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what if there is a door for which our immune system has no key?

And as a B cell matures, it develops the ability to determine friend from foe, developing both
  immunocompetence -- or how to recognize and bind to a particular antigen -- as well as
  self-tolerance, or knowing how to NOT attack your body’s own cells.
  Once it’s fully mature, a B lymphocyte displays at least 10,000 special protein receptors
  on its surface -- these are its membrane-bound antibodies.
  All B lymphocytes have them, but the cool thing is, every individual lymphocyte has
  its own unique antibodies, each of which is ready to identify and bind to a particular kind of antigen.
  That means that, with all of your B lymphocytes together, it’s like having 2 billion keys
  on your immune system’s keychain, each of which can only open one door.

This is what Hank said in Crash course. So the b cells, each are having several unique antibodies and I also saw that this is true for T cells too and the dendritic cells  look for a helper T cell that can bind the parts of the intruders which the dendritic cell has presented on its membrane.
my question is
What if there is no antibody in any cell against an antigen?
Does the immune system has antibodies against all antigens in the world?
What happens if an antigen came into our body which has no antibody matching for it?

A clarification: each individual B cell has only one type of antibody. They can have many thousands of copies of it, but the copies are all identical.

@Matt this information is very useful for me.  thank you for the clarification

No problem. Incidentally, T cells are the same way - they have tons of T cell receptor (TCR) complexes on their cell surface, but all have exactly the same sequence, and are specific for exactly the same antigen. Now, as Joe Healey points out below, there can be cross-reactivity between antigens (sometimes substantial cross-reactivity, something he doesn't mention), which is the basis of a polyclonal immune response.

@Matt All the comments and answers are really a learning curve for me.I learned a lot like v(d)j gene, cross reactivity, polyclonal response. So thank you very much.

Most likely, another antibiody matching another antigen from the same infectious source takes care of it.

The same thing that happens to the native american when they were first exposed to smallpox. Extermination of 90%-95% of the population. https://en.wikipedia.org/wiki/History_of_smallpox
The immune system is unable to attack bacteria or virus which makes unrecognizable antigen. As a result the bacteria/virus continue to grow and grow unopposed, until the person dies.
The disease goes wild, spreads like wild fire, killing every single individual it infects. In the worst case scenario, the species may go extinct.
EDIT
Why do vaccines work.
Firstly the adaptive immune system is adaptive. The immune system generates new antibodies (ie new keys) by splicing together different version of the V(D)J genes in a big round of mixing and matching. Then it uses an enzyme called AID to induce hypermutation to that combination. The end result is a nearly limitless number of antibodies (keys).
https://en.wikipedia.org/wiki/Somatic_hypermutation
https://en.wikipedia.org/wiki/Antibody
However this process takes time. And during that time the bacteria/virus is growing and growing. Weakening the body. So it becomes a race. Can the body generate an antibody that recognizes the bacteria/virus, before the body dies.
A vaccine helps in this respect, because the vaccine is can expose the immune system to the antigen of the deadly virus/bacteria without actually using the active/live virus.
ie Some vaccines only uses pieces and parts of the bacteria/virus. The antigen is there. But the virus is dead.
In other older vaccines, the virus used in the vaccine has been weaken/mutated so much that it has a low probability of beating the body before the immune system. https://en.wikipedia.org/wiki/Edward_Jenner
In the Edward Jenner cowpox vaccine... the cowpox virus so happened to have antigens similar enough to smallpox, that antibodies against cowpox works on smallpox. And cowpox is not deadly to humans.
Now..  here is the interesting part. The arms race between host and disease has gone on for a very long time. So many viruses develop what is equivalent to chaff. These are proteins that stick out on the membrane surface and thus easily recognized by the immune system, but are rapidly changed. So by the time the immune system launches an aggressive response, the protein changes again. Kind like a disguise that a thief changed every time he robs a bank, so the police are always one step behind. The bacteria grows and grow. Constantly switching its antigen coat and eventually the person dies.
https://www.ncbi.nlm.nih.gov/books/NBK27176/
https://en.wikipedia.org/wiki/Relapsing_fever
A vaccine in this case, presents the immune system with the one part of the bacteria antigen coat that does not change. So an effective immune response can be made. However as experience with HIV antibodies has found, those constant parts tend to be protected by the parts that do rapidly change. So antibodies have trouble reaching it. And this is why we do not have vaccines for HIV. The constant regions are too well protected.
One response to this can be seen in flu vaccine. Here the virus changes it antigen coat not every few days, but on average once a year. So we try to predict what is the flu strain of the year.. and raise a vaccine to the antigens of the year. Sometimes the predictions are spot on, so the vaccine works perfectly. Sometimes the antigen predictions are a little off... so the vaccines don't work so well. And on a rare bad year, the predictions are completely off. And the flu vaccine do not work.

That's a great answer. I never read anywhere about production of new antibodies for new antigens. So I doubted how then we survived several diseases which are always evolving. you cleared it greatly.thank you for adding additional informations. thank you very much.

All the comments and answers are really a learning curve for me.I learned a lot like v(d)j gene, cross reactivity, polyclonal response. So thank you very much.

The Native Americans and smallpox
First I want to note that some of the posted answers are not quite accurate. For example, smallpox ravaged the Native American population because they did not have high-affinity MHC molecules for it, which is an evolved trait. MHC molecules must be capable of binding to a large class of peptides, at least weakly, to allow their presentation. There are only a finite number of MHC alleles in a given individual, and they tend to represent the most commonly found classes of foreign organisms.
The Native Americans were equally capable of creating anti-smallpox antibodies as any European, but that process was significantly slowed down due to not having MHC alleles which promote the presentation of smallpox, allowing the virus to accumulate to lethal levels before a sufficiently mature immune response could be mounted. You can bet that the survivors were the ones with MHC alleles that promoted rapid recognition of the virus!
Somatic hypermutation and affinity maturation
The way antibodies work is, B cells undergo both genetic recombination and an intentionally increased mutation rate called somatic hypermutation. This results in a virtually uniform distribution of new antibodies. These new antibodies are actually pretty bad at binding antigens, and at best, only roughly approximate them. This is one reason the first exposure takes so long to eradicate. When an antibody that weakly matches is found and the number of B cells rise, some of them begin to induce additional mutations to their antibody, a process called affinity maturation. The mutations that result in breaking the antibody end up discarded (those B cells die), whereas those that have an even stronger affinity result in the clone of B cells being positively selected for. This goes on and on until the resulting clone of B cells produce extremely high-affinity antigens.
The result of this is that virtually any possible "door" will have a "key", even if it is poorly fitting. Over time (and subsequent exposures), the key is fine-tuned. The only way a persistent antigen could evade an immune response, short of interfering with the immune system is if the antigen is extremely similar or identical to a self-antigen.
Some pathogens can avoid an immune response in indirect ways, such as frequently changing exposed antigens either by switching genes or through rapid mutation, covering the cell surface with self-antigens or innate, non-protein material, tucking conserved regions that act as epitopes deeply inside a protein, releasing molecules that inhibit the immune response, etc.
Foreign antigens resulting in production of anti-self antigens
An interesting thing to note is that, even if the antigen is similar to self, it will still often be detected. This can be highly problematic because selection against anti-self antibodies occurs when the B cell is first developing, during somatic hypermutation, but not during affinity maturation. A weakly binding antigen that is similar to a self-antigen may then stimulate the production of anti-self antibodies since the antigen is different enough from self that B cells specific to it are not negatively selected, but similar enough to self that the changes in affinity maturation are sufficient to convert it into an anti-self antigen (in other words, an antibody x steps away from targeting self-antigens results in negative selection, but affinity maturation results in y changes to the antibody, where y > x). This is one reason why some viruses can trigger auto-immune diseases.
Answering your questions directly

What if there is no antibody in any cell against an antigen?

If for some reason no antibody were even had the slightest affinity for an antigen, then there would be no problem, and a pathogen would trigger an immune response because of another antigen. If for some insane reason every single antigen on a pathogen (there are many) was not even slightly matched, then no humoral immune will be invoked. There still may be a cellular immune response (e.g. for viruses), and the innate immune system would still be active.

Does the immune system has antibodies against all antigens in the world?

The immune system has antibodies that bind a wide range of antigens, albeit weakly, and with high overlap. As a result, you could say that all possible antigens that are not too similar to self are countered by antibodies with at least some level of affinity. There is only a finite number of possible antigenic peptides, and of those, all that's needed is a weak interaction to trigger a full-blown adaptive immune response.
It's like going to an ophthalmologist. They don't have lenses for all possible refractive indexes, but they do have enough samples that, by trying them out, you can see which ones improve your vision. Going through this process allows gradual improvement, and eventually they are able to proscribe a perfect match.

What happens if an antigen came into our body which has no antibody matching for it?

A single antigen, as opposed to a pathogen with many antigens? Ignoring the cellular immune system, nothing would happen. It would be treated virtually identical to self-antigens (i.e. it would be ignored). Depending on how the pathogen behaves, it could be wiped out by the rest of our immune system, contained in a local cyst, or even result in a lethal infection.

If you have no antibody to a particular antigen, you have no immunity to that molecular pattern (and the organism it belongs to).
That's the basis of immunity.
This is why you have vaccinations. You are artificially exposed to an antigen your immune system hasn't seen before, so you sero-convert and then have immunity.
That passage is a little misleading though, its not quite one key-one lock, as it's possible for antigens to have slight crossreactivity (which is why you can be vaccinated against one thing, with a related thing (e.g. the old Jenner cowpox vs smallpox example).

Thank you for adding information like cross reactivity. I thought the same as in your answer i.e. we will die if we dont have any antibody against an antigen. But I cant understand sero conversion. I saw in  Wikipedia and they said it  is the time period during which a specific antibody develops and becomes detectable in the blood. I read it fully and understood what sero conversion is. But how is this is related to your answer. And if our immune system produce antibodies for vaccines why can't it directly produce antibodies for new antigens that enters our body? Thank you for the timely help.

You mix up two things: If there is no antibody, there is no immunity. And there will be none. If you vaccinate, you have at least low affinity antibodies, which are then adapted to fit better. This happens during infection, but this takes some time (around two weeks until full production of new antibodies, which might be too long for some diseases). Immunisations short-cut these time, as they mimic the infection and give the body the time to produce the necessary high affinity antibodies without being terrible sick.

@Chris The comment that you wrote, Is it  for cumulonimbus(me) or for Joe Healey?

@cumulonimbus It is to Joe's answer.

@Chris You're saying I'm mixing up 2 things? I don't see how? Your comment says exactly the same thing my answer did.

You say on one hand that if there is no fitting antibody, there will be no reaction, which is correct. Then you say that this is the reason why we vaccinate. Which is wrong, because if there is no antibody, which fits at least a little bit (low affinity antibodies), there will be no reaction to the vaccination. We vaccinate to train the body and have memory cells present in the case of an infection. This allows an immediate reaction, which otherwise takes some time.

@JoeHealey one thing I would mention is that cross-reactivity between antigens can be substantial, not just "slight" as you put it. I used to work making antibodies for research (Western blotting, IHC, flow cytometry, etc.) and I've made antibodies that cross-react with practically everything - sometimes intentionally, usually not. For example, my company has some monoclonal anti-phospho-tyrosine antibodies that just recognize a phosphorylated tyrosine residue, mostly independent of the surrounding sequence. There are many other examples - just search for motif antibodies.

@joe  All the comments and answers are really a learning curve for me.I learned a lot like v(d)j gene, cross reactivity,sero conversion, polyclonal response. So thank you very much.

@chris  All the comments are really a learning curve for me.I learned a lot like affinity, cross reactivity, polyclonal response. So thank you very much.

@MattDMo that's interesting. I was underselling it for simplicity, granted. I didn't realise it could be that extensive though, good to know!


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DNA adaptation in human life
Does our DNA adapt by human lifetime? Or do we have the same genetic information from birth to death?
I mean: What is usually called "evolution" means "natural selection" like this:
http://www.youtube.com/watch?v=hOfRN0KihOU&list=UUsXVk37bltHxD1rDPwtNM8Q
-stronger animals have more descendants, so they make bigger percent of strong animals.
But does evolution work by some primitive genetics-engineering too? Thank you.

Lewontin's recipe
A very nice way to consider natural selection is through the lense of Lewontin's recipe. Evolution of a given trait (tail length for example) through natural selection occurs whenever the three following conditions are met:

There is variation for this trait in the population

This variation is caused by mutations

Part (or the totality) of this variation is heritable

Heritability is the part of the variance in a trait that is explained by genes. It can be measured as a parent-offspring correlation.

The variation of this trait is correlated with fitness

loosely speaking, fitness is an index of both fecundity and survival

You can take two minutes to think about how logical it is that changes in frequency of variants (natural selection) occurs whenever these three conditions are met. You can imagine any objects you want (pencils of colors for example) and simulate these three steps:

Variation

different pencils have different colors

Heritability

simulate that your pencils reproduce (asexual reproduction is conceptually easier to understand) and offsprings have similar (or even the same) color than parents

Correlation between trait and fitness

Pencils of different colors have different fitness.
For example each red pencils create two red pencils the next generation while blue pencils do not manage to replicate at all.

You can quickly see how the red pencils become more frequent in your pencil population through time. If you wait long enough your pencil population will be totally composed of red pencils. And you'll need to simulate a mutation in order to create a blue pencil. I think you understand the how different are the roles of mutations and natural selection in evolution with this example.

Genetic Adaptation During Lifetime of a multicellular organism
For a beginner in evolutionary biology, saying that a multicellular individual's genome does not change during its lifetime might be considered satisfying. In reality it is slightly more complicated. Two elements that are mostly influent very early in the lifetime of an individual have to be considered.

While most mutations occurs during reproduction, some mutations does also occurs during body growth or stated differently during cell reproduction (Mitosis). In consequence, some pairs of your cells share exactly the same genome while other pairs of cells have a sligthly different genome.
Moreover, once some mutations had occurred within the development of an individual, these mutations might influence the fitness of the cells and therefore some alleles (variant of a gene) might raise in frequency while others decrease in frequency (Natural selection). It is important to understand that this process of natural selection select for cells that have a higher fitness and therefore do not necessarily select for the cells that allows the individual to increase its own fitness.

I don't fully understand what you mean when saying: "But does evolution work by some primitive genetics-engineering too?" Could you try to rephrase this question?
Please, let me know if I answered your question!

Note:
Here is a good way to understand the difference between "gene" and "allele". A gene might be a called the "eyes color" gene for example, while the three alleles of the "eyes color"  gene might be callsed "blue eyes", "brown eyes" and "green eyes". In this sense, the alleles are the different variants of a gene. Mutations increase the number of alleles and natural selection reduces the number of alleles by selecting for the allele that cause its holder to have the greatest fitness. If you understood that, it is already good!
Note: Natural selection does not necessarily reduce the number of alleles, several alleles might be kept (polymorphism) in certain "types" of natural selection (frequency dependent selection and overdominance (heterozygote advantage), fitness varies in space and/or time, selection acts on different levels). The "type" of Natural selection that reduces the number of alleles after some time is called directional selection.

Yes, you answered my question excellently. Thank you.

The concept that the environment directly changes DNA and alters the characteristics of the offspring falls under the heading of Lamarkism. In the context of DNA the  Lamarkian view would be that the giraffe got its long neck by stretching its neck cells reaching up to tall trees for leaves, which then (somehow) changed the DNA in its gametes and thus produced offspring with longer necks.   There's no compelling evidence for Lamarkism and Remi.b 's  nice answer describes DNA and evolution/selection/adaptation in its standard form and how giraffes would evolve such features.
OP initially asked 'does our DNA adapt during our lifetime'.  Certain regions of the DNA in each of our immune T-cells and B-cells change (recombine) to code for specific protein molecules that bind to antigens.  These are the genes for the T-cell receptor in T-cells and antibodies in the case of B-cells.  So the DNA in a T-cell or B-cell is different compared to other cells in the body including the gametes.  These regions of altered DNA help us fight infection.
You can easily imagine that an individuals ability to fight infection may affect whether they can survive to reproductive age.  Genes involved in immune system function might be selected for during deadly epidemics. And paradoxically, some genes responsible for debilitating or deadly diseases can persist in human society due to their protective effect against other diseases.
For completeness there is also some emerging data that neurons have some alterations in their DNA but its not clear what, if anything, that means and whether its of functional significance.  Unless similar types of changes are made in gametes,  DNA altered by this mechanism will not be passed on to offspring.
Finally, DNA in cells can be modified by a process called epigenetics.  Epi- means 'around'. In epigenetics various regions of the DNA strand (and some related proteins that keep DNA coiled up called histones) are chemically modified by a set of enzymes.  Epigenetics affects how certain genes are switched on and off and is perhaps best known for inactivating one of the two X chromosomes in female cells.  In epigenetic modifications the DNA sequence remains the same but the epigenetic 'decorations' around the DNA can vary and this process can be influenced by the cells environment.

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Cancer a method for early Earth Evolution?
Something I have been wondering for a while is looking at cancer from an evolutionary standpoint.
It's easy to conclude (from observations today) that cancer is something we would rather avoid. However I kept asking myself what would be the purpose of cancer existing in the first place? In my experience of studying biology if a organism or mechanism in nature exists it is because there was a pressure to create it.
It has led me to think that perhaps early on, when cells were just beginning to clump together forming very very primitive organisms, that cancer was a way for a cell to proliferate very quickly and make their particular genomic sequence more common within what would have been organisms made of a lump of cells. Perhaps the different organs we have today exist not just because there was environmental pressure to have a specific organ with a specific function. Perhaps the cells descended from a "cancer" that proliferated faster over other cells in a primitive ancestor of that organism.
The answer that "cancer exists because our bodies make mistakes" doesn't satisfy me when everything else around us evolved and formed due to a multitude of different pressures.
In an effort to make this question less broad my question is basically this:
Is it plausible that cancer is a phenomenon that began to occur relatively early in Earth's evolutionary history as a form of survival for cells in primitive organisms or am I applying evolutionary theory incorrectly?
(I know there is a better word for "pressure" to describe the variables that guide evolution but right now my brain can't come up with anything better).

The majority of cancers occur around or after the end of reproductive viability of the organism. Therefore there is no selection against it. Had it been a disease that predominately affects embryogenesis or early development, then there would be spontaneous abortions or young dying prior reproduction, thus taking the genes out of the gene pool. That it occurs later in life means that the organism's genes, with all of their strengths and weaknesses get passed to the next generation. Those can then be offset by a more fit mate so that it continues to keep cancer at bay until after reproduction

There is a lot of terminology, semantic and biology to be discussed if one was to fully answer your question and it would take a whole book. Below I am just trying to push you to reading more on the subject.
Evolution of cancer prevalence
The probability of getting a cancer is under selective pressure for sure. Citing cancer.net, here is some information on the genetics of cancer:

Many of the genes that contribute to the development of cancer fall into broad categories:

Tumor suppressor genes are protective genes. Normally, they limit cell growth by monitoring how quickly cells divide into new cells, repairing mismatched DNA, and controlling when a cell dies. When a tumor suppressor gene is mutated, cells grow uncontrollably and may eventually form a mass called a tumor. BRCA1, BRCA2, and p53 are examples of tumor suppressor genes. Germline mutations in BRCA1 or BRCA2 genes increase a woman’s risk of developing hereditary breast or ovarian cancers. The most commonly mutated gene in people who have cancer is p53. In fact, more than 50% of all cancers involve a missing or damaged p53 gene. Most p53 gene mutations are acquired mutations. Germline p53 mutations are rare.
Oncogenes turn a healthy cell into a cancerous cell. Mutations in these genes are not inherited. Two common oncogenes are:

HER2, which is a specialized protein that controls cancer growth and spread, and it is found on some cancer cells, such as breast and ovarian cancer cells
The ras family of genes, which make proteins involved in cell communication pathways, cell growth, and cell death.

DNA repair genes fix mistakes made when DNA is copied. But if a person has an error in a DNA repair gene, these mistakes are not corrected. And then they become mutations, which may eventually lead to cancer. This is especially true if the mutation occurs in a tumor suppressor gene or oncogene. Mutations in DNA repair genes can be inherited, such as with Lynch syndrome, or acquired.

Somatic Evolution in cancer
A cancer is a group of cells that proliferate. In other words a cancer is a group of cells having a higher fitness than other cells.
See Wikipedia > Somatic Evolution in cancer
Can a cancer be beneficial?
I am here attempting to answer your specific question.
We define a cancer based on the fact that it is detrimental to the organism carrying it. If a group of cells divide a lot more than the others and this is beneficial to the organism, then it is not a cancer but an adaptive developmental process.
Let's generalize the definition of cancer
To generalize the definition of cancer, one can say that a cancer is a group of individuals that proliferate to the detriment of the group. In other words, we need a social group of individuals (such as a multicellular organism) to get a cancer. Depending on your definition of a social group, one could consider a criminal organization as a cancer to human society.
If you push the definition a little further by either leaving out the need of a close phylogenetic relatedness between individuals of the group, one could say that "humans are a cancer of the earth". If you google this sentence you will get many hits!

The majority of cancers occur after the age of reproduction, so they are absolutely not under selective pressure. Selective pressure only occurs if it affects getting genes to the next generation. That is why Huntington's disease has survived as long as it has, the onset of the disease isn't until the 40s or later, after people have reproduced.

Just because something is genetically heritable does not automatically mean that it is selective. It is only selective if it helps or hinders the organism from reaching reproductive age and producing offspring.

Yes, absolutely. Prevalence of cancer is a trait that evolve with age-specific effect. See Mutation Accumulation (MA) hypothesis and Antagonist Pleiotropy (AP) hypothesis. Wikipedia > Evolution of Ageing. Do you feel like your comments are contradicting my answer?

Why are you linking to an article that has this warning This article is written like a personal reflection or opinion essay that states the Wikipedia editor's particular feelings about a topic, rather than the opinions of experts. (October 2009)
This article contains weasel words: vague phrasing that often accompanies biased or unverifiable information.

This is what prompted my comments. "The probability of getting a cancer is under selective pressure for sure. "

That is a very insightful question.  In general terms, you're right that cancer is unregulated cell division, which hijacks the mechanism of cell division which is ancestral to all multicellular life.  In early multicellular life, it may well be the case that faster reproduction was selected for, while it has been selected against for most organisms as they became more complex.
The mutations which cause tumors are usually two-fold: first there is a mutation which causes a cell to get genetically switched on.  This might be a mutation causing an overproduction of a protein signalling molecule which tells the cell it is time to grow.  The second is usually a mutation in cancer prevention genes, since a cell going haywire is likely to be spotted and destroyed relatively quickly.  If both of these mutations happen in the same cell, the cell can form a tumor (and if the tumor spreads to other parts of the body, it is called cancer).
Some people have suggested that cancer be thought of as "cell-level selection."  This idea of levels of selection takes a little explanation.  When evolution was first proposed (and the way in which it is introduced still) is individual-level selection.  Individuals compete against other individuals to survive and reproduce.  However George C. Williams suggested (and Dawkins later popularized in "The Selfish Gene") that genes might compete against other genes.  This is called the gene-level view.  In the mid 1980s, Leo Buss suggested that a cell might also be a level of selection, and that cancer represented cells trying to reproduce at the expense of the individual which carried them.
In some cases, such as instances of transmissible tumors (there are only a few such tumors known in the wild, none in humans).  These cancers spread from individual to individual, rather than just within one individual.  In that way, the cancer's evolutionary strategy was successful.  However these are rare, so if we view cancer as an evolutionary strategy, it is not usually a successful one.  As such, thinking of cancer as a cell-level selection has not yielded many interesting ideas so it is not widely used in biology today.  It is not incorrect, but it doesn't further many research projects so it is not commonly taught or studied.
There's one exception to that, however.  Thinking of cancer itself as an evolutionary process, where cells survive and die off according to their mutations, is very useful to understanding the progression of a tumor.  If you're interested in this line of thought, there's a summary paper Merlo et al 2006 which you might want to take a look at.

You are wrong and right. Remi.b's answer is describing the idea is not right and the answer is generally accepted.
The cells in muticellular organisms have to be regulated tightly--some has to differentiate into skin to protect bodies, other, into stomach to secrete digestive enzymes, etc. This regulation was established when multicellular organisms appear.
In other words, unicellular organisms do not care about the regulation. They do not have to be skin, stopping cell growth. Not much problem that they grow as cancer cells do, although you don't call such unicellular cells "cancer" probably because they are not abnormal.

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How do human cells respond to mechanical pressure such as heel contact during walking?
Basically, I'd like to do a full accounting (inventory, assets, liabilities) of a human cell under mechanical pressure.
For example, if in steady-state, does the cell consume more or less energy under pressure?
Is membrane transport affected? For example are ion gradients or cell fluid levels changed in response to pressure. If there is a change, how does the cell sustain this over a period of time.
Conversely, if a gradient is disturbed by mechanical pressure, what are the energetic consequences? Does the system behave like a spring such that if the concentration gradients are perturbed out of balance, there is a restoring force (say passive) that will rebalance after the mechanical pressure is removed?
Any focused sources or references would be greatly appreciated.

What is the difference between a cell's inventory and a cell's assets in this context?


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Diazepam with Aluminum Hydroxide
Some common medicinal preparations contain diazepam with aluminium Hydroxide, there may be other compounds [e.g. magnesium trisilicate and polydimethylsiloxane with Aluminum Hydroxide and Diazepam as ingredients of Tablet Peptica ( Geno pharmaceuticals)]. These drugs are commonly used as antacids. We can see in the drug Peptica that Aluminum Hydroxide and Magnesium Trisilicate were included for neutralizing the acidity (HCl) of stomach.....thus serving their purpose as antacids. Polydimethylsiloxane is a carminative preparation ('Carminative' means preparations that expulse gas from the gastrointestinal tract or prevent its formation). But what is the need for adding Diazepam here?


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Accommodation mechanism.
Can anyone explain how contraction of the ciliary muscles causes relaxation of the zonules? Please explain it anatomically i.e. the attachments of ciliary muscles and its relation with the accommodation process.

If you explain in more detail what confuses you and why (i.e. show us you've researched this and tried to answer it on your own), I'm sure it would have a better chance at attracting an answer.

When we study the attachment  of ciliary muscle, it appears to produce more tension on the ciliary zonules (& thus also on the capsules of the lens)-thus should cause flattening of the lens(i.e lesser convexity or more redius of curvature). But according to Von Helmholtz's capsular theory on accommodation, contraction of ciliary muscle causes releases of the zonular tension on lens capsule. My point is..... Ciliary muscle surrounds and holds the lens capsule, so when it contracts it should shorten in length....thus causing more tension on lens capsule(which is clearly against the theorem)

I searched medical books on anatomy and physiology and different medical websites for it. I also tried to find an explanation in YouTube but found no video satisfactorily explaining it. So I posted it here.

I think the problem you're having is in the way you're thinking that all contracted muscle shortens, and all relaxed muscle lengthens. But the cilia is different. The ciliary muscle is a circular or radial muscle (like the orbicularis oris of the mouth.) Thinking of it like a sphincter muscle is much more helpful.
The ciliary muscle is attached at its periphery to the lens by suspensory ligaments (aka the zonules). Think of the the lens, the suspensory ligaments, and the ciliary muscle as a single unit with only two components whose length can change dramatically: the cilia and the lens. The length of the suspensory ligaments is more or less fixed.
This may be counterintuitive, but for seeing at a distance, the ciliary muscle relaxes, and the muscle in effect becomes "thinner" (think of the capitol letter O in a thin font, or think of a shpincter muscle; when the latter relaxes, it becomes thinner and more spread out). This means the "decreased distance" taken up by the ciliary muscle must be made up for by the suspensory ligaments and the lens: The tension on the suspensory ligaments increases, causing the lens to assume a flattened shape.
For near vision, the opposite occurs; The ciliary muscle contracts (think of the letter O now very bolded - it takes up more of the fixed distance.) This allows the ligaments to relax, allowing the lens to assume a more rounded shape.
Does that make any sense at all? I hope so, because it is essentially how it happens.
I did find a YouTube video; unfortunately it explains it pretty much like I did varying in a few details.
Morphological Study of the Accommodative Apparatus in the Monkey Eye Way way complicated; it's better to just believe me.


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Could there be any effects from low powered infrared being used to track eye movements long term?
Basically,  looking  into infrared LED's and a camera with an infrared bandpass filter for tracking eye movements; my concerns are whether there would be any potential negative long term effects from constantly illuminating the eye with low power infrared?
TIA
A

Most likely not. We are exposed to IR light every time we step out into the sunlight, so a very small amount from an electronic device designed to follow the eyes is not going to matter much at all.

I would have said that IR is safe, but some studies have suggested otherwise.
This is a vague study on rabbit eyes:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116568/
https://academic.oup.com/annweh/article-abstract/35/1/1/170395
So there may be a dosimetric exposure limit of some kind that you have to aim for. LED's are very controllable. I'm amazed that they talk about cataracts with a chemically soft, non -ionizing wavelength like IR, because we get IR all day from the sun. If you control the levels to be less than a sunny day, you may find that you can use equivalent of 1hr of sun exposure to run many hours of eye tracking. the figures are a matter of research.

Heat waves are probably infra-red waves. We have these all around us (with great intensity) all the time. A small intensity Infra-red from an LED shall not cause any problem at all even in long terms. Our eyes are evolved to withstand far greater(i.e. around temperature of 45°C)  intensities. So, no need to worry.
But since, water is lost from heat waves, do allow subject to blink his eyes frequently.

LEDs are near IR, while low temperature radiant heat is far IR. Near IR behaves much more like visible light. Like others have said near IR is significantly present in the solar spectrum, so to a degree effects are bounded by what we observe with sunlight exposure.

@Real sorry, what do you mean, i don't understand ? Is there any clarification you need?


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Pigment returning to my grey
In the past I dyed my hair to cover the grey, but it became a more frequent event so I decided to just go grey.  My hair has been almost entirely white for nearly 20 years.  The pigment has been returning to my hair gradually for the last 18 months.  Do you have any explanation for this?  I have tried to research this, but have not found any answers.  There is information for reasons why hair looses pigmentation, but not for its return.  Any ideas?

Hello, and welcome to the site! Personal health questions aren't allowed here, but your question might be adaptable into a more general question about pigmentation that could be answered. Check out the Help.

I can't explain the phenomenon, but have experienced it to a lesser extent as well. And I studied dermatology. I thought it was impossible. Clearly it's not.

Do you get any new medications in that time?

There have been more questions on exactly this phenomenon on this site. Unfortunately it's off topic as said by others.


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Are Sloth tongues soft or rough?
Are Sloth tongues soft or rough?
Dogs have soft tongues, while cats have rough tongues, so the feeling when they lick e.g. a human hand is quite different. So what about sloths?
This question came up in a recent discussion but I was unable to find any materials as google queries for sloth tongues leads to tons of cute pictures.

Cats have hairs like structures called papillae on the upper surface of tongue that's why they are rough. The same could be for sloths if they have any.

Sloths have long, thick, sticky tongues covered in a carpet of tiny, rear-ward pointing spikes that they can pull leaves in with.
So the tongues are quite different from human tongues and likely much less "soft" to touch and more "rough".
According to scanning electron microscopy studies on the topography of a sloth's tongue, the following results were found:

The results revealed that the rostral part of the tongue presents a
  round apex and covered by filiform and fungiform lingual papillae and
  a ventral smooth surface.


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Which biological process causes the feeling of having "Butterflies in the body"?
If someone is under stress, he or she may feel a strange feeling in the belly; it can be said that he or she feels that butterflies spread through the belly.
For other emotional reactions like being in love, similar, but different feelings can be caused.
What causes this symptoms? Is it because of the muscle tension varies, is it an electric current through the nerves?

"Butterflies" are caused by adrenaline (or nor-epinephrine) released by stress. It is one of the first stress hormones released. Love is a bit different. This question is very broad, and you can easily google part of it and show your research. If you narrow this down, and add your research, I'd be happy to withdraw mt close vote.

Why we can feel the adrenalin or nor-epinephrine release?

Do some research. I wasn't writing for nothing.

These sorts of behaviors are mediated through activation of the sympathetic pathway of the autonomic nervous system.

it would greatly strengthen your answer if you could expand it a bit...FYI


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Is mucus significantly affected by the presence of ions?
In mucus, there is besides water and the mucins (Proteins for mucus), there are Ions like $Ca^{2+},Na^{+}$, etc. I have read that These Ions can Control the mucus swelling, i.e. the volume that the mucus occupies. Moreover, I have heard that some polymers can be affected by the presence of Ions, These are called "electroactive polymers". Is mucus a substance that changes ist consistence dramatically, when Ions are added or removed (equivalently, if pH value is changed due to $H^+$ ions)?

Do you mean the mucus, or the mucins? By bringing up "electroactive polymers" it seems like you are thinking in terms of the mucins, but that need not have anything to do with the effects of ions on the volume/viscosity of mucus. In fact, I don't quite see the connection of electroactive polymer and ions, because the former is referring to sensitivity to an electric field, which ions don't necessarily need to be involved in (at least on anything but an atomic scale) due to the presence of other ions of opposite charge.

Yes.  Mucus is hydrated by the movement of ions.
Cells cannot move water.  Cells can only move ions, and water follows the osmotic gradient.  When hydrating mucus, cells move ions into the mucus and water follows.  A failure of this system is seen in cystic fibrosis.
Targeting ion channels in cystic fibrosis

CFTR, the protein that is defective in cystic fibrosis (CF), directly
  mediates the transport of chloride and other anions through the apical
  membrane of several types of epithelial cells [1], [2]. Therefore,
  mutations impairing CFTR function cause a severe imbalance in ion and
  water transport that leads to a variety of negative effects in various
  organs. In the lungs, impaired secretion of chloride and bicarbonate
  appears to have multiple consequences. First, reduced secretion of
  electrolytes, and consequently of water, causes dehydration of airway
  surfaces with impairment of mucociliary clearance [3]...

People with cystic fibrosis have a defective chloride channel, and it cannot move chloride into mucus.  They therefore have thick mucus with abnormally low water content, and much of the trouble they have with their lungs is because this thick mucus does not perform its functions well.

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


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Which proteins are most sensitive to electric fields?
Many Proteins have ionic charges that can attract each other (e.g. Formation of salt bridges) or repel each other. On the other Hand, Proteins are mostly immersed in water that screens most of the Electric charges of the proteins. The reason is that water is a dielectric, the H2O-molecules can be polarized easily. So the Electrostatic Forces are reduced in aqueous solution.
Now I am asking which Proteins can be easily affected when applying an Electric field? That means which Proteins will Change their conformation substantially even when weak Electric fields are applied?
Can some proteins immersed in water also be dependent on external Electric fields?

There are various proteins sensitive to changes in electric field. More precisely, they are activated by changes in voltage (surrounding the protein), and immersed in water, as all cells are mainly composed of an aqueous solution. You are correct that most charges in the side chains of the proteins' amino acids are 'masked' by the dipole character of water molecules, but the electrochemical potential of the cell is primarily due to ions, and not to the interaction between side chains in a protein. However, it is important to note that within these proteins sensitive to changes in the electrochemical field, there are domains that contain charged aminoacids (i.e. not covered by water), very important to be able to 'sense' the changes in voltages.
You can check out some of the voltage-sensitive ion channels, which participate in different cellular pathways, including the generation and transmission of the action potential in neurons:

Wikipedia has a good entry about them.

As you mentioned water is a dielectric and because of that and the presence of ions in  solution, electrostatic forces have a very short range inside a cell.
If you apply a potential difference (voltage) in solution, you will generate a constant electric field between the two electrodes. Proteins will respond to this electric field by moving towards the anode or cathode depending on the charge of the protein. This is what we know as electrophoresis (note that for the electrophoresis of proteins you usually need tens to hundreds of Volts)
Now, when you have the same voltage difference but there is an electrical insulator in the middle, most of the electric field will be concentrated within the insulating material.
This is what happens in the cell membrane which insulates the small voltage difference between the inside and outside of the cell (-40 to -90 mV depending on the cell). This small voltage difference generates a huge electric field with the membrane which now can be sensed by charged residues of proteins within the membrane such as the arginines in the voltage sensor of a potassium channel. The electric fields sensed by these channels are in the order of 10^8 to 10^9 V/m.

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


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Conjugation in bacteria
I was studying about conjugation in bacteria, I have a doubt. In conjugation F- cell transforms into F+ cell when there is a formation of sex pilli in between the two. The doubt is if the F- cells convert into F+ cells how can F- cells form again...?
If all the F- cells convert into F+ can we expect F- cells to form again?

Within a bacterial cell exists circular chromosomes, and plasmids. During cellular division, chromosomes are always conserved - passed to both daughter cells.
As you are aware, plasmids can be passed between cells by a form of horizontal gene transfer called conjugation - whereby plasmid DNA is replicated, and passed through a sex-pilli into an adjacent cell.
When a cell divides in to two daughter cells, it is possible that one cell will not receive a plasmid. Thus, the result is one F+ daughter cell, and one F- daughter cell.

The partitioning of the F plasmid between daughter cells is tightly regulated https://academic.oup.com/nar/article-lookup/doi/10.1093/nar/gkr457. Loss of F takes place if this mechanism fails.

That's an interesting article. But regardless of mechanism, I think the important point to OP's question is the fact that reversion to F- cells can occur during cellular replication.

Agreed, I was commenting on the (now deleted) use of the word 'stochastic' which conjured up a picture of a rather random process. Clearly it isn't. I certainly wasn't suggesting that loss of F can't happen, but I haven't found any data on how frequently it does happen. Probably that is to be found in very old literature.

As extra genes generally cause increased stress to a cell, unless the cell is actively taking advantage of plasmid DNA, I believe they will get rid of them. But I do disagree with your statement that plasmid replication does not ever display stochastic characteristic. http://www.sciencedirect.com/science/article/pii/S0147619X14000559?via%3Dihub

What about the process of duplication of plasmids and the production of pilis? My understanding of comments is that it's connected: duplication of plasmids (that is not that trivial to me, should be mentioned) should be a prerequisite for sex pili transfer, so no pili without duplication? I mean,  there's more than "never get lost on you" than a very good song.


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Flowers in Arachis hypogea, are they clestogamous or chasmogamous?
I have seen the flowers of groundnut, they open and remains open for one day, so they should be chasmogamous, but in my school book, they mentioned it as clestogamous, and I searched for it in wikipedia but it wasn't clear. So how to classify it?


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What happens to the enzymes produced by the digestive system?
Our digestive system produces a lot of enzymes and they help to catabolize the food, and after completing their work are they excreted out or as they are also made up of proteins are they catabolized and assimilated back?

Yes,Enzymes too get degraded and catabolised, if not then we would be wasting a lot of proteins.

@JM97 ,Which enzymes help in degrading the other enzymes?

Proteases, being themselves proteins, are cleaved by other protease molecules, sometimes of the same variety.

The answer is autodigestion fascilitated by denaturation of the digestive enzymes.
EVIDENCES OF AUTODIGESTION OF THE DIGESTIVE ENZYMES
1.The concentration of digestive enzymes is found to decrease from the small intestinal ileum to the large intestine.

There is a general trend to a decrease in the enzyme concentration the furthur down in the intestine the samples have been collected inspite of a concentration of the intestinal content in the same direction (see Figure1).This fact must indicate that the enzymes are partly inactivated or autodigested in the lumen of the small intestine.[pg 1529].

2.Essential amino acids have been found in the small intestinal lumen even if the food ingested didnot contain them which suggests that their source was the hydrolysed digestive enzymes which would eventually be re-absorbed in the small intestine to prevent their loss from the body.

Amino acids from dietary digestion are not alone, because the ingestion of food-even non-nitrogenous food-stimulates the digestive tract to secrete endogenous protein, derived from the sloughing of intestinal cells and used up digestive enzymes. These recycled proteins are a rich source of essential amino acids.Studies by Nasset show that regardless of the amino acid mix of the meal, the intestinal tract maintains a remarkably similar ratio of essential amino acids.[source]


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What Animal is This Skin From? A Wooly Mammoth?
I was at the American Museum of Natural History in New York City today, and I saw the skin pictured below. Because it was next to stuff about wooly mammoths, I thought it might be a mammoth skin. However, there was no sign accompanying the skin. What is it from?

its looks like an elephant's leg on the right. close enough to be a mammoth then.

Yes, this is the remains of a wooly mammoth. Many mammoths have been found frozen and well preserved in Siberia.


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Why does DNA have two sets of bases?
DNA has two sets of bases. Why is this the case? If one gets mutated, does the other as well?

Can you please clarify what you mean by "two sets of bases"? Are you asking about the paired strands of a double stranded DNA molecule? Purines vs. pyrimidines? Something more obscure? ——— The way you have phrased this question suggests that you don't have a background in molecular biology — if this is true you may find the resources in the following comment to be helpful.

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.

Does this answer your question? Why is thymine rather than uracil used in DNA?

One could argue that any informative polymer must have more than two different monomers in its primary structure in orden to contain biological information. One could make an analogy to having a language in which any word contains two letters. Any word contained on such languague, like aaaabbbbb or ababababa for example, would essencially be devoid of information, as we can predict the the sequence of letters. So it is clear that if DNA was to be the molecule carrying the genetic information of a particular cell, then its primary structure must contain more than two different monomers. Now, asnwering why exactly does it use 4 different nucleotides is quite hard.
When you use an even number of nucleotides, all the nitrogen bases can have its complementary base, which allows for the formation of two or three stabilizing hydrogen bonds, in sort of a one-to-one relationship (cytosine to guanine and adenine to thymine). These hydrogens bonds can form because the functional groups of the complementary bases are arranged in space in such a way that allows the formation of these stabilizing eletrostatic interactions. If DNA used any odd number of nucleotides, like $3$ or $5$, this one-to-one relationship would not be possible, since you would always have an extra base without a complementary partner. If DNA uses $3$ different nucleotides, let's say, thymine, adenine and cytosine, we can see that in this example, cytosine lacks a complementary base to bind to. The same can be applied to an usage of $5$ different bases, and in general, to an usage of $2n + 1$ bases. Then, the extra base must bind to a non-complementary base and form a much weaker interaction with it, as the functional groups of the bases will not complement in space well enough, which will decrease the stability of the molecule. So, we can see that, any DNA molecule that used an odd number of nucleotides would be far more unstable than any other that used an even number of nucleotides.
Now, in terms of an even number of nucleotides, from above, we can see that DNA could not use $2$ different nucleotides, as it will hardly contain any biological information. The usage of an even number of nucleotides that are greater than $4$, such as $6$ or $8$, seems to be quite unfavorable, as this would imply that we would have to recognize hundreds of different codons. If we pick greater even numbers than these two, the situation only becomes worse, as the number of codons would exponentially grow ($n^3$) into the thousands. So it seems that using $4$ different nucleotides is, by far, the best pathway to take in terms of stability and practicality.
As for the second question, no, a gene mutation on a particular base will not necessarily alter the complementary base, but it will affect the number of hydrogen bonds the pair can form, and therefore, the stability of the molecule.
NOTE: Credits to Bryan Krause for his insight.

There is another big problem with having 3 or 5 nucleotides that you seem to be missing...

Yes, you are right!


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Pathogenesis of type IV hypersensitivity
In hypersensitivity, as I understand it, a normal immune response gets excessive, misdirected or wrongly regulated to cause tissue injury. The various types determine the various ways in which the tissue-causing responses are effected, at all times the ultimate cause being either excessive response (the normal amount being harmless), misdirection or wrong reglation. Hence, the ultimate cause beneath all hypersensitivities is some factor which just unleashes the immune machinery on normal tissues.
With this in mind, as Type IV Hypersensitivity is typically described under the headings of a granulomatous reaction, DTH (Delayed type hypersensitivity) or a contact dermatitis type response, involves the stimulation of $T_{h1}$ and $T_{h17}$ subsets of $T$ cells (along with $\text{CD8+}$ cells). What I fail to understand is that,
What goes wrong along the normal T-cell effector pathway to ultimately cause the injury?
(In type I, it is the IgE arsenal release on parasite mimicking allergen, in type II it is the self-antigen directed or hapten mediated self-tissue direction of Ab, and in type III it is the precipitation of immune complexes owing to the overburdening of the Ag-Ab response due to continued influx of Ag which cause the problem)
The events of stimulation, cytokine release and macrophage proliferation and activation is exactly what you would expect to be, in case the cells are doing what we want them to, to ward off a normal invader. But it ends up damaging the tissues.
Moreover, a lot of books say some variant of

"DTH is necessary to fight some specific pathogens"

Since hypersensitivity, (and hence DTH) by definition is immune-mediated tissue injury, do they mean that this tissue injury is indispensable in the fight against these pathogens (in which case, is worrying about DTH necessary?) or that the normal unaltered form of the pathway of immune response (the altered form of which results in DTH) is necessary for the fight (in which case there is a minor semantic error in the quoted statement)?

In some cases where your hypersensitivity reaction is due to autoreactivity it's cause for alarm. In other cases, though, nothing is going wrong with the development of the T cell response except for some reason they can't clear the infection in a reasonable amount of time or effort. The situation escalates as more effector cells are recruited, producing more and more cytokines/TNF-α/etc. as a part of their normal response. In fact, you end up with chronic DTH reactions when phagocytes uptake microbes but fail to get rid of them, such as Mycobacterium spp. that prevent lysophagosome formation.

@Kendall So, the tissue injury is just the result of a prolonged activation of the immune mechanisms or of pathogen-mediated misdirection of the system? Thanks. Can you also shed light on the questions following "Moreover, a lot of books....."

It's not 100% misdirection; while the pathogen remains the immune system is getting signalled "We need to clear this infection." So it's the normal response, just over an abnormal period of time and circumstance. I tried to answer that last part w/ the Mycobacterium spp. example. They infiltrate cells and are difficult to clear, so the DHT is actually an attempt to clear out the microbes by scuttling the infected tissue.


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Sodium levels and blood pressure

Why does low Na+ levels cause hypotension (low blood pressure).
  Alternatively, why does excessive intake of Na+ cause
  hypertension or high blood pressure?

From what I understand, there are two different mechanisms at play. Renin secretion from kidneys occur during low salt levels in blood and hence, under low sodium concentration, high amount of Renin secretion from kidneys should actually raise the blood pressure, via the Renin-Angiotensin loop, constricting the arteries. Under high sodium concentrations, low renin secretion should be accompanied by low pressure. If the osmotic entry of water into blood raising the blood volume and thus pressure, plays a role here, will not, on increase of blood volume, decreased Vasopressin increase urinary output and thus control the blood volume, not allowing it to cause any body changes? Why isn't the first effect (renin) significant here as compared to the second (osmotic entry).

Renin angiotensin is for regaining homeostasis. If you have lost salts, blood pressure and blood volume will decrease due to loss of fluids. But the renin angiotensin mechanism will try to undo this by stimulating uptake of Na and water.But still, they can not fully compensate for loss of Na , INTAKE of Na is NECESSARY.

By the way, the main stimulus for triggering renin angiotensin is Blood volume and pressure rather than Osmolarity of blood. In conditions like hemorrhage where blood loss occurs but there is no change in osmolarity, Renin-Angiotensin will still respond ( but ADH(vasopressin) will not as ADH responds only to change in osmolarity.)

@biogirl Thank you. This helped to a considerable extent. :)

I think it will help you a lot if you read these topics from Tortora and Derrickson or other physiology books.

Renin angiotensin is for regaining homeostasis. If you have lost salts, blood pressure and blood volume will decrease due to loss of fluids. But the renin angiotensin mechanism will try to undo this by stimulating uptake of Na+ and water. But still, they can not fully compensate for loss of Na+, INTAKE of Na+ is NECESSARY.
By the way, the main stimulus for triggering renin angiotensin is Blood volume and pressure rather than Osmolarity of blood. In conditions like hemorrhage where blood loss occurs but there is no change in osmolarity, Renin-Angiotensin will still respond (but ADH(vasopressin) will not as ADH responds only to change in osmolarity.)     —  biogirl


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Charge distribution to neuron connections
How is charge generated by the action potential is distributed to all of the neuron connections? From what I understand the total charge transmitted by a neuron once it fires is same for every neuron. Is it divided based on synaptic weights?

The action potential is an active process, its mediated by voltage sensitive ion channels that shuffle ions around in order to create an electrical gradient that travels through the whole cell. When it reaches an axon, some of these positive ions bind to pockets of molecules (vescicles) that fuse with the cell membrane to release their neurotransmitters. Check out this very good answer to a similar question. Once these neurotransmitters bind to receptors in the post-synaptic membrane of the subsequent cell it produces an EPSP.
Each synapse is unique, meaning that although the action potential is the same synapses are changed depending on their activity some synapses might have more vescicles, more neurotransmitter, more sensitivity to the change in voltage. Postsynaptic membranes can also grow and increase the density of receptors in order to make the synapse more effective. The effectiveness or weight of a connection is just a measure of how good that connection is at eliciting a spike or action potential from the postsynaptic cell.
Once a cell fires it fires, but not all the connections count the same to elicit a response from the next cell down and there are a bunch of interesting sub-threshold dynamics.

I understand this much, but I am more interested in the mathematical side of the exchange in order to build a model. I wonder if it is safe to assume that every neuron produces same constant charge X when it fires, which is divided to all its output connections based on their weights?

Oh,well, I guess either a modeling tag or some indication in the question that it was a modeling issue would have saved me some time.

In this case the answer is yes, as I mentioned neurons either fire or not, once they do you go through all the connections and modify the input current by the weight of that connection, update the weight according to whatever rule and move on. I assume its a spiking model (https://en.wikipedia.org/wiki/Biological_neuron_model)?


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Evolutionary pressure of vaccines towards a virus
I am trying to understand the following quote from one of the Twitter threads
:

A change in the spike protein which allows the coronavirus to enter and infect human cells that is radical enough to make our vaccine completely ineffective would also, almost certainly, be so extreme as to make the virus non-functional. -- Sara Gilbert, Oxford Team.

What are the underlying principles that backs this claim?

In biology, especially molecular biology, a common and important principle is that the structure determines the function. If the structure of spike protein changes so drastically that antibodies cannot recognize it anymore, this would very likely mean that the part of the spike structure responsible for infecting the cells (by binding to cell receptors) has also changed, making it unable to bind to the cell receptors. Therefore, it would become "non-functional", as the author put it.

See also: https://www.sciencedirect.com/science/article/pii/S2666379121000410 (on non-evolution of vaccine escape mutants in measles)

@Domen - That would make a good answer.

Does the quote refer to and include a situation where mutation is improvement of function, not deterioration?


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Is differential equation modelling in molecular genetics useful?
I graduated last year with a degree in Applied Mathematics and just this month I started a PhD in molecular genetics. I was accepted into a program specifically for individuals with a quantitative background, though the differences between my program and the general graduate program seems fairly minimal.
The department is fantastic and I'm enjoying learning the experimentation, but I haven't had the opportunity yet to use my actual skills.
The more talks I attend, the more I realize that much of the "computational" side of molecular genetics seems to be split between machine learning, bioinformatics and statistics or some combination of the three. In my undergrad I studied topics such as differential equations (partial and ordinary, extensively), dynamical systems, vector calculus (though I never took any fluids courses, I was more of a systems guy), computational mathematics, control theory and some computer science (about 5 courses).
I've talked to a few of the faculty so far and when I mention the possibility of differential equation modeling, they don't seem comfortable giving me guidance. In addition, I read a review paper today that seems to suggest this kind of modeling is fairly uncommon.
So, my questions are these: Are differential equation models useful to geneticists and biologists? Why are they not done more often? How difficult would it be to create my own project that involves differential equation modeling coupled with experimental parameter finding and model verification?
Nobody seems to be able to give me an answer, so I hope the Stack Exchange community has some insight.
Thanks in advance!

@WYSIWYG This hardly seems a matter of opinion. I cited two seminal papers in biology and genetics that model biological phenomena with differential equations. Clear diff. eq. are useful in biology.

@CharlesE.Grant It is opinion based. OP is seeking opinion on how easy or difficult something would be and whether something would be useful or not. Moreover, it is also broad and not really about a biological question. There are several papers on mathematical models of genetic systems (I personally also work on such problems). This question is off-topic on several grounds.

Are differential equation models useful to geneticists and biologists?

Well yeah, of course they are. Look up Alan Turing and "The chemical basis of morphogenesis", or look up "differential equations and gene regulatory networks" But folks have to specialize, and not every department studies every aspect of a field. You may just have ended up in a department where nobody is studying an aspect of genetics that can be well modeled by differential equations. At lot of molecular genetics is still figuring out the coarse grained phenomenology of the genome, like "How does a cell figure out which copy of the X chromosome gets condensed into a Barr body?" A lot of these problems involve picking out subtle signals from noisy data, thus the interest in statistics and machine learning.
If diff. eqns. are the passion of your life, you might have to look 'next door', to departments studying biochemistry and population genetics, both of which do huge amounts of modeling using differential equations. There are also applications of differential equations to molecular genetic methods like QPCR and next generation sequencing, but you'll either have to sell your mentor on the topic, or move to a different department.
On the other hand, if it's just a matter of diff. eq. being your undergrad emphasis, you may want to find a biological problem that interests you, branch out beyond diff. eq., and use your general mathematical maturity to pick up the relevant mathematical tools: say statistics, optimization, or dynamic programming.


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Extinction of species
I barely know anything about biology and realize that this might be a stupid question, but I'll ask anyway! I know that species "transform" into other species through the process of evolution. Many species around today still co-exist with the species in which they evolved from, right? Actually, is it correct to say that all species coexist with some common ancestor?
Anyway, my question is; if the monkeys that we evolved from are still around today, then where are all the in-between species. Are there still early humans, like Neanderthal's or Hominids or what have you still roaming around some where?
If all early forms of humans are gone, is it because the more modern humans had a greater evolutionary advantage? But wouldn't these less modernized humans have those same advantages over the less evolved monkeys?

This 'missing link' question has been posed many times here. I think a reading list is the best response and should be posted in context of closure process.

I disagree about this question being off topic.  The help center specifically states that "general questions about biological concepts" are suitable. This question addresses common misconceptions about the evolutionary process. Of course, I'm new here but I wanted to share my opinion.

I too do not see how this question is off topic. If it is a duplicate, then you could perhaps link it, or perhaps suggest a source in which I could find it? I have found some of the answers here helpful

This is a common misconception about evolution, many skeptics ask something along the lines of "If humans evolved from monkeys, why are there still monkeys?" The answer is that evolution is not a linear process of one species becoming the next species becoming the next. Species branch off much more like a tree. At some point in the past the last common ancestor of humans and monkeys split into two directions, one that became the apes including humans, and one that became modern monkeys. Evolution did not stop for either branch, but only our branch became humans, after several more branchings. Sometimes species adapt and evolve without major changes in morphology, for example modern turtles look a lot like turtles from 100 million years ago, but this doesn't mean they haven't evolved.
The intermediate species are often lost with time as environmental conditions and competition changes. For example, if one early human group found itself competing with a slightly more advanced human group with better tools, the more primitive group would have trouble getting enough food and eventually die off, leaving the more advanced group to pass its genes on.
Now, if those more primitive humans were more suited to a particular niche, they could survive there. Lets say they could climb trees better ( assume REALLY primitive ancestors, barely out of the forest ), they might survive in the forested areas while the more advanced groups become dominant in the grasslands. Something like this is why our ancestors didn't totally displace monkeys, the monkeys were better suited for their forested ecosystem. If those same monkeys had to live on dry savannas we would have eaten them all long ago.

Cool, thank you for your answer. I agree completely that it makes perfect sense why there are still monkey's around today. So I think what you're saying is that I can (vaguely!) think of it like this:

At the branching point between the common ancestor of modern monkeys and modern humans, there were sort of two scenarios which evolution acted on, one in which the "to be monkeys" were better suited and the other "to be humans." In the former, the monkeys won and still strive in those areas today. In the later, the "to be humans" won. But in this setting, the modern humans were just evolutionary superior, and so the in between species of human eventually died out?

Worth noting that they took a fairly long time to die out everywhere. The Denisovans(Siberia), the Neanderthals(Europe), and probably some others all stuck around for thousands of years after modern humans evolved and spread out of Africa. As these 'more human' hominids shared ecological niches(bipedal, relatively smart, thumbs) with early humans, we outcompeted them for resources(small game, territory) while we don't compete as much with say, orangutans. They live in trees and eat leaves and fruit, but we need protein and fat for brain-making.

I think other answers have explained natural selection, but I think it is also important to note that species boundaries are applied in retrospect. This sounds blindingly obvious, but when presented by skulls from two species, such as Homo erectus and Homo sapiens, many will then ask where the evidence is for the species that came between those two.
There are several reasons why you can't see all of these in-between forms:

The fossil record is imperfect. Although there are no longer any "missing links" in the fossil record for the evolution of humans from our most recent common ancestor with chimpanzees, not every change in skeleton shape has been preserved for us to look at.
Species boundaries are applied retrospectively. This means that when we find a new set of bones that seem to be in-between two species, we give these bones a new species name, because they clearly don't belong to the other species we've already identified. The bones actually represent one of the "in-between" forms that people are asking about, but we can't just label it "intermediate" or "missing link". It has to be categorised as a new species or sub-species.
You're not technically looking for an "intermediate". It's not that chimpanzees are an "intermediate" between humans and some ancestral species. It's that humans and chimpanzees share a common ancestor. When you see a pictures of a neanderthal, they might superficially look like an intermediate between humans and chimpanzees, a sort of hybrid between the two, but that's not quite right. It's not that chimpanzees eventually became neanderthals, which eventually became modern humans. It's actually that humans and neanderthals share a common ancestor and that ancestor is no longer around for reasons given in other answers. Similarly, neanderthals and chimpanzees share a common ancestor that is now extinct. My point is that if you're looking for something like a "crocatoo" that's a hybrid between a crocodile and cockatoo, you won't find it. Yes, crocodiles and cockatoos share a common ancestor somewhere in their family trees, but there's no reason that it will look half like one species and half like the other! It might look nothing like either of them!

If you're looking for more information on evolution, I'd highly recommend "The Greatest Show on Earth" by Richard Dawkins. If you want citations for the points I make, you'll find all of it in there. It explains this stuff quite clearly, with ample evidence to back it up (assuming you can put up with his occasional rants about young earth creationists...)

If all early forms of humans are gone, is it because the more modern
  humans had a greater evolutionary advantage?

If you take an environment where species dwell, three things could have happened:

The population got smaller and smaller, in a given environment, and then bam the last ones disappeared without producing any offspring. This is because population as a whole wasn't  reproducing as fast as they disappeared, for a variety of reasons. By disappeared I mean: went away to other environment or died out.
In another environment, so much changes had spread through the population that at one time the new offspring was born with their genotype now "too much" different and thus incompatible. By "too much" I mean this: they could still mate with both partners from their population and with "less changed" neighboring populations, but they could only produce a fertile offspring with former but not with the latter. We nowadays refer to such situation as "they became new species". From this point they obviously couldn't spread "their" genetic changes anymore to other environments via reproduction (spreading parts of genotypes). Their offspring would be infertile. They only could spread "their" genetic changes by sending whole groups of folks (complete genotypes) to other environment to try and cope there. And sometimes to kill others interfering, because, hey, that's what living creatures sometimes just do.
The population lived without "too much" change in the genotype and still exists today in the given environment. Without "too much" change means they were unchanged or rather changed slow enough that at any given time they could leak their changes to other populated environments via reproduction (they kept being the same species as their neighbors).

I have written about genetic "changes". You call these "advantages" and even "modernizations", but for the sake of argument it just doesn't matter (and only blurs the picture with the unnecessary concept of "superiority"). Advantages in one environment are disadvantages in another.
I use "environment" here for simplicity, but a more proper term would be a "habitat".

We don't observe any early humans today. It seems that all their populations have met one of these two former fates.
Also, you tend to overuse high-level abstract terms that distract you from thinking what have actually happened at low level. "Evolution" does not "act" on any "scenario". This is just a bit too much of anthropomorphism.

It would be fantastic if you included some references in your response!

I know that species "transform" into other species through the process
  of evolution.

I don't think you are thinking about that right.
We have a population of organisms that are breeding together.  We humans label that a 'species'.  That population has descendants, and over time, the population changes, and when we humans think that the new population look sufficiently different from the old, we label them a new species.

Many species around today still co-exist with the species in which
  they evolved from, right?

You might have founder situations, where a small sub population breaks off and inhabits a new environment, and changes a great deal more over time than the original population does, such that we continue to label the original population the same species, while we label the offshoot a different species.  But I think what happens more often is that the alleles that cause humans to label a population a distinct 'species' dwindle to nothing in the descendants, and then we say that the original species is extinct, replaced by the new one.  but that's a matter of labels: there is continuity in that the new 'species' is just the descendants of the older one.

Actually, is it correct to say that all species coexist with some
  common ancestor?

No.  Can you even name any examples where you think this is true?

if the monkeys that we evolved from are still around today,

What on earth makes you think that's remotely true?  For one thing we aren't descended from monkeys.  We are descended from primates that were more like apes, not monkeys.  There is no living population of primates that we would categorize as being the same species as that non-homo sapiens ancestor population.

Are there still early humans, like Neanderthal's or Hominids or what
  have you still roaming around some where?

I'm confused how you think an organism or a population existing in the 21st century could be "early". All the hominids walking around today are members of homo sapiens sapiens.


text:
What should be the distance between plant promoter and gene?
I am trying to clone a rice gene under a different endogenous rice promoter.I will be cloning the CDS of the rice gene.So I wanted to know what is the minimum or maximum distance I should put between the rice and the promoter so that I can get good expression levels.
Should I check the expression of the construct in E.coli before transforming it?
What should steps should I follow before finally transforming the construct into rice?

where do you want to express the protein?

I will be overexpressing the protein in rice.


text:
Is an adaptation against impact of fall a factor in babies' bones' structure?
Obviously, babies' bones need to be flexible to get through the pelvic bone. But is that the only reason? Could it be that as babies aren't able to maintain stability, they need bones less prone to damage?


text:
How do colds and flu not infinitely recur?
I'm in my third week of university, and a large number of people I know, including myself, still have "fresher's flu", which is probably just a cold and a cough. My lectures are constantly punctuated by the sound of violent coughing. What I don't understand is: how do colds ever go away, given these conditions? Surely by the time you've gotten rid of your cold you've passed it onto someone sitting near you in a lecture, who could then spread it back to you directly or indirectly later? Why don't we have an infinite recursion of colds, coughs and other minor infections throughout the year?

In one word, because of immunity (in particular adaptive immunity). Related question and answer with somewhat opposite reasoning here.

Atl LED says in that question that we can never develop immunity to the HRV. If that's so - and assuming, though I could of course be wrong, that HRV is the most common viral infection at this time and place - then why does the HRV not infinitely recur throughout the year? How do we ever have quiet, relatively healthy periods?

Short answer:
Because your immune system adapts to the virus causing the flu or the common cold and, thus, you become immune to it.

Longer answer:
When B cells first encounter an antigen (usually a protein on the surface of a pathogen), the antigen attaches to a receptor, stimulating the B cells. Some B cells change into memory cells, which remember that specific antigen, and others change into plasma cells. Plasma cells produce antibodies that are specific to the antigen that stimulated their production.
After the first encounter with an antigen, production of enough of the specific antibody takes several days. Thus, the primary immune response is slow and that's the reason you experience the symptoms of the disease.
But thereafter, whenever B cells encounter the antigen again, memory B cells very rapidly recognize the antigen, multiply, change into plasma cells, and produce antibodies. This response is quick and very effective.
This means that, theoretically, you shouldn't be able to become sick twice by the same virus.
However,
virus are very prone to mutations. If these mutations occur in the genes that code for antibody-binding sites, the antibodies produced by B Cells become less effective. This is called Antigenic drift and the reason you might catch the Flu every year (because, with enough time, the virus antigens become different enough to "fool" your immune system).

Also, there are a few explanations why the flu has a seasonal pattern, with a peak usually at winter. One of the theories postulates that in cold weather, people tend to stay indoor, favoring virus transmission.
Recently, an interesting article was published that found that:

transmission of influenza B viruses is enhanced at colder
temperatures, providing an explanation for the seasonality of
influenza epidemics in temperate climates

source


text:
Is there a period after you have had a cold when you cannot get a cold again?
I always assumed colds ran on a 'no tagbacks' principle: once it's out of your system, it takes a while before you can get a cold again. Is there any truth to this, or can rhinoviruses hit you at any time?

The problem with a cold is that there is nothing like "the" cold. It can be caused by a number of different viruses (Adeno-, Rhino and Coronavirus for example).

you can't be affected by the same virus that caused the cold, but a new virus could affect you to cause a new cold.

You can't catch a cold twice. But you can catch one cold and then catch another one.

The short answer is no, there is no minimum time between two colds. The reasons for this are different.
Mostly it has to do with the viruses which cause the common cold. There is a bunch of them causing what we call a cold, including rhinoviruses, coronacviruses, adenoviruses, human parainfluenza viruses, human respiratory syncytial virus, enteroviruses other than rhinoviruses and metapneumovirus. As much as 200 different virus serotypes are connected to this disease, alone 99 from the rhinoviridae. See the references 1-3 for more details.
Different serotypes means that two viruses of the same family (a rhinovirus for example) have different surface antigens on the virus and are not recognized by the same antibody. And this is what makes it difficult for the immune system. When it has learned to recognize and defeat one virus which causes a cold, it still has to learn how to do this with another (serotypically different) virus. So the adaptive immune system has to make highly specific antibodies every time it is faced with a new virus (which is of course not limited to cold viruses).
Once you have been infected with a virus and developed a sufficient immune reaction to develop antibodies, you are usually immune against this specific virus (with its specific serotype). Cold viruses live in communities, so when you move or travel, you will most likely encountered with different viruses, which your immune system doesn't know...
Finally there is another point which adds to the problem: Mutations of the viruses. The viruses are mutating constantly (RNA viruses at high rates) which changes their appearance and also their surface molecules (which are important for the recognition through the immune system). This leads to new serotypes, which are unknown to the immune system. See reference 4 for some more details.
References:

Understanding the symptoms of the common cold and influenza.
Sequencing and analyses of all known human rhinovirus genomes reveal
structure and evolution.
Common cold
Mutation rates among RNA viruses

If you are cured from the exact same virus, there is a less chance you will get it again.
As Chris already mentioned in the comment, one part of the problem, that different species causes similar symptoms which you know as cold.
Another part of the problem that the same species can have different subtypes and different antigens, so the immune system does not necessary recognize the same species with different surface antigens. The most well known from this group is influenza (flu) surface antigens e.g. H5N1.

Technically, I would say no. There is no period after a cold in which you can't get a cold again. This is because as mentioned in the comment, there are many species of rhinoviruses which all give very similar symptoms (not to mention mild flu viruses), to which the body will have no immune response.
However, it's important to remember how you get colds. It tends to be from people in your general area, and due to how colds spread this is all likely to be the same strain. Re-exposure to the strain that you have just recovered from would not cause the same infection again. It's also worth mentioning that the immune responses the body generates are in part non-specific (see innate immune system), and as such may help in preventing reinfection.
If you were to be exposed to a different species it is possible get a second cold after only just clearing the first one, but within real-life this is unlikely to occur.

Just like that while a cell is infected with a virus, other virus can not enter that cell
As long as your body has not fully recovered and did not acquire full health so not be affected by another cold. The experience in cell culture and virus replication is observed exactly.
This includes all viral infections. When the cell (as conceptual you'r body) were infected with virus A, B virus unable to replication in the cell's and enter the host cell, untill host cell recovery.
The virus antigens that experss on the cell membrane prevents that other virus entering and until complete recovery those antigen is present in you'r cells membran's so cannot get a cold again, At least not the same cells infect

authors: Максим Бондаренко


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Droppings of mystery: What are they
I have noticed the droppings below, quite visible on snow, next to an inner-town building situated next to this place in Luxembourg, central Europe. There are quite a few, but I have not noticed them anywhere else. What animal creates these and why do they have this red color which stains the surrounding snow? Is it a cat being fed colored food?
Local wildlife is mostly city pigeons (with digestive tracts of steel), huge flocks of crows (inhabiting parks and occupying the construction cranes at nightfall), maybe a few stray foxes and rabbits. House dogs and cats of course although these don't run around unattended.

How big are they? Is the snow melting? (Otherwise it looks like whatever left it did it without leaving tracks.)

@picapica As big as the the half the pinky. The snow is not melting in this picture, temperature about -4°C. The picture shows the border of a decorative plant-holding trough, rather overgrown, so it's likely there are mice living in there and probably cats doing regular inspections.


text:
What constitutes as the death of a bacteria?
I've read that some bacteria can survive a long time without food.
What constitutes the death of a bacteria ?
What process needs to take place for it to be considered dead?

When you talk about organisms like fungi and bacteria which can have a dormant form, and viruses, "dead" becomes somewhat harder to define. In fact, it has not been definitively defined for bacteria.
I would have guessed "when they are permanently unable to reproduce", but I may be wrong.
From one source[1]:

The observed coordinated gene expression continued even after cell death, in other words after all bacteria permanently lost their ability to reproduce. Transcription of a very limited number of genes correlated with cell viability under the applied killing regime. The transcripts of the expressed genes in living bacteria – but silent in dead bacteria-include those of essential genes encoding chaperones of the protein folding machinery and can serve as molecular biomarkers for bacterial cell viability.

From another[2]:

it is a challenge to determine if bacterial cells are dead, or viable but non-culturable (VBNC), and what is an agreed upon correct definition of dead bacteria.

Some viable but nonculturable cells (VBNC) can be "resuscitated" into dividing cells. [3]
Also4,

However, the simple binary definition live/dead probably does not accurately describe the complex physiological states possible with microbial cells.

Unfortunately the actual conclusion is behind a paywall.
Finally, another country heard from5 :

Programmed cell death is a gene-directed process involved in the development and homeostasis of multicellular organisms. The most common mode of programmed cell death is apoptosis, which is characterized by a stereotypical set of biochemical and morphological hallmarks. Here we report that Escherichia coli also exhibit characteristic markers of apoptosis—including phosphatidylserine exposure, chromosome condensation, and DNA fragmentation—when faced with cell death-triggering stress, namely bactericidal antibiotic treatment.

So, perhaps the answer is, a bacterium is dead when it is unable to reproduce, cannot be resuscitated, gene expression has ceased, and shows characteristic markers of apoptosis
[1] Transcriptional activity around bacterial cell death reveals molecular biomarkers for cell viability, Remco Kort, Bart J Keijser, Martien PM Caspers, Frank H Schuren and Roy Montijn, BMC Genomics 2008
[2] Can dead bacterial cells be defined and are genes expressed after cell death? Trevors JT1, J Microbiol Methods. 2012 Jul
[3] A matter of bacterial life and death Gregg Bogosian, Edward V Bourneuf
[4]Advances in microbial food safety: 23.
[5] Antibiotic-Induced Bacterial Cell Death Exhibits Physiological and Biochemical Hallmarks of Apoptosis, Daniel J. Dwyer, Diogo M. Camacho1, Michael A. Kohanski, Jarred M. Callura1, James J. Collins, Molecular Cell, Volume 46, Issue 5, 8 June 2012, Pages 561–572


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


text:
What is the name of the category of viruses that affect only one side of the body?
The Varicella zoster virus causes chickenpox in children and shingles in adults.
When the virus attacks as shingles, one of its distinguishing characteristics is that it only affects one side of the body. (As shown in the link and verbally identified by a doctor I spoke to). This happens because the nerve cells themselves are infected - and are partitioned on different sides of the body.

At first the rash appears similar to the first appearance of hives;
however, unlike hives, shingles causes skin changes limited to a
dermatome, normally resulting in a stripe or belt-like pattern that is
limited to one side of the body and does not cross the midline.[13]
Zoster sine herpete ("zoster without herpes") describes a person who
has all of the symptoms of shingles except this characteristic
rash.[16]
 From Wikipedia

My question is: What is the name of the category of viruses that affect only one side of the body?

I don't think there is a name for the "category", or that it really is a category unto itself.

"unilateral" would make for a convenient shorthand.

Short answer: Viruses that affect only one side of the body are not categorized by this information.
Long Answer: For people who likes details
Several types of virus classification exists:

Baltimore: Classified by the type of DNA or RNA that is carried by the virus
Holmes: Classified by the target organisms of the viruses (plants, bacteria, animals)
LHT: Classified using several physical differences (More specific and complex)

For example, Shingles would be classified as:
Baltimore: Group I (double DNA stranded viruses)
Holmes: Group III Zoophaginae (animals)
LHT:

Order: Herpesvirales
Family: Herpesviridae
Subfamily: Alphaherpesvirinae
Genus: Varicellovirus
Specie: Human herpesvirus 3 (HHV-3)


text:
Identifying flying insect from southern Poland / Upper Silesia area
Yesterday evening, I spotted this quite huge insect at my home in southern Poland (the exact location of the place). Unfortunately, I have only a very low quality pictures available at the moment:

Some details:

found in southern Poland / eastern Europe,
about 3 cm long,
quite fat (if I may say so),
seems to have 4 pairs / 8 legs in total,
airborne / able to fly (though quite slowly).

The quite huge (as per typical insect in Poland) size of this species was kind of surprise for me, but its behavior was even more surprising to me:

As pictured, it was able / willing to rest (copulate?) one on another even in groups of three (I failed to picture this), remaining still / not moving at all even for as long as half of hour.
After such resting / copulation ended or was interrupted the species on top was thrown off, falling down to the windowsill beneath.
It was then lying there up-side-down on its back, again remaining still and not moving at all even for 10-15 minutes.
Then it was kind of waking up from some kind of stasis, turning over walking a little bit around the windowsill.
Then it was flying up, flying around a little bit.
Finally, it was trying to rest / copulate with the species still on my window's mosquito net (or with the couple being there).

And then, the whole cycle was repeating until (late evening) only one species remained on mosquito net, which was also gone late in the night (not found the following morning).

Did they make any sounds while flying?

I believe, not.

Found it, with a lot of help from my local neighbors. It is Melolontha melolontha or cockchafer.

From English Wikipedia:

The cockchafer, colloquially called May bug or doodlebug is a European beetle of the genus Melolontha, in the family Scarabaeidae.
Once abundant throughout Europe and a major pest in the periodical years of "mass flight", it had been nearly eradicated in the middle of the 20th century through extensive use of pesticides and has even been locally exterminated in many regions. However, since an increase in regulation of pest control beginning in the 1980s, its numbers have started to grow again.

Here, where I spotted this insect (Upper Silesia) it is called in local language (in Silesian language) "julik", which is quite correct, since they seems to appear in July.
However, as per above cited part and as per Polish counterpart to above cited article, officially this insect is called after May, either "May bug" (English) or "Chrabąszcz majowy" (Polish). Most likely because adult forms of this species appears mature by the end of April and through May.