text:
Examples of creating a new animal species by humans
So recently, I was arguing with my friend who happens to be creationist. As he does not believe in the "theory of evolution" I asked him how he can explain such a big diversity in the dog Canis familiaris sppecies. (The example taken from Charles Darwin's on the Origin of Species saying that humans made to dogs what mother nature has done to every species)
My friend replied something like:

Well, having chihuahuas or huskies is one thing but, getting a tetrapod from a fish is a something which can never happen.

I realized that indeed the Darwin's example isn't perfect... Even though, due to size chihuahuas and hounds can't copulate efficiently their semens and ovaries can start a new life.
I can't give a counterexample of a species which was bred artificially by human for so long in a new direction that a new species (whose specimens by definition were not able to reproduce with the specimens of the base species) was created.
It's not that I am becoming creationist... but is there any exception from that rule for any artificially bred animal species?
[Edit]
This question has nothing to do with this
I am strictly asking about examples of an artificially bred animal species which got bred into two species.
[Edit 2]
Also to be exact, I am not interesed in specimens that can't reproduce due to various "external" circumstances like environment's temperature or size (chihuahuas&hound example). I am interested in specimens which come from the same base species and can't reproduce even with the help of in vitro fertilization (I know this is not exactly the definition of species). I just want to avoid getting answer similar to this.

Note that there are many definitions of "species", and you've chosen one that was specifically devised for evolutionary theory. In any case, rather than animals you might look into crops such as corn and its ancestor teosinte, the Brassica family, etc. It's pretty pointless, though, to try to reason someone out of a position they didn't reach by reason.

On top of the marked duplicate which seems very central to your misunderstanding, you might want to consider having a look at Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?. Of course, crops are also examples that come to mind (such as corn and teosinte for example).

@Remi.b,  I don't agree this is a duplicate of the ancestor-of-birds question that you marked up; this one asks about humans breeding organisms, not natural evolution. The drosophila question you mention in you comment does answer this question though.

That is exactly my point

@Roland. Ok, I've reopened the post. Thanks for feedback. The question might arguably be a duplicate of Have we ever observed two drosophila lineages that evolved reproductive isolation in labs? though but an answer based on some crop would probably be a better fit. Note that there is likely reproductive isolation between a chihuahua and a wolf despite taken as example of something of no interest in the question

You many want to tell your friend that saying evolution can happen but not to the point of new species is like saying you can walk around the block but its impossible to walk across the country. The mechanism is identical all that changes is how long the mechanisms runs.

This page contains a list of observed speciation events including a breakdown by mechanism and starts with a rather good introduction to the concept. http://www.talkorigins.org/faqs/faq-speciation.html

Why - and I'm not saying your question is wrong - but why does it have to be a new species? Doesn't any significant mutation (e.g. the mutation allowing lactase to be expressed into adulthood) suffice? Does not the fossil record suffice? Your friend's arguement is based on the difference between selective breeding and the cumulative effect of many mutations. I don't think you finding a new species through selective breeding proves anything. imo.

@John I’d like to give you some advice in order to be more effective when talking to creationists.  As I pointed out in this post , creationists challenge evolutionists with what they call the bait-and-switch (see their link I posted).  AGAIN, creationists fully believe in adaptation via genetic variation and NS.  To them this is NOT evolution that will turn worms into women.  Your ‘walk around the block/across the country’ falls directly into that, and is completely ineffective against a creationists.

No offense Runz but I know all this, I also know that if what the believe is wrong you do them no service by pretending it is not. The mechanisms are identical are the same thing and pretending otherwise only helps them deny reality. It plays right into their false belief in "kinds" by acting as if there is some great diffrence between a change in a population and and change in population we happen to label as speciation.

@John, No offense as well, but do understand that there IS a difference between N.S. based on variation of existing genetic variety, and the CREATION of new phenotypes via genetic material that did not exist before.  Creationists are well aware of this difference.  You need to be as well.

Yes there is a difference new genetic material and existing.  However new genetic material is NOT speciation and new genetic material  is actually quite common in the "population level" evolution they accept. furthermore new material is not necessary for speciation. Again both "types" of evolution are the same mechanism both may or may not have new genetic material but do have a selective process. They are trying to create an distinction where there is not one and using ambiguous terminology to make it seem as if they are not. If you want to continue this in discussion feel free.

There are indeed many examples of new species created by humans, and observed to arise by humans. Many via deliberate experimentation. You can find examples googling "examples of speciation", looking at the Wikipedia page for speciation or the Talk Origins one:
http://www.talkorigins.org/faqs/faq-speciation.html
http://www.talkorigins.org/faqs/speciation.html
https://en.wikipedia.org/wiki/Speciation
The issue is that there are two events of interest in "the origin of species" that are related but not the same thing: there is speciation, and then there is overall change. And as far as change itself goes you can have genetic change and phenotypic change which themselves aren't perfectly correlated.
Speciation is a very important evolutionary event, as it's the point at which genetic material is no longer exchanged between two groups and so they start evolving independently, meaning differences will accumulate over time (steadily and inevitably for genetic differences, more variably for phenotypic ones as that depends on the environment). But you can have differences accumulating without speciation (especially not with your "in vitro fertilization" criterion, which allows gene flow to be stopped for a long time without "speciation" by that definition happening), and you can have speciation happen without much genetic or phenotypic change.
And so on our human timescale we'll tend to see three categories of events:
1) large phenotypic change without speciation (especially by the in-vitro definition), because natural selection can cause large phenotypic change but random mutation cannot be rushed and that genetic drift is usually what will make groups no longer inter-fertile,
2) Speciation without large phenotypic change, again because speciation is just the beginning and all you need for "speciation" is just enough change to make interbreeding impossible or difficult, and so many examples of observed speciation involve just that, and
3) Speciation with large phenotypic change, which will usually be single-generation events with hybridization and polyploidy. Those are the most likely to fit your criteria that in-vitro fertilization shouldn't work. And they are legitimate and important evolutionary processes; polyploidy has happened many times in our lineage, it's an important source of genetic diversity, and hybridization and polyploidy are a major mechanism in the evolution of plants in particular. But they're not the major mechanism for the evolution of large vertebrates, so it's easy for Creationists to dismiss them.
Still, looking at the links I gave you I see a few examples that involve genetic change sufficient to block even in-vitro fertilization. The second Talk Origins link in particular refers to examples where speciation was determined by the offspring being sterile. There is also an article in the notes of the Wikipedia page about a recent discovery about the kind of genetic changes that can lead to speciation:
https://www.scientificamerican.com/article/wandering-fly-gene-suppor/
The general problem with giving Creationists examples though, is that the examples they want don't exist (and would usually contradict the theory of evolution anyway) and the ones that do exist they're not satisfied by (because the change involved isn't dramatic enough, or IS dramatic but as a result makes the dramatic look trivial because it happened via a small gradual underlying change - which, you know, is how evolution is thought to work).
I notice in fact that you are the one asking about the speciation with in-vitro fertilization, not your friend; your friend apparently just said that huskies and chihuahuas are not comparable to fish vs tetrapods. If this is personal curiosity from you then that's fine; if you are looking for arguments for your friend specifically then it looks like you're on the wrong track, since no amount of lack-of-interbreeding will make flies any less flies, which is usually the issue for people who focus on "fish to tetrapod" as a scale of change.
You might have better luck figuring out exactly what claims your friend makes, where they set the boundaries of what they think is possible and what they think it isn't, and then find an example that breaks that specific boundary. So they say "speciation can't happen !", you reply "speciation happened in fruit flies", and they answer "so what, fish haven't become tetrapods" - but, what is it they meant by "speciation can't happen" ? What mechanism do they think makes it impossible, what do they think this "speciation" is that's impossible, where do they set the boundary for themselves between "ordinary change that can happen" and "stuff that can't happen so evolution is false" ? They probably don't know clearly themselves, but figuring it out and addressing it is a better way of moving forward, and you both can learn things. And it makes it a bit easier for you too - you don't have to worry about finding proof that fish can become tetrapods, you can be like "OK fish can't become tetrapods whatever, but you said that new species cannot arise through genetic change, but here is a paper saying that a gene transposition makes it impossible for those two flies to interbreed, wouldn't that be an example of speciation via genetic change ? What do you think ?"


text:
Can Fluoride be absorbed into the blood from within the mouth without swallowing?
I'm having a discussion with somebody regarding Fluoride usage. I told him that even if he doesn't like the idea of ingesting it, brushing and spitting it out will do you no harm. He then said this:

You have missed the point of ingestion massively! Brushing with fluoridated paste is NOT fine.
The mouth, with its gum entry and under tongue glands are the PERFECT entry point to the blood, without even swallowing? What do you think oil pulling is all about? Fluoride passes those barriers as easy as the shit that resides in your blood can!"

Now I call BS on this, but I'd just like an expert opinion with cited sources if possible. Can Fluoride be absorbed purely by the mouth without ingestion?

Absorption in the mouth doesn't happen, see this answer. But this will probably not persuade your friend.

@Chris definitely not a friend of mine, haha :)

@Chris whilst that links explains remineralization very well, it doesn't really talk about gums or the tongue or digestion in the mouth and why fluoride can't be absorbed that way. That's more of the kind of thing I'm looking for

If fluoride can't be absorbed through the mouth, then why do dentists recommend fluoride-containing dental rinses?

@jamesqf because it can be absorbed onto the teeth that way, but my question is can it enter the blood through the gums, tongue etc. I know it can be absorbed into the teeth through the mouth

@Charlie: If that's what you're actually asking, perhaps you should consider editing the question.  As of now, it says "absorbed into the body", and the teeth are part of the body.

@jamesqf ok will do

Oil pulling?  You know you are talking to someone who has bought quackery hook, line and sinker, right?

Sorry I'm a lil late at finding this but thought I'd share two studies I found proving 'absorption of fluoride through the oral mucosa of rats' https://doi.org/10.1016/0003-9969(68)90140-4 https://doi.org/10.1016/0003-9969(78)90219-4 *the second link is a study on radioactive fluoride.

Although I'm having a hard time finding a source that provides specific information on fluoride in toothpaste, this review explains that fluoride is most readily absorbed through intestinal epithelia and that fluoride absorption through other tissues, such as oral epithelia, depends strongly on other chemical properties of fluoride-containing compounds: their

"reactivity and structure, solubility, and ability to release fluoride
  ions."

This suggests that you would need additional information concerning the overall toothpaste formula.
This review shows the rates at which fluoride ions are released from various toothpaste formulations. Figures 2 and 3 show that the highest discharge rate is roughly 1.7ppm and the lowest was just under 0.5ppm, both occurring after a 24hr period. The authors note in the discussion that these measurements are likely higher than what would occur in the mouth, since they had to use deionized water for their experiments, in which fluoride is more soluble than in saliva.
Wikipedia lists fluoride toxicity levels as being between 0.5 and 1.0mg/L. Fluoride's molar mass is 18.9984 g/mol and this calculator shows that 0.5mg/L of fluoride translates to about 0.5ppm. While at first this makes the above results sound a dire, it's important to note that toothpaste remains on your teeth for far less than 24hrs and to remember that less fluoride is released into saliva than into deionized water.
Wish I could find better results on how much fluoride might be released during a typical toothbrushing session, but I'm inferring from the linked review that it would be small enough to not merit a health concern.
I emailed a dentist friend for more info and will update this post as I hear back from him.
As for the comment about glands, it's important to understand that the glands found in the mouth are secretory glands, which means that they are optimized for discharging fluids and not for accepting them.
--Update--
My dentist friend wrote back, confirming that no significant fluoride absorption occurs through the gums. From him:

the only significant absorption would be through swallowing fluoride.
  Any that was just in the mouth would not be well absorbed...
  that is why we do the high dose swish and spit treatments is to avoid
  fluorosis but deliver sufficient fluoride to the teeth.

In short, it looks like the answer to your question is: no, fluoride is not significantly absorbed into the blood from within the mouth without swallowing.

thanks for the info! I'll keep this open for now to allow time for you and others to find out more.

source: Stack Exchange

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

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

sort: votes


text:
Why do death cap mushrooms not warn of their poison?
This has been puzzling me for a long time now. There is an evolutionary predilection for living things which have evolved strong defensive measures (that may not themselves be visible) to give distinct visual or audible warnings advertising these measures.
Wasps, hornets, snakes, and bees are all brightly coloured. Snakes may even have rattles to advertise their venom. These things by in large don't want to have to use their poison in a defensive capacity. Getting revenge on a predator who has mortally wounded you is a Pyrrhic victory.
These warnings are so potent that many animals without such measures will mimic these warnings in order to piggy pack on a general evolutionary bias towards an instinctive avoidance of anything that warns of being poisonous.
But take the death cap mushroom.

This innocuous fungus looks identical to completely harmless mushrooms. It has no foul smell. In fact, evidence shows that it actually has a pleasant taste! That picture above actually looks pretty tasty in my opinion.
This fungus has gone to the trouble of developing one of the most potent poisons in nature (humans have a seriously robust digestive systems by animal standards, and yet a single death cap can easily kill an adult human).
So why so secretive about its arsenal?
I know this same question about evolving poisons that are not well advertised could be applied to a large number of animals, insects, and particularly fungi, but I think the death cap is the most extreme example in both the lethality of the poison considered, and combined lack of advertising.

I collect and eat wild mushrooms and that Amanita looks very frightening to me.

Two questions need to be asked, 1) Was the mushroom's poison evolved specifically to serve as a poison, or does it serve some other function and just happens to poison humans?  (Given the long-delayed effect, this seems possible.)  2) Was the poison evolved for humans, or for some other species (insects, perhaps), which can detect warnings like odors or UV markings that humans can't?  Or a third possibility: the mushrooms are fruiting bodies.  A critter that eats them gets dusted with spores, goes somewhere else, and dies, providing a food supply for the spores.

Related https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont?noredirect=1&lq=1

Most of this type of evolutionary question are generally worthless, IMHO. You can rationalize anything post hoc and then go away with the misapprehension that you have been involved in science.
To add a few of those possible post hoc explanations (which took longer to type  out than think up):
1) The poison is only accidentally a poison.  It serves some other function in the mushroom's metabolism.  There are numerous possible examples of this.  For instance, the stalks of rhubarb are edible, while the leaves are poison; potatos are edible unless they've turned green from exposure to sunlight...
2) The poison might not be directed at humans.  The mushroom might have some warning that would be obvious to other species, for instance a smell or markings visible in UV (such as many flowers have).  We have lots of examples of poisonous plants that we grow because they're attractive to us: datura, lily of the valley, foxglove, oleander, delphinium...
3) If I'm not mistaken, mushroom poisoning takes rather a long time to kill, which argues against it being a defense.  The poison might have evolved as an aid to reproduction.  Mushrooms are the fruiting body of the fungus.  If an animal eats it, it consumes the spores.  If it dies hours or days later, it has transported those spores to a distant location, and the corpse provides nutrition for the new fungi.
However…
Doesn’t the all-white toadstool look distinctive and memorable to you? It doesn’t look remotely like the field mushrooms or other edible mushrooms I would collect. What edible fungus would you confuse it with?

The death cap is infamous for looking like safe mushrooms. For instance https://www.mushroomguru.co.za/uploads/5/5/2/1/5521125/4187215_orig.png
This is also totally safe, albeit not as tasty. https://www.wildfooduk.com/wp-content/uploads/2017/06/White-false-11.jpg
All evolutionary questions are post hoc, unless you have a couple of million years to spare to actively observe change.

@Stumbler — One of your links is broken, but I am only speaking from experience and my post hoc reasoning may be faulty. All evolutionary questions may be post hoc, but that doesn’t mean they have the same level of uncertainty. Speculating about why something is the way it is is in a different league to calculating the time of the last common ancestor of mice and rats from their DNA sequences, for example.

I'd be okay with this sort of "we can't really know" answer if you included some of the different likely competing explanations. Jamesqf's comment is a decent starting point that hits most of the basics (might not be primarily a poison, might not target humans, might not be necessarily selected to prevent predation, etc).

Bryan — Well my main point was really that the “Exterminating Angel” whiteness appeared distinctive to me and my wife (who knows more about fungi than me). I suppose it depends on where you live. But I invite @jamesqf to edit my question with his comment to improve it. That’s supposed to be acceptable, here.

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


text:
Why isn't meiosis II called mitosis (as the chromosome number doesn't half)?

Meiosis: a type of cell division that results in four daughter cells each with half the number of chromosomes of the parent cell, as in the production of gametes and plant spores.
Mitosis: a type of cell division that results in two daughter cells each having the same number and kind of chromosomes as the parent nucleus, typical of ordinary tissue growth.

After meosis II we have the same number of chromosomes as before. So why isn't meiosis II called mitosis instead?

Well, in my opinion, the entirety of the meiosis is a process (reproduction of sex cell) in which two levels of division occur, it's all kind of one process. Though meiosis II may seem to have many similarities with mitosis, meiosis II can only occur with sex cells, to my understanding that is the main factor which differentiates meiosis I and II from mitosis. Furthermore, regardless of the similarities, to call meiosis II the same as 'mitosis' (whilst meiosis II is still in the entirety of the meiosis process) is not only confusing but impractical. I'm sure, though, that somewhere along the line there are several detailed differences between the technicality behind the cellular division in mitosis as in meiosis II. But, don't listen solely to my answer, that's just my opinion since your question is subjective to my personal opinion...

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


text:
Examples of Differential equations in Biology
I am a mathematician currently teaching some math classes at a university. Next semester, I'll have bachelor's degree biochemistry students. I want to know where certain math tools might be needed in such a field.
Where do differential equations arise naturally in professional Biology? Maybe from some data analysis of a complex phenomenon? What scenario?
I was thinking of a scenario where, for a complex set of variables, you would take one of them, say $x$ and plot $\frac{\Delta x}{\Delta t}$ vs $x$ and find that the relationship was e.g. polynomial ($\frac{\Delta x}{\Delta t} \propto x^{3}$).

Unless you’re teaching in Harvard or MIT, the most you can expect from biochemistry students is simple algebra. That doesn’t help you, but “Blessed are they that expect nothing…”.

@David I was interested in numerically approximating systems of differential equations to model metabolic pathways when I was an undergrad. I was not allowed to pursue this. Not because it was explicitly disallowed, but rather because I was kept too busy memorizing multisyllabic terms (a little bit of physics and graph theory would have been better IMO) that I promptly would forget after finals.

@Galen: Did those multisyllabic terms include "multisyllabic"? =P

@user21820 Who knows! I forgot!

I'll just say I don't miss reciting "Phosphoribosylformimino-5-aminoimidazole carboxamide ribonucleotide isomerase".

All the posts are very helpful! Thank you to everyone!
I am quite familiar with the use of Differential equations in population biology, but I sensed that wouldn’t be that satisfying to biochemists. You provided me with a lot of useful references :)

The only time I ever used my Ti-89 calculator to do anything of use was calculating sedimentation of proteins in an ultracentrifuge.  It totally worked though.

For biochemistry students the obvious link to differential equations is the Michaelis–Menten equation which is a simple model of the kinetics of reactions involving enzymes. Your students will be hearing a lot about Michaelis–Menten in their biochemistry classes if they haven't already. It's also very accessible to students having their first exposure to differential equations.
Considering the wider field of biology there are several major topics that revolve around differential equations. Population Biology and the related field of Population Genetics are heavily mathematical with lots of differential equations involved.
Expanding beyond ordinary differential equations there is Alan Turing's Theory of Morphogenesis which tried to explain striping and spotting in animal hides using a system of coupled partial differential equations to model reaction rates and diffusion.

Michaelis-Menten is super obvious, can't believe I didn't think of it.

Update
please follow Charles E. Grant's advice and do Michaelis-Menten!
Hodgkin-Huxley as suggested by commenter ctwardy is a great idea too.
Original answer
I would strongly recommend the book mathematical ideas in biology by J Maynard Smith.
A couple of examples that spring immediately to mind with relevance to biochemistry might be:

gene expression
structure of the coiled-coil protein fold (see e.g. equation 4 in Quine's book)

Less biochemical but still very fun is Lotka-Volterra modeling of predator-prey interactions.
Another book that seems to directly address your question is this one.

Also neurophysiology! The Hodgkin-Huxley equation won a Nobel prize.

Are Twelve ODEs for mitochondrial membrane potential (ΔΨm), and matrix concentrations of Ca2+, NADH, ADP, and TCA cycle intermediates, used to model the response of mitochondria to changes in substrate delivery, metabolic inhibition, the rate of adenine nucleotide exchange, and Ca2+ good enough for you?
Generally speaking, many biochemical process would often be modelled on the macro-molecular scale by differential equations. These include rate equations for the chemical processes, as well as diffusion kinetics within the cytoplasm or across membranes.
On the larger scale of organs and entire systems, we also have alveolar gas exchange, digestion and absorption processes, renal filtration, homeostasis, and of course many others.

Logistic differential equations in modeling population dynamics is the first to come to mind.
Populations grow under the constraints of limited resources, capturing the transition from initial exponential growth to a plateau as the carrying capacity of the environment is approached.
For a detailed exploration of logistic differential equations you can refer to this comprehensive guide on Brilliant.org.

The other answers offer many examples of differential equations for initial-value problems where you solve an (most often here) an ODE or a PDE. There are also boundary-value problems in biology, for example when modelling the strengths and elasticity of various structures supporting a plant (e.g. https://doi.org/10.34133/ehs.0007) or of animal bones (e.g. https://doi.org/10.1007/s12018-015-9201-1 for human medicine, but the principle is the same for other living and fossil vertebrates) or modelling the elasticity of plant leaves based on the plant's turgor (https://doi.org/10.1111/tpj.12042). Similar simulations had also been done for individual cells. In these cases the PDEs are elliptic and are most often solved by the finite element method or similar methods.


text:
Why didn't Rosalind Franklin's X-Ray crystallography photograph contain any histones, methyl groups, or transcription factors?
When DNA is condensing, it wraps around histones, where it can also be methylated with the addition of a methyl group. On top of this, DNA has transcription factors which determine what can be transcribed into RNA.
I understand that Rosalind Franklin had pure DNA from Signer which she converted to a paracrystalline form by raising the humidity of the specimen. How was it that none of these structures that we know DNA attaches to or are attached to DNA didn't show up in photo 51?

That's actually a great question, and it makes a lot of sense to wonder why we don't see histones, methyl groups, or transcription factors in Rosalind Franklin's famous Photo 51. The key to understanding this lies in the context of the experiment and the type of DNA Franklin was studying.

When Franklin took the X-ray diffraction image that became Photo 51, she was working with highly purified DNA fibers, not DNA from inside a living cell. This purified DNA had been isolated by the Swiss scientist Rudolf Signer and was stripped of any proteins, histones, or other cellular components like transcription factors. The DNA was essentially "naked" and free from the structures it normally associates with inside the nucleus.
Another important point is that X-ray diffraction only reveals the overall repeating structure of molecules, especially those that form highly ordered, crystalline or paracrystalline patterns. In Franklin's case, she hydrated the DNA just enough to form a paracrystalline structure, where the molecules were aligned in a regular, repeating pattern. The repeating nature of DNA's helical structure is what generated the characteristic "X" shape in Photo 51, which provided critical information about the double helix.
Histones, transcription factors, or even methyl groups would not form such regular, repeating patterns. They are more varied in size and shape, and they don't contribute to a uniform diffraction pattern like the helical backbone of DNA does. Furthermore, their presence would have been too sparse or irregular to significantly affect the X-ray diffraction image. In the purified conditions Franklin was working with, these additional elements weren't present to interfere with the image, which is why they didn't show up.
So, the reason why you don't see those other components in Photo 51 is simply because Franklin was working with DNA in a highly purified, idealized form, and the X-ray diffraction method specifically highlighted the repeating, regular structure of the DNA itself.

Chemist here. I would further note that when DNA is doing what it is best known for (replicating) it isn't wrapped around histones. It is floating free, where the polymerase can run along the chain and replicate. Histones are not required for the base pairing and would get in the way during replication. The bases and the sugar-phosphate backbone are primary structure; the base pairing is secondary structure, and the coiling around histones is tertiary structure.

Note that the use of generative LLMs is banned on SE and this answer, as did others from your hand, are suspected of being AI generated. Please refrain from using ChatGTP (yup 'GTP', biologist here) or other generative AI tools in the future, or the mod team may have to undertake action.

@AliceD I went to the comments as my AI sense tingled around the second sentence already.

@htmlcoderexe- thanks for the comment, and if that sixth sense tickles again, please also hit that 'flag' button.

@AliceD - ChatGTP for a DNA answer. Love it!

@anongoodnurse, why thank you <3


text:
Shouldn't recording electrode have as low resistance as possible?
Following quote is from this wikipedia page on single unit recording.

Intracellular single unit recordings require electrodes be inserted through the cell membrane to record from within the cell. Glass micropipettes or metal electrodes may be used for intracellular single unit recordings, but glass micropipettes are preferred because their high input resistance allows more precise recordings for measurement of resting potentials.

How high input resistance helps better recordings? Shouldn't recording electrode have as low resistance as possible?

Can you please offer your proposal for the situation? Do you know which variables are relevant there? What is your measurement setting?

Could it be that you mean impedance instead of resistance? It is one of the electrical properties that is the least understood by biologists (like me) and in the biological community there are lots of myths and rumors about whether impedance should be high or low. This might help: https://electronics.stackexchange.com/questions/21787/why-is-high-input-impedance-good or this: https://www.quora.com/What-is-the-influence-of-electrode-impedance-on-EEG-data-recording (though it refers to EEG)

For accurate measurement of the membrane potential, it is crucial to have as little current flow through the measurement device as possible. Otherwise, the equilibrium of leak channels that generates the resting potential would be disturbed. See diagram and text from Axon Guide 3rd edition below:


text:
can somebody please Identify this queen ant?

hi, i found this queen in France and i want to know if it is a species i can take back home to England. i cant identify her since the only queens I've ever kept are Lasius Niger so i would like some help please!!

Please don't. It is never ever a good idea to import insects. The species is irrelevant, even a native species can be genetically different.

Oh, ok, i had no idea. im still kinda new at ant keeping. I only go to France for the Summer holidays so will i have to let her go?

that would be my advise, yes.

+1 to RHA's suggestion, but it isn't just genetic difference: insects (and any other animal or plant) can carry disease as well.

Just to add: it is often not only a bad idea biologically to carry insects to new locations (even different habitats within the same state/region/country), it is also often times illegal. Glad to hear you're releasing it where you found it :)

There are 4 main families in France. Formicinae, Dolichoderinae, Myrmecinae ans Ponerinae. This is a an ant in the subfamily Formicinae because it is large and has only one segment between the thorax and the abdomen. You can deduce that because the thorax and the abdomen seem very close. This particular ants is a queen of the genus Formica (wood ants) from the general aspect. The presence of wings indicate this is a reproductive individual and because the eyes are small compared to the rest of the head it is a female. The color and the general shape and the size would allow any trained observer to identify the genus Formica, although no formal criteria can be seen on this picture. Formal criteria require inspection of the funicula, a part of the antenna, which cannot be seen on this picture. For references please visit http://antarea.org, http://cle.fourmis.free.fr and read Seifert - Ameisen Mittel und Nordeuropas. Lutra.

Your answers need to be backed up with some sources and explanations.

The issue is that most of the time, when identifying insects on bad pictures, there isn't any formal character available. Identifications are often based on the general aspect of the insect by a trained observer.


text:
What kind of grasshopper-like insect is this?
We found this thing in our basement. Not quite an average grasshopper. Any ideas?

Please include your location, or at least a country and state. That will make your question much easier to answer.

This is potentially a duplicate of the question asked here; if not a duplicate, the species involved appear closely related.

That is a "cave cricket", in the family Rhaphidophoridae. These are common in basements, and harmless.


text:
Does Povidone-Iodine that penetrates through the skin stays in the body (cells, liver etc)?
Here it says on povidone-iodine:

"Route of Elimination: Povidone-Iodine is intended for topical application and is not eliminated"
"Clearance: Povidone-Iodine is intended for topical application and is not eliminated"
"Metabolism: Povidone-Iodine is not absorbed or metabolised"

Now Povidone-Iodine is a very widespread antiseptic used directly on open wounds and there are cases of people using it as a disinfectant before and after microneedling (ie: inducing micro-injuries with a dermaroller device over the skin) which ensures penetration of the substance through the skin and blood circulation and into the body.
What happens with it once it's inside the body - even if some is excreted what happens with the rest which isn't? does it forever lingers within the body (cells, liver etc)?

Your source (DrugBank via PubChem) is describing the typical pharmacokinetic information (ADME, absorption, distribution, metabolism, excretion) on Providine-Iodine, under the assumption it is not absorbed. It's true, a thing that is not absorbed has no volume of distribution, is not metabolized, and is not eliminated.
Though Providine-Iodine is not absorbed as is, Iodine is.
From the Lexicomp drug information for prescribers:

Absorption: Absorbed systemically as iodine; amount depends upon concentration, route of administration, characteristics of skin

Other pharmacokinetic properties are as for Iodine. It may be taken up by the thyroid. Clearance is primarily unchanged (as Iodine) by the kidney.
The absorption through the skin as iodine and elimination by the kidneys are the reasons for the prescribing precautions:

Use with caution in patients with burns (excess absorption)
Use with caution in patients with renal impairment (impaired excretion)
Use with caution in patients with thyroid disorders (taken up by the thyroid)

This case report of Iodine toxicity following prolonged povidone iodine administration is available on pubmed central. It's from the 80s, but it is still relevant and the comments section has a good overview:

The reports of iodine absorption from topical povidoneiodine
  solution suggest that absorption is enhanced when the
  compound is applied to denuded skin, mucosal surfaces with
  high absorptive capacity or extensive areas of intact skin. The
  evidence for iodine absorption includes documented serum
  iodine concentrations and thyroid function abnormalities.

I see, it wasn't understood from the text I've quoted that these claims were under the assumption that the Povidone-Iodine is not absorbed. I don't have access to the Lexicomp info so two questions: 1. I guess my original question concerns the PVP compound - what happens with the PVP that isn't excreted? (question continues in the following comment)

On the PVP page it says that: "THE RETENTION OF PVP IN THE BODY IS PROPORTIONAL TO ITS MOLECULAR SIZE, SINCE ONLY THAT OF LOW MOLECULAR WEIGHT CAN BE EXCRETED. THE RETICULOENDOTHELIAL SYSTEM RETAINS PVP WITH A MOLECULAR WEIGHT IN EXCESS OF 110,000" so does it mean it lingers forever in the cells of the body (possibly liver)? 2. I know that Iodine is metabolized but does this necessarily imply that the povidone-iodine molecule is?

@Amit none of my references are able to measure any absorption of the polyvinyl polymer, just the iodine (released by PVP). The question of excretion vs. retention in the reticuloendothelial system is one of metabolism and excretion, or excretion unchanged. Theoretically, if you were able to absorb  a high molecular weight polyvinyl polymer somehow, it wouldn't be excreted unchanged by the kidney (because it wouldn't be filtered by the glomerulus. It would have to be metabolized by the liver first, which would break it down into something that would be excreted by the kidney.

@Amit the point here is that it's the Iodine that people are/have been worried about (as far as the toxicity of PVP-Iodine is concerned). It's the iodine that is absorbed, and it's the iodine that is (potentially) toxic.

@Amit is there a particular reason you're interested in the idea that the polymer would accumulate and be retained forever in the liver?

I'm specifically interested in povidone-iodine use to disinfect the skin before and after microneedling (which I guess will have the side effect of allowing even high molecular weight PVP to enter through the skin) hence was wondering whether some may remain in the body (possibly disrupting normal functioning). I'm aware of the iodine toxicity risks :) BTW since I'm not a chemist is it likely that the commercial povidone-iodine solution is made such that it doesn't contain high molecular weight PVP or maybe it's not even possible since they'll be spontaneously created?

Let us continue this discussion in chat.


text:
What is the status of the "Free Energy Principle" as a theory of living organisms?
The free energy principle states that biological organisms maintain their order by minimizing a function called variational free energy (VFE).
While it is the case that the minimum to VFE also minimizes Helmholtz free energy under certain assumptions, VFE is distinct from Gibbs free energy or Helmholtz free energy and is borrowed from statistics (variational Bayesian inference). It measures the degree to which the approximate posterior deviates from the exact posterior.
It has been argued that the free energy principle explains many facts about brain function. However, I would like to learn about biologists' views on the broader claims as a principle that seeks to explain all aspects of the function of living organisms. I would be grateful for direct answers and for any references that discuss this issue.

I think the vast majority of biologists has never heard of this paper you linked (Karl, 2012; published in "entropy", a journal that I suppose few biologists ever read). So biologists's view are probably very inexistent for the moment. But maybe someone will be willing to read the paper for your post as the question can be interesting.

While this paper may not be the most popular (although it has been cited at least 300 times) this: https://www.nature.com/articles/nrn2787 is the "canonical" reference for the application of the free energy principle in neuroscience (since you used the tag). I am not (yet) an expert on the subject but I do feel that it is one of the most powerful theories in neuroscience at the moment. Some people feel uneasy as it explains too much.

Thanks, I‘m trained as a neuroscientist myself and I‘m roughly familiar with the applications of FEP there. However, FEP is often used as if it were a fundamental and universal biological principle, and I wanted to know whether this has been discussed within the biological communities. In particular, the distinction between free energy and its variational counterpart seems interesting.


text:
What is the relatedness of sisters in a haplodiploid system if you mate virgin queens with 1 of their sons
So I'm having trouble wrapping my head around this. In haplodiploid insects, sisters are related by 75% on average due to all sharing 100% of dad's genetics and 1/2 of mom's. (males are produced from haploid eggs)
The question I have is, if you take a son of a queen and mate her with her own son, what is the genetic relatedness of her resulting daughters to one another?
Here is an illustration of the haplodiploid system in insects.

Thanks in advance!
source: https://en.wikipedia.org/wiki/Haplodiploidy

Possible duplicate of How to calculate relatedness in haplodiploid organisms (mainly full sisters and full brothers)?

It is not a duplicate to me, it is related for sure but the question here is more precise. Maybe we sould rename the question so that it is easier to understand what is asked

This question may not be duplicate but I would reconmmend reading the answers of this question first How to calculate relatedness in haplodiploid organisms (mainly full sisters and full brothers)?
I think an image is worth a lot of words so here it is:

To calcul relatedness, I used the formula
$ \text{relatedness} = \ce{prop_{mother}} \times \ce{shared_{mother}} + \ce{prop_{father}} \times \ce{shared_{father}}$
The little trick here is that we know the father (son of queen) is unique, so we can focus on either of the two possible son of the queen. This gives us a 0.875 relatedness between sisters with a father being the son of the mother.
I hope it is clearer now.


text:
Genotypes of gametes produced by an F1 individual?
I have an urgent question as I have an exam tomorrow. I was skimming some past exam papers and one question came up which has me completely confused.

A cross was made between a pure breeding diploid pea plant with round, yellow seeds and a pure breeding diploid plant with wrinkled, green seeds.
R and r for round and wrinkled respectively, and Y and y for yellow and green respectively. Assume dominant allele of each gene is upper case, and that the two genes are on different chromosomes and so are independently assorting.
a) Give genotypes of two pure breeding parents
RRYY, rryy
b) Give the genotype of resultant F1 progeny
RrYy
c) Give the genotype and respective frequency of the gametes produced by the F1 individual and indicate whether the gametes are parental or recombinant.
This is the question I am having trouble with and confused about

The reason I am confused is primarily I do not understand what is being asked when referring to the "gametes produced". Is this an F1xF1 cross and the question is asking about the F2 generation? I assumed not as the next question is:

Two of the F1 individuals obtained from the above parental cross were crossed to obtain the F2 generation
d) Give the phenotypes of the F2 progeny and their ratios

If someone could please shed some light on this it would be much appreciated

Gamate is a haploid germ cell produced by either male or female parent. In your question,two homozygous dominant and recessive parants produce RY and ry gamates respectively. F1 would have four types of gamates if we think about their genotype.They should have any one of  RY, Ry, rY, ry as their genotype.
RY and ry are parental gamates. They have the genotype of the gamates that F1's homozygous parents produced. Other two are recombinant genotype. Since they behave independently, you can go with mendelian genetics and draw a punnett squre.write RY Ry rY ry horizontally and vertically then get the F2 cross genotypes. Dominant genotypes will determine the phenotype.


text:
How does the brain regulate its temperature?
I recently ran into a bio-physical paradox while trying to solve an engineering problem, using nature's way as a guide; namely the brain.

I'm working on designing a totally new system of liquid/gas cooling for a project. In Normal systems, the coolant is first cooled at a point, then sent along to the target areas; however, the coolant gets too hot along the way and cannot meet my target at one of the end components. Additional external cooling fins along the path still do not compensate.
I took biology classes in college and recall some mechanisms of the brain and pictures too (usually depicting the brain as all white internally). So, I theorized that maybe the coolant (blood) was not in direct contact with the brain in a substantial volume; however that was debunked: Why is the brain white?
From what I gather from the major answer, the brain's way of achieving homeostasis might present the answer to my problems. There is a lot of blood in the brain. This blood comes from the carotid arteries, which means it comes from the main circulation, and is hence at body temperature {considering homeostasis of all the body organs i.e. the lungs in this case}. By connotation, the brain should be the hottest organ in the body!
Considering the volume of blood in the brain, how does it regulate its temperature?

Great question, thanks for posting it as a new question. +1

Well, blood is highly toxic to the brain, which is why there is a blood brain barrier and there are astrocytes and glial cells that interface between blood vessels and the central nervous system. Homeostasis is maintained chemically much more than mechanically and it is more the task of the glial cells to maintain homeostasis in the CNS. As for heat dissipation, the majority of that happens through the enormous surface area of the skin. Basically the entire body acts as a radiator. And no, core body temperature is 37°C, barring an infection or inflammation. There is no hotter or colder organ.

What you saw in the post that you linked to is the amount of vasculature that is circulating around the cranium, but that is hardly any different from the amount of vasculature in the rest of the body. Yes the body is able to shunt blood flow to different areas under different conditions using hormones, but the network of blood vessels is still there. If you really want to compare that to a cooling system then calculate the volume and surface area of of all of those blood vessels to the volume and surface area of the brain, then compare that to the cooling components in your project,...

... and if you had a 1000th of the amount of cooling capacity running through your device as compared to the brain, or any part of the body for that matter I would be very surprised... the average human has 96 thousand kilometers of blood vessels in them. Cells are usually never more than 50 micrometers from a blood vessel, and the entire environment is aqueous which dissipates heat much better than air. Either you need to go really cold, N2(l), or you will need better tolerances for the downstream components. Or do like the body does, lots of pipes close together running for short distances.

Amazing! I believe I just got my answer. The chemical cooling you mentioned. All I need is to find an intermediate coolant fluid whose volume at any component along the path will regulate the amount of heat removed along that path before the end component. Though that is easier said than done. Thanks.

@AMR -  blood is highly toxic to the brain? If I would pump demineralized water around it would readily die :)

@AliceD Yes it absolutely is. Just think of the effects the Complement proteins would have if the got anywhere near the tissue of the brain.

@AMR - Agreed, it's just that OP's distant knowledge about Bio may make him interpret it as whether blood's a bad thing in the brain. It's not.

@AliceD. Blood flow through highly specialized vessels is not. There are two types of strokes. One is obstructive, the other is hemorrhagic. Both can cause severe disability and both can be fatal. His question says the "(blood) was not in direct contact with the brain in a substantial volume; however that was debunked," but it is not in direct contact. You have extremely tight endothelial cells of the blood vessels of the brain. You have astrocytes that surround the blood vessels and glial cells that protect the neurons. The architecture of the brain has evolved to keep blood out.

@AMR oh yes definitely. Blood's kept confined anywhere in the body, only a bit more in the brain via BBB. I am not arguing against, just the tone of the statement.

@AliceD. The use of homeostasis in their question is also problematic, as it is much more than just temperature regulation, but I let it slide. And the BBB is a lot more than a bit more when compared to the rest of the body. It is like the access point to a top secret military installation to the screen door on a porch, or to use an example from Biology, a BSL 3 or 4 facility to a freshman lab. And as far as tone, spend a day on a Neuro ICU and see what they think of blood and brain coming in contact with each other.

The gaming sector and data centers have done a lot of work on using liquid cooling. Also if you look at Texas Advanced Computing Center or CERN, they will likely have published plenty of material on component cooling.

There is an assumption that the OP is making that is problematic and that is that biological systems and man-made systems operate under the same principals. Man-made systems tend to be run a maximum efficiency or we push the envelop, over-clocking a CPU, afterburners on a jet engines, etc. and we then develop robust cooling systems to try to keep the components at the threshold of failure without exceeding it. Biological systems almost never do this, and metabolic activity is tightly control with enzymes that catalyzes chemical reactions in a controlled manner and with negative-feedback loops.

It is only in rare occasions that a biological system pushes the envelop, and that usually has to do with survival mechanisms that are for organism preservation, even if some deleterious effects are endured... Fight or Flight signals, inflammatory response to infection, chasing prey, etc. That is why these things happen in short bursts for short periods of time, because failure in a biological system leads to severe disability or death.

From what I can make up from your question is that you assume the blood in the brain is a bad thing in terms of temperature control. It is not. On the contrary, blood circulation is crucial in maintaining brain temperature.
Under conditions where the brain is heating up, which seems the focus of your question, there are mechanisms in place to extract this heat and dissipate it. Ambient temperature is often lower than body temperature, and even in hot climates, transpiration and water evaporation may cool the skin nonetheless.
Indeed, during hyperthermia, venous blood flow from the skin of the face and scalp fed to the dura mater (the brain's membranes) is enhanced and cools the brain (Brinnel et al., 1989). Moreover, blood from the nasal and paranasal mucous membranes flowing to the dura mater cools the brain due to the evaporative cooling of sweat or mucus. The dura mater may also transmit temperature changes to the cerebrospinal fluid compartment (Zenker & Kubik, 1996).
References
- Brinnel et al., Arch Dermatol Res (1989); 281(1): 66-72
- Zenker & Kubik, Anatomy Embryol (1996); 193(1): 1-13


text:
Why are sight and sound prerequisites for intelligence?
Edward O. Wilson, in The Diversity of Life wrote (emphasis mine):

Ninety-nine percent of the animals find their way by chemical trails.  […]
Animals are masters of this chemical channel, where we are
idiots. But we are geniuses of the audiovisual channel, equaled in
this modality only by a few odd groups (whales, monkeys, birds). So we
wait for dawn, while they wait for the fall of darkness; and because
sight and sound are the evolutionary prerequisites of intelligence, we
alone have come to reflect on such matters […]

I'm getting this from an anthology (Dawkins' "Modern Science Writing") so I don't see how Wilson supports this statement, and my google-fu is bringin up nothing relevant-seeming.
My question is: why are sight and sound prerequisites for a species to evolve intelligence?

To answer your question, we must first ask the question What is defined as intelligence?
A googling will tell you that most people believe intelligence to be something related to apes or even more conservatively to humans. But, I find this to be a bit unpragmatic. The closest level of abstraction I find towards defining intelligence is this wiki on Animal Cognition. Having said so, I personally would define intelligence on a much more abstract level.
Intelligence can be broadly defined as a learned response towards an external stimulus, providing the organism with an increased fitness/survival within it's ecosystem.
So Intelligence can be broken down into two parts

Memory of a stimulus
A programmed response towards that stimulus

This is a very famous video showcasing intelligence in the animal world; Crow Intelligence test
But My objective is to state that sight and sound are are not at all prerequisites of intelligence.
This paper from way back in 2014 is I think the best that I can state
Memory and Fitness Optimization of Bacteria under Fluctuating Environments
In this particular paper the authors test the capacity of E coli to produce a response within fluctuating environments, and they find that as the generations progress the later generations take lesser time to produce a response towards the stimulus. They also note that what happens if the prior external environmental state is restored. In such a case later generations become optimised for that particular state.
This is a very good example of memory which is stored at the level of DNA, and a level of intelligence is manifested in a microbial system. So therefore, can you really state that "sight- and sound" are pre-requisites of intelligence. I would say No They are not, that would be an over-simplistic way of what intelligence really is.

He may be referring to the fact that many nocturnal animals wait for the cover of darkness to be able to get their food safely or in order to cloak themselves to approach their prey better. However, this seems to be a matter of personal opinion. He wants you to think that we are smarter because we have to hide and hunt in broad daylight. I haven't been able to support his theory as bats can be considered very intelligent - and they primarily hunt at night.
In fact, we also consider dogs - and their wolf counterparts - to be intelligent as well, and you typically only see wolves at night.
Also, studies are showing that humans who are "Night Owls" are smarter than people who are "Morning Larks" according to a study in Psychology.
If you're interested in different kinds of behaviours and how intelligent they are you can look at BBC Animal Adaptations, which has a really cool list of what abilities each animal has split into categories. Particularly, they have an "Animal Intelligence" section which goes into detail about particular behaviours humans consider to be signs of intelligence. Personally, I think their list is a little out of date - where it is missing a few animals - but by their standards, many of the nocturnal animals have not made it onto the list.
A reason that hearing could be a prerequisite for intelligence is that communication is considered to be a HUGE part of intelligent behaviour. Tool use could be a reason that sight is considered a prerequisite for being intelligent. Really, the five senses (sight, hearing, touch, taste and smell) allow us to really take in the world and adapt to it properly. Sight, hearing and smell typically allow us to be warned of dangers but the fact is that we have to be intelligent enough to know what to do with the information.

Summary: Intelligence can be measured in many different ways. Edward O. Wilson could have been looking at a number of different things when he came to his conclusion (where sight and sound were required for intelligent beings). The truth is that it is all speculative.

If you judge a fish's intelligence by its ability to climb a tree, it will grow up thinking that it's stupid.

Subsequently if you judge my intelligence by my ability to spell, I will also go on thinking I'm stupid ;)

I have not judged you by your ability to spell English words, I have merely corrected them.

With all due respect to Dr. Wilson, this is just an anthropocentric, post hoc ergo propter hoc logical fallacy. Dr. Wilson looked around the world we live in, saw that most intelligent creatures navigate by sight and/or sound and concluded that those sense are a prerequisite for intelligence. I see absolutely no evidence to support this theory.
First of all, that is a classic fallacy. It is the equivalent of a 17th century European going to Africa and concluding that having pinkish skin is a prerequisite for the development of technology. Or if I were to go to Japan and conclude that having an epicanthic fold is a prerequisite for making good sushi.
The fact that the paths chosen by the evolutionary process on this planet are skewed towards sight and sound for more intelligent species does not in any way imply that those senses are needed for intelligence. What is needed are ways of detecting and reacting to the environment as quickly as possible. Light and sound are indeed particularly well suited for this since they travel several orders of magnitude faster than chemical diffusion. That's a good reason to conclude they might have given a selective advantage to the species relying on those two waves to detect their predators or prey.
There are, however, other options. Radar (bats) and sonar (dolphins) can be thought of as sight (or hearing) but are quite different. They both involve the emission of a wave and analysis of what is reflected back. Sight involves the analysis of light emitted by the sun and reflected by the environment. Being able to use your own body to emit the energy needed for your perception would seem to be a huge advantage. Our wonderful sight only works half of the time.
You could also, conceivably, have very fast perception based on things like:

Quantum entanglement; actually faster than light.
Magnetoception;
Electrolocation;
Gravity;

Some of the above already exist in species on this planet, others do not. Admittedly, using quantum entanglement would be kind of tricky. On the other hand, I see no reason why tiny disturbances in the gravitic field could not be detected just as tiny disturbances in the electromagnetic fields are by animals like sharks and cockroaches.
The main point of all this is that the fact that intelligent animals on this planet tend to do X does not in any way imply that X is a prerequisite for intelligence. Quite frankly, I expected better of someone like Dr. Wilson than such baseless speculation presented as fact.


text:
Is there a complete connectome of a cortical minicolumn?
I know that there are projects that try to map brain connectivity. Given that a cortical microcolumn has only around a hundred neurons I wonder whether there is a dataset available with the complete connectivity of just a single minicolumn of the neocortex. Doesn't have to be human.
I posed this question on cognitive science stackexchange already, but it doesn't seem to be happening.

I'm voting to close this question as off-topic because it has cross-posted to cogsci.se and has an answer there: http://cogsci.stackexchange.com/questions/16090/is-there-a-complete-connectome-of-a-minicolumn-of-the-neocortex

Perhaps the first place to look would be the Allen Brain Atlas
 (for mice, this is a paper about it), and also [this paper].(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4169118/)


text:
How does the cardiovascular system improve upon repeated, strenuous exercise?
New here, hopefully this is the right place to post this question.
It's widely known that repeated, strenuous aerobic exercise gradually improves the capacity of one's cardiovascular system — $\text{VO}_2$ max, cardiac output, etc. The U.S. NIH, for example, states the following:

Over time, regular aerobic activity makes your heart and lungs stronger and able to work better.
When done regularly, moderate- and vigorous-intensity physical activity strengthens your heart muscle. This improves your heart's ability to pump blood to your lungs and throughout your body. As a result, more blood flows to your muscles, and oxygen levels in your blood rise.
Capillaries, your body's tiny blood vessels, also widen. This allows them to deliver more oxygen to your body and carry away waste products.

Unfortunately, I have not been able to find information about the actual biological processes that happen during repeated exercise which trigger these effects. Is it some combination of hormones? Is it a form of muscle hypertrophy of the heart?
Frankly, the subject fascinates me, and I'd be grateful if someone with knowledge about this could share it!

Regular exercise results in "increased oxygen demand," which, via the hormone epinephrine and sympathetic nervous system, stimulates the heart and, in long term, the growth of new capilaries in the muscles. Yes, heart muscle hypertrophy is also one of the results. You may want to search for something like "adaptation of circulatory system to exercise" and you'll get results like https://www.ptdirect.com/training-design/anatomy-and-physiology/chronic-cardiovascular-adaptations-to-exercise and https://www.youtube.com/watch?v=OLGy1a3w08s .

Interesting resources, @Jan — thanks for your time! :)


text:
Is addiction adaptive?
Addiction and addictive traits seem common amongst animals.  A pubmed query shows it's been studied in everything from humans to worms.

My personal favorite of these is: "Individual Consistency of Feather Pecking Behavior in Laying Hens: Once a Feather Pecker Always a Feather Pecker?"

Is there/was there something adaptive about addictive behaviour?
Alternatively, how it is that addictive behaviour survived/persists if it is not adaptive?

First, I think you are mixing up obsessive compulsive behavior with addiction, which isn't exactly the same. From a strictly biological perspective, addiction generally has to do with the reward pathways. What usually happens is the chemical that the organism becomes addicted to binds irreversibly to a receptor on a neuron. In order to stop the signal, the cell pulls down the receptor, as there are less receptors, more of the chemical is needed to induce the same response. Also the body tends to develop a physical need for that chemical and without it there are severe withdrawal consequences.

See this related ? Here.  http://biology.stackexchange.com/q/36620/6061

Albeit used in the keywords of the paper, feather pecking is not an addiction, but normal behavior turned pathological in artificial (overcrowded) environments.
Addiction typically arises through overstimulation of reward centers in the brain, most notably the dopaminergic pathways involving the nucleus accumbens. Massive dopamine release, e.g. through cocaïne or meth intake, results in euphoria (Wise & Bozarth, 1985). When the drug's effects wear off it is followed by the 'crash', characterized by dysphoria and a longing for more drugs (CSAT, 1999). Gambling addiction works much in the same way.
Addiction develops because of an interplay of dependence and tolerance. Dependence is caused by downregulation of dopaminergic responses in the reward centers. Notably, dopamine receptors are downregulated when dopamine agonists like stimulant drugs of abuse are chronically administered. Downregulation of dopaminergic responses causes the physiology of the reward pathway to adapt to the presence of dopamine agonists. While the drug is in the system, everything is OK. However, once the levels of the dopamine agonist wears off, the body enters a state of lack of dopaminergic responses, causing dysphoria and depression. Tolerance develops as the liver and other tissues start breaking down the drug more efficiently due to upregulation of the necessary catabolic enzymes. Hence, more of the drug is needed, and the user becomes more and more tolerant. The interplay of dependence and tolerance form the dreaded vicious, downward spiral of addiction.
The reward centers have been crucial in evolution, as they provide motivation to vital acts of life, including eating and sex (University of Colorado, Boulder). Without a proper reward system, why eat or reproduce? However, drugs and other addictive acts such as gambling also activate the reward system.
Highly purified drugs such as crystal meth and cocaïne result in massive dopamine release that is unparalleled by normal physiologic processes such as eating. Before the occurrence of stimulants and things like gambling, the reward system was nothing but essential to life and evolution. Now, things are different and man needs to adapt to these novel, artificial pleasures in life.
References
- Treatment Improvement Protocol (TIP) Series, No. 33. Center for Substance Abuse Treatment. Rockville (MD); 1999
- Wise & Bozarth, Psychiatr Med (1985); 3(4): 445-60

Although addiction as a coping mechanism may help in the short term. Ie.preventing a depressed person from killing themselves through temporary relief of symptoms. In the long run addiction causes many more problems then it solves. The type of addiction also needs to be considered. Many alcoholics can go years before health and financial problems begin to cause trouble. Enough time to raise a family. Possibly the reason addiction genes haven't been removed from the pool. If you look at possibility the most extreme form of addiction, wires directly into the pleasure center of the brain. You see how completely maladaptive it can be. The monkeys will sit and press the button over and over. They neglect grooming behavior, other external stimulation,food and water. Loosing interest in anything beyond the pleasure button. Eventually succumbing to exhaustion. If allowed they will continue pushing the button and die as a result. This is an extreme case because with electronic stimulation the regular negative feedback that results from overstimulation of the pleasure centers appears to be absent. chemical stimulation of the pleasure centers causes tolerance and the feeling becomes harder to obtain the more one uses. Although many addicts chase the high until it kills them as well.

can you add some references to your answer? we always appreciate external references to questions and answers on BiologySE - thanks!


text:
Do "scars" in humans replace all the skin layers or only some layers?
When someone has a cut or surgical incision that results in a "scar", is the scar tissue replacing all 3 layers of the skin (epidermis, dermis, hypodermis)? Or only the first one or two of them?

Scarring can be internal also so it would depend how deep the cut was and how successfully it healed along with many other variables.

@Tusky it is clear what the OP is asking. Problem is there's to many critical variables to consider to be able to provide a straight answer. The OP didn't mention anything about why scars don't go away.

This depends on how deep was the initial wound, and how that wound healed. There are mainly two ways a wound could heal, either by primary intention (like in surgically closed wounds), or by secondary intention (like in wound left to scar up with the edges not closed properly).
In very well closed wounds that involves all layers of skin, such as primary intention healing following plastic surgery on previously healthy skin, the skin would regenerate all the layers after a long process that could last for 2 years or longer and involves constant life long remodelling of the remaining scar.
In wounds healed by secondary intention, such as following a third degree burn without treatment with skin grafts, there is extensive scaring (mainly consistent of collagen which could be thought of as a filler and adhesive that allows the epithelial skin layer only to grow over it, without renewing the deeper layers). In such cases the scar is large, adherent to underlying tissue, and has only a thin overlying layer of epithelial skin cells. This scar might also be insensate (numb) as a result of superficial nerve injury due to the initial wound.
Most scars are somewhere on the spectrum between the two extremes mentioned above. A badly sutured surgical wound, or a surgical wound that gets infected later, might still heal by secondary intention causing extensive scaring that doesn't replace all the skin layers. A good plastic surgeon might later remove that scar and allow the wound to heal by primary intension to improve the outcome.
If you would like to expand on how wounds heal, here are a couple of links to start you off:
http://teachmesurgery.com/skills/wounds/wound-healing/
https://emedicine.medscape.com/article/1298129-overview


text:
Inhibition of beta-oxidation by acetyl- or malonyl-CoA

Which molecule, in excess, inhibits beta-oxidation?
a. Acetyl-CoA
b. Malonyl-CoA

The answer to this question seems debatable to me, as I think both are correct.  However, according to my professor, only one is correct — which one I  don’t know because it was a question from the final exam.
Acety-CoA can inhibit thiolase, and malonyl-CoA can inhibit CAT I (Carnitine- acyltransferase), both of which lead to the same outcome — inhibiting beta-oxidation

Mammalian $\beta$-oxidation occurs in the mitochondrion, whereas fatty acid biosynthesis is cytoplasmic.

The rate-limiting in mammalian fatty acid oxidation is considered to be carnitine palmitoyltransferase (CAT), a key enzyme in the transport of acetyl-CoA across the inner mitochondrial membrane.  This enzyme is inhibited by low micromolar concentrations of malonyl-CoA (see Beta oxidation of fatty acids by H. Schulz).

Malonyl-CoA, of course, is a key intermediate in fatty acid biosynthesis.  Salih Wakil showed that CO2  is required for fatty acid biosynthesis, but that carbon atoms from CO2  do not appear in fatty acids, and it is now known that this is due to the formation of .malonyl-CoA by acetyI-CoA carboxylase, the rate-limiting reaction of fatty acid synthesis.

Thus when fatty acid biosynthesis is taking place, the concentration of malonyl-CoA is high and CAT (and therefore $\beta$-oxidation) is inhibited (Schulz, 1991).

However, as the OP points out, micromolar concentrations of acetyl-CoA inhibit 3-ketoacyI-CoA thiolase when the concentration of CoASH is low, and the Acetyl-CoA/CoASH ratio within the mitochondrion may also play a role in the regulation of beta-oxidation (Schulz, 1991).
As the OP says, it is a debatable point, and it seems to me, an example of a badly worded exam question.  I think the 'expected' answer is probably malonyl-CoA, and there is no doubt that this molecule plays a key role in the regulation of both fatty acid oxidation and fatty acid biosynthesis.  Nevertheless, the inhibition of thiolase by Acetyl-CoA may also play a role in the regulation of beta-oxidation.
Perhaps your Professor is an example of the type that Warburg told Hans Krebs to attach himself to? :-)

Your Google books link tells me I have reached a page I cannot access. Perhaps you can give us the Warburg quotation, in the German original if possible.

Taken me a while to get to it, but I finally found the quotation in Krebs’ (English language) autobiography of 1981, Reminiscences and Reflections. On p. 26 he gives this account of his interview with Warburg “I could learn a lot in his laboratory, he said, but if it were my aim to make a university career, ‘Then you had better attach yourself to some old ass of a professor.’” He goes on to write: “Warburg kept his word on both counts: he taught me a great deal, and he did not actively help me find a post…”


text:
Common properties of herbs in creating anaphrodisiac effect?
Recently came across Wiki article about anaphrodisiac herbs and other products.

An anaphrodisiac (also antaphrodisiac or antiaphrodisiac) is something
that quells or blunts the libido. It is the opposite of an
aphrodisiac, something that enhances sexual appetite. The word
anaphrodisiac comes from the Greek privative prefix ἀν-, denoting
negation, and aphrodisiac, from the Greek goddess of love, Aphrodite.
Reference

The article mentioned some of the herbs and plant related putative anaphrodisiacs like,

Marjoram (Origanum majorana) (Family: Lamiaceae)
Humulus lupulus (Family: Cannabaceae)
Heracleum mantegazzianum  (Family: Apiaceae)
Morton Arboretum  (Family: Salicaceae)
Vitex agnus-castus (Family: Lamiaceae)
Ruta graveolens (Family: Rutaceae)
Coriandrum sativum (Family:  Apiaceae)
Tropaeolum tuberosum(Family:  Tropaeolaceae)

I am not sure that is there any relevance in these claims that these herbs triggers anaphrodisiac effect.
The question is,
Is there any common alkaloid, aromatic hydrocarbons or any other chemicals present in these herbs which triggers the anaphrodisiac effects ?

Why down vote ?

This might answer part of your question: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3731873/

@skymninge:Which part ?

I did not read all of it, but it looked to me like it mentioned at least some of the herbs and the chemicals you were asking for.

@skymninge - that article deals with aphrodisiacs


text:
What specific sensory nerves act as receptors for "pins and needles" (neuropathy)?
According to this excellent answer, the difference between "pain" and "pins and needles" (neuropathy) is that different receptors (sensory nerves) trigger in reaction to different stimuli.
Different types of pain receptors (hot/cold, pressure, etc.) send pain signals to the brain.
Different receptors are responsible for sending neuropathy signals to the brain. These receptors are usually triggered when the nerve receives a shortage of blood flow.
According to the Wikipedia Article on Sensory Receptors, there don't appear to be any nerves that produce pins-and-needles sensations to the brain...
So I ask: What are the specific types of nerves/receptors that send "pins and needles" signals to the brain? What are they called?
I would imagine that it either has to be a specific, specialized receptor that (perhaps) starts firing if its senses "something is wrong" (such as decreased bloodflow to the area, etc.), or it's that all sensory receptors are capable of firing "pins and needles" signals under special circumstances.

Pain is an active neural response (nociceptive pathways). Neuropathy is a neural dysfunction. Where is the confusion?

Thanks @WYSIWYG (I'd upvote you if I had the rep to do so) - You are correct: neuropathhy is neural dysfunction, however, you cannot deny that pins-and-needles does in fact register with the brain as a sensation, otherwise we would never know about it (that our nerves weren't functioning correctly)! So clearly, neuropathy communicates to the brain via signals. Clearly, so does pain. Pain feels different than pins-and-needles. I want to know why.

Are you specifically asking about neuralgia and general pain. Pins and needles dont feel painful.

Thanks @WYSIWYG - I feel like perhaps you're either not reading my question carefully, or you're reading too much into it. I am asking: why do pins-and-needles feel different than pain? And I'm looking for a biological/physiological explanation, not something high-level and lofty that a monkey would understand.

Well.. okay.. I didnt get why you were comparing the both. You should see this post. This one too.

Thanks again @WYSIWYG - so the first post you referenced has one of those high-level, lofty answers that I don't want ("The feeling you describe is called "paresthesia," and ... it happens "when sustained pressure is placed on a nerve."). The second post you referenced almost hits the nail on the head, but still falls short in the specific thing I'm looking for...(continued in next comment)

In that 2nd post, the accepted answer states that pain receptors send one kind of signal to the brain, which interprets those signals as pain, whereas other sensors send different signals to the brain, which the brain interprets as pins-and-needles. So to me this implies that the difference is the kind of sensory nerves that are firing. I'm asking: what are the sensory nerves that send pain, and what are the sensory nerves that send "pins and needles" signals?

Pins-and-needles (PAN) sensation and pain stem from the same nerves. The pathophysiologic process is different, though. PAN is characteristic of nerve lesion, and is therefore a pathologic reaction. Pain is a physiologic reaction to a stimulus perceived as ominous.
Pathophysiologically speaking, the PAN sensation is a distortion in somatosensory stimulus processing due to injury to peripheral nerves.
Of course, the PAN sensation will stem from somatosensory nerves. Pure motor nerves will not cause such a sensation.


text:
Do repetitive movements on EEGs show up as discernible patterns?
Here is a typical EEG reading:

(source: frontalcortex.com)
If I am connected to an EEG, and am sitting perfectly still, and then begin doing some repetitive motion, say, 10,000 times, will we see discernible patterns emerge in the output?
In other words, would it be possible to categorize a particular pattern in the output and say "Waves with this signature correspond to the subject wiggling his left pinky"?
I would imagine that, over time (and many trials) wave patterns converge to predictable signatures for a given movement.

Specific events, e.g. finger flexions, generate synchronized neuronal responses in the brain that can be measured on the scalp with EEG. However, a voltage response to a single event typically generates a low-amplitude response relative to the background EEG. One way to enhance the signal-to-noise ratio is to repeatedly record the EEG in response to the same event. By time-locking the event with the EEG and averaging the individual event-related EEGs, the random background noise will be reduced (stochastic noise) and the event-related potential (or ERP) can be extracted from the EEG (Woodman, 2010). An example of an ERP to repeated index finger flexions is shown in Fig. 1. Such a wave doesn't need 10,000 repeats. 25 may be sufficient.
If you characterize this ERP and determine specific features of it (duration, amplitude, latency after event etc.) you can generate algorithms that detect these features in the raw EEG, without the need to do repeated measures. In fact, thinking of a motor movement (e.g. grasp that coffee mug) generates very similar EEG activity as the factual act of grasping that mug. By recording the ERPs using events like think of grasping that coffee mug from a person missing a hand, and subsequently designing the necessary algorithms to detect that waveform near-realtime in the person's EEG, one can design brain-computer interfaces to control prosthetic limbs (Guger & Pfurtscheller, 2016).

Fig. 1. ERP to voluntary index finger flexions. Motor activity was recorded from the motor area. Source: Ball et al. (1999)
References
- Ball et al. NeuroImage (1999); 10: 682–94
- Guger & Pfurtscheller, AAATE 5th European Conference Advancement of Assistive Technology (2016)
- Woodman, Atten Percept Psychophys (2010); 72(8): 10.3758


text:
What are wave frequencies in the EEG?
Here is a typical EEG reading:

(source: frontalcortex.com)
I understand that each row corresponds to the signal read between two sensors on a standard 10-20 (or 10-5) distribution setup (e.g. C3-P3).
What I'm missing here is: what waves are we actually seeing here - alpha, beta, etc.? Or do EEGs not really contain wave types, and instead just show voltage differentials between sensors?

Actually I believe you may be seeing all the bands and will need to do a fast Fourier transform to get the actual frequency, however, I could be wrong as I am studying the MEG currently, not the EEG.

Thanks @SolarLunix (+1) - so I assume there's a way to use FFT to decompose V(t) (voltage as a function of time) back out into constituent waves?

EEGs are often analyzed in the frequency domain, where signals are subjected
to spectral analysis, typically by Fast Fourier Transformation, or FFT.
What an FFT basically does is decomposing a signal in the time domain into one in the frequency domain. It does this by decomposing the input signal (any signal, including EEG) into a series of sinusoids. These sinusoids are not present in the original signal; it is a mathematical trick. If you would add all the sinusoids back together, the approximate original signal is restored.
Typically not a single frequency is analyzed, but a band of frequencies, because the frequencies within these bands are associated with similar brain states. The frequency bands that are typically reported on are shown in Table 1, including the brain state they associate with as well as sample EEGs:

Table 1. Typical analyzed EEG frequency bands. Source: Conorrus Somanno
Reference
- Nelson Garcia et al. Device and method for cognitive enhancement of a user (2014). Patent EP 2681729 A1


text:
Why is freezing bacteria not a problem?
I have a follow up question to this question: Does freezing microorganisms such as probiotics kill them?
If freezing bacteria kills some of them, then you are effectively putting selective pressure on bacteria when you freeze them (the bacteria more resistant to low temperatures survive, bacteria less resistant die). Why then is it a good idea to freeze bacteria?

Hmm ok you have a point. So bacteria are killed in a non-discriminant way by freezing? i.e. some just happen to die during freezing while others survive.

I was thinking of heterogeneous bacteria, but that's not correct it seems.

I don't understand why selection like this would be a problem, even if it occurred. What's the issue with having more cold-resistant bacteria? As Hallur mentioned, even if the bacteria survive being frozen, they won't reproduce at such cold temperatures, so it wouldn't be a problem for food safety. And I don't think anyone uses freezing to try to sterilize things.

I was thinking about its use in research. If you selected for cold resistant bacteria then it could possibly confound your experiment.

The ice crystals that form tear and shear the bacterial cells, unless you add a cryoprotectant (for example, glycerol) to the cells beforehand.
Remember, when water freezes its volume increases.  This is why a closed soft drink can that you put into your freezer to chill faster, will burst if you leave it in until the contents are frozen.
Exactly the same thing happens to cells (animal cells, plant cells, yeast cells, etc.) if they are frozen without a cryoprotectant.

This does not answer the question.

The long-term effectiveness of freezing or incinerating bacteria is rooted in how brutal and difficult to withstand such actions are.
Freezing generates ice crystals which, as mdperry points out, "tear and shear the bacterial cells."  In theory this could create a selective pressure to survive these temperatures, and indeed akinetes are known to survive the freezing process.  However, that is a non-trivial evolutionary step.  To fit such a state into the lifespan of a bacteria would call for a substantial mutation.  Freezing bacteria for a few hundred million years will likely be sufficient to "teach" them how to survive!  Without such a step, it's just not reasonable to survive the abuse.
The same goes for incinerating.  Once you get hot enough, the chemistry of organic molecules starts to become a permanent terminal issue.  Evolving to beat this is simply really hard.  In fact, an autoclave is enough to kill virtually everything, though one strain of Pyrolobus fumarii did survive at 121C in an autoclave.


text:
Cis and trans linkage
Question:

Two dominant non-allelic genes are 50map units apart, the linkage is:
(A) Cis type
(B) Trans Type
(C) Complete
(D) Absent/Incomplete

My take:
After a lot of searching on the net I found that 50 map units =50% recombination frequency. And no recombination happens  when it is 50 map units or more than that.
But there is no information given about cis and trans linkage with that of map units.
Even though the answer for the above question is absent or incomplete (d),the options bugged me to ask this question
Is it possible to guess cis /trans linkage when map units are given? If i am wrong please correct me. Thanks in advance !

50cM ≠ 0.5 probability of recombination. See Difference between crossover rate and recombination rate?

Yep...i understood that ! Only genes  less than 50cM apart  can be recombined right?

It would be better if you post the question from your textbook (or exercise) as a text instead of an image.

As far as I know, cis and trans require the knowledge of which alleles of two traits are present and how they are linked. But based on the "two dominant" thing in the question, if there were linkage, it would have been cis type linkage. A random page on the first page of Google search, if it helps.


text:
What does "dissipated" mean here?
This is the context:

You know cardiac muscle cells are small cells relative to skeletal muscle cells, but unlike skeletal muscle cells that are arranged in parallel and their contraction is dissipated onto a tendon to bring about movement at a joint , cardiac muscle cells aligned end-to-end.

I've googled it, but it didn't make sense

Dissipate
to (cause to) gradually disappear or waste

● Can anyone change it into an easier text?
● What does dissipated mean?
● What does end-to-end mean?
● I wonder whether skeletal muscle contraction is disappeared onto a tendon or not.
● Is there an another scientific word for dissipated?

& apparently, I think end-to-end here means that cardiac muscle cells  join strongly to each other, but actually this is not a specific definition, I suppose.

Source:  Cardiac Muscle: Function & Main Parts – Histology | Lecturio.

Have you made any attempt to understand these words with tools you would use to learn english outside of science? Dictionaries, translation tools, finding other contexts, etc? We expect some effort from askers before we answer questions here.

@Bryan Krause Yes, of course, but it didn't make sense at all.

What does dissipate mean?

It's a word from a thermodynamic context. Heat can dissipate. Doing work causes energy to be lost in the form of heat, which is called dissipation. It means to spread out your energy, as in, a hot object - like a cup of boiling water - dissipates heat to its environment. The cup cools while the environment gets warmer. Likewise, a concentrated force (like tension across a skeletal cell within a muscle) can spread over lengthwise to connected tendons, and the energy is transferred to the bones that move.
It's really not the most precise use of the term, but it's understandable and gets the point across. To waste or to disappear is the colloquial meaning of the word. To dissipate, scientifically, means to spread out energy which was once concentrated relative to its environment. The energy can take the form of heat or work (mechanical work, in our case).

What does end-to-end mean?

End to end means in series, as in, not parallel.
Cardiac cells arrange end-to-end:
beginning -- CARDIAC CELL -- CARDIAC CELL -- CARDIAC CELL -- end

Skeletal cells arrange like so to form a muscle:
beginning ---------------- SKELETAL CELL ------------------- end
beginning ---------------- SKELETAL CELL ------------------- end


text:
Confusion about the duration of different phases of the cell cycle such as G1, G2 & S
We all know that normally most of our cells (which are alive and have nuclei - except for cells such as "stem cells", "red blood cells", etc) spend most of their lives in interphase.
But the Interphase itself is also composed of other parts, other stages, including G1, S, and G2.
Is the staying duration of the most human cells in each stage(G1,G2 & S) is comparable to the other stage?
For example, is it true to say that:

"Most human cells, which have the ability to divide(passing the cell cycle), spend most of their lives on stage G1 than S phase or vice versa."?

Usually, which stage is the longest or shortest?
It is quite clear that the G1 is normally longer that G2 and as far as I know the G2 is the shortest stage in interphase, but what about G1 and S?
Is stage S usually longer than G1?
Is there any information?

It depends on the conditions, cell type or state of the cell.
I don't think anyone here can do better justice to the question for a beginner than this web page.
To show you why your answer is not answerable, by way of example: some cells exit the cell cycle and enter a stage called G0. This can be a permanent state for some cells, or, for instance, others may return to the cycle if they receive (external) signals.
Here is a very loose approximation, circles are to scale with respect to cycle time. Notice, for instance, the human circle is for an immortalized cell line under laboratory conditions, rather than for cells in your body. A neuron (brain) or an enterocyte (gut) have vastly different cell cycle states, so it's impossible to give you a single straight answer without misleading you totally.

Bonus food for thought: notice that the fraction of time cells spend on G1, S, G2 and mitosis is also different between different cell types.
Bonus food for thought #2: In fruit fly embryos (pictured bottom right in the above picture), you have an extreme example of unconventional (non-textbook) cycling. Rather than synthesizing new cytoplasmic materials, the size of the developing embryo is constant except for the replication of the genetic material. This happens in the growing larva for ~10 cell divisions, in thousands of cells. One of these cycles takes about 8 minutes to complete fully. That's an impressive time to copy a genome; most* bacteria can't do it this quickly!
(*any that I am aware of)

Is it true to say "Most human cells, which have the ability to divide(passing the cell cycle), spend most of their lives on stage G1 than S phase or vice versa."? Is there any information?

I don't think this is known definitively. We can only guess. Most cells are in interphase (i.e. not mitosis+cytokinesis). There is an important cell-cycle checkpoint at the end of G1 which, when passed, means that the cell is preparing for eventual division (S or synthesis phase means it's duplicating its genome). I would hazard to guess most cells in the body, by sheer number, are in G1 or have entered (semi)permanently into the G0 phase. Even some adult stem cells await signals to enter the cell cycle again and divide, and these are the most proliferative cells. Don't quote me on this.

I wonder whether entering the G0 is only done through G1. Is it possible for the cell to go from stage S or G2 to step G0?

By definition G0 is prior to S phase. Cells can remain for a long time in G2 but if they are not 'actively readying for division', they are either in G1 or out of the cell cycle entirely, in G0.

@AmirhoseinRiazi also have a look at https://biology.stackexchange.com/q/13703/3340

A typical eukaryotic cell cycle is illustrated by human cells in culture. These cells divide once in approximately every 24 hours (Figure 10.1). However, this duration of cell cycle can vary from organism to organism and also from cell type to cell type. Yeast for example, can progress through the cell cycle in only about 90 minutes. The cell cycle is divided into two basic phases:
Interphase
M Phase (Mitosis phase)
The M Phase represents the phase when the actual cell division or mitosis occurs and the
interphase represents the phase between two successive M phases. It is significant to note that in the 24 hour average duration of cell cycle of a human cell, cell division proper lasts for only about an hour. The interphase lasts more than 95% of the duration of cell cycle. The M Phase starts with the nuclear division, corresponding to the separation of daughter chromosomes (karyokinesis) and usually ends with division of cytoplasm (cytokinesis). The interphase, though called the resting phase, is the time during which the cell is preparing for division by undergoing both cell growth and DNA replication in an orderly manner.
The interphase is divided into three further phases:
G1 phase (Gap 1)
S phase (Synthesis)
G2 phase (Gap 2)
G1 phase corresponds to the interval between mitosis and initiationof DNA replication. During G1 phase the cell is metabolically active and continuously grows but does not replicate its DNA. S or synthesis phase marks the period during which DNA synthesis or replication takes place.
During this time the amount of DNA per cell doubles. If the initial amount of DNA is denoted as 2C then it increases to 4C. However, there is no increase in the chromosome number; if the cell had diploid or 2n number of chromosomes at G1, even after S phase the number of chromosomes remains the same, i.e., 2n.
CELL CYCLE AND CELL DIVISION
In animal cells, during the S phase, DNA replication begins in the nucleus, and the centriole duplicates in the cytoplasm. During the G2 phase, proteins are synthesised in preparation for mitosis while cell growth continues.