what prompts me to ask this question is my wondering if it is possible to have a multicellular prokaryotic organism. For instance, can a biofilm be considered a single organism? Why or why not?
Why is it that multicellular prokaryotes do not exist (if they do not)?
At what point can a collection of cells be considered one whole -- do they need to all share identical DNA?
Fire away.

What defines a single organism is ongoing debate in biology. It will probably never be answered because it is a human attempt to create discreet categorizes for something that exists in a continuous spectrum.  Because there is a lot of gray area, generally when dealing with an edge case an author will say what definition they are using.

I agree with John. See here for an example of a discussion of issues and proposed definitions. I don't necessarily agree with the proposed definitions, but I think the article does an ok job of pointing to some literature for further discussion.


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Ways cancer cells spread through blood
If I understand correctly when tumor grows, it can reach blood vessel and then spread through it to another organ - it called metastasis.
How do cancer cells then are spreading through blood? Do they just flow the same as another  blood cells? Or maybe they connect to erythrocyte and drive on them?
Also, it will be useful if you provide metastasized cancer cells sizes, at least ranges

Sorry I'm having a hard time understanding how the first sentence connects with the rest of the question... What is the relationship between angiogenesis and metastasis?  Also, you'd be better to narrow it down quite a bit... "Cancer" is a huge subject with tons of different types.  Please [edit] to clarify

@rotaredom, sorry maybe I used wrong words, English is not my native language. Is it more clear now for You?

A short and abbreviated summary:
When tumors grow to a certain size, they will start to develop a "tumor microenvironment", which is a umbrella term for all kinds of cells and tissue beneficial to the tumor, in most cases fibroblasts (cancer-associated fibroblasts) and macrophages (tumor-associated macrophages), but it depends on the specific kind of tumor and its organ.
As tumor cells exhibit a drastically increased metabolism, they will begin to suffer from hypoxia (low oxygen concentration), which is signaled via several different biochemical pathways to the microenvironment and leads toward angiogenesis, the creation of new, often malformed, blood vessels, towards the tumor mass.
The tumor can now increase its mass further due to the continual metabolic supply and the cells can undergo a process called "epithelial-mesenchymal transition", which will allow the tumor cells to "detach" themselves from the primary organ (intravasation), enter the blood system and colonize "pre-metastatic niches" => new tissues and organs.
Some tumors are able to prime distant organs for metastasis via the secretion of specific factors and in many cases tumors show a distinct preference to metastasize in particular organs.
Sources:
Ralf et al (2007): Molecular regulation of angiogenesis and lymphangiogenesis
Costa-Silva et al (2015): Pancreatic cancer exosomes initiate pre-metastatic niche formation in the liver
Egeblad et al (2010): Tumors as organs: complex tissues that interface with the entire organism
Bu et al (2019): Biological heterogeneity and versatility of cancer-associated fibroblasts in the tumor microenvironment
Jang et al (2019): Integrins, CAFs and Mechanical Forces in the Progression of Cancer

Thank You, this answer is informative and useful, but, unfortunately doesn’t directly answer the question (minus not from me)


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Why is muscle force more dependent on cross-sectional area than on fiber length?
I was looking up why smaller animals are proportionally stronger than larger animals. The answer that comes back everytime is that muscle force depends on the number of muscle fibers, which is proportional to the cross-sectional area of the muscle.
However, I don't understand why muscle force wouldn't depend on fiber length.
I'm not a native english speaker, so I'll try my best to articulate my reasoning in the most concise way possible.

Force is exerted by the myosin motors. Force is therefore proportional to the number of myosin motors.
The number of myosin motors is proportional to the fiber length.
The number of myosin filaments is proportional to the cross-sectional area.
Then, muscle force is proportional to muscle volume, and therefore to muscle mass.

What am I missing ? Why is muscle fiber length not that important to muscle force ?
Thank you in advance for your help.

Here is a thought experiment that might help. Consider a single muscle fiber as being like a rope. Granted, a rope won't shorten on its own, but if you think of an isometric muscle contraction, then it's closer to what is happening when a single fiber contracts.
Now think about two situations:

You double the length of the rope. Does the total force that the rope can hold get larger, smaller, or stay basically the same?
You halve the length of the rope by doubling it up (so two ropes instead of one). Does the force that the rope can hold get larger, smaller, or stay basically the same.

So lining up more fibers in series is like making a longer and longer rope. It's still basically as strong (or weak) as a single rope. But when you bundle more ropes, increasing the cross-sectional area, the overall force that they can hold increases.
I'm not sure why a thought experiment needs citations, but here you go:

The canonical source for discussion of muscle fiber architecture is Gans C. 1982. Fiber architecture and muscle function. Exerc Sport Sci Rev 10:160–207.

I see... but I was thinking of the myosin motors kinda like people in a game of tug of war. If you increase the number of people, don't you increase the force ?

To expand on the rope analogy, is it correct to think of the protein strands as ropes which would be glued together in some places (similar to how myosin binds the actin strand) ? If so, then wouldn't it be correct to think that glueing the ropes in several places is more robust than glueing the ropes in only one spot ? I'm sorry If I'm missing something obvious about how muscle works... I feel like my brain isn't wired correctly today

@Gabel Luc, I was a part of game of tug war without a rope as a kid. The kids did hold each other hands as a substitute. They also decided to put the older stronger kids at the ends so they can better pull. Stupid. I was in the middle. It was painful. Imagine seven people puling your one hand and eight puling on your other hand. There was no question of me contributing, I was just holding myself together. My joints felt like giving in any second and I did let go the hand very fast. Ever since I understand that the force the chain of people can exert is only what the weakest link can withstand.

There is a distinction to be made between the tensile strength of the muscle, that is, how much force can be applied to it before it breaks, and the strength the muscle is capable of applying to move something. In an actual game of tug-of-war, the rope is very strong, and what is being contested is the motive strength of the two teams. But the motive strength of a muscle is obviously no greater than its tensile strength, which as a matter of materials science is measured on a per-area basis. There may be more to it than this, but I think this is at least part of the answer.
To extend the tug-of-war example, if you had unlimited staffing to pull stones up the ramp to the pyramid, you would add pullers to each rope until you were afraid to add any more because the rope might break. So the pulling strength would ultimately depend on the number of ropes.


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Is it possible for virus infected cells to continue to present a self-antigen on the MHC1?
Forgive my ignorance, as I'm new to immunology, however it seems like there would be some amount of positive selective pressure for viruses to develop the ability to continue to present the host's self-antigen on the MHC1 of a newly infected cell, thereby disguising the infection from the body's immune system (or at least from the cytotoxic T cells).
Is this in theory possible? Or is there a reason it cannot occur.

Self antigen is presented throughout viral infections.  You seem to think that cytotoxic T lymphocytes respond to absence of self. That’s backward. CTL respond to their specific peptide target no matter how much self antigen there is. In a typical response, there may be 100,000 self peptide/MHC complexes and 100 viral peptide/MHC complexes, and that’s enough for a CTL response.
One trigger for NK cells is absence of self, so perhaps that’s the source of your confusion.

So viruses cannot avoid displaying at least some viral peptides on the MHC complex?

Many viruses, especially members of the herpesvirus family, try, in that they express inhibitors of MHC Class I antigen processing. Even those viruses don't seem to completely succeed. So no, viruses can't avoid it completely

From what I know, the cell does not actively choose to display viral antigens on its MHC 1 receptors. As proteins within the cell are inevitably degraded as a part of garbage disposal, these peptides are transported to the ER, where they bind to MHC 1 and display on the cell surface. When a virus infects a cell, some of its proteins are similarly degraded, either by the cell's own defenses or as a part of their normal life cycle.
So, there will inevitably come a time when a viral antigen will make its way to a cell's surface. The only way to stop it would be to stop protein degradation in the cell entirely, which is not a good idea. What viruses do try is downregulating MHC 1 molecules themselves, so there are less receptors to display antigens, but a reduced MCH 1 expression attracts the attention of NK cells.


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How to biologically interpret path weight summation in weighted and directed gene regulation network?
I've considered asking this question on Bioinformatics SE, Mathematics SE, and Stats SE, however I've judged that my question belongs on Biology SE because I am interested in a biological (domain-specific) interpretation rather than a further development of the mathematics or software.
My question pertains to applying graph theory to biology, so first I will describe the graph in its mathematical properties and how they reflect biological properties.
The graph
Let's consider a weighted and directed graph whose nodes represent genes and whose edges represent the binary relation gene A regulates gene B. The directionality of the edges is imposed in order to reflect that gene A regulates gene B does not imply that gene B regulates gene A. The magnitudes of the weights are to represent some measure of how "strongly"  one gene is regulating another, and the signs of the weights are to represent whether the regulation is upregulation (positive) or downregulation (negative). For this graph, edges with a weight of zero are considered equivalent to 'no regulation' and should be excluded from the graph.
Path Analysis
Restricting ourselves to paths that do not visit the same node twice, what is the biological interpretation of the sum of the weights (of the edges) of a path between two nodes in the aforementioned graph?
I have conflicting intuitions. For example, why would these weights be additive? I'm not imposing that such weights have to be correlation coefficients, for example, but they are commonly used weights in networks that are not additive so it warrants some consideration in the more general case. If they're not additive, then their summation is not necessarily meaningful. Conditioned on being meaningful in the first place, my other inuition is that the meaning of such a summation would reflect the strength of 'indirect' regulation

There's quite a bit of use of graph theoretic approaches in gene regulation, so I'd suggest you start there and Stand on the Shoulders of Giants rather than reinventing gravity:
https://scholar.google.com/scholar?hl=en&q=graph+theoretic+gene+regulation
Although this isn't my area of expertise, I think the thing most obvious to me as a biologist and statistician is:
Sums are misleading in non-linear systems
Biology is very non-linear. You can probably get closer to linear in the graph you are describing if the weights reflect log-transformed ratios: this transformation makes a multiplicative system linear. But even after this transformation, you are making substantial assumptions. The only way to verify those assumptions would be with either a more complex model of the underlying system (since the graph you describe is quite abstracted) or the old-fashioned way: by experiment.

We have the same concern about the weights, as additivity is one of the conditions of linearity. Since posting the question I've been thinking about how to refine my question to be particular weight function, otherwise my question has multiple answers depending on what properties we can assume about these weights.

Yes, there are transformations that can linearize. A good point in general, although it doesn't answer my question. Partly my fault as I have not specified what operations are valid on these weights.

@Galen Overall, I think the question is a bit ill-posed. Rather than starting from graph theory and thinking about how graph theoretic measures should be interpreted biologically, I think you want to start from biology and figure out what biological question you want to answer. Then, the hard step that represents an intellectual contribution to science is deciding how to use the graph theoretic tools you have.

I think my question is ill-posed because it isn't specific enough. I think more would have to be said about the weights before an interpretation is possible.


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How to Identify Astragalus Species
I have several photos of a plant I believe to be in the genus Astragalus. I would like to determine the particular species in my area, the foot hills of San Diego County. Do I need a microscope to determine species, or can it be determined from the naked eye? How exactly should I proceed?


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An online tree of life with extinct species present?
There are awesome online phylogenetic trees such as OneZoom.
But they all only list living species.
I want to see dinosaurs between birds and crocodiles.
I wanna see that humans are reptiliomorphs and eupelycosaurs.
species.wikimedia.org seems to contain this info, but it's not presented in a navigable tree structure.

The tree of life project is your best bet, its not 100% complete but it is more complete than any other project I have ever seen, and unlike most actually includes many if not most extinct taxa. http://tolweb.org/tree/phylogeny.html
It also includes citation and brief descriptions of links and groups to make it easier. Some extinct lineages suffer from unresolved phylogenies but many of those are in constant flux or are actually unresolved in the fine scale so I can't blame them, especially considering they were originally based entirely on genetics, and is updated constantly.

Had this same question, and after a lot of digging, came up with this http://lifemap.univ-lyon1.fr/explore.html
Very cool tool!!

cool but dinosaurs are not included other than a footnote.

A link is not an answer in terms of SE Biology. Please finish the [Tour] and read the help on answering questions.


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Coronavirus capsid missing?
According to several sources, Coronavirus is a helical virus, i.e. it should have a helical capsid. Although most sources did not labelled or pointed any kind of capsid. It was mysterious to watch diagrams of spherical envelops with no underneath capsids.

Cutaway view of coronavirus from Wikipedia
David Goodsell painting on PDB

No mention of capsid.
Initially I guessed the proteins around the RNA fibre formed the capsid, not labelled otherwise. Alternatively I was speculating whether coronavirus is lacking the capsid.
However a researchgate paper picture (heavily diagrammatic) shows a polygonal capsid, the picture is captioned as coronavirus.

It makes me think of whether the capsid is like a hollow spherical or polygonal thing spirally wrapped.
Now my questions are .

What is the actual/ realistic shape of coronavirus capsid?
Does it really contain a capsid?
(Just speculating) Is it SARS-CoV2 lacking a capsid, and thus special exception from g eneral description of coronavirus?

Just to clarify - are you asking about coronaviruses in general, or about SARS-CoV-2 specifically?

Yes I am asking about Coronavirus in general but is Sars cov2 an exception?

"helical" does not mean "spherical". Who says coronaviruses are "helical" (esp. their capsids)?

Does it really contain a capsid?

Yes. Coronaviruses have a capsid, but it's not reminiscent of the polygonal (icosahedral) capsid depicted in the Research Gate picture you referenced. Icosahedral capsids form a sort of shell around the viral genome, where helical capsids actually bind the viral nucleic acids, holding them in a more rigid shape.

Is it SARS-CoV2 lacking a capsid, and thus special exception from general description of coronavirus?

SARS-CoV-2 is not an exception. In fact, its nucleocapsid is a target for diagnostic tests.

What is the actual/ realistic shape of coronavirus capsid?

It is actually depicted in Goodsell animation you referenced. The nucleocapsid proteins are the squigly bits in and around the genomic RNA (labeled "N", for Nucleocapsid). The actual capsid is the complete complex of N proteins bound to genomic RNA, so it doesn't have that polygonal outline that maybe we're used to when we see depictions of viruses. If you want a more detailed look at the actual capsid protein structure, there's a depiction of its crystal structure in this New York Times piece co-authored by Carl Zimmer.


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Mutated and unmutated PCR product
If I have a mutated colony containing the fusion protein, mCherry instead of the stop codon TAA, and an unmutated colony which does not contain the protein. Why will the PCR products of the two colonies have the same size?
I thought that since the mutated colony contains the protein instead of the stop codon, this would cause this product to be larger in size than the unmutated product. However, from experimental data it shows that both products are of same size. Could someone please explain why this is?
Thank you!

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, your question should show evidence of prior research and some familiarity with the relevant area of biology. Note that it is extremely unlikely that you have replaced the stop codon with a protein. ——— Please do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

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

If mCherry was successfully cloned replacing the stop codon, you would indeed expect a fusion protein that is about 27 kDa larger than the original protein.
However, with a PCR you are not testing for the full length protein, but rather for a part of the target gene sequence.
The length of the PCR product very much depends on the position of your primers: If both primers are targeted at your unmutated sequence, the product size will not change by adding mCherry behind the targeted sequence. The product size of the PCR would only change, if one primer is located before or in your unmutated protein and the other one behind mCherry. This would probably result in a very large PCR product and hinder the PCR reaction from being effective.
To check for correct integration of mCherry, you would need to design a primer pair with the forward primer in your unmutated protein and the reverse primer in mCherry. This should result in a product in the fusion protein colonies, but not in the unmutated ones.
Alternatively, you could sequence your products.

Whoever gave a -1 to my answer, could you please explain why?


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Are there any solid inorganic compounds that are part of the human body?
I'm more interested in parts physically attached to the body, if that makes sense.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, your question doesn't seem to make sense as currently written — the title is asking about solids, but your examples are liquids. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

bone and teeth are calcium phosphate.

@tyersome Sorry, I corrected the error.

@John Thanks. I'm surprised I did not think of that

Calcium carbonate stones in the utricle and saccule of the vestibular system are pretty interesting (I think they could be what you're looking for).  They are part of the response to acceleration; if they're messed up, you can get vertigo.

Neat! That works just fine, thanks


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Is there any other sources of hydrogen carriers for the Electron Transport Chain other than the 3 main metabolic pathways?
I am learning about the 4 main metabolic pathways for cellular respiration. I learned that NADH and FADH2 hydrogen carriers are essential in the Electron Transport Chain, because they deposit their hydrogens (which consist of protons and electrons), which are used to power ATP synthase (reattaches ADP and Pi together to form ATP) in the inner mitochondrial membrane. The reduced hydrogen carriers must come from glycolysis, pyruvate oxidation, and the Krebs cycle. I'm wondering if all those pathways were inhibited (and essentially broken completely) let's say, is there any possible way for the Electron Transport Chain to get hydrogen so that it can still work?

Hey welcome to the site!  Just to clarify the start of the question slightly... We generally speak of the electron carriers carrying electrons, not hydrogens... it avoids confusion with the hydrogens which are being pumped across the mitochondrial membrane, which are not the hydrogens attached to NADH, for instance.  In fact, the energy from the electrons on NADH pumps 10 H+ across the membrane (and it only loses one in the process).  Also, NADH actually drops off four electrons, two of which are not associated with a hydrogen at all but rather the pyrimidine rings.

Yes, but you should wait until you meet them in your studies. And you seem to be looking at things backwards. It's not a question of getting the ETC to "work", it's a question of whether there are any oxidative pathways that produce NADH or FADH2 to provide energy for an organism through using the ETC. You're very welcome to this site, but finish reading the Tour (you'll get a badge so that we know you have), and look at the Help on asking questions.


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What are these lentil like eggs? (Utah, United States)
I've found these (what appear to be eggs) attached to an apple tree in central Utah USA.

The eggs are less than 1/2cm in length, have a waxy appearance and are attached to the branch at one end. Visually and tactilely they are quite similar to lentils.
I thought they were Box Elder bug eggs, but after a google image search I am convinced that is not what they are. What are they?

They look just like katydid eggs.
Image for comparison from the Missouri Botanical Garden:

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Sickle-cell trait : Why is only one type of beta chain found in any one hemoglobin molecule?
I was reading a textbook (iGenetics, 3rd edition page 71), and came across the following passage:

Homozygous bS bS people make Hb-S, the defective hemoglobin, with two
  normal a chains specified by wild-type a-globin genes and two
  abnormal b chains specified by the mutant b-globin bS allele: these
  people have sickle-cell anemia. Heterozygous bA bS people make both
  Hb-A and Hb-S and have sickle-cell trait. Because only one type of b
  chain is found in any one hemoglobin molecule, only two types of
  hemoglobin molecules are possible—one with two normal b chains, the
  other with two mutant b chains.

(Emphasis mine)
My question is: Why is only one type of beta chain found in any one hemoglobin molecule? Or is this statement simply false?
I did search biology SE for similar questions, and found this one, but it is phrased poorly and the only answer does not address my question.

For one specific hemoglobin molecule, yes it's just one type of beta chain.  In the case of a heterozygote, this hemoglobin molecule could be expressing from the bS gene OR the normal beta gene.  Let's call it a 50/50 chance for each hemoglobin to be expressing bS.  Because RBCs have a ton of hemoglobin in them, this 50/50 or so expression of bS wouldn't be enough to cause RBC sickling and disease, and it also helps explain the heterozygote advantage vs malaria.

"Let's call it a 50/50 chance for each hemoglobin to be expressing bS." What? Hemoglobin is a protein, not a cell , it doesn't "express" anything.
Each hemoglobin molecule has two beta chains: the question is: why do we never find one normal and one bS chain in the same hemoglobin tetramer.


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Tiny worms found inside my house
I noticed spider cob hanging of my light bulb. That spider web was full of moving creatures. I quickly removed them and threw in the big. Wanted to find out what could that possibly be. I opened up light bulb and no traces to the ceiling. I found hundreds of them fallen on the floor, some where still moving. I do not have a good quality picture, but I have taken a video of it. Would anyone be able to identify? I live in Australia QLD, i think this could have been seeded by some fly?


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Why is untreated trypanosomiasis invariably fatal in humans?
If left untreated, African trypanosomiasis will invariably kill the patient. The human immune system is unable to clear the infection.
I am aware of a few other infectious diseases with this property and I have a rudimentary understanding of the reason why. For example, I'm told that rabies has evolved to be uniquely good at attacking the brain because that's the only way it can spread to other hosts, and the neuroimmune system, being quite different from the peripheral immune system, is not capable of dealing with a virus that has this property.
I do not understand why the human immune system is ineffective against trypanosomiasis. One explanation I was offered is that the human immune system is just not very good at fighting parasitic infections (compared to viral and bacterial infections). However, this can't be the full answer, because there are other parasitic infections that may go away on their own without treatment.

Welcome to SE Biology. As a veteran contributor to StackOverflow you will know how important it is to follow the guidelines of a SE community. Our guidelines, like most, specify the audience (biology researchers, academics, and students) which is important in that answers will assume a certain level of knowledge, just as on SO) and that posters are expected to show that they have researched a question before asking it. If you search for "trypanosome immune evasion" you will find many articles on a very broad field.

African trypanosomiasis, or sleeping sickness, is caused by the protozoan Trypanosoma brucei, a single-celled eukaryote.  Being eukaryotic, it has a cell nucleus and a larger genome than most bacteria; it also has a flagellum with which it can propel itself.  Infection with T. brucei occurs via the bite of a blood-sucking fly, one of several species of tsetse fly.
The mammalian immune system has a difficult time with T. brucei because of an effective set of adaptations.  The protozoan's surface maintains a dense coat of a particular glycoprotein on its surface which generally hide other necessary surface features such as chemical receptors and ion channels. Since it is this glycoprotein that the adaptive immune system will encounter, that molecule is the one which it will develop antibodies to recognize.
Within a few days the protozoans would be recognized and soon eliminated by the immune system except that T. brucei at random times changes the glycoprotein used as its surface coat.  The mechanism that does this is called a variant surface glycoprotein (VSG) expression system.  The organism has a repertoire of about 1500 different proteins to  select from to use for a new glycoprotein coat.  The overall effect is that by the time the immune system is able to flood the body with the antibody type it has developed, most of the T. brucei population is not recognizable by those antibodies. T. brucei devotes a significant portion of its genome and its protein production to this immune evasion system.

good answer!, also, the trypanosome gets through the blood-brain barrier where immune system options are fewer, and fewer chemicals can get there.

This makes sense. I wonder if you have an opinion as to why a VSG-like mechanism hasn't evolved in other kinds of infectious parasites, though? It seems that it the trade-off involved would be similar for them (i.e. the benefit of being more effective at infection versus the cost of the additional genome size and protein production)

@Brian That's probably wide enough topic for a separate question, but I think the fly-mammal-fly lifecycle might have something to do with it. Malaria has a somewhat similar, but apparently separately evolved, mechanism of varying its surface characteristics. More here: https://en.wikipedia.org/wiki/Antigenic_variation

I hope you're not trying to give a new idea to our newest coronavirus, @brian!

Viruses are dumb, eukaryotes are smart.

@Brian Evolution isn't forward-looking. It doesn't seek out adaptations which would be useful; it merely preserves any adaptations which it happens to come across which turn out to be useful. (Of course, there isn't really any "force of evolution" which causes these things to occur. Evolution is merely the name we give to the self-evident fact that adaptations which propagate themselves propagate themselves.)


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How can a joint extend or flex?
The idea of a joint flexing or extending doesn't make sense to me, I can see how a leg or an arm might extend or flex but how does a joint extend or flex ?
"The hip joint is most stable when it is extended and the ligaments are taut."
Does that mean in the state that is most right in this picture ?

It is really unclear what you are asking, the picture you show is that of the hip joint extending and flexing.

Which is why I specify the “figure/state which is most right”

That doesn't help, lets start with whether you mean right as opposed to left or right as in correct?

 Short Answer
The words extension and flexion actually mean to increase or decrease the angle of a joint, respectively. In other words, the terms are directly related to the joints themselves. Bones can only move relative to each other at joints, so when the angle between two bones increases or decreases, that action is occurring at the joint. In other words, the joint acts as a vertex of the angle of movement.

 Long answer
In general, one should think of extension as "increasing the angle of a joint" and flexion as "decreasing the angle of a joint" (see here, here, here, here, here, here or here for reference). From Saladin's 2015 Anatomy textbook$^1$:

Flexion = a joint movement that , in most cases, decreases the angle between two bones.

Put differently,

Flexion refers to a movement that decreases the angle between two body parts.

I think where you are confused is that you do not understand what a joint is. A joint is anywhere where two bones articulate (or touch). Although various types of joints exist, those that readily move well enough to receive movement terms such as flexion/extension are called synovial joints.
At any given synovial joint, two bones are able to move relative to each other due to a cavity that provides space for movement -- the synovial cavity. Put differently, bones (which are solid, unbending objects) move relative to each other during our body movements, and this relative movement occurs at joints.
Using your example of arms and legs:
When your arm flexes/extends, what's happening is that the head of your humerus is moving inside the glenoid cavity of the scapula. This movement at the "glenohumeral joint" results in the entire arm (humerus and all distal components) either swinging forward or backward  due to the angle of the glenohumeral joint increasing or decreasing (though, actually, other movements are possible as well). The same applies to the hip.
Another example is the "elbow" joint -- which actually consists of 2 joints: the humeroradial and humeroulnar joints. Consider when you "flex your arm" as in showing off your bicep. Yes, your lower arm (forearm) moves, but the movement all occurs at the point of the elbow at these two joints. In other words, the elbow joints form the vertex of the angle between your upper and lower arm bones. When you "flex" your arm, the angle of these joints decreases. When you return your elbow to being straight (i.e., "extend" your elbow), your are increasing the angle of the humeroradial and humeroulnar joints.

$^1$ Saladin, K. S. 2015. Anatomy & Physiology: The Unity of Form and Function. Seventh ed., McGraw-Hill, New York, NY. 1248pp.


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Why some plants can be propagated from a leaf cutting but some can not?
I understand the process of leaf-cutting propagation as following:
1) with the help of auxin from the leaf, callus is forming on the wound and then roots are forming from callus,
2) with the help of cytokinin from roots, shoots are forming.
Is it wrong or too simplified or do I miss something? Why some plants can do this and some can not?

Can we ever really know the plant cannot do this? All we can know is that combinations of conditions that have been tested did not work for that particular species/genotype.

You have a point. It seems like theoretically any plant can be propagated by leaf cutting in some specific conditions within some time. In this case are there any clearly identifiable characteristics of particular species/genotype that affect this ability, ceteris paribus? Or is it rather complex thing?

What I have seen people to do is mostly trying protocols that work for related species and trying large matrix of conditions on large set of genotypes etc. Once the protocol is established people seem to move on to using it instead of researching deeper reasons. If you find any overarching theoretical work on this matter I would be very much interested.

A major factor would be how fast a leaf dries out, A leaf that dries out quickly will not be able to keep photosynthesizing long enough to grow roots to collect more water.

The plant has to be able to develop meristems from the leaves, and plant stem cells for the roots?

@John it is necessary but not sufficient condition, isn't it? There is at least a problem of "blind" cutting: the cutting roots but does not produce any shoots to develop new full-fledged plant.

I have mostly experience with plant tissue culture on agarous media where drying of leaf is not problem. Still, some plants respond and some don't. Species I work with has been considered recalcitrant to in vitro for decades but then a different cytokinin molecule was tried and shoots started to form.


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What spider is this
Live in London I have this in my backyard. Want to know what kind is it...Also does it bite?

Please provide approximate size

May we get a view from the front? The eye pattern can be very helpful.

looks like a kind of wolf spider. legs not quite long enough for a dolomedes


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Modeling the production of mRNA
I have the following example of how an equation for the production of mRNA in a particular organism could look like:

Consider the following equation for the production of mRNA for a gene Y. Gene Y is expressed from a promoter that is repressed by protein R. For example, if Y is GFP above, then R would be TetR.
  $$
\beta_{Y m}=\left[\frac{\beta_{y \max }}{1+\left([R] /_{K_{R Y}}\right)}\right]
$$

And now I am trying to understand what the different variables of the equation are.
$\beta_{ymax}$ must be the maximum rate at which mRNA can be produced and $R$ is concentration of a repressing protein, but what must then $K_{RY}$ be? Is it as simple as that it is an inducer for the production of mRNA?

Where did you get the equation from?

At a first guess, $K_{RY}$ is a dissociation constant for the repressor binding of the gene Y promoter, but it's hard to say without more information. e.g. David's question. Also, it is best practice to reproduce the equation as text rather than as an image, to make it easier for screen readers.

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Image Dataset for Cardiac cells for Mus musculus?
I'm working on developing a transfer learning model to detect cells in a culture using microscopic images.
for that i require data set of images having microscopic images of various cell types. Is there any such database present? Any open source research work having  microscopic images of cardiac cells that can be used?

Sure help yourself with the broad institute image sets collection
Broad Bioimage Benchmark Collection - Annotated biological image sets for testing and validation:
https://data.broadinstitute.org/bbbc/image_sets.html
And the EMBL-EBI:
https://www.ebi.ac.uk/bioimage-archive/
No mouse cardica cells, but I am confident you can easily do transfer learning after training on those.


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Search engine for biological/medical/epidemiological science literature
I hope this question is appropriate for this exchange (I think it is too specific for meta?).
We are looking for a search engine that is capable of performing a search of all available biological/medical/epidemiological scientific literature (So more on the scope of Google than Elsevier or similar subscription services) and providing as many as possible of the following features:

Keyword search
Range of dates
Boolean terms (AND NOT etc.)
Option to download and sort
Email alerts.

Does anyone know of a search engine or service that has these capabilities? (A paid subscription is fine).
Thank you in advance for your patience.

Yes, this exists. The portal is called "Pubmed" and looks like this:

This portal allows you to search (have a look into the search-Faq) in various ways as well as getting email alerts, download your searches in different formats and so on. It indexes most (but not all) scientific literature for medicine, biosciences and all related topics and is probably the biggest database in this field. And its free.
Another possibility would be Google Scholar, which is focussed on scientific literature and can also be adapted to your personal needs. However, I usually prefer using Pubmed, but sometimes it is useful as well to use Google Scholar.


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What current evidence supports the use of hydroxycloroquine used as a prophylactic for (corona)-viral infections?
I've also read comments from doctors suggesting that hydroxychloroquine has been studied in the past as a potential prophylactic for viral infections.  A search through US clinical trials yields many results which mention this drug in connection to lupus, arthritis, and cancer.  But I have yet to find completed clinical trials which revolve around viral infections - does this exist somewhere or has this never been studied?

What has your research shown?

SE Biology is a question and answer site concerned with the mechanisms of biological processes, as you will see if you finish reading the Tour. Your question is about the results of clinical trials, which do not come into this category. There are ample reputable sources that provide expert and up-to-date information about efforts to combat the coronavirus, some of which are listed on our meta site. Please consult that.

The only double blind randomised clinical trial I am aware of is this one, examining the use of hydroxychloroquine for the treatment of HIV-1-infected patients.  It finds significant reductions in viral load, but not improvement of CD4+ counts.  How much change could be expected in 8 weeks I do not know.  There are in vitro studies, such as this one looking at dengue virus.
In combination with azithromycin it has been examined for the use in COVID-19 (pre-print, not peer reviewed), but without a control group I find it hard to call it a clinical trial, and there are other criticisms of the work.


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How to filter the PBD databank for "single-domain proteins with full length 3D-structures solved"
I am trying to reproduce a machine learning model that has been developed here. As one of the datasets, they use single-domain proteins with full length 3D-structures solved. Since I don't have a background in biology, I am not sure how to filter the PDB databank for these kind of proteins. Any help would be appreciated.

This question would probably be a better fit for the bioinformatics.SE. If I were you, I would take a look at the ftp/download section of the PDB and see if the documenation for that let's you figure out the appropriate filters. It may be necessary to downlaod the full pdb & filter then.

I'm voting to close this question as off-topic because it is about bioinformatics rather than biology. Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site for descriptions of what is (and is not) a good fit for this site. Thanks!


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Are there any "thermotroph" lifeforms?
I only found chemotroph and photoroph examples of life, but are there organisms that can use a temperature gradient to convert energy?

No, because temperature is a quantity related to the motion of molecules (or particles) in an ensemble (thus, kinetic energy) but such motion does not have a mechanism to transduce it into some form of useful energy for biological purposes. Chemical gradients are easily stored because of the highly specialized biological membranes (via specific ion channels, etc). Light (photons) can also be used via some proper transducers (photoreceptors), given that there is transduction into chemical energy (i.e. in photosynthesis). But there is no way to 'store' energy from temperature directly in biology because there is no transducer. Temperature differentials in purely physical applications exist, but there is no parallel for biology. All life forms depend heavily on chemical potential and physicochemical gradients, which is deeply rooted in the evolutionary history, you can find an interesting lecture on this topic here.