text:
What makes tones sufficiently useful that it would lead to the evolution of tonal processing?
I will define a "tone" as  a steady periodic sound. As an example, I consider a sinusoidal wave to be a tone. By "tonal processing", I mean ratio relationships between the notes. For instance, if I play 220Hz sine wave then a 440Hz wave will be perceived as an octave higher.
I don't understand why humans have the ability to perceive frequency relationships between tones. I have read several evolutionary anthropology books like The Singing Neanderthal and Finding Our Tongues and, between these two books, they suggest that the obvious evolutionary purpose of music is for communication. Each author takes a slightly different approach but the basic underlying point remains that tonal processing exists because it gives us advantageous communication abilities. But even accepting this hypothesis, it doesn't explain why humans have a tonal processing mechanism that is specific enough to perceive ratio differences between notes. The tonotopic organization of both the basilar membrane and the precortical auditory pathways might partially account for the machinery used for tonal processing and why the advanced forms in music could have developed. But this still leaves us with the question as to why would such information be useful?
I remember reading somewhere one person hypothesized that the purpose of perceiving these differences was to identify "relative pitch", i.e. the ability to identify or re-create a given musical note by comparing it to a reference note and identifying the interval between those two notes. But this hypothesis doesn't really make complete sense to me because it doesn't explain why the brin can have such specificity when identifying the ratio between two notes.
Another phenomena that seems pertinent is the idea of a "drifting reference point" which Glimcher discusses in Foundations of Neuroeconomic  Analysis. In Chapter 12, he explains how our perception of color isn't fixed but depends on context and in this sense drifts. IIRC, there is a literature that discusses possible neural mechanisms for this. Perhaps something similar would be relevant here for explaining why humans can process tones so precisely.
My Question:
What are the accepted arguments for why would ratios between tones would be be useful information for social communication?
Just to clarify, I am expecting the answer to this question to involve a discussion of the physical properties of tones and why a hominid brain would find this useful information for communication purposes.

I don't understand the question. Is it "why can we process multiple frequencies" or "why do we appreciate music". If the former, then you have to realize that not only music contains various frequencies, but e.g. speech contains a range of frequencies as well.

In short, I suspect that the answer is not so much that it is useful to recognize tonal relationships, but that it is easy.
It sounds like why or how we can distinguish pitch at all is a separate question which you have already accepted. So let's take as a given that whatever purpose our hearing serves, what we have ended up with is machinery which can usually tell higher tones from lower tones.
Now, it turns out that this by itself is not a simple problem to solve. Real, natural sound is never a simple sinusoidal wave. If you hear a pure sinusoidal wave played over a speaker, it sounds synthetic, like maybe a pitch fork, a singing bowl, or a computer - definitely something man-made. That's because absolutely nothing natural makes a sound like that. Consider any natural thing that for even a moment holds a single tone, like a long tone from within birdsong, or the long tone at the peak of a wolf's howl, or wind whistling through a cavern. If you heard samples of each at exactly the same pitch, they would still be distinguishable, just as a clarinet is distinguishable from a flute, or in fact, to the trained ear, two clarinets are distinguishable from one another. This is because the wave that reaches your ear is actually much more complex than a simple sine wave.
In fact, if you saw the high-fidelity digital wave representation of almost any sound which we would consider to be a single tone of one steady pitch, you might have a lot of trouble identifying the period of that wave (which correlates to it's pitch). In digital processing, to identify the tone in a digital wave, or for that matter, the many tones represented in a piece of music, we run a complicated calculation on the wave called a Fourier Transform.
Our aural machinery came up with a fascinating solution to the problem of distinguishing frequencies. Rather than discovering the mathematical method for calculating a "Fast Fourier Transform", our inner ears contain thousands of stereocilia - little hairs of varying lengths which vibrate at different frequencies. Rather than trying to determine the periodicity of a wave by any sort of analysis, these hairs automatically vibrate when any frequency within the wave resonates precisely with their length. This allows us to hear the various frequencies within the sound wave that reaches our ear, so that we can take in the whole ensemble of our environment.
Now here's the catch. A hair that vibrates at exactly 440Hz, also vibrates pretty well at 220Hz. In a sense, this actually represents a weakness in our hearing strategy. Even though the one frequency is twice as fast as the other, they actually sound a lot alike to us. It is harder for us to distinguish middle C (C4) from the C an octave above (C5) than it is for us to distinguish middle C from the D-flat right above it. We can still recognize the difference, but when we do, part of what we recognize is their likeness. Other intervals share the same characteristic in different ways. For example, double a frequency is one octave higher, but three times that same frequency is a fifth above that.
So, from an evolutionary perspective, this is a coincidence of the handy solution found to distinguish tones. However, the joy we find in music is so serendipitous as to beg for a more divine explanation, which you will find echoed throughout our history and surely our future, and within any moment in which you find yourself appreciating the beauty of well-tempered harmony.

This was really interesting! Thanks very much. A bunch of things you mentioned I knew already but you helped me fit them together very nicely. Like I hadn't completely gotten what Fourier transforms were used for. Thx :D

As I understand it, Fourier Transforms are used in the breakdown and analysis of all kinds of signals. But I personally had the opportunity in school to see how they operate on the vibration of a single guitar string. G, I think it was. The transform breaks down the wave (which is a function of point intensity over time) into a display of frequency intensity (where frequency is on the X axis and cumulative intensity is on Y). I was fascinated to see that although the correct frequency for that G was the strongest frequency present, numerous other undertones and harmonics were in the signal.

I think the whole issue is that you put all your focus into music. The ability to tell apart different tones hasn't evolved with the culture of music playing. It is much older.
Ability to distinguish different tones in non-human animals
Humans are of course not the only animals that are able to recognize tones. Mice for example can as well accurately tell the difference between two close tones (ref.).
Perceiving its environment
So why is the ability to tell different tones apart important. It is important because it allows one organism to better perceive the elements in its surrounding. For example, consider being in the savanna and you can't tell the difference between a lion roaring and a water fall. It seems to be a pretty important handicap.
Tones recognition in social contexts
A very large part of animal's communication is based on tons. Very primitive forms of language are mostly based on tones. Courtship display for example is often based on the tone of the other gender (the tone is correlated with the size of the organ producing the tone). A very large part of human's communication is based on tone as well. You might want to have a look at Albert Mehrabian.
If you have more questions about the importance of non-verbal communication you will need to ask your questions to psychologists (on CognitiveScience.SE) and not to biologists. Note btw, that the condition of being unable of recognizing different tones is called tone deafness.

+1 Interesting. I didn't realize mice could perceive differences between tones.


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Does a gene need to be transcribed for every single protein made?
There is one set of DNA in the nucleus and one instance of any particular gene. That gene is transcribed into mRNA and then it is translated by a ribosome. A cell has millions of ribosomes. So it seems strange to me that the cell relies on transcribing this one gene over and over again to get mRNA to supply its excessive amount of ribosomes. I feel like there should be some way to replicate the mRNA after transcription. Otherwise, it seems like it is way too slow and having millions of ribosomes makes no sense.

mRNA is not destroyed immediately after it is translated once. There can be multiple ribosomes translating a single strand of mRNA, as well. Depending on the regulation of the system, a single transcription event (producing one mRNA strand) could produce tens to hundreds or perhaps even thousands of protein molecules.

Image from here, which also provides much more in-depth information and calculations.

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Is Chimpanzee mitochondrial DNA identical to human?
How similar is chimpanzee mitochondrial DNA to human?
Does it show the same single ancestor?

I have removed the first part of your question "I know human mitochondrial DNA is "identical" for all humans…" at it is quite wrong. See, for example, https://www.nature.com/scitable/topicpage/mtdna-and-mitochondrial-diseases-903/. I suggest that in future you look for sources to support any assertions you make in questions and quote them. Also, the first part of your question can be answered by research.

@David: I don't think you should remove a statement from a question simply because it's false; such statements help answerers understand and address any misconceptions that may be underlying the question. (Ideally an answer should tackle the statement head-on.)

@ruakh In this case I disagree, as it is only background to the main question, which has already got an answer. One function of editing is explicitly stated as being to improve questions. That is what I have done.

@David: If that's so, then how come you commented on the answer to suggest that it address the false assumption that you've removed from the question?

@ruakh — An analysis of the thought processes behind my historic actions is irrelevant. I am not a politician and this is not an undergraduate debating society. What is important is that I did the right thing. I may have just changed my mind, or thought a note in the answer would help the poster and anyone who had seen the original. If you wish to discuss the principle behind this I suggest you raise it on Meta.

There are many mitochondrial haplogroups, which by definition means we don't all have the same mtDNA.

While the mitochondrial DNA (mtDNA) from humans and chimpanzees is not identical, it is highly similar. The nucleotide difference between the complete human and chimpanzee sequences is 8.9%, the difference between the control regions of the two sequences is 13.9%, and the difference between the remaining parts of the sequences is 8.5% (see reference 1).
Interestingly, humans have substantially lower levels of mitochondrial genome diversity compared to chimpanzees. The nuclear mutation rate on the other hand is higher in humans than in chimpanzees. This has been explained by differences in the mutations rates (see reference 2).
The high homology between chimp and human mtDNA does points to the same single ancestor. The divergence between human and chimpanzee ancestors dates to approximately 6.5-7.5 million years ago (see reference 3).
References

Comparison between the complete mitochondrial DNA sequences of Homo
and the common chimpanzee based on nonchimeric sequences
Comparative nuclear and mitochondrial genome diversity in humans and
chimpanzees
Differences between human and chimpanzee genomes and their
implications in gene expression, protein functions and biochemical
properties of the two species

You might have emphasized the false assumption in the question, even though your answer implies this, the poster doesn't appear to have taken the point.

@David Yes, good point. I think of some addition.

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Repetition of "Clade" in a taxonomic tree
Animals and plants are somtimes classified (organized) into a taxonomic tree data structure. The term "tree data-structure" comes from the fields of computer science and software development.

On Wikipedia this taxonomy sometimes has more than one field named "Clade". How is it possible for more than one tier of the taxonmic tree of life to be named "Clade"?
Kingdom:
Clade:
Clade:
Clade:
Clade:
Order:
Family:
Genus:
Species:

Why would "Clade" be repeated more than once?
Are the instances of the text "Clade" supposed to be "phylum", "class", and "Order"?

Have you read about what a clade means?

Possible duplicate: https://biology.stackexchange.com/q/55457/27148

Minor note: the tree structure for representing knowledge does not derive from CS/software. CS/software probably adopted it from biology and related disciplines (would be interested to know where exactly). Recall that biological taxonomy in its modern sense derives from Carolus Linnaeus, who had no knowledge of CS or data structures.

Wikipedia employs multiple taxonomy databases. The page gives an idea of conflicts of consensus and for official species classification. The ball python has 10 levels of classification and the rose has 11. One is a plant, the other is a reptile. Biology didn't give them tidy class and phylum ranks.

I don’t think we need to get rid of [taxonomic ranks]
[...]
What we need to abandon is the unwarranted connotations that higher-level taxa are comparable. Because they aren’t. They are abstractions. They are information storage boxes. That’s all they are.
Ronald Jenner, a phylogeneticist

Linnaeus invented ranks (uniform levels of nesting that he applied across groups of organisms) to organize his understanding of diversity. The original ranks designated by Linnaeus were kingdom, class, order, genus and species, and others, including the phylum, have been added since. As phylogenies improve, some have called for the abandonment of ranks to avoid implying that different clades given the same rank are comparable.

There have never been clear objective criteria for designating a clade as a phylum. There is, for example, no known property that is shared by all echinoderms or all molluscs, both of which have been designated as phyla, and that would distinguish these clades from more or less inclusive clades that aren’t phyla, such as deuterostomes or bivalves. This has provoked considerable discussion about whether the categorization into phyla says more about the way humans perceive animal diversity or the biological processes that generated this diversity
 Ref.: Andreas Hejnol, Casey W. Dunn, Animal Evolution: Are Phyla Real?, Current Biology, Volume 26, Issue 10, 2016, DOI: 10.1016/j.cub.2016.03.058

UK and USA textbooks don't have the same number of kingdoms, one has 5 and the other has 6, other theories have 32.
Super and sub ranks also exist, like superfamily and subphylum.
Taxonomy is most often a spectrum of variety with unclear or overlapping divisions, like a rainbow, and words are attempts to put labels onto the divisions of the spectrum.
Different cultures and regions employ words that segment the spectrum of knowledge into different compartments, artificially. That is especially mired by the complexity of taxonomy grouping.

For taxonomic hierarchy, there’s some sense in which the phylum and the species both have rigorous currency, however the intermediary levels are a kind of construct.
Ref.: https://www.quantamagazine.org/phyla-and-other-flawed-taxonomic-categories-vex-biologists-20190624/

The idea of a clade and taxa (phylumn, class, order, etc.) are two different, but sometimes overlapping approaches to the classification of organisms. In short, a clade is any group of organisms that contain a common ancestor and all of its descendants, and is sometimes said as monophyletic. On the other hand, a taxon is a group of organisms that fits in to the taxonomical ranking system. Due to the limitation of technology and molecular evidence in the past, not all taxa reflect the evolutionary relationship.
On the wikipedia page, many clade are included as a result that an organisms can fit in groups within group. Take the clade Angiosperms and Monocot, an angiosperms is any flowering plants and this clade contain another clade within. That is, the Monocot, which are flowering plants with a single cotyledon (embryonic leaf) in the seed. Keep in mind the Angiosperms and Monocots are clade, meaning that is a natural group in the sense that it reflects the evolutionary history of the organisms within the group.
So, to answer your question, a clade does not always represent, or equal to a taxon. The purpose of including the clades is to provide finer details with regard to the evolutionary history and phylogenetic relationship to a given organism.
Suggested readings and relevant question:

What is the difference between these terms: clade, monophyletic group and taxon?
Monophyly (wikipedia)
Clade (wikipedia)

Hi MKJ, I don't understand the last phrase of the first paragraph, if clades are related, "and technology hasn't always confirmed the eveoltionary relationship of taxa" that should be the same with clades?

@bandybabboon Hi, I was refering to some taxa like the class Reptilia traditionally didn't include birds. I made an assumption that birds were excluded due to limited molecular evidences, but I might be wrong and tbh I haven't really researched about it before I answered. I'll edit it out of this answer if this is not the case. Apologize for the confusion.


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Do humans produce an immune response to their own antibodies?
As far as I know, T and B cells form a part of the adaptive immune response in humans. In their early stages, these cells undergo genetic recombination to produce a diversity of antigen receptors/antibodies, before maturing in the thymus/bone. As a part of this maturation process, I understand that the body presents the lymphocytes the full set of molecules present in the body, and ones evoking an autoimmune response are eliminated. This maturation process allows lymphocytes to recognise the difference between pathogens and body cells/molecules.
My question is this:

Since the maturing lymphocytes are not exposed to
pathogen-complementary antibodies before the primary response to a
pathogen, does the body recognise the variable regions of these newly
synthesized antibodies as foreign, generating a second wave of
antibodies?

This might cause the body to produce antibodies it doesn't need to, or unnecessarily remove useful antibodies from the blood by agglutination/phagocytosis.

Are you asking about anti-antibody antibodies?

@MattDMo — Seems quite clear to me what the poster is asking. He explained his problem — asking him to put a (your) tag on it is neither required, reasonable nor helpful. If you don’t understand, say what it is you don’t understand.

In short, the body CAN produce antibodies against antibodies (although it is not desirable and is a form of autoimmunity).

This happens e.g. in rheumatoid arthritis (see https://en.wikipedia.org/wiki/Rheumatoid_factor); RF is an autoantibody against Fc portion of the immunoglobulin.

Antibodies against other antibodies can also be produced by one species against another's antibodies (e.g. anti-rabbit antibodies), which have applications in biomedical research. Production of antibodies against another species' antibodies is also a potential adverse reaction in monoclonal antibody therapies (when using antibodies originating from another species, e.g. mouse; 'humanising' the antibodies reduces that risk).

The question arises, why this does not happen more frequently. For simplicity, I will continue to focus on B-cells (and antibodies, rather than T-cell mediated immune responses). The key is to understand the process for mitigating self-immunity, in general, with a few points that might be antibody-specific.
The journey of a B-cell goes from bone marrow (HPSC > pro-B-cell > pre-B-cell) via mature B-cells (in peripheral circulation, tissues and lymph nodes), first naive, then activated, to plasma cells. The key points for preventing autoimmunity are:
BONE MARROW: VDJ rearrangements. This is antigen-independent. There is negative selection too: B-cells whose receptors are bound to an antigen undergo either receptor editing, apoptosis or anergy (to prevent auto-immunity).
The limitation here is that B-cells are only exposed to limited number of antigens available in the bone marrow. However, because of access to blood/serum and bone marrow containing plasma cells (up to about 3% bone marrow cellularity), it is reasonable to expect that developing B-cells encounter immunoglobulins. As a result of this, in theory there should be no cross-reactivity to antibodies, or at the very least the constant antibody fragments.
(Note that some B-cells get activated and become plasma cells via interactions with T-cells outside of germinal centre, but these are thought to be more important for fast immune response, and generate more short lived cells)
GERMINAL CENTRE: somatic hypermutation (SHM), isotype switching and affinity maturation
After encountering an antigen (in amount meeting a certain threshold), B-cells become activated and migrate to primary follicles and form germinal centre, where they become centroblasts and centrocytes. There, they depend on interactions with follicular dendritic cells and T-follicular helper cells to undergo the above processes. All these events can (in theory and in practice) cause the previously non-self-reactive B-cells to become self-reactive. This is to some degree filtered against. The key points here are:

there needs to be sufficient antigen (that the B-cell has good affinity for) to allow the B-cell to survive; it is quite unlikely that the B-cell will have a good affinity for a completely new auto-antigen
the process needs to occur in the right context (antigen alone is not sufficient), with the right support (i.e. FDCs and TFHs), for example co-receptor binding needs to also occur, complement complexes will be present etc. Usually the antigens are displayed by FDCs in the form of immune complexes, which were delivered to them by circulating macrophages.
in general, there is an excess of rapidly proliferating and mutating activated B-cells, that need to compete for a limited amount of antigen, so only the best B-cells are selected (that can bind to the antigen best). This, for example, means that a B-cell with weak affinity to a (novel auto-)antigen not displayed by FDC will be less likely to succeed than one that has a strong affinity to the (non-autoimmune) antigen on the FDC

Finally, note that antibodies are secreted by plasma cells (i.e. the end stage in the differentiation of B-cells). The earlier stages have instead B-cell receptors, which are membrane-bound immunoglobulins (i.e. antibody on the cell surface).
However, in case of high rates of apoptosis and inadequate clearance of apoptotic debris can increase the chance of autoimmunity developing...
Some background:
https://pathologia.ed.ac.uk/topic/the-germinal-centre/
Basics of germinal centre
Vinuesa, Carola G., Iñaki Sanz, and Matthew C. Cook. "Dysregulation of germinal centres in autoimmune disease." Nature Reviews Immunology 9.12 (2009): 845-857.
https://doi.org/10.1038/nri2637
A relatively aged, but quite informative article on germinal centre in autoimmunity

Very nice answer!

The short answer is this happens all the time - it's called self-aggregation and it can be perfectly ok as a regulatory mechanism, most of the time. HOWEVER has bad name in the pharmaceutical industry.

This might cause the body to produce antibodies it doesn't need to, or unnecessarily remove useful antibodies from the blood by agglutination/phagocytosis.

^EXACTLY
The bodies antibody regulation is under tight control. A lot is known about this subject because of the modern approach to using antibodies in therapeutics (ADC) - I'll avoid the specifics.
The crux of the question is - it's not long lifespan that is of primary concern but the short lifespan of antibodies - so there are clearly defined mechanisms to overcome this, mainly recycling (below). Aggregation, described below - in therapeutics is a bit of a problem because causes the antibodies to mess-up in their primary function.
The key is antibodies do bind to themselves it's not necessarily bad however (below), it's sort of a natural process for excretion (which might be the basis of the question), but it can be bad. Again to reiterate in therapeutic antibodies it's not seen as good and actively screened against.
Getting rid of antibodies is the primary function of the kidneys and  not self-aggregation (its a lesser mechanism).
Kidney Filtration and Recycling
How antibodies end up in the kidneys as part of protein excretion.
Your kidneys constantly filter the blood, removing waste and small proteins, including antibodies. However, IgG antibodies escape this fate thanks to the neonatal Fc receptor (FcRn). This nifty protein grabs IgG molecules inside cells, shielding them from degradation in lysosomes. After hitching a ride on FcRn, the antibodies are spat back out into circulation. Without this recycling system, IgG levels in your blood would plummet, as they'd be filtered out and destroyed.
Neonatal Fc Receptor (FcRn)
FcRn isn't just a one-hit wonder for neonates/babies—it’s a workhorse in adults and very interesting for the pharmaceutical industry. In endothelial cells, FcRn binds IgG under acidic conditions (like inside endosomes) and protects it from being digested. This recycling process extends the half-life of IgG to about 21 days, keeping your immunity sharp. FcRn is also key in therapeutic strategies; targeting this receptor can reduce IgG levels in diseases like myasthenia gravis.
Self-Aggregation of Antibodies
Antibodies like to team up sometimes—this is called self-aggregation. As I keep reiterating it seen as bad and can be bad, but it can be useful. By clumping together, antibodies help the immune system identify them as ready for clearance. It’s like raising a flag for excretion (kidneys above). However, excessive aggregation can lead to issues, as you mentioned about function, also forming immune complexes that might clog things up in autoimmune diseases in the other answers here.
Polyspecificity
In therapeutic antibodies polyspecificity is the current buzz word (recent Nature paper). Its not really related to the question - but its where the field is at. It means they can recognize and bind to multiple antigens, even unrelated ones. This feature is like having a Swiss army knife in your immune arsenal. It boosts adaptability, especially when encountering novel pathogens, but it also carries a risk—misidentification can trigger autoimmune responses.
Vidarsson, G., Dekkers, G., & Rispens, T. (2014). IgG Subclasses and Allotypes: From Structure to Effector Functions. Frontiers in Immunology.
Antagonism of the Neonatal Fc Receptor as an Emerging Treatment for Myasthenia Gravis. (2020). Frontiers in Immunology
See also
Pyzik, M., Kozicky, L.K., Gandhi, A.K. et al. The therapeutic age of the neonatal Fc receptor. Nat Rev Immunol 23, 415–432 (2023). https://doi.org/10.1038/s41577-022-00821-1
Polyspecificity is a very recent full Nature paper.

Yes, one of the problems that sometimes humans face is when the immune system is recognizing it's own "proteins" as a source for responding to it.
That said, this is a process that cannot be avoided as there's always a try to eliminate pathogens, and to check them.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

My naive response it as follows.
The antigen-binding sites on an immunoglobulin are generally concave in shape. Hence I would anticipate that the antigen-binding site on immunoglobulin-1 would have difficulty binding to the antigen-binding site on immunoglobulin-2.
There may be additional considerations, such that the overall difference of the antibody from its un-mutated precursor is too slight to elicit a strong response.


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Why do stem cells injected into muscle become muscle cells?
In this article published in Science Daily, researchers injected teratoma-derived stem cells into mice with muscular dystrophy, and the stem cells regenerated 80% of the lost muscle. But what is the mechanism that results in their becoming muscle cells, rather than any other type of cell?
I'd have to assume some sort of cell signaling is responsible for this directed differentiation into muscle cells, so what is it? Can it be reproduced in vitro?

Looking at the paper itself, we find that they prepared the stem cells to have myogenic (muscle-specific) properties. They first injected stem cells into the irradiated (which kills muscle stem cells) muscles of immune-deficient mice. This resulted in tumor growth (teratoma - a stem cell derived tumor, where different kinds of tissues are spontaneously formed. Growing in a muscle environment increases the chance of muscle tissue formation.). The tumor cells, which expressed muscle-specific markers, were isolated from the other tissues and then used for regeneration of an injured muscle.
In their teratomas they checked for cells expressing α7-integrin and vascular cell adhesion molecule-1 (VCAM-1), which are markers expressed in satellite cells (muscle stem cells). These factors were expressed in about 10% of the fraction that did not show any hematopoietic and endothelial markers (meaning: there were a lot of other tissues formed as well). They also showed expression of Pax3 and Pax7, which are muscle-specific transcription factors, important for differentiation of myogenic progenitors. These cells were therefore already muscle-specific cells before they have been transplanted for regeneration.
The researchers did, in fact, do in vitro and in vivo differentiation experiments. For in vitro differentiation they subjected their muscle-marker expressing cells to a myogenic medium. This mimics the muscle environment and enables cell differentiation signaling. Here is an example protocol how this can be done. Then they transplanted their muscle stem cells into a muscle and they also managed to differentiate in vivo and regenerate the injured muscle.
The entire process of pluripotent stem cell to muscle cell differentiation can be performed in vitro, but seems to be tricky (1,2). Medium factors or genetic activation of transcription factors can activate different steps in the differentiation cascade.


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Why do athletes see a dip in performance in their thirties?
I have noticed a lot of athletes hit their prime when they are in their 20s and that by the time they reach their 30s they are past it and start to decline. Great athletes tend to prolong their careers by adjusting their game strategy, but even so they can't do the things they used to do when they were younger. Examples of this are abundant in the NBA, NFL, MLB, NHL, football, etc.
Why do athletes suddenly have such a drop off in performance? What happens to their bodies,  muscles, etc that prevents them from doing what they once did? Can someone explain the biological/physiological reason for this?

A lot of sports cause damage to the body, compare the average retirement age of gymnasts and footballers to that of golfers and cyclists

That is a great point. I never thought of it like that.

The decline in athletic performance is a result of senescence; the question then becomes "why do we senescence?"
A number of questions on this site have addressed this. These include Why does evolution not make our life longer?, Why do we age?, and any number of others that one can pull up with a search for senescence. It is key to distinguish between proximate (how, physiologically ) and ultimate (why, evolutionarily) explanations. It's not entirely clear to me from your question which of the two you are asking.

I am asking about the physiological mechanisms. And I don't think simply saying they are getting old is succifient. By any normal person's standards, they can still compete at an exceptional level.

@StanShunpike Yeah, but normal people also drop off the same way.  By your mid- to late-twenties, your body is basically finished getting better simply through development and now only gets worse.

But why physically as opposed to mentally? Why doesn't the mind drop off the sane way?

Who says it doesn't?  We can keep learning of course but there's solid evidence that brain development has largely wrapped up by our mid- or late-twenties.

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Does taking a shower have the same effect on muscles as warming up?
When playing sports, coaches and trainers are always very clear that it is necessary to warm up and stretch. But sometimes athletes sometimes want to get an extra stretch in and don't want to go through the hassle of warming up.
Will taking a hot shower warm up muscles or does an athlete sctually have to do physical exercises like jogging in order to be ready to stretch?
I know this sounds like a question I could go on the physical fitness SE, but I'm really hoping for an answer involving thermodynamics and I doubt I'll get that there.

Hot shower will definitely affect your muscles health. Hot water shower results in Vasodilation,which will decrease the vascular resistance and allows blood to flow easily through the blood vessels. As the vasodilation (increase in diameter of blood vessels) allows blood to move without resistance and which in turn nourish the tissues with sufficient oxygen and nutrients. Also it affects in the removal of metabolic wastes from cells. There is another process called  Vasoconstriction (decrease in blood vessel diameter) which makes the blood vessels to contract and may lead to increased blood pressure.
There is a technique called as Heat therapy which will be effective in muscle and body health.

Heat therapy, also called thermotherapy, is the use of heat in
  therapy, such as for pain relief and health. It can take the form of a
  hot cloth, hot water, ultrasound, heating pad, hydrocollator packs,
  whirlpool baths, cordless FIR heat therapy wraps, and others. It can
  be beneficial to those with arthritis and stiff muscles and injuries
  to the deep tissue of the skin. Heat may be an effective self-care
  treatment for conditions like rheumatoid arthritis.
Heat therapy is most commonly used for rehabilitation purposes. The
  therapeutic effects of heat include increasing the extensibility of
  collagen tissues; decreasing joint stiffness; reducing pain; relieving
  muscle spasms; reducing inflammation, edema, and aids in the post
  acute phase of healing; and increasing blood flow. The increased blood
  flow to the affected area provides proteins, nutrients, and oxygen for
  better healing.Reference

While taking a hot water bath we are just making our muscles and tissues nourished, which means the muscles will be in a healthy state for expansion and contraction. So it is recommendable to take a hot bath before exercising.

I am not an expert but I would definitely say never replace a warming-up by a hot bath. However, this depends on the activity to be undertaken. When you go for a round of chess or a stroll through the forest on a Sunday afternoon, sure, take a bath. When you're getting ready for a bout of sparring in a martial arts tournament, a hot bath is the perfect recipe to get injured (and beaten).
The Australia Sports Commission says that a warming-up aims to:

prepare the body and mind for the activity
increase the body's core temperature
increase heart rate
increase breathing rate.

None of these are targeted with a shower, on the contrary even I would say. The only thing that a hot bath can do is superficially increase temperature, flexibility and blood flow in the muscles. But this can never replace a warming up. I would save the bath for after exercise, as everyone does :)

Wouldn't a hot shower increase the body's core temperature, or does it only affect the body's surface temperature?

@CactusWoman: Just superficially I guess. Depends on the temperature and duration. A shower just above our core temperature is already pretty hot!

I am going to address only the stretching portion of the question since some misinformation is out there. When you say stretching, I hope you mean dynamic as opposed to static stretching especially if you are about to compete in a sport. If you are referring to static stretching, taking a shower may be a better option then, but if you mean dynamic stretching, a shower will not provide a greater benefit.
For peak performance, athletes or weekend warriors should use dynamic stretching prior to an event.

In previous research it has been recommended to use dynamic stretching as the primary method of stretching pre-event warm-up before high speed, and power activities (Little & Williams, 2004). The findings of this study agree with that recommendation for agility activities as well. This study supported the use of dynamic stretching in eliciting the greatest performance in agility movements by decreased T-Drill time. The findings
  of the current study are consistent with those of Fletcher and Jones (2004), and Young and Behm (2003) who determined that dynamic stretching elicits the best performance in power and high-speed activities [1].

However, static stretching does not improve performance and can actually lead to injury.

The current study found static stretching to have a negative effect on agility, and acceleration (Fletcher & Jones, 2004; Nelson et al., 2005). As acceleration is a component of agility, these findings support those of Fletcher and Jones (2004) and Nelson et al. (2005). Agility also involves components of braking, and change of direction. Static stretching prior to agility activities was found to have a negative effect on agility performance [1].

To read up on dynamic and static stretching as well as other types of stretching, I would recommend MIT's Types of Stretching page.
Additionally, the references to my reference one provides many more useful articles to look into.

Static versus dynamic stretching effect on agility and performance

Stretching and warming up are indeed a different thing altogether, +1.

@AliceD the OP said some athletes want to get an extra stretch in but dont want to go through the hassle of warming up. To me, they are implying substituting a hot shower to stretching in order to warm up the muscles.

I agree - the question should have been specified first. Nice addition, hence the upvote :)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Are there more true codes found in biology besides the central dogma?
I know each element of the central dogma is a code in the mathematical sense of finite-state machines. That is, DNA is transcribed into RNA, and RNA into proteins.  What other examples are there of codes that exist naturally in organisms?

Developmental patterning(?)

Stepwise polymerization of monomers, Operons for catabolism, operons for anabolism. Inducible and Repressible genomic expressions. Your question is very general. Also, besides methods of mathematical analysis, central dogma is mathematical in what sense exactly ?

@Macedona93 I am no expert. However, I believe FSM theories define a particular class of mathematical objects related to what are known as free monoids. I believe the conversion of DNA to RNA or vice versa follows FSM processing of this type. I think this is a well-established fact and is really the true definition for what we casually call a "code".

I see, perhaps im not enlightened in Finite State Machines and their philosophical relaton to cell and molecular biology. I just know that the rules of cellular biology follow those of physics, biological thermodynamics (Free energies and what have you) amongst others. Like the fact that DNA is coded in respects to monomerical polymerization. Regardless, i up-voted the question as i find it quite interesting. Seriously check out operons, they're quite amazing.

DNA is a code that occurs via stepwise polymerization, like all major macromolecules. In respects to DNA, it is Nucleic Acid sequences that polymerize to create the DNA. In eukaryotic cells this happens at multiple replicons (regions of replication). So you can look DNA as code for itself. You also have rRNA, mRNA, and tRNA. All of these code for and do specific things. rRNA facilitates the creation and movement of the ribosome, where mRNA and tRNA "code" for the final protein. tRNA serves as the principle code strand for the correct Amino Acids. This is read as a series of three N.A's (codons) One codon for a respective Amino Acid. mRNA actually guides the synthesis of these polypeptide chains. You also have something called operons. These are groups of genes with related functions that are clustered together. This allows for rapid initiation and termination of gene expression. Im sure there are a few others but these are those that come off the top of my head. The term "code" and molecular bio are very much intertwined.

I answered the question before his edit

Yea in respects to these situations rather than editing my answers I'll leave them as they are. And comment if I see fit. The only other situation where a "code" would represent its intrinsic definition would be with operons and genomic expressions.

I thought this was a nice answer for how I phrased the question previously. Your answer isn't what I had intended the original question to imply.  Hence I changed it immediately. But had I meant to ask that particular question, this answer would have been succinct and sufficient. I am new to SE, so if there is a better way to edit questions in the future I am open to suggestions. I would have liked to retain the information in how I phrased it originally so that your answer wouldn't seem so unrelated to the current phrasing.

wait, is the lac operon an operon of the type you mentioned? I don't remember much about it, but i remember learning about that in my intro bio class

Yep Lac Operon is a good introduction to the functioning and mechanisms behind operons. I also first heard of the Lac Operon in my Cell and molecular bio undergrad course

I am not very familiar with them, but I hear that bacterial non-ribosomal peptide synthases are made of catalytic modules, lined up in series, paralleling their product. My suspicion is that there is some promiscuity / ambiguity in the nonribosomal code.
Also, N-glycosylation in the ER / Golgi occurs in a defined series of events, but that includes backtracking (that is, sugar cleavage), which I am not sure would belong in a finite state machine.


text:
Do cells in healing ligaments or tendons have deformation processes? If so, what are they?
I am trying to better understand how non-muscle tissue in the muscuoloskeletal system heals. Specifically, I am interested in how ligaments or tendons heal once torn.
I read the following text:

If the muscle pulls the damaged tendon and then releases it then we have a deformation cycle that the cells are able to detect. They also then receive the information they require regarding orientation. This is why the elasticity of the early callus is important; the tissue must be able to be pulled out and then return to its original shape in order to receive information about orientation.

Source:
http://www.peraspenberg.com/texts/how-do-tendons-and-ligaments-heal/
I don't understand what they mean by "deformation cycle" and how cells detect it.
Is there a name for this cycle? If so, how do the cells detect tissue deformation?
Also, if there is any literature that specializes in the tissue of ligaments or tendons, recommendations would be appreciated. I have plenty on muscle tissue and some on bones, but not ligament or tendon tissue regeneration.

Are you asking about tendons or ligaments, or both? Your quote only discusses tendons. Your title only mentions ligament. And in the question's details you asked about "the tissue of ligaments and tendon formations"

You are correct, it was ambiguous. I updated it. Is it clearer?

Thanks, that's clearer. Why did you reject my edit? it was pretty much the same as yours and in addition to it was fixing tags, typos, and dead link.

@FranckDernoncourt Because I didn't read it clearly enough and did a bad job. If there was a way to resurrect your edit and do it again, I would approve it. At the time, I read the title and the first few lines, and it seemed to be changing the content. Then you called my attention to it again and I realized it was probably an experienced person editing it or they wouldn't care. When I reread it carefully, I realized you were right. I get a lot of edits that just make small changes, so I might have been trigger happy on reject.

@FranckDernoncourt Sorry about that :/


text:
How much difference in genome is enough to prevent interbreeding?
I am not a biologist. I am a software developer interested in genetic algorithms therefore i am probably talking to biologists who also have a knowledge of genetic algorithms. I need to "breed" different solutions to a problem while allowing the number of genes in my solution to vary because i don't know in advance how many genes i need. This is why i need to be able to cross solutions with N genes with solutions with M genes and this is a serious problem. If N and M are very different the problem would be even more serious. I want to know what happens in the biological world. I am trying to understand how much difference in genome is "enough" to prevent interbreeding between different organisms. Would it be possible to say that if less than (approximately) X% of the genes of two organisms are different then they can probably mate and have offspring?
Thank you
Wentu

It is not just genomic differences that prevent interbreeding. The synteny also matters.

Welcome to Biology SE! I think this question holds potential, but probably it needs some narrowing down or splitting up in multiple questions: e.g. (1)  On the other hand, members from different species have genomes different enough to make interbreeding impossible. Is it possible to explore what happens in-between these two cases? and   (2) what happens during evolution? is it just geographical separation that allows genomes two diverge up until the point when two species exist instead of one? are quite different questions.

A first idea would be that inbreeding is only deleterious because of the possibility of creating homozygous recessive genotypes which then cause lethal phenotypes. If there were no deleterious recessive alleles in either parent, it could perfectly be the case that interbreeding would still be possible.

MarchHo, i personally can't have offspring if i mate with a chimp female but i can have it if a mate with a human female. The genes of these two organisms differ for something like 1-2%, right? But i don't know my genome differs from the average woman genome. I suppose that 1% difference is already too much but... how much is too much?

@JohannesWentu It isn't as simple as genomic %-difference. If there is a mismatch in crucial systems, this can be enought for incompatibility, even if the genome difference is miniscule. You also need to consider other barriers for reproduction, such as behavioural and mechanical barriers.


text:
What is meant by “genes at the trunk of the evolutionary tree”?
Recently I went through a paper about hepatocellular carcinoma in which they talked about trunk genes (p. 26, second paragraph):

Branching tumor evolution complicates efforts to implement
  personalized medicine and suggests that targeted therapies might be
  directed to genes that are mutated at the trunk of the evolutionary
  tree. Transposons provide powerful tools for identifying trunk genes,
  as insertions in trunk genes are more likely to be associated with a
  higher number of sequencing reads.

I really don’t understand what are the trunk genes. Can anyone please explain them clearly.
Thank you

I've tidied up you question a little and given focus to the key concept at issue — the "genes at the trunk of the evolutionary tree".

I think the article is using a phylogenetic tree to explain the stages of how the tumor has evolved.
According to Nature.com >>

All trees have a shared 'trunk', which represents the complement of
  mutations shared by all malignant cells within the cancer.

Or simplified by Britannica.com >>

Phylogenetic tree, also called Dendrogram, a diagram showing the
  evolutionary interrelations of a group of organisms derived from a
  common ancestral form. The ancestor is in the tree “trunk”; organisms
  that have arisen from it are placed at the ends of tree “branches.”

For a visual representation, this is a phylogenetic tree for evolution of breast cancer >>

Image Source: Phylogenetic Cancer Trees

My first few readings of the sentence, I thought the article meant the ontogenetic tree -- that is, the mutation occurred early in the life of that specific individual.  From the word "evolutionary", though, I think you are right.  Still, the confusion is a warning to technical writers to use metaphors only very carefully.

@Malvolio I had the similar confusion, although upon reading the abstract the OP has provided, I am pretty sure the trunk genes they have mentioned in the context of evolutionary trees is what I have answered. Needless to say, I totally agree with you about the careful use of these terms.

@user3351523 My pleasure. Glad I could help.


text:
Hydrogen Peroxide on Open Wounds
I know that H2O2 is a chemical with high oxidative potential. It can deliver nascent oxygen which can destroy bacteria.
I understand that open wounds have cells that are dividing at a fast rate to effect healing. Is it good to add a substance that can cause damage to cell membrane and possibly cause mutation in the DNA of these fast growing tissues?
Can H2O2 be safely used to sterilize wounds?

H₂O₂ is used only at the time of first cleaning afaik; good against Clostridia. For regular dressing it is not generally prescribed.

There will be few rapidly-dividing cells in a fresh wound (which is the wound to which H2O2 is applied). In general, it is a good idea to avoid applying irritants to rapidly dividing tissue.
Hydrogen peroxide is a weak mutagen. It is produced in many body tissues, ingested in drinks, produced by mouth bacteria, etc. It may well cause some cancers. Some OSHA-mandated literature does warn that it is a mutagen and must be handled with care, but these are warnings to people who work with concentrated solutions.
However, a relatively weak hydrogen peroxide solution, even if it is mutagenic, would need to be left in place and active (or renewed) for a long period of time to produce skin cancer. As it has been a staple of first aid kits for decades, and this association has never been made clinically, my best guess is that the benefit (as a bacterocidal agent) far outweighs the risk in the treatment of minor wounds. As in all things, however, prudence is advised. (I myself don't use it because soap and a lot of water is quite effective. Nor is it used in the care of wounds in Emergency Rooms where it is considered to be detrimental to wound healing. If I were in a country where clean water and soap were in short supply, I might well use it if necessary.)
Because it is an irritant (and many irritants can be considered mutagenic), it is actually used to treat precancerous skin lesions, the finding being that it affects the more rapidly dividing pre-cancerous cells than the rest of the epithelium.
Far more potent peroxides have been used topically, which may increase the risk of skin cancer.
Interestingly, one of the responses of skin cells to H2O2 is the generation of an oxygenase to fight the effects.
Topical sulindac combined with hydrogen peroxide in the treatment of actinic keratoses
Effects of Peroxides on Rodent Skin: Epidermal Hyperplasia and Tumor Promotion
Heme oxygenase is the major 32-kDa stress protein induced in human skin fibroblasts by UVA radiation, hydrogen peroxide, and sodium arsenite
Recent Advances in Wound Care, Michael K. Abraham, MD, MS, and Jason S. Oh, MD

Nice answer. I shouldn't ask new questions, but what about chronic repeated exposure to peroxides via mouth wash, given that epithelial cells in the mouth are quite rapidly dividing?

@ChrisStronks - Almost any irritant has the potential to be mutagenic. One weighs risks to benefits. When there are specific benefits (to whiten teeth, for example), it's unlikely to do more damage than good. But where there's little benefit, I wouldn't do it on a daily basis.

Ahem, I think you may have teased out the self-helpness there.... But yeah. That helps :-)

@ChrisStronks the epithelial cells in your mouth also shed fairly quickly, so even if a cell were to develop enough mutations to become cancerous, it likely wouldn't be around long enough to start dividing into a tumor.

@MattDMo - while it's true that epithelial cells in the mouth have a high rate of turnover, it's also true that oral cancers occur still. 43,250 Americans will be diagnosed with oral or pharyngeal cancer this year, of those, only slightly more than half will be alive in 5 years. Alcohol has long been a risk factor because it is held in the mouth, and it's an irritant. So, no pleasant daydreams about this are helpful. I've seen people with their lower jaw removed due to oral cancers. :-O (Not recently, though.)

@MattDMo - also, hydrogen peroxide is readily absorbed into tissue, which means it can easily reach more permanent cells. I'm not a cancerphobe. I think the risk from using a peroxide mouthwash is lower than alcohol and smoking, but as they have been on the market for far less time, we don't know their long-term safety. The good thing I can say is that it is produced by our own bodies, and we seem to have means to fight it. But, prudence in all things is not bad advice.

@anongoodnurse I completely agree with both of your comments. My thinking was that since H2O2 would only be in the mouth for 30 seconds to a minute once or maybe twice a day, it wouldn't be quite the same level of exposure as would be seen in a smoker, smokeless tobacco user, or chronic consumer of alcohol. I was also primarily thinking of the cells on the inner cheek, which shed rapidly, while other epithelium, such as gums or the roof of your mouth, may turn over less quickly and allow mutations to accumulate (...)

(...) Still, it's a matter of degree as far as risk is concerned - you need to think about the cumulative exposure over time - 1 to 2 minutes of H2O2 exposure/day is nothing compared to a 1-2 pack/day smoker, or a heavy drinker. It all comes down in the end, however, to how much risk you're willing to take.

@MattDMo - I agree completely. I think we are agreeing in principle, and perhaps differing in the details. :)


text:
Horns in animals and birds
Are there any carnivores with horns (whether extinct or currently alive)?
Do any flying creatures have horns?
By horns I mean horn like structure.

Why do you want to know, and what do you know from before? Are you aware of the distinction between e.g. horns and anthers (and other types of hornlike structures)? What types you include as "horns" make a big difference to your question.

honestly, @OneFace this is a bit of a 'let me google that for you' question :)   http://lmgtfy.com/

Males of the carnivorous Jackson's chameleon (Trioceros jacksonii) have three hornlike structures on their heads (also found in a couple of related species). From what I know, these are true horns, which means that they are pointed keratin-covered protrusions that have a core of living bone, see e.g. this website from Toronto Zoo (this page also claims that their horns show annual growth rings). However, there are many definitions of horns (some only consider the horns in Artiodactyla to be "true" horns), so you need to be specific in what you are asking for. Used casually, the antlers of Cervids or other similar structures, are often considered as horns.

As for birds, the closest thing to a horned bird I can think of are species of the Australian Cassowary (Casuarius). They have a bony crest on the top of their heads, which is covered by keratinous skin. However, the bony crest is supposed to be relatively soft and spongy, and can hardly be counted as a horn is the strict sense of the word.

(Southern cassowary, Casuarius casuarius, from Wikipedia)

As far as alive carnivorous land animals go, there are non. But let's search in the sea:

Narwhal (Monodon monoceros)

 courtesy: http://i.huffpost.com/gen/1625488/images/o-NARWHAL-facebook.jpg
Longhorn cowfish (Lactoria cornuta)

 courtesy: Wikipedia

They are omnivourus and feed mainly on microorganism. There are loads of sites claiming them horned puffer fish.

Extinct

Carnotaurus (Carnotaurus sastrei)

 courtesy: https://img1.wikia.nocookie.net/__cb20141130153854/dinosaurs/images/e/ed/084d14_0ce4968fba228be913b757cc8ba15f88.gif

Horned Flying Bird

Gread hornbill (Buceros bicornis)

 courtesy: http://www.livepterosaur.com/LP_Blog/wp-content/uploads/2011/05/Lip-Kee-Malaysia-Hornbill-5110157612_e1e078296f_z.jpg

What definition of "horn" are you using? The included examples represents different types of structures with different functions, and several of them are not horns in the strict sense of the word. Based on your examples, you also seem to use such a wide definition of "horn" that your own first sentence is factually incorrect.

Great horn bills do have a horn shaped bill, but its not a horn.


text:
What determines whether a cell divides by Mitosis or Meiosis?
What I learn from biology class is that mitosis is for producing somatic cells in animals and the gametes of some plants. And meiosis is for production of animal's gametes.
I am curious about what determines whether it divides by mitosis or meiosis.
What signal does it need before it starts mitosis or meiosis?


text:
Reversal of reactions and enzyme catalysis
Enzymes increase the rate of a reaction. They cannot affect the rate constant, thus the rate of both the backwards and forwards reaction is increased. This means the same enzyme catalyses the forwards and backwards reaction.
Then why do cells sometimes have different enzymes for the backwards and forwards reaction (eg alcohol hydrogenase and dehydrogenase)?

Which specific enzymes are you referring to, in what species and cell are these two enzymes present, and what are the entire reactions that each one catalyzes? "Alcohol dehydrogenase" is a name for many different enzymes. I'm not sure what "alcohol hydrogenase" is.

Welcome to SE Biology. Please do us the courtesy of reading to the end of the [Tour] to find out how this site works and what is required of questions. One thing is research on the topic, which would perhaps have given you the answer that I have provided instead.

Enzymes do change the rate constant. Maybe you meant equilibrium constant?

There are two things to consider in relation to an enzymic reaction. The rate is one consideration, but that has no influence on the direction in which the reaction proceeds.
The direction in which the reaction proceeds is determined by the Gibbs Free Energy change — dependent on the intrinsic chemistry, in the form of the standard free energy change (ΔG0), and the concentration of reactants and products. This determines the position of equilibrium. Speeding up the rate of the overall reaction (the combination of forwards and backwards reactions, the rate of both of which increases) has NO effect on the position of equilibrium, and hence the overall directionality.
This is basic enzyme biochemistry, covered in all textbooks on the subject.
So, how can a different enzyme reverse a reaction, if its ΔG0 and equilibrium constant are fixed? The solution to this apparent paradox lies in discarding the lax terminology:

what is happening in the example cited is not the reversal of a reaction, but the reciprocal of an inter-conversion of two metabolites by a different chemical reaction, involving other metabolites. These two reactions have different values of ΔG0, and, being different, are catalysed by distinct enzymes with different catalytic mechanisms.

I am not familiar with the enzymes the OP refers to as alcohol hydrogenases, but this point is illustrated more easily with the familiar glycolytic enzyme, hexokinase, and its gluconeogenic counterpart, glucose 6-phosphatase:

It can be seen that the two reactions interconvert glucose and glucose 6-P, but are different in that one involves ATP (the hydrolysis of which produces an overall negative ΔG0, whereas the other involves a hydrolysis to produce inorganic phosphate.

Yes now I understand . Different catalysts are involved because different reactions are occurring not the backward and forward part of same reaction. Beauty of biochemistry .

@Location — glad to hear that. I did an internet search for enzymes entitled "alcohol hydrogenases" but drew a blank. Are you sure this is correct? Have you a reference of an EC number?

https://images.app.goo.gl/13ky2sGSiK4UBZNMA this image caught my attention and I

It actually says it's a class of enzyme not a particular enzyme

@Location — The link you posted is to alcohol DEhydrogenases, which are well known, not hydrogenases.


text:
Why don't women continue to produce ova indefinitely?
Why has the human body not evolved to produce more ova?
Is there some technical reason that makes is easy while the fetus is developing, but much harder later in life?
Or, perhaps more likely, is it just that during the majority of the evolution of our species, people would not have lived long enough that menopause would be a significant factor, combined with the quite long gestational period, whereas a male can fertilise comparatively far more in the same period; thus the ability to indefinitely produce sperm is far more valuable?

Welcome to Biology.SE! There may not be a good answer to your specific question, so I'd suggest reading Why do some bad traits evolve, and good ones don't?

they probably aren't , https://www.nih.gov/news-events/nih-research-matters/egg-producing-stem-cells-found-women your question might be better considered as why does menopause exist. in either case one question at a time, this fails the would a complete answer be a textbook check.

Most female mammals have reduced or no ability to reproduce in later years. Why should humans be different? If anything, it's an advantage, as it allows for a longer lifespan. Having babies is taxing (both before birth and after.) Having an extended family, e.g. grandmothers with life experience, able to share in caring for family members is beneficial. Teleological arguments, admittedly, but so is the question.

Welcome to SE Biology. I have edited your question to remove the misuse of the word "finite" and put your question it into plain English. Even though we are scientists, we understand and even prefer this. I have also removed your irrelevant and incorrect paragraph about oocytes. If you want to know what an oocyte is you can look it up on Wikipedia: it is a precursor of a mature ovum.

Also, there's a consideration of mutations. Germline mutation rates in sperm increase substantially with age, but remain consistently lower in oocytes throughout the woman's reproductive life. I imagine having completed all meiotic division by the time they are born contributes to this low and consistent rate of germ-line mutations. It also makes sense evolutionarily considering the resources females expend on gestation, birthing, and parenting. They more invested in the genetic fidelity of the offspring, whereas males are built for quantity more than than quality.

Maybe because it's better to have the mother present to care for the offspring for childhood and adolescence. Assuming menopause occurs at 45-55 years of age and the average life expectancy of a female is 75 years, there is an overlap of 25 years on average. I don't know if this makes sense, especially when we consider that life expectancy used to be much lower, around 30 years on average throughout history and that old mothers are less able to take care of children anyway. The latter is more plausible; older mothers are less capable of child care.

Just to add a postscript, the fundamental difficulty with the specific question from biological viewpoint is we evolved as a species as hunter-gathers and most of that history has been erased. Urbanisation/"civilisation" has only occurred for our species for at best 5% of its history (more like 2.5% and less).
Society and survival are very different for hunter-gatherers; I once attended a talk by a PNAS Academy member whose work specialised in the differences. What's a norm to us, is weird to hunter-gathers because we do stuff that has no practical benefit for survival.
Purely as wild speculation the menopause in hunter-gather societies could have had a pivotal advantage, such as the extensive knowledge, or knowledge base, leveraged via kin selection.
Survival and eventual dominance of our species was a consequence of adaptation to selection pressure.

Original answer
This is a really good question, because few other species are known to go through menopause, one of these is the killer whale (as well as the pilot whale and toothed whales). The phenomenon in killer whales has been subject to extensive studies.
To specifically answer your question, I don't know. Given the research and debate in killer whales I'd suggest that menopause here (i.e. specific to whales) is an important evolutionary strategy that enhances the overall success of the pod.

In female killer whales, menopause typically occurs around the age of 40 to 50 years, and they can live another 30 to 40 years after they stop reproducing.
There are loads of hypotheses of why killer whales have a menopause, these include but are not limited to:

Mother hypothesis
Grandmother Hypothesis or Ecological hypothesis

Point 1 has been well researched and the idea is that female orcas select mates on the size of the male, i.e. how physically big the male orca. This selection pressure is extreme one male orca can sire offspring from multiple females. Male killer whales, unlike females, continue reproducing throughout their lives. So the selective pressure is for the mother not to maximise the number of offspring but to have bigger sons (and grandsons). They do this by feeding their sons throughout their lives, the menopause is considered part of this process, to ensure resources are maximised on maximising the reproductive success of their sons. Thus the idea is the more the male orcas eat, the bigger they get.
Point 2. Kin Selection. The idea is that the menopause in orcas enhances the survival and reproductive success of their descendants by focusing on helping raise and protect younger generations. Reproduction has cost in longevity. One very clear mechanism is the pod is a matriarchy and the older females retain extensive knowledge, for example of a diverse range of feeding grounds. Their knowledge can be invaluable for helping younger generations find food and survive in changing conditions.
Summary. Instead of reproducing, older female killer whales invest their time and energy into helping their offspring and grandchildren survive and thrive.

Citations: "Menopause in killer whales: A review of the evidence"
This is a really good Nature journal podcast presented as a YouTube video. Highly recommended.

As extracted from reference source:

The ovaries are filled with follicles. Follicles are fluid-filled structures in which the oocyte (also called egg) grows to maturity. Current knowledge indicates that females are born with their entire lifetime supply of gametes. At birth, the normal female ovary contains about 1-2 million/oocytes (eggs). Females are not capable of making new eggs, and in fact, there is a continuous decline in the total number of eggs each month. By the time a girl enters puberty, only about 25% of her lifetime total egg pool remains, around 300,000. Over the next 30-40 years of a female's reproductive life, the entire egg supply will be depleted. Although no one can know with absolute certainty the number of eggs remaining within the ovaries at any given time, most women begin to experience a significant decrease in fertility (the ability to conceive a child) around the age of 37. At the time of menopause, virtually no eggs remain.

The large supplies of eggs within each ovary are immature, or primordial, and must undergo growth and maturation each month. The eggs are stored within follicles in the ovary. Within a woman's lifespan, large numbers of follicles and oocytes will be recruited to begin the growth and maturation process. The large majority, however, will not reach full maturity. Most will die off in a process called atresia. Thus, only about 300-500 of these eggs will mature over a women's life span.

https://www.rogelcancercenter.org/fertility-preservation/for-female-patients/normal-ovarian-function#:~:text=At%20the%20time%20of%20menopause,within%20follicles%20in%20the%20ovary.


text:
Molecular Docking - a guide
I have a question regarding molecular docking, as I am far for familiar with it.
I started with generating the models of a ligand (which is a F(ab) part of an antibody).
I obtained the structure of a receptor from the Protein Databank.
Using two tools, LightDock and PyDockWEB, I have obtained docking models. The options I included, were the restraints - as for the antibodies, there are regions (CDRs) that will be most likely in contact with a receptor.
However, the best-score docking models are different for the two tools and alternatives using the same tool. There is contact with receptor in many regions, some of which are in agreement in the different cases, but others differ.
How do I choose the one that is most probable, except by using the score returned by the tool? What else can I do? Are there any additional steps that I could take to make sure that a chosen model is also probable?
Additionally, I am not sure if the antibody model is correct. It is stated to be a best model, but it has not been refined. What tools should I use to relax, minimize energy and so on? I used the model straight from the modelling software, without altering the options.
I have tried to go through the procedure by consulting the available information, but I feel lost and would like to find a guide to this topic.

Welcome to SE Biology. Please finish reading the [Tour] so as to find out about this site, and, in particular, the Help on asking good questions. You will see that we deal with one question at a time, whereas you are asking many questions or asking to be pointed to a general book or article. In addition I would  point out that the tools you mention are quite specialized, and only few biologist on this list are likely to be familiar with them. Have you tried to see if there are user groups or mailing lists associate with the software?


text:
Does ATP drive cellular work solely from energy release during hydrolysis, or is additional work done by repulsion of ADP and inorganic phosphate?
After ADP and Pi are no longer bound to each other but still bound to an enzyme, do they repel each other? If so, does that contribute to the work that ATP hydrolysis can do?

I have written my answer in more detail. I suggest a better title for your question. It is up to you whether you adopt it or not. If you do I will modify my answer accordingly.

Definition of Terms: Energy and Work in metabolic interconversions
The title of this question uses the terms “cellular work” and “energy release” in a very general sense, so I think it is important to start be establishing what ‘energy’ and ‘work’ mean in relation to biochemical reactions, in order to relate them more rigorously to the role of ATP in metabolism.
Energy. Biochemists — and  biolochemical texts — consider metabolism energy in thermodynamic terms, specifically in relation to what is known as the Gibbs Free Energy (G). This is not as it applies to individual compounds (which is difficult or impossible to measure) but in relation to the overall change in this Gibbs Free Energy (ΔG) that occurs during a particular chemical reaction, considering both the reactants and products. The basic precept is that if ΔG is negative, the reaction proceeds ‘spontaneously’.  I would emphasize that this is a ‘black box approach’: we do not need to know, and do not consider how the change is accomplished in molecular terms — that is the realm of reaction mechanism and kinetics, not thermodynamic energy.
Work. A general definition of energy I remember from school physics is “the ability to do work”, and searching the internet I find this is still used (with ‘capacity’ replacing ‘ability’).  Elsewhere I find it defined as “… the energy transferred from one thermodynamic system into another thermodynamic system”. This is most easily envisaged in terms of mechanical work, but, although ATP is involved in this in biological systems, the question is about the ‘work’ done in facilitating a non-spontaneous reaction — one with a positive ΔG. (The difference of this from mechanical or electrical work means that the term ‘work’ is quite infrequently used in biochemical texts in relation to metabolic reactions.)
Restating the question
The phrases “drive cellular work” and “energy release” in the title do not fit well with the definitions above. I suggest it would be best to rephrase the question as:

“Does ATP perform cellular work solely from the free energy change
during its hydrolysis, or is additional energy obtained by repulsion
between ADP and inorganic phosphate?”

Thermodynamics of ATP hydrolysis in coupled biochemical reactions
Two things are required for ATP hydrolysis to facilitate a non-spontaneous chemical reaction:

The unsigned value of the negative ΔG for the reaction of ATP hydrolysis must be greater than that of the positive ΔG for the reaction that is being enabled. i.e. The overall ΔG for the two reactions considered together must be negative.
There must be a mechanism to couple the reactions, i.e. to ensure that the energy of the phosphoanhydride bond is used to form bonds in other reactants and not lost as heat.

An enzymic reaction mechanism will involve a pathway that differs from an uncatalyzed reaction and will have intermediates with different energy states (e.g. below), but the details of this have no relevance to the thermodynamics of the overall change involved. This depends solely on the overall free energies of the reactants and the products, and the change in their combined reaction.

[Example of the energy changes during a simple unimolecular enzymic reaction]
Answer to the question
From this it can be seen that the answer to the question of whether additional energy is obtained by repulsion between ADP and inorganic phosphate is

“No, The energy driving the reaction arises solely from the free
energy change during hydrolysis”.

Any repulsion of ADP and Pi on the enzyme has no bearing on the energetics. If such repulsion does, in fact, occur, its influence would be on the release of the reaction intermediates at some point along the reaction pathway of the type illustrated. The energy changes along the pathway have no effect on the overall free energy change.
Coda: Does direct hydrolysis of ATP to inorganic phosphate actually occur in metabolism?
The assumption in the question is that in coupled metabolic reactions involving ATP, inorganic phosphate is released directly by hydrolysis of the phosphoanhydride bond. This is generally not the case, as multi-step reactions normally occur in which the phosphoryl group is transferred to another participant, ‘activating it’ for the energetically unfavourable reaction. (Or the ADP (or AMP) moiety is transferred to another compound and phosphate released.) I have addressed this point in more detail in an answer to a related question from the poster.
Bibliography
A good place to read about biochemical thermodynamics is in Biochemistry, by Berg et al. It should be possible to pick up an older edition cheaply on eBay etc. Although not as good in my opinion, there is a freely accessible chapter in a book on NCBI Bookshelf in which the section on Metabolic Energy explains this generally accepted approach to biochemical thermodynamics.

To perhaps clarify for a lay audience, work done by repulsion of the hydrolysis reaction products is still work done by the reaction.

@timeskull Not sure what you mean but my expanded revised answer tries to deal with this in terms of the reaction pathway. I'm also not sure that a layman can deal with thermodynamics…

I do not mention the term "energy charge" in my answer, so whether or not it is controversial seems irrelevant to this answer. I am following the views expressed almost universally that the Gibbs free energy change in any reaction determines its spontaneous direction, and that it is possible to for a reaction with a negative free energy change to be coupled to one with a numerical smaller positive free energy change. Are these views controversial?

I beg to differ. I think it is extremely relevant as it addresses the basic misunderstanding of the poster. If I spend several hours on an answer I make sure it is relevant to the question asked. You can see this in my highlighting the crux of the question in precise terms, and flagging my answer.

"This is most easily envisaged in terms of mechanical work, but, although ATP is involved in this in biological systems, the question is about the ‘work’ done in facilitating a non-spontaneous reaction — one with a positive ΔG." Unlike my other question, this question was meant to be about mechanical work. I'm not sure if that changes much to your answer? I would like to keep the answer you've posted in existence; would it be easiest for me to ask another question about mechanical work and edit this one to be explicitly about non-spontaneous reaction stuff?

@elijahwhipple — I strongly agree with your proposal. I know less about coupling to mechanical work, and have started (very slowly) reading what is know in different examples. I happened to be reading an old question on Physics SE which asked about ATP activation energy in relation to mechanical work, and didn't have very satisfactory answers, but I decided not to answer myself until I had studied the topic a little more.


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Why is the transfer of a phosphoryl group used by ATP to drive reactions rather than simple hydrolysis?
I’ve been thinking a lot about ATP, and here’s what I’m thinking so far:
It seems like ATP can do work via hydrolysis, where an enzyme will manoeuvre a water molecule so that the last phosphoryl group is no longer bonded to ADP. Then, the phosphate and ADP repel each other strongly, which can change the enzyme’s shape.
ATP also commonly transfers phosphoryl groups. It seems like there’s still a strong repelling force between ADP and Pi, which enables the phosphoryl group to be pushed onto a molecule. The work done is converted to potential energy in the molecule. Now that the molecule has a higher potential energy, it is able to proceed in reactions that previously would have needed an “input of energy,” like the force produced by ATP hydrolysis or heat.

Would reactions driven by phosphoryl group transfer also be feasible through ATP hydrolysis alone (e.g., could ATP hydrolysis force two reactants together in an enzyme's active site)?
If so, why is phosphoryl group transfer preferred as a mechanism for enabling subsequent reactions rather than ATP hydrolysis alone?
Why is the phosphoryl group in particular widely used to ensure the progression of cellular reactions, rather than some other group?

Please review the comment under your last post; finishing the tour would be helpful, as would reading the help section about asking. It's standard on this site to ask one question per post; also expected is evidence of research (a quote and a link) attempting to answer your own question. What you're thinking may not be correct, and framing it that way is an invitation to discussion.  For many reasons, "Why doesn't it happen [this way]" questions are generally not very well met here. Biology is more the study of what is than what is not and why it is not so.

As a Christmas present I decided to provide you and the List with an answer to one of your questions. I had to edit your question to retract my downvote, although I personally would scrap point 3 in your list and ask a specific question on this point. I have ignored it as it took enough space to answer the main question.

Answer Summary
There are two distinct questions here:
Q1 “Could ATP hydrolysis force two reactants together in an enzyme’s active site?”
A1 No. Reaction coupling always involves formation of an ‘activated’ intermediate comprising the phosphoryl or adenosyl component of ATP and one of the substrates. This, or a subsequent activated intermediate, combines with the other substrate in a subsequent step.
The suggestion reveals a relatively common ignorance of the way that ATP can be used to drive ‘non-spontaneous’ reactions. My answer will address this point.
Q2 “Why is the phosphate group in particular widely used to ensure the progression of cellular reactions…?”
A2 This is an aspect of the question “Why is ATP used as energy currency?”, which has already been asked on this site in various forms, one of which I have already answered, and another with a relevant answer from someone else. I shall not address it here.
General Answer
I will start by reminding the reader that it is the free energy change in a reaction that determines whether it proceeds, irrespective of whether it is enzyme-catalysed or not. I have already considered this aspect of ATP hydrolysis in the answer to a previous, related, question.
A ‘black-box’ approach is valid in relation to the thermodynamics of whether ATP can drive an unfavourable/non-spontaneous reaction, but a mechanistic approach is required to answer the question of how ATP hydrolysis can be ‘coupled’ to an overall reaction such as:
ATP + X + Y → ADP + Pi + X–Y
The answer is that ATP reacts with one of the substrates to form a ‘high free-energy’ intermediate that can then react with the second substrate. In the above case we can represent this as:
ADP~P + X  → ADP + X~P
…followed by
X~P + Y  → X~Y + Pi
with the ‘~’ symbol being used as a crude representation of the bonds made or broken in the transfer of ‘energy’†.
The crux of the matter is that ADP and inorganic phosphate are never released in the same reaction step, as the overall reaction might suggest. There is no trimolecular reaction.
The schema emphasizes that what is important is the bonds being formed, not the phosphate group or phosphoryl transfer. Indeed the alternative manner in which ATP drives reactions does not involve phosphoryl transfer, but transfer of AMP to give an acyl adenylate intermediate:
AMP~PP + X  → PPi + X~AMP
…followed by
X~AMP + Y  → X~Y + AMP
In instances of the second type — where the intermediates are generally more easily demonstrated — one often reads that the substrate X is ‘activated’ so as to be able to drive the subsequent reaction. The term ‘activation’ applies equally well to instances of the second type.
Although important, the mechanistic details of the formation and reaction of these activated intermediates on the enzyme will not be covered here — they vary from enzyme to enzyme — and would require a question of their own. Studying them would dispel the idea that electrostatic repulsion (obviously not between ADP and Pi) is somehow the key to ATP coupling.
Examples
Examples of synthetic reactions coupled to the overall hydrolysis ATP are now considered, in order to illustrate and provide evidence for the proposition above. I challenge the reader to provide any example of a reaction which violates this proposition.
(1a) Glutamine formation from glutamate and ammonia

In the first phase of this reaction (catalysed by glutamine synthetase) an acyl phosphate is formed, which then reacts with ammonia to form the carbon–nitrogen bond of the amide. In fact this is an example of general reaction scheme involving an acyl phosphate intermediate shared by members of the so-called ATP-grasp superfamily that also includes glutathione synthetase, D-Ala-D-Ala ligase, and succinyl-CoA synthetase:

[From a 2012 review by Waldrop et al. For glutamine synthase both R′ and R″ are H.]
(1b) Carboxylation reactions
There are several reactions (e.g. pyruvate carboxylase) in which ATP drives the addition of carbon dioxide to a compound via an intermediate in which the carbon dioxide is covalently bound to the co-enzyme, biotin, through a bond the breakage of which has a negative free energy change. In effect the energetic potential of ATP has been transferred to carboxy-biotin, and this is thought to proceed through the formation of a carboxyphosphate intermediate:

The initial reaction is complex, involving another cofactor, acetyl-CoA, but I mention this class of enzymes, not only to reinforce the idea of transfer of ‘bond energy’ through phosphoryl intermediates, but because the ultimate reaction of the carboxy-biotin with the other substrate takes place on another site (actually another subunit) of the enzyme.
(2a) Asparagine formation from aspartate and ammonia

Here the AMP is transferred to the substrate, with the other phosophoanydride bond being hydrolysed and pyrophosphate liberated. Reaction with ammonia does not occur until the second phase of the reaction. Another metabolic pathway in which adenylate transfer occurs is fatty acid synthesis.
(2b) Amino acid activation for peptide bond formation
Transitory reaction intermediates in an enzyme-catalysed reaction are often difficult to identify, and this may be the reason for some of the initial ‘magic’ thinking about ATP. But a type of reaction in which adenylate transfer occurs and the intermediate product was identified quite early on, is the ‘activation’ of amino acids by the aminoacyl-tRNA synthetases. The energy potential of the phosphoanhydride bond is maintained in this intermediate and the subsequent bond between the amino acid and the tRNA, which will be used on the ribosome to form a peptide bond.

Conclusion
A sledgehammer to crack a nut? Perhaps. But the topic of how the free energy of hydrolysis of ATP is coupled to synthetic reactions is seldom considered outside biochemical texts, and perhaps not given sufficient emphasis even there. Popular accounts tend to ignore thermodynamics or chemistry for cartoon explosions, and students coming from the more numeric sciences tend to think on a higher plane. The latter is typified by a poster on
SE Physics who had arrived at the idea that breakage of the phosphoanhydride bond released “electromagnetic energy at some characteristic frequency which bonds in the enzyme could absorb, hence changing its shape”.  He would probably react to this answer as John Ruskin is said to have done on discovering that his bride had pubic hair.
† Although to some the ‘~’ may recall Lipmann’s ‘squiggle’, it is here used solely to allow the reader to follow the bonds formed following the initial breakage of a phosphoanhydride bond in ATP. Lipmann’s ‘squiggle’ would certainly not apply to the final product, for which emphasizing a single bond may also be an over-simplification.


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Do color-blind people have more rod cells in their retinae than the normally sighted?
All types of color-blindness are said to be caused by the defect or lack of cone cells in the eyes[1]. Since cone cells sense color[2] and rod cells can only sense light intensity[3], the lack of cone cells would mean that the eye cannot detect color. However, rod cell function better in low light than cone cells. Color-blind people have fewer cone cells than other people. My question is, is it possible that they also have more rod cells than other people?
I am color-blind, and I have observed instances where I was able to see better in low light than other people. For example, most often when I read at night or in low light, people have wondered how I'm able to see in the low light condition. I also do not turn on the light most of the time when I walk around the house at night, whereas other people in the house often cannot see well enough to walk without turning on the light. I also recently noticed that my favorite theme (for VS Code), is actually meant for people who work in low light conditions or at night. But they have also noted that it is suitable for people with color blindness.
All these occurrences made me wonder whether color-blind people have more rod cells than average people, and hence can see better in low light too.
[1] ‘Color Blindness’ entry in Wikipedia
[2] ‘Cone Cell’ entry in Wikipedia
[3] ‘Rod Cell’ entry in Wikipedia

The other people in the house should be around your age for a fair comparison. Because in my experience people 60+ tend to be night blind.

Not an answer, but from a cursory search it appears that only a few samples are known where the counting has been done, individual variation seems to be as much as a ratio of 11:18 or possibly more, and no colour-vision capacity was stated in any case. Lots of confounding factors and little useful data there. Perhaps someone else might dig deeper.

@DKNguyen that's a fair point. I'm only 13, so it will be hard to compare the results, since the "other people" I mentioned are basically just my parents.

@ARogueAnt. I was hoping that there might be some experiments done regarding vision, instead of just counting the cells manually. But again, like DKNguyen mentioned, there are a lot of factors affecting vision, so it might be hard to conduct a controlled experiment.

A friend at lawn bowls remarked that he is red/green colour blind but that he can see movement much more clearly than others. We believe he is correct in this assumption.

Short answer
There are not many studies that have counted rods and cones in the human retina, let alone compared healthy retinas with those of color blind people. Yet direct evidence, as well as circumstantial evidence, point toward a degeneration of cones, rather than substitution of cones with rods.
Background
There are a few points of importance. For one thing, as Fig. 1 shows, rods outnumber cones by a factor of 20 in the human retina (Purves, 2001). Secondly, their distribution is very different, cones being clustered in the center of the retina (the fovea) and rods more eccentrically (Fig. 1) (Wells-Gray et al., 2016). Lastly, and most importantly, the scarce studies out there that actually counted photoreceptors in human retina of colorblind people found that deviant photoreceptor counts were the exception rather than the rule. In those rare cases where a loss of cones was found, it manifested itself as areas in the retina lacking photoreceptors altogether, and not by a substitution of cones by rods (Caroll et al., 2004).
The patchy photoreceptor loss found by Caroll et al. (2004) shows that degeneration can be a hallmark of color blindness, but no evidence is yet found to support de novo appearance of rods.
More circumstantial evidence comes from the facts above that rods appear eccentrically, whereas cones are clustered foveally. So any appearance of rods where the cones are lost is not a parsimonious assumption. Secondly, because rods are so much more abundant, patchy increases in rod numbers replacing cones would, likely, not add noticeable differences in night vision. Lastly, rods wire with rods (to amplify light), and cones with cones (for color vision), so substitution of patches of cones with isolated functional circuits of rods would be quite unlikely to occur in my opinion secondarily to degeneration of cones, as the retinal circuitry is quite complex.

Fig. 1. Retinal distribution of rods and cones. Cones (left) are clustered in a densely packed fovea. Rods are more abundant overall and their distribution is reversed from the cones. source Purves et al. (2001)
References
-Caroll et al., PNAS (2004); 101(22): 8461–6
- Purves et al. (eds.). Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001). Anatomical Distribution of Rods and Cones
- Wells-Gray et al. Eye (2016); 30: 1135–43

that makes sense. Thanks a lot for answering! I've just posted another question (somewhat related), check it out if you're interested https://biology.stackexchange.com/q/107212/68669
Thanks again!

Many people are claiming both experimental and anecdotal evidence that colorblind people see better in low-light, in this question here: https://biology.stackexchange.com/questions/44140/what-is-the-evolutionary-advantage-of-red-green-color-blindness/44147#44147
@AliceD, do you think that although the number of rod cells might be the same, the sensitivity might be more for colorblind people? This might explain why most people report better low-light vision.

@Zo-Bro-23 - To be frank, I have no idea. It's an interesting observation though and I'll look into this further.

@AliceD thanks, that works. Please do let me know if you find out anything else about it...

This paper seems relevant ...


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Dinosaur bones found
I found a bone in 120 metres under the ground which has nuclear radiation. Can you help me to recognize this bone?

It was found in a clay quarry near Odessa Ukraine.

Not with just that image. You want pictures with something for scale from all sides including the broken section. We need to get a good idea of the shape and size. The formation it is found in would also be helpful but not absolutely necessary. The radioactivity is irrelevant.


text:
What are the white spots?

What are these white spots? It's like Braille writing or something.
How is the appearance encoded in the plant? (which I think is a Pine, though I am not sure).

If I manually made the "spot sequences" into binary strings, would it be possible to search them against some database? GenBank?

Questions should be asked in the question, not as a comment.

What do you want to know about the white spots? The name? Function? If possible please list the questions in a concise manner


text:
Two mice heterozygote and black are reproduced. Find the probability of getting the filium dark and heterozygote
Well, here's what I did: P: Aa*Aa
F1: 1/4 AA, 1/2 Aa, 1/4 aa, SO the answer is 1/2, but out teacher did this:
AA(1)    Aa(2)    aa(1) and she said we divide the number of filium for the phenotypes number and get 2/3. This is the probability. I don't get it.

why didn't you ask your teacher to explain when you didn't understand

You know in India it is very unlikely a student will ask a teacher about something (s)he does not understand. In many cases I have found out that the teachers themselves don't properly understand what they teach. The language is a huge barrier @WYSIWYG

@OneFace (a.k.a CRags :P) That is a problem with the education policy. We cannot do anything about it. We also cannot do a background search of a user before answering the question. Plus, you cannot generalize this for an entire country.

What is a "filium"? I would assume Latin for "children", but it isn't even correct Latin.

Okay so in your teachers answer there are four offsprings. . You used all offsprings when you made the division so 2/4 = 1/2.Your teachers 2/3 comes from the fact that 3 out of four is black, but only 2 out of that 3 black is heterozygote so 2/3 is good by this logic. I think that your teacher's logic faulty because you have to take into consideration all the offsprings. Basic genetics and Mendel's law tells us that crossing two heterozygotes with independent alleles result in a 3:1 ratio in phenotype separation in the next generation with 1:2:1 genotype separation -- that is what basically both of you have wrote. The fault is in the getting the probability - basic maths tells us that in an independent experiment, the probability variables have to sum up to one. In your teacher's logic this basic rule is not kept, because finding homozygous non-dark offspring would be one (there is only one non-dark filium and that one is homozygous). So by this logic all filium are non dark-homozygous, but then what about the others. I hope you see the problem with that logic.


text:
Does the duration of the head-hair growth phase differ between men and women?
I found one website which claims the following

The growth phase of the hair is called the anagen phase. It lasts
about 3 years in men and 5 years in women.

Another website makes a very similar claim.
The problem is I can't find any journal article which supports the idea. Is it true that the anagen phase lasts longer in women than in men? And is there published research to prove it?

Both these articles are from companies that sell cosmetic products. If their "research departments" have any data to support any scientific statements they make they are unlikely to be interested in publishing it. It sounds uncontroversial and may be old observations or old wives' tales nobody has cared enough about to investigate. Not where modern biology is, for sure, but you never know whether your bounty will bring something out of the woodwork.