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Heart Rate being normal when under treatment for the bends
When you surface from diving too quickly; you get "bends" - these are caused by gas bubbles forming in your lungs (especially nitrogen). This causes breathing problems if not treated since the bubbles are essentially blocking oxygen transport.
For treatment, you have to be in a hyperbaric chamber for several hours.
Why is it you don't get nitrogen and carbon dioxide bubbles in your bloodstream while being treated? I would think that in the machine the nitrogen, carbon dioxide and water concentrations would rise causing you to start having signs of low oxygen like loss of brain function.
As I stated previously, nitrogen bubbles block oxygen transport and thus carbon dioxide transport. Since there is nowhere else to go, it goes into the bloodstream where oxygenated blood is supposed to be. This is detected by the chemoreceptors in your arteries; this then tells the heart to beat faster in attempts to rid the body of CO2. Once again; however, this doesn't happen because now there are more nitrogen bubbles from breathing in more nitrogen and water. This leads to a progressively higher heart rate (Ventricular Tachycardia - V-tach) which is dangerous as it can lead to MI (Myocardial Infarction) symptoms - like chest pain. Ventricular tachycardia that lasts a maximum of a few minutes can then lead to V-fib (Ventricular Fibrillation) which, if not treated with epinephrine or defibrillation on time, will lead to asystole and death.

Summary:

When someone has the bends and is being treated in a hyperbaric chamber; how do they not end up having an acute MI (due to accumulation of nitrogen gas in the bloodstream)?

Can you please explain your abbreviations and also rephrase your question? At the moment it's hard to understand.

Does “a machine” refer to a hyperbaric oxygen chamber? I’m having trouble understanding the logic of the last sentence or what that has to with heart rate.

The point of "the machine" (hyperbaric chamber) is recompression, which stops the dissolved gases in the body to form bubbles in the blood. Then after treatment you can do a controlled decompression, similar to what you do during ascent in normal diving.

What makes you say there's no change in heart rate? Both the heart rate and the respiratory rate increase. But if you're talking about the effect of hyperbaric hyperoxia's effect on the parasympathetic nervous system, please clean up your question by editing it.

I ran some edits - hopefully you all will be able to understand the drift here :)

Allot of misconceptions regarding rapid decompression and the bends in this post; mostly none of what is mentioned happens unless the diver goes through extreme rapid decompression, and embolism is more likely to kill the diver in that case.  Recompression in a chamber re-dissolves the N2 bubbles and slow decompression prevents the return.

You have misunderstood bends, effects of high pressure on body and the need for recompression. If this question gets re-opened, it will receive great answers from a lot of people

You are wrong on several accounts:

Bends occur due to bubbles that form in muscles and joints and not lungs - They fall under Mild or Type 1 Decompression Sickness (Type 1 DCS).
Formation of bubbles in blood stream do occur in the Decompression process - Hyperbaric chamber is used to treat this condition.

What happens when diving:
During deep sea diving the pressure surrounding a person increases at the rate of 1 atm (atmospheric pressure) for every 10 m in sea water and 10.3 m in fresh water. This relation is linear.
The pressure inside the body equalises with the pressure outside to prevent any deformation. The solid and liquid components of the body can withstand pressures upto 151 atm (depth of 1.5 km underwater) without undergoing any noticeable compression. But air, being extremely compressible undergoes compression.
So at 2 atmospheric pressure the space occupied by the air in our body is halved. This would shrink the lungs to half the total volume. To circumvent this the divers breathe air compressed at the same pressure as the water pressure around them, so that the pressure gradient across the chest wall is normal.
Pressure Concentration relationship:

Dalton's Law:
This law states that the Barometric Pressure is the sum of the partial pressures of the individual gases in the air mixture.
Barometric Pressure - The total pressure measured

In air at 1 atmospheric pressure (760 mm Hg) the partial pressures of various gases are:

Nitrogen ~ 593 mm Hg
Oxygen   ~ 159 mm Hg
Co2 ~ 0.2 mm Hg
Others   ~ 7 mm Hg

According to this Law, as the pressure inside the Lungs increase, the partial pressures of each gas increases. At 2 atm, the partial pressures of every gas doubles.
The gas exchange in the lungs is based on partial pressure of the gases. Thus due to increased partial pressure, the amount of gases dissolved in blood increases (This increase is proportionate to the pressure levels).

During a extended dive (one lasting several hours) the body tissues gradually equilibriate with the high-pressure gases. At sea level our body contains 1 L of dissolved nitrogen, equally distributed between body's water and fat. As partial pressure of Nitrogen rises, the nitrogen equilibriates with the body's lipid stores because adipose tissue is relatively underperfused.

Once equilibrium is achieved the volume of nitrogen dissolved in tissues is proportional to the alveolar partial pressure of nitrogen. Thus at 4 atm the body will contain 4 L of nitrogen.
The same principle applies to oxygen as well, though the solubility of oxygen and the speed at which equilibrium is attained are different.
Decompression
During ascent from the depths, the Barometric Pressure (surrounding pressure Pb) falls. As the Pb falls the pressure inside the alveoli fall as well. This causes a fall in the partial pressures of all gases in the lungs creating a gradient of gases from the tissues to the alveoli.
So the diver has to ascend slowly to give enough time for the gases to move into blood from the tissues and then get washed out. If the ascent is too rapid, gases dissolved in the tissues - due to high pressure - attains the gaseous form (due to pressure drop) and become bubbles. This is similar to opening a pressurised coke can where one can observe gas bubbles forming.
The bubbles are the reason for the bends. Bubbles can also cause serious problems like arterial gas embolisation, CNS disorders (due to formation of bubbles in the myelin sheath of axons which compromise nerve conduction), pulmonary symptoms (due to pulmonary emboli), sometimes even Disseminated Intravascular Coagulation.
Solution
The decompression is done in stages - in which the divers spend various amount of time at various under water levels to allow complete diffusion of dissolved gases into blood and into the alveoli which is consequently breathed out.

Hyperbaric Chamber
The hyperbaric chamber is used when the above solution is not applied i.e. the diver has surfaced rapidly without spending sufficient time at various levels to allow proper decompression.
In a hyperbaric chamber the diver is recompressed to the pressures equal to the pressure experienced at the level to which the diver dived. Due to the increase in pressure, the bubbles get dissolved again. This instantly relieves many symptoms - like the nerve conduction delay, bends, niggles etc... Now the decompression is carried out by under controlled environment, simulating the various intervals the diver has to stay at various pressure levels under water.
Hope this explains your doubt.
So coming to myocardial infarction, the hyperbaric chamber redissolves the gas bubbles thus preventing myocardial infarction.

For more info read chapter 61 of Medical Physiology, 2nd edition, by Walter F. Boron and Emile L. Boulpaep.


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How does ANF increase GFR?
ANF as we know reduce the Na+ uptake and K+ removal in the distal tubules and it also functions as a Vasodialator (?) But again it says that ANF increases the Glomerular filtrate ? But if it is acting has a Vasoldialator (ie, antagonistic to Vasopressin) how is it increasing the GFR ? Shouldnt it lower the GFR ?

ANF - Atrial Natriuretic Factor also called Atrial Natriuretic Peptide
GFR - Glomerular Filtration Rate

ANF (Atrial Natriuretic Factor more commonly known as ANP - atrial natriuretic peptide) squeezes (vasoconstricts) the efferent arteriole. This means the pressure in the glomerulus is higher (like if you squeeze the end of a hose) and so more fluid is squeezed out i.e. the glomerular filtration rate (GFR) is higher. It also dilates the afferent which means more fluid is going in, further increasing GFR (Marin-Grez et al.)

Why is this answer down voted?

Someone has been downvoting all my answers for whatever reason. Assume they're trying to get me under 4000.

I found two downvotes and I upvoted once to get the -1 status. Good answer though. I think it will be reversed soon! Good luck

It seems the community is very reluctant to upvote good answers. Most of my rep comes from answers to silly questions vs well researched answer to good questions

I downvoted because of the lack of references, the unclear picture, the use of acronyms and the ample use of technical terms. Should have let you know earlier. I also downvoted the question for similar reasons, but after@CRags made the edits I removed the downvote and close-vote as well. I am not downvoting person-based btw - everyone is free to like or dislike particular questions and answers isn't it?

And don't assume the worst when folks downvote. Downvoting helps to  improve questions and answers. My downvotes have nothing to do with personal missions to bring someones rep <4k, nor has it anything to do with a reluctance to upvote! Personal vendettas can be reported to moderators btw.

@ChrisStronks: Thank you for your feedback. Comments and feedback help improve answers whereas simply down voting leave the author of an answer confused. In the future make sure to leave comments when you down vote to avoid not being helpful. I have improved the answer by explaining acronyms and adding a reference. There isn't a better picture than this which has ANP on it.

@AndroidPenguin - you are totally right. Normally I leave a comment. My bad. +1 :-)

So the summary is that ANP vasodilates the afferent arterioles and constricts the efferect arteriole ?

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text:
Are small CO₂ concentrations devastating to certain cognitive tasks?
A new study shows strong effects of what should be a negligible CO2 concentration.
The paper "Is CO2 an Indoor Pollutant? Direct Effects of Low-to-Moderate CO2 Concentrations on Human Decision-Making Performance" exposed people to three levels of CO2: 600, 1000, and 2500 ppm while keeping constant other factors such as ventilation, humidity, temperature, and indoor pollutant concentration. Of course, the participants didn't know how much CO2 was in the air.
At the 2500 ppm level, most cognitive performance measures were temporally reduced (they used the SMS management test). Some changes were drastic.
Since normal air is 400 ppm, 2500 ppm sounds like a lot. However, it is dwarfed by internal production. Humans exhale 50,000 ppm CO2 in the lungs, meaning that the lung air averages 25,000 ppm (as a rough approximation). The extra 2500 ppm is only a 10% increase in the average "atmosphere" that the blood is exposed to. Furthermore, people partially compensate increased P(CO2) with deeper ventilation (the effect takes much larger concentrations to be noticeable). Why would this extra 10% have such a strong effect?
Personally I am skeptical. This study has such high impact (millions of people's performance) that it needs replication. Maybe the hissing sound of the injector got people worried (more hissing at a higher concentration!). Maybe an experimenter (who knew the concentration) was watching the people and that subconsciously affected them.

Interesting question. I will take a look at the original paper, but this can take a day or two.

@Chris: Thanks. I am not the best at including links and other formatting. Can editors be rewarded 5 rep when the asker likes it?

You only get rewards for accepted) edits when you are below 1000 reputation points (and only 2). Good that you like it. :-)

I have read it now but I am not decided yet. The first and biggest problem I see is the relatively small number of participants (only 24). This is pretty small to do real statistics (it can be done, but needs extra care and is not as conclusive as larger groups). And I am not sure, if the differences are really so big. If you look on the single results in figure 1, than these results vary quite a lot. So personal factors seem to play an important role here, too. I am not too convinced by this study.

I think that the diffusion of carbon-di-oxide in the alveolar surface depends on the residual P(CO2) in the inhaled air. If the partial pressure of CO2 is high in the inhaled air then the amount of CO2 that diffuses out of the blood decreases

That and the carbon-di-oxide dissociation curve is not linear. This means even a small increase in the partial pressure of CO2 in the inhaled air can cause dramatic shift in the CO2 exhaled. See this:http://www.umc.edu/Education/Schools/Medicine/Basic_Science/Physiology_and_Biophysics/Core_Facilities(Physiology)/Physical_Exercise_-_Bicarbonate.aspx

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Is it possible that a set of functionally related proteins in a pathway fulfill different functions?
Could it be that a given pathway of enzymes (or proteins in general) may fulfill different purposes in a cell by for shifting partners? Say protein A activates B, B activates C and C has a specific action X (e.g. X = phosphorylation of protein D). Now do pathways exist where, e.g., A can activate C directly resulting in action Y (e.g. dephosphorylation of protein D)?
At this time I am in need of real-world examples of this scenario, but I can't find any. Can anyone help?

Hello Costa, and welcome! I don't understand your question. What is supposed to connect to what, what do you mean by property? It's a very broad tem. And maybe you man exhibit, not execute. I know it's not easy if English is not your first language, but people can't answer if they don't know what the question is. You can edit it to add detail, else it's possible that it will be temporarily closed until you explain more.

Hi Costa Welcome to Stack Exchange! - Thanks for your question! @rumtscho is right. I took a bash at improving your wording a bit, but you may have to elaborate a bit yourself. SE users, and particularly those at Biology SE (myself included :-) can be picky in accepting questions :)

ps: please feel free to roll my edits back if it is not to your liking

Just summarizing my current understanding: A -> B -> C effects X. Then, through some mechanism, A -> C effects Y.

Do you mean C has two X and Y actions and this different actions results from its different stimulator?

I don't understand the question...

If Y can be seen as the inverse or absence of X function, it sounds to me like an incoherent type 3 feed-forward loop, where
A activates B
B activates C
A inhibits/reverses C
example from literature, E.coli: fnr as A, and arcA as B, cydAB as C
source: http://www.pnas.org/content/100/21/11980.long

I3FFLs are quite rare. I haven't really encountered an example of I3FFL. I1FFL is quite common. This you can intuitively guess because A acts as both inhibitor and activator. Though this phenomenon is possible it is not very common.


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Why White Blood Cells (WBCs) do not react to foreign bodies like sperm?
Why do the white blood cells allow foreign bodies like sperm to exist inside body cavity without any reaction?
White blood cells function is to fight against foreign bodies (from the text books).

Majority of white blood cells in general are present only within blood vessels, lymph vessels and lymph nodes. In addition various organs have locally adapted specialised immune cells. For example brain has microglia, Liver has kupfer cells, etc... Specialised immune cells are present along the mucosal linings which are named differently in different regions - Peyer's patch in the jejunum and ileum, tonsils in oral cavity, adenoids in the nasopharynx, etc...
As sperm do not enter blood vessels, only local mucosal immunity will act on them. There is a local immune response to the sperm in the vaginal mucosa. However, the immune response to the sperm is transient. Several hypotheses have been put forth to explain this:

The seminal plasma suppresses the immune response. This is supported by the fact that sperm, if introduced without seminal plasma, do elicit an immune response--however this suppression seems to be inconsistent
Insemination might activate a sequence that results in active immune tolerance to paternal antigens (antigens present in sperm)

For details see here:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782486/

Studies show semen does mount a considerable immune response in the female mucosa, however:

Seminal plasma redirects the differentiation of human dendritic cells (DCs) toward a regulatory profile. By promoting a tolerogenic profile in DCs, seminal plasma might favor fertility, but might also compromise the capacity of the receptive partner to mount an effective immune response against sexually transmitted pathogens.

Semen promotes the differentiation of tolerogenic dendritic cells.


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Human leukocytes (re)circulation/migration in homeostatic state
One can easily find information on the topic of leukocytes trafficking between vessels and peripheral tissues during inflammation.
But what happens during normal states when there is no pathology? Do all the subtypes of granulocytes, monocytes, and lymphocytes leave the blood vessels and enter healthy tissues in the same way they do under pathological (inflammatory) conditions?
References and thoughts are very welcome.
Thank you.

Which leukocytes do you mean? Peripheral memory b cells?

I have edited your question a bit. Please feel free to roll back if you think it alters your question.


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What happens to the second strand in single-stranded / prime editing?
Articles about ’prime’ CRISPR editing generally state that a major advantage is that it only affects one strand…
…But what happens to the second, complementary strand of the genome?  Doesn’t it have to eventually change to match the first?
Or is that edited portion of the genome forever ‘open’, which would surely cause problems in replication etc.?

Of course, both DNA strands must be changed.
The way this is done can be found,for examlple, in the Wikipedia article “Prime editing”. In brief, there have been several modifications of the main approach to this, which in essence is as follows:

After the editing of one strand has been completed, a nick is
introduced in the unedited strand. The cell’s natural repair
mechanism will act on the nicked (unedited) strand and, in so doing,
copy the intact edited strand.

Details of how the specific nicking of the unedited strand is achieved can be found in the cited article.
Postscript
It is perhaps worth clarifying why editing a single strand, rather than both, is advantageous. As I am no expert in this area, I merely quote verbatim from the Wikipedia article:

“The prime editing tool offers advantages over traditional gene editing technologies. CRISPR/Cas9 edits rely on non-homologous end joining (NHEJ) or homology-directed repair (HDR) to fix DNA breaks, while the prime editing system employs DNA mismatch repair. This is an important feature of this technology given that DNA repair mechanisms such as NHEJ and HDR, generate unwanted, random insertions or deletions (INDELs).”

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Why does conjugation occur in Spyrogyra if it reproduces via isogametes?
I've read in my book(NEET EXPLORER-By Sanjaya Sharma and Sudhakar BanerJee) that Spyrogyra sexually reproduce through conjugation, I have also read many articles which say that it's by isogametes. I thought that in this conjugation hologamete/vegetative cells of opposite strains would merge each other’s cytoplasm and form a diploid zygote from which meiospores would be produced.If isogametes are involved, then why is conjugation necessary? Or does conjugation with isogametes occur?

By far I get the true definition of Isogametes! So, isogametes are of same size, but not merely must be flagellated. They are either motile or non-motile pairs. Then the conjugation here is served for the union of the isogametes. And conjugation may also serve for union of unlike(anisogametes) ones too!

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Why is it often stated that Riccia has both type of rizhoids which are present attached to mid rib on the ventral surface of the thallus?
In liverworts, Phyllids lack midribs.
Then why is it often stated that Riccia has both type of rizhoids which are present attached to mid rib on the ventral surface of the thallus?

Welcome to SE Biology. Please finish reading the [Tour] to find out how this site works, and the help on asking good questions. It is important in a question that queries a common opinion that you quote an example. This both supports your assertion and allows others to inspect the source to see if it provides an explanation or has been taken out of context. I am not a botanist and know nothing whatever about this subject, but I think it would increase the likelihood of an answer from someone in this area.


text:
Which brain structures are most involved in the construction of the motion image in motor imagery?
I have several possible answers. They are motor cortex, somatosensory (sensorimotor) cortex, cerebellum, insular cortex, premotor cortex, cingulate gyrus, occipital cortex and temporal cortex.
Obviously, the motor and premotor cortex are suitable. But then... the cerebellum is involved in motor movements, but I am not sure that it is used in the construction of images, because it is a separate part of the brain, which is responsible for execution, and not for representation
Probably somatosensory cortex is used to represent tastes and tactile sensations
I found an article about the participation of the insular cortex in this process, but perhaps it is not used much - https://pubmed.ncbi.nlm.nih.gov/
The cingulate gyrus is definitely not there, it has other functions
The occipital cortex of the brain is used for the primary processing of visual information. Although he is not involved in the construction of images, perhaps this is the right answer. For example, athletes can imagine how they would run an obstacle course, they see themselves from the outside, they see how they jump, run. The occipital cortex is most likely involved
The auditory cortex is needed to represent sounds, it is part of the temporal cortex
This was the information that I could find in open sources. Perhaps it will be useful

The correct answer is motor cortex, premotor cortex, somatosensory (sensorimotor) cortex and cerebellum


text:
Gas exchange in the alveolus
When our teacher was talking about the gas exchange inside the alveoli, he mentioned the flow of air and the flow of blood was going in opposite directions so that there always would be a concentration difference.
Because of this the gas exchange between the alveolar space and capillary continues and reaches ~99%.
I could not understand how the air would always go in the same direction so I researched the topic. All resources I found state that when the air enters the alveolus there is a pressure gradient for both oxygen and carbon dioxide between the capillary and the alveolar space.
But I found nothing mentioning the opposite direction of flow for air/blood.
So does that mean gas exchange for oxygen and carbon dioxide stops when diffusion equilibrium is reached?
(I'm not a native English speaker so I hope this question makes sense.)

I think that is about fishes, and most aquatic creatures. They exchange gases from their gills. Most advanced animals have blood vessels in their gills that flow on the opposite direction to the water that is flowing through the gills.

Welcome to Biology.SE. Please take the [tour] and consult the [help] starting with [ask] for details on using this site, which promotes self-learning with some expert help. See also the "homework" policy. Please [edit] this down to a single question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. ——— In particular this seems like the sort of question your teacher could best answer ...

oxygen will go into the blood and co2 will go into the alveola never the oposite.

@trondhansen Bingo. I'm sure that's what the tutor meant.

@cc12amu This seems to be the case. I dont think my teacher would get it wrong. Probably my sleep-deprivated brain is recalling the whole thing very differently, thanks for the answer.

is down voting answers the best peole at this part of SE can do,had it not been better to make an answer that correct the mistakes(if any)in the other answers?

The air in the alveoli has a higher oxygen concentration than the blood, and the blood has a higher carbon dioxide concentration than the air. Due to this concentration gradient, the carbon dioxide will diffuse from the blood to the air, and the oxygen will diffuse from the air to the blood. My guess is that this is what your teacher referred to as "opposite flow".
However, you are right in noting that this flow will eventually reach equilibrium, and gas exchange will cease between the air and the blood. This is where the role of the lungs come in. The lungs constantly exchange carbon dioxide rich air for oxygen rich air, and hence the gas exchange continues happening. Cellular respiration also converts the oxygen rich blood to carbon dioxide rich blood.

Difference in the Partial pressures of Oxygen and Carbon Dioxide in the alveoli and blood capilariess respectively cause respiration.

In alveolar blood, PO2 is low while PCO2 is high, whereas in atmosphere its vice versa, so it diffuses out to the atmosphere.

In capillary blood, PO2 is high and PCO2 is low, whereas in the cell its the opposite, so it diffuses into the cell.

Even if the diffusion equillibrium is reached, the negative pressure gradient of the lungs make sure that there is a constant exchange of gases.
You are good at observing that bro. I didnt even this of that when i studied respiration.


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Source for "The human body recycles its body weight of ATP each day"?
I have read in many biology textbooks and scientific journals that "you create your own bodyweight in ATP each day", but they are all just stated as facts.  I have yet to see a study or article that explains how this was determined and what assumptions or observations were used.
For example in the Wikipedia ATP entry "Other processes regenerate ATP so that the human body recycles its own body weight equivalent in ATP each day."  This has a footnote which links to Opening and Closing the Metabolite Gate in PNAS.  Once again it is just stated as a fact "On any given day you turn over your body weight equivalent in ATP" this time with no footnote.
Has anyone come across anything with actual calculations of how this was determined?  Is it based on calories eaten, or oxygen consumed, or extrapolation from a single cell, or something else?

If this doesn't work out as a question here on biology, then our sister-site [skeptics.se] would certainly take it. You should take the [tour] and refer to the [help] on each site before posting (in an ideal world).

As @Domen demonstrates in his answer, it is quite easy arithmetically to come up with this sort of statement. But why are you interested in it? It is just hyperbole used by the self-important to imply their topic is of importance. It may or may not be, but this sort of thing doesn’t make it so.

Hi @david, I agree with you that the weight part of this is stupid. I think it misses the really impressive part which is how many times the body is converting ADP to ATP.  Something like 6x10^25 a day, or 150 million /every cell in the body (excluding RBCs) /second !  I asked my question because the "body weight in ATP" is commonly stated and I hoped someone knew where it came from.  I disagree it is "quite easy" to determine due to uncoupling proteins and mitochondrial membrane permeability that make heat rather than ATP from protons.  And other things I am unaware of, hence my question.

But are big numbers really impressive? How many water molecules are there in a filled tumbler? A lot. And someone will always say "Wow". But one hopes only the first time. Yes, the microscope world is amazing, but the aim of investigating it is rather wider than finding throw-away lines with which to start a lecture.

The following is a back-of-the-envelope calculation to get a reasonable order of magnitude.

An average person has a daily caloric intake of $E \approx 2000 \; \rm kcal$.
Assume all of the caloric intake goes into the production of $\ce{ATP}$.
The free energy cost1 for synthesizing $\ce{ATP}$ from $\ce{ADP}$ in cellular condition is $\Delta G \approx 50 \; \rm kJ/mol \approx 12 \; \rm kcal/mol$.
Molar mass of $\ce{ATP}$ is $M(\ce{ATP}) \approx 500 \; \rm g/mol$.

Therefore, each day our body produces:
$$m(\ce{ATP}) = \frac{E}{\Delta G} \times M(\ce{ATP}) \approx 85\; \rm kg,$$
which is approximately the mass of a human body.

1 http://book.bionumbers.org/how-much-energy-is-released-in-atp-hydrolysis/

Wow............

While this calculation works out, I think it's worth considering that it's kind of bizarre to think this way for any purpose besides trivia. If a 70 kg person takes about 1000 steps over an 8-minute run, you could say that they've moved 1000X their body weight = 70,000 kg in 8 minutes, but has that actually told you anything about how much useful work they've done? Not really, you've come up with an impressive number but it hasn't really meant anything without other context.

@BryanKrause Well, yes and no. You example is meaningless, but the ATP production is, I think, not. It means that indeed there is an enormous churning and recycling of compounds in our body. (I for one would not have thought that it's so much, hence my previous comment.) For example, it becomes clear that the ATP, once it has delivered its energy load, must be readily available to be "recharged" -- we see from the numbers that it cannot be metabolized and excreted, for example.

@Peter-ReinstateMonica Sure, but there's nothing in ATP that comes from the food being 'burned' for energy, it's just part of the "machine". Why count just the ATP, and not all the other molecules that were part of some chemical/electrochemical reaction in the process? What if you summed up the mass of a weak acid/base in solution every time a proton bounces on/off? I do see your point, though, that it may be useful to countering some particular misconceptions of what happens in a cell at a molecular level, which can be quite difficult to intuit.

@BryanKrause Yes, true, it's mostly within the cell, and there it is less meaningful. Although (excuse my layman-ness) I suppose it's the product of some oxidation of glucose or such in the cell?

But note the conjurer’s sleight of hand. The molecular weight is immaterial. If Adenosine had a MW of 1 million, the fact would  remain that all that is happening is one phosphate is being added and taken away. I edited the title to try to show how this sort of statement morphs into nonsense.

@David True, it's not that 80 kg of mass is synthesized from scratch!

Yes, David's slight of hand point is basically the point I was trying to make about the jogger. It doesn't really matter what the weight of the phosphate is, either, you could do the whole thing with just a rearrangement within one molecule, too, without any appreciable change in mass.

@BryanKrause, I agree that such calculations and final results can be a bit misleading if one isn't careful when interpreting them. However, I think that the "usefulness" of this particular one can be revealed if you actually see it from another perspective: "How much ATP do I need to power (by converting ATP to ADP) a human being for one day?" This interpretation then gives you some rough idea on the amount of ("useful") energy that ATP can store (or more precisely, its energy density), which you can compare to the energy density of food (2000 kcal ≈ 85 kg of ATP ≈ 800 g of bread ...).


text:
Different enzymes catalyzing the same reaction but in opposite directions

Nelson, D. L., & Cox, M. M. (2017). Principles of Biochemistry 7e. W. H. Freeman. 13.3: Phosphoryl Group Transfers and ATP: Inorganic Polyphosphate Is a Potential Phosphoryl Group Donor.
(This part has been removed from the eighth edition of the book.)
PPK-1 and PPK-2 are essentially catalyzing the same reaction, however, PPK-1 is used when polyphosphate synthesis is thermodynamically favorable and PPK-2 is used when the reverse reaction(ATP synthesis) is favorable. What is the need for having 2 different enzymes if 1 enzyme is enough to catalyze the forward and reverse reaction?

Welcome to SE Biology. Please indicate the source of the graphic, with date.

Oops, I forgot that! thanks for reminding me. Nelson, D. L., & Cox, M. M. (2017). Principles of Biochemistry 7e. W. H. Freeman. 13.3: Phosphoryl Group Transfers and ATP: Inorganic Polyphosphate Is a Potential Phosphoryl Group Donor.
(This part has been removed from the eighth edition of the book.)

Thanks. I’ll have a look at this. You have written polypeptide synthesis, but I presume you mean polyphosphate.

Thank you. Yes, I meant polyphosphate.

I don't see the mystery. Having 2 enzymes doing opposite things allows for better activity or specificity (each can be much better suited than a "general" catalyst) and regulation, over multiple levels (e.g. localization, transcription, post-translational modification, inhibition, degradation, etc.). Don't you think a single enzyme catalyzing forward and reverse reactions would be rather difficult to regulate, or be very functionally limited? For purposes of ATP production, I think an enzyme strictly producing ATP would have viability over another enzyme simultaneously producing/degrading ATP.

Well, what you said about the different regulations of the two enzymes makes sense. I'm looking for a more specific answer, however. Also, I have a comment on your last sentence. In reversible reactions, all the enzymes catalyze the forward and reverse reactions simultaneously and equally. And in this case, since these two reactions are reverse of each other, any enzyme catalyzing either of these two reactions would catalyze the other too. The existence of an enzyme that strictly produces ATP contradicts what I have in mind about enzyme function. Am I right?

This is a complex area that I was completely unaware of and know nothing about. The first question that I ask is how you reverse a reaction with a ΔG˚ of -20kJ per/mol? Two possibilities occur to me — either a high ratio of polyphosphate to ATP or that there has been some mistake and the two reactions are not the reverse of each other. The few papers I looked at on PPK2 did not address the thermodynamics. Without further information I cannot be of any help.

The textbook is either incorrect or very poorly worded. You are correct that all enzymes catalyze both both the forward and reverse reactions. The enzyme could only lower the activation energy of this given reaction, affecting both the forward and reverse reaction rates. To drive them in the forward direction, enzymes must couple endergonic reactions (i.e. $\Delta G > 0$) with exergonic reactions (i.e. $\Delta G < 0$).

Please add sources to support your answer


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How are correlations between genes and observed traits made?
If a given organism has a certain characteristic (a chemical that's produced, a place an organ or organelle is in, a particular behavior), what's the general procedure for correlating that characteristic to a particular gene?
As I understand it, there are two main ways of doing, the first being to take a sample from two populations that do and do not have the characteristic respectively, then find the genetic correlation between the two populations. The second way I've heard of is by inserting or removing a particular gene and then observing the organism after it has grown, either inserting some marker gene (fluorescence is a popular one) or removing a gene believed to be responsible for the characteristic (something like leaf or petal pigmentation).
Are these the only effective ways of forming these correlations? What sorts of correlations could be made in silico? If two different species create the same chemical, and you know the gene responsible for that chemical's creation in the first species, would you be able to somehow infer which gene is responsible in the second species? What happens if you don't have a population without the given characteristic you want to correlate?

Have a search for the terms gene and homology; that'll get you started on most of an answer.

Ah thanks! I figure the subject is a pretty common question, but I couldn't get the right keywords for what I was looking for.

I have edited your title, despite voting to close the question, because what you are asking is the correlation is between a gene and a trait, not genetics and trait. Genetics is the overall study of this topic, and the methods of making such correlations have varied historically with the development of scientific methodology and knowledge, and differs between organisms. Your question is therefore impossibly broad for this site, and what you need to do is read a book on — yes — genetics.

Ok do you have a recommendation?

I recommend looking into genome-wide association studies, genetic mapping, etc.


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History of ideas about the form of the genetic code
In preparing a lecture on mRNA translation and the genetic code, I remembered a talk given at a symposium where they mentioned the origin of the code and how, before the code was established, various other mathematical possibilities were proposed that turned out to be incorrect.
Does anyone know about these alternative proposals?

The Nobel Prize speech of Marshall Nirenberg maybe interesting: https://www.nobelprize.org/nobel_prizes/medicine/laureates/1968/nirenberg-lecture.pdf

Before it was established that there was a triplet, non-overlapping, comma-less genetic code* for what at that time were thought to be only 20† amino acids, there was uncetainty about:

The codon size (must be more than 2, but...)
Whether the codons overlapped (e.g. in a stretch ABCDEFG with triplet codons, whether ABC, BCD, CDE etc were the codons)
Whether there were ‘commas’ as demarcation betwen different codons

These and other problems were disscussed by Crick et al. in Nature (1961) 192 1227–1232. There is an introductory gloss of this on Scitable, with a link to free-view of the original paper.
Footnotes
*We now know there are variants on the standard genetic code, but all the codes have the characteristics mentioned.
†In addition to the standard 20 amino acids stop codons can be subverted in certain circumstances to encode selenocysteine and, in some bacteria, pyrrolysine.


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Immunotherapy for tumours which do not have TSA
Is immunotherapy possible for tumours which do not have Tumour Specific Antigens (TSA)? If so, doesn't targeting those tumour cells also target other healthy cells, thus causing autoimmunity ?

chemotherapy kills a lot of cells, but tumorigenic cells die first. Same can be true with immunotherapy

During chemotherapy , it is true because tumour cells have weaker dna repair system compared to healthy cells.  But when it comes to immunotherapy, cancer cells are good at immune evasion.

Yes, in some circumstances.
In some cases the antigen being targeted, even if it leads to loss of normal cells, can be targeted. This is most evident in the targeting of CD19 to treat various forms of B-cell derived tumours. Example of such an application and response biomarkers are described here
https://www.ncbi.nlm.nih.gov/pubmed/28291388
Secondly, opportunities may be created by the generation of epigenetic states. Cancer-germline antigens are usually only expressed in gonad tissues (which enjoy immune privilege) but are often aberrantly reactivated in tumours, but not in other somatic tissues. This too can create specificity to immunotherapy even if the antigen is not truly tumour-specific, and is rather striking as a phenomenon in testicular cancer.
https://www.ncbi.nlm.nih.gov/pubmed/28555838

Monoclonal antibodies can have a range of uses: Avastin (Bevacizumab) directly targets VEGF to inhibit angiogenesis (with obvious side effects). Some mAbs are chemolabeled with a cytotoxic drug that can be delivered to tumor based on normal antigens, but the obvious downside is healthy tissue expression.
There's a fair overview of immunotherapies available here.


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How does the immune system recognize pathogens?
There are useful and pathogenic bacteria in our body. How does the immune system differentiate between them?

Pathogens will often have non-peptide antigens, peptide antigens, and pathogen-associated molecular patterns that are recognized by innate and adaptive immunity mechanisms. Useful bacteria are not differentiated, and often sit beyond the grasp of our immune system, or have mechanisms to escape an immune response. When contacted they do, however, produce an immune response and due to their location, this often involves mucosal immunity:

This portion of the immune system varies greatly in response to the systemic immune response because it is constantly stimulated, and in a way trained, by the presence of all microbes, such as gut flora. As a result, it often resolves infection quickly with low severity, and little lasting tissue damage. Keep in mind that self cells have mechanisms which desensitize them to autoreactivity with immunity. Microbes don't share these same mechanisms, but can evade or escape the immune response through their own methods. But by no means are microbes of any sort, for the average immune system, disregarded.
Unfortunately, to respond more specifically would go into textbook chapters of material so to that end I'm going to cut the explanation here, and recommend you do some research of your own.


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Why is a DMSO-only Control Important?
Why is it necessary to have a DMSO alone control when DMSO has been used as the solvent (vehicle) in the treated conditions?
And, in this case, why is the viability of the untreated condition lower than the vehicle (DMSO alone)?

It could simply be that the reagents or drugs involved dissolve well in DMSO and poorly in other solvents. Vehicles are a way of saying this is the drug/reagent + solvent. As always, when DMSO is the solvent, include DMSO-alone controls so you know the effect you're seeing isn't a result of the DMSO.

@CMyosychuk So we use it in order to know whether the drug or reagent itself that has effect on cell viability, right? And based on the above graph, why do the graph of Vehicle is higher than None?

@Sokviseth Its not possible to give a clear 'why' answer to that question. The most probably reason is just biological variance, from your two different samples. Also note that the SD (which doesnt make a lot of sense for 2 samples anyway) for the vehicle control is very large.

As @Nicolai said, this is most likely simply variance, with more independent samples, the difference will probably be smaller. Additionally, given these error bars, I would see the untreated and the DMSO samples as the same. The treated samples are pretty much different from them.

@Sokviseth What's your measure here (the axis values)? If it's indeed a measure of viability, basically you're saying your drugs are dissolved in DMSO, and you want to see the effect of the drugs vs. no drugs. But, the DMSO can affect viability, too, so you have to do a DMSO alone condition. Your goal, however, is you actually want to say that the DMSO had no effect so you can see the pure effect of your drugs. The p-value between your none and vehicle is like 0.5, which means they aren't different, which is good because your drug readouts will have no/little background.

In my opinion, you want to get a third replicate though to give yourself the best statistical power, and make those error bars a little tighter.

I edited the question so it may be reopened

@CMosychuk Why do you think this question should be reopened? This is a pretty simple homework-style question.

@CMosychuk Thanks for your explanation :-)  I learned a lot from you!

@BryanKrause Every question should be welcomed. It is might be simple for you, but it is not for someone else. I just need to get some ideas from this forum. :-) Science is about discussion.

@Sokviseth The reason for the prohibition on homework questions is that homework is designed to direct your learning, and asking on SE bypasses the normal ways to obtain that information. A lot of what you are supposed to be learning about is actually how to obtain the information, not just obtaining the information itself.

@BryanKrause The way I worded it in my edits probably made it more homework than it is. To the layman, seeing a DMSO control in a scientific figure might not immediately make sense. I know that it's for when DMSO is involved in the treatments, but I don't think it jumps out at people who aren't used to drug preparations. This is a good question for basic experimental design: looking for, and controlling for confounding variables.


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What are senescent cells doing in our bodies?
I'm reading a paper that mentioned the elimination of senescent cells delays aging. I'd like to receive more information about it.
The Baker study published in Nature demonstrates that targeted elimination of senescent cells in mice results in remarkable protection from several age-related pathologies, cancer, and makes cancer cells resistant to chemotherapy. I know that senescent cells drive aging, and induce cancer. Can we grow them in cell culture as a kind of stem cells ? How might they contribute to the aging process ?

Welcome to Biology. Could you provide a source for this claim? Also, have you done any research on this topic, such as performing a simple Google search for "senescent cells", reading the Wikipedia page, or clicking on the [senescence] tag in your question and reading some of the linked questions? If not, please do so, then [edit] your question to include what you know so far, and what specifically you still have questions about. Otherwise, this post may be closed as "homework."

@MattDMo Did you actually review this one? I'm asking because it isn't in queue, and I thought it would be.

@L.B. nope, I just saw it appear on the main page

Hi,my question is the senescent cells is kind of aging cells? What are the similarities and differences between them?

Voted to re-open. Although there are some misconceptions here this question is well within the realms of an overview answer of our current knowledge, in my opinion.

Edited the question, prepared a comprehensive answer.

@MattDMo I know that was a strange question on my part... I was just confused! Thanks!

Sorry for not being more specific. I would like to further clarify my question by stating that cells reach senescent state after prolonged cell stress caused by DNA damage.The study published in Aging Cell indicates that senescent cells are seen with increased frequency in premature aging skin and are thought to cause age-related dermal thinning thus, accelerate aging of the skin. I'd like to know are both terms (cell aging and cell senescence) the same? Is a senescent cell an aged cell? If a young cell undergo a stress or damage can be induce senescence? Thank you .

@Microbiologist please include a direct link to the paper you are asking about (PubMed, DOI, etc.) so that we can answer your specific questions. "The Baker study published in Nature" is not very helpful...

Senescent cells are cells that go into permanent cell cycle arrest. Although they may be metabolically active, they are not actively dividing. This may occur when cells in our bodies undergo damage from an extraneous or endogenous source. I understand that its role in cancer and aging is a great topic of study.

this is a rather incomplete answer, and could easily skew a newcomer's viewpoint. Many, if not most of the cells in the body are senescent, and will never divide again. However, they is programmed to do this, it is not as a result of damage.


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How does the placement of it's motor domain affect the directionality of a motor protein?
I'm going over some of my notes, and I have written down that motor proteins with + cytoskeletal directionality have a reversed schematic representation relative to - directed motor proteins. Then I have this sort of image drawn. I just want to clarify it, since I don't remember this part of lecture at all.

Schematic representations

Kinesin: N terminal - |Head||Coils||Tail| - C terminal
Dynein: N terminal - |Tail||Coils||Head|| - C terminal

Does this look right?

I don't understand your question. Both schematics are the same, just written in reverse. The 5' end of an mRNA always codes for the N-terminal end of a protein. Perhaps your asking which protein domain (head or tail) occurs at the N-terminal end in each type of motor?

Sorry! It's been a long day. I fixed it to what it should've been. Now their motor domains are at the opposite termini.

"The direction in which cargo is transported is dependent in part upon the position of the motor domain, which can be located N-terminally (N-kinesins), C-terminally (C-kinesins) or internally (M-kinesins).  In general, kinesins with N-terminal motor domains move their cargo towards the plus ends of microtubules located at the cell periphery, while kinesins with C-terminal motor domains move cargo towards the minus ends of microtubules located at the nucleus." Source

@drowsy Feel free to roll back my edits if my understanding is inaccurate.

No. DNA, and RNA have a polarity in the orientation of their sugar-phosphate backbones, based on the numbering of the carbon atoms in the sugar rings. So, for example, we say that the sequence of this RNA is being read from the 5' to the 3' end, which indicates that the first nucleotide is exposing the hydroxyl at the 5’ carbon on its sugar ring.  At the other end of the linear polynucleotide the sugar is exposing the hydroxyl on its 3’ carbon of the sugar ring.
All mRNAs are translated in the 5’ to 3’ direction and all proteins are synthesized from the amino terminus to the carboxylate terminus, because the peptide bonds in the protein also have a directional polarity.
You appear to have mislabeled the N and C termini of Dynein in your diagram. Perhaps the  lecture was about the domain structure of these two motor proteins? And the point might have been that they each have three equivalent domains but in one case the part we call the head is synthesized first and in the other case the tail is synthesized first(?).

I did. Thanks for catching that. But thanks for your response. It makes sense. Basically one is translated motor first and one is translated tail first, right?

I don't know if that is true, because it has been a long time since I thought about motor proteins, but yes, that is what your diagram shows must be the case. I would go so far as to say that these two very large ATP-ases that Carry cargo along microtubules share related structural domains but since the proteins are modular you can mix and match the modules in different combinations

So, as I pointed out in comments, and requoting:
"The direction in which cargo is transported is dependent in part upon the position of the motor domain, which can be located N-terminally (N-kinesins), C-terminally (C-kinesins) or internally (M-kinesins). In general, kinesins with N-terminal motor domains move their cargo towards the plus ends of microtubules located at the cell periphery, while kinesins with C-terminal motor domains move cargo towards the minus ends of microtubules located at the nucleus."
And that was a short excerpt from Jennifer McDowall on Interpro. And then just surveying kinesins from the mouse genome,

Source: Kinesin superfamily motor proteins and intracellular transport
In terms of dyneins, however, I believe they're all (-)-directed motor proteins with the following general structure,

Source: The 2.8 Å crystal structure of the dynein motor domain
Keep in mind these representations are always expressed N-terminal (left) to C-terminal (right). So while your model for dyneins is correct, for kinesins this depends on the location of the motor domain.

authors: علیرضا سجادی


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DNA content doubling in interphase
Why does the DNA content of a cell get doubled in interphase? Why doesn't it become tripled or quadrupled? What's stopping it from doing so?

So in mitosis, the cell has to split itself into two cells; each daughter cell has a functional genome that may again split into more daughter cells. The cell replicates the DNA before dividing, so the error in replicating 3x or 4x is that upon division, the daughter cells will have more DNA than the initial cell, and every generation will have more DNA than the last. One replication ensures both daughter cells receive one functional genome. We can see the result of extra DNA in cases like Down Syndrome (trisomy of chromosome 21).
The cell controls this process by controlling the cyclins present in the cell temporally, namely cyclin-A and cyclin-E when we talk about DNA replication in S-phase,

From wikipedia,

Cyclin A resides in the nucleus during S phase where it is involved in the initiation and completion of DNA replication. As the cell passes from G1 into S phase, cyclin A associates with CDK2, replacing cyclin E. Cyclin E is responsible for initiating the assembly of the pre-replication complex. This complex makes chromatin capable of replication. When the amount of cyclin A/CDK2 complex reaches a threshold level, it terminates the assembly of the pre-replication complex made by cyclin E/CDK2. As the amount of Cyclin A/CDK2 complex increases, the complex initiates DNA replication.
Cyclin A has a second function in S phase, in addition to initiating DNA synthesis, Cyclin A ensures that DNA is replicated once per cell cycle by preventing the assembly of additional replication complexes. This is thought to occur through the phosphorylation of particular DNA replication machinery components, such as CDC6, by the cyclin A/CDK2 complex. Since the action of cyclin A/CDK2 inhibits that of cyclin E/CDK2, the sequential activation of cyclin E followed by the activation of cyclin A is important and tightly regulated in S phase.

Source: Cyclin A


text:
Examples of genes involved in plastic responses
Adaptive plasticity involves sensing the environment and responding adaptively to it. Intuitively, I would think that this process may ask for a more or less complex genetic machinery of regulation of gene expression.
Can you give me examples of genes and genetic pathways that are famous for their role in adaptive plastic response?

You might want to check out the work of people like Amanda Bretman and Tracey Chapman, they've done some stuff with plasticity and gene expression if I remember correctly

Instead of genes you can ask about pathways.

Yes, indeed, that what I meant by "genetic processes" as you noticed in your question. I edited my post. And I think I'll checked your your answer!

I assume that you mean gene expression regulation when you say genetic processes. The best example for your question would be that of synaptic plasticity in neurons.
The immediate responses are obviously that of protein modifications (cell signaling). These are fast responses that have immediate effects but are also quite short-lived. During the long term potentiation (LTP) some stable changes happen via gene regulatory mechanisms.
It is to be noted that in a polarized cell such as neuron the distance between the nucleus and the point of action i.e. the synapses (at dendritic spines), is huge. Any event leading to transcription regulation would take a long time to act. Therefore there are post-transcriptional regulatory mechanisms in place. The mRNAs are localized at the spines and are kept in a repressed state; poised for translation when the signal is received. Finally, if the signal is sufficient enough, transcriptional regulation (sometimes stable due to epigenetic changes) takes place.
You can look for the genes involved in this pathway which also include ncRNAs (lncRNA and miRNAs).
Other examples:

Acute stress response (such as Unfolded Protein Response [UPR])
Acute inflammation
Chemotaxis

Here is a paper I just read about translational regulation in LTP, if the OP is interested: http://www.cell.com/molecular-cell/abstract/S1097-2765(12)00400-5


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How many Endogenous Retroviruses do we share with other primates?
Is there a list of Endogenous Retroviruses that we share with other primates? I would like to map all (or most) of them into a hierarchy and see how it fits in our evolutionary branch.

Please do not use abbreviations in a title that may be unknown to many, and in your question only if you repeat it. This is a barrier to comprehension and indexing. I have made the changes for you.

There are several papers that cover this. Briefly, humans share the vast majority of their ERVs with other primates, but not all; and this is mainly because other primates have acquired ERVs that humans have not (rather than humans acquiring new ERVs themselves).  The third link, in particular, seems to cover your proposed reconstruction and concluded that in general "these sequences gave trees that were consistent with the well established phylogeny of the old world primates".

Divergent Patterns of Recent Retroviral Integrations in the Human and Chimpanzee Genomes: Probable Transmissions between Other Primates and Chimpanzees
The decline of human endogenous retroviruses: extinction and survival
Constructing primate phylogenies from ancient retrovirus sequences


text:
Getting Started with ELISAs
I'm interested in designing an ELISA to detect the presence of Aflatoxin B1, but I'm having a hard time finding information about designing an enzyme and some sort of guidance on how ELISA protocols are designed, and generally where I can get more information. I'm in Grade 9 and am extremely unexperienced to a lot of the terms I'm coming across, but I'm very interested and would be grateful if anyone has a book or a website I can visit to get started or give me some sort of direction.
Thanks,
Joshua


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Which are the most genetically different mammals to humans?
According to this Human and Chimp DNA is 98.8% identical

In terms of actual genes, though, we’re 98.8 percent alike, meaning
only 1.2 percent of our genetic material is not found in chimpanzees.

and according to this,
unequal-nature-geneticists-perspective-human-differences

we share roughly 90 percent of our DNA with mice, dogs, cattle, and
elephants

Even though, this article states
Researchers map genome for cats, dolphins, birds, and dozens of other animals

Mammals, a subset of vertebrates that includes primates, dogs, cats,
mice, and humans, share 50% to 99% of the same DNA and nearly all the
genes from a common ancestor that lived roughly 200 million years ago.

So there are mammals which share much less genes with us than mice, dogs, cattle, and elephants. Which are those mammals who are the most genetically different to humans?

I have replaced your incorrect reference to the genetic code, which you will realize after consulting the Wikipedia page on the topic is identical for all mammals.

google mammal phylogeny

The monotremes (platypus and echidna) are the most genetically distinct mammals from humans. They are also the most genetically distinct mammals from all other non-monotreme mammals. The monotremes are found in the image below on the black line with Ornithorhynchus.
After the monotremes, the marsupials (pink lines) are the next most genetically distinct group from humans (and other placental mammals). Generally, the deeper the divergence between two species in the tree below, the lower the genome similarity between those species (though this might differ a little depending on the exact measure used, see below).

One needs to use caution when comparing statistics about the percent similarity between genomes, as this can be measured in many different ways and is often ambiguous. For example, one statistic might refer to the percent of genes that are shared between species, while another might refer to how similar the sequence is between shared genes.

Species
Gene 1
Gene 2
Gene 3
Gene 4

Blue
ATCG
CCGA
ATTC

Red
ATCC
CAGA

GAGC

In the table above, the blue species shares 66% of its genes with the red species, with those genes being 75% similar in sequence.
Genomes also contain a lot of DNA that is not part of a gene, and similar stretches of DNA can be arranged differently along a chromosome or on different chromosomes. This all means that it's difficult to boil down genome similarity to a single number unless the author is very precise about how they are using the term.
(For what it's worth, 82% of the genes in platypus had readily identified analogs [the technical term is ortholog] in other mammals [opossum, mouse, dog, human] or birds [chicken].)

The image is a work by the OrthoMaM team at the Institute of Evolutionary Sciences of Montpellier (ISEM) and at the University of Montpellier. Original paper: "OrthoMaM: A database of orthologous genomic markers for placental mammal phylogenetics." Ranwez V., Delsuc F., Ranwez S., Belkhir K., Tilak M. & Douzery E. J. P. BMC Evolutionary Biology, 2007, 7:241. CC BY-SA 4.0

This is a really good and challenging question because it involves rare areas of taxonomic controversy.
From the list you present elephants are easily more genetically diverse than an other species in your list. There's nothing controversial about this.
The answer to your question has two different answers regarding the evolution of mammals:

The most ancestral mammalian group are the Xanarthra, according to morphology (older tree "a" in the diagram), so edentates such as armadillos, this also includes anteaters and sloths. Those are the most diverse mammals to humans using the diversity of their phenotypes and traits. Armadillos are very cool BTW.

The most ancestral mammalian group are the Afrotheri , according to phylogenetics (emerging tree "b" in the diagram), so elephants, aardvarks and various shrews.

As this is a question on genetic diversity, rather than the evolution of mammals, then it is without question the Afrotheri, thus the elephants and aardvarks. That is rather surprising (to me), but thats the answer.
HOWEVER the Afrotheri are a big diverse group and I would be really surprised if all their genomes have been sequenced, thus which member of the Afrotheri is more diverse? I very much doubt that can be answered down to the level of a species.
It's one of the few discordant observations between cladists and phylogenetics, usually they are highly congruent approaches: hence it's a good question.
The most basal relative to the mammals are the Monotremata - platypus, i.e. far more genetically diverse, but they are not mammals.

The tree is from the American Museum of Natural History, originally from MS Springer et al. (2004), "Molecules consolidate the placental mammal tree", Trends in Ecology and Evolution 19: 430-438.
I do like controversy, but not in this specific fields of methodology.

@bryanKrause wrote:

Since when is a platypus not a mammal? Also, I do not think you are using the phrase "genetically diverse" with an ordinary meaning.

I am an internationally recognised phylogeneticist - take a look other sites on SE for evidence. Some of the tenants of specific higher and lower eukaryote evolution came from my early work.
Let me answer this is in very simple words:
A PHYLOGENETIC TREE = GENETIC DIVERSITY  .. and that is a very ordinary meaning in biology today (30 years ago maybe it wasn't).
As things evolve the genetic diversity between then increases (except for mammals) and that information is represented in a tree. What is hard to understand about this?
I do question where this criticism of molecular evolutionary theory and its relationship to genetic diversity coming from? Evolution per se has come on significant criticism and molecular evolution was no exception. The majority of those criticisms were not based on empirical science but other principles.
Let me go through the basics:
Criticism 1
Platypus, in a field where the relationship between genetic diversity and evolution is contested - which for placental mammals its nice to have a clear definitive outgroup that is not controversial. It is helpful for technical reasons. If you look at tree a and tree b they are both rooted at the platypus. Why? I clearly stated in the answer that a platypus was not a mammal.
The platypus roots the tree unequivocally and therefore positions the next stage of the controversy, which is the disparity between genetic distance and evolution of the placental mammals. Usually the most evolutionary distant ancestor is the most genetically diverse and that relationship holds across the tree of life. In mammals that is not the case, a basal evolutionary lineage isn't the same as a basal lineage based on genetic diversity.
Criticism 2
GENETIC DIVERSITY I am embarrassed by the second part of the criticism. That is to misunderstand the fundamental tenant of phylogenetics and its relationship to genetic diversity. It is not unordinary but very ordinary.
Phylogenetics is the representation of genetic diversity AS A TREE.
Genetic diversity is quantitated as genetic distance and the relationship between those genetic distances is represented as a tree.  The more basal the branch the more genetically distant the relationship. Thus the most basal (ancestral) branch in the placental mammals is Afrotheri and one of the most recent were humans, i.e. we're at opposite ends of the tree.

THUS if I draw a 1x2 matrix between humans and the other 6400 mammalian species the Afrotheri will collectively show greater genetic diversity than EVERY other species of mammal. Do you see that?
THUS if you do PAIRWISE comparison of genetic diversity for all placental mammals (around 6400 species) and root it at the platypus  distance you will recover tree b. Do you see that?

Thus every member of the Afrotheri is more genetically diverse against humans than any other species of placental mammal alive today AND THAT IS WHAT TREE B represents. I do repeat that this is old science.

I've worked with marsupials and even at publication level "mammals" are shorthand for "placental mammals", i.e. distinguishing them from marsupials, and everyone understands that. Technically marsupials are mammals but a different order, in the same way Monotremata are the order for platypus. "Mammals" is shorthand for the Order of placental mammals, their Linnaean taxonomy is rarely used.

More comments: there is a technical gulf here about how concepts are worded and how they are interpreted, leave it at that.

I started to wonder this because, doesnt seem odd that there are non mammals  (like white sharks) which share more DNA with humans (65%) than other mammals (50%)?

@Pablo I'd suggest this is not a like for like comparison in this specific case, however ichthyology (fish) is outside my expertise. For example, one might DNA diversity the other might be protein diversity, or nuclear genome and the other mitochondrial genome.

Since when is a platypus not a mammal? Also, I do not think you are using the phrase "genetically diverse" with an ordinary meaning.

@Pablo This confusion comes up a lot. There is no single type of "percent shared" that makes sense for this sort of measurement, and it gets less and less sensible the less related the species are. If you're comparing numbers you better make sure they're the same sort of number.

@BryanKrause is categorization of living organisms changing based on DNA? I understand traditionally  taxonomists categorized living organisms based on morphology and physical traits, and that is still being used today

@BryanKrause I have responded to your question in detail

Perhaps there is some debate in your community I am not aware of, but my understanding is that a platypus is in fact a mammal, albeit a quite unusual one compared to species most familiar to humans. By what criteria are you determining that it is not?

The platypus are not placentals (they lay eggs) and all the examples in the question were placentals. Had the OP said "kangaroos" that would be different - they didn't.

The question said "mammals"; your answer says "mammals".

Did you really expect the OP to say the most genetically diverse Eutheria and do you refer to yourself as a member of the Eutheria? No! The examples were all Eutheria and commonly referred to as mammals.

No, but they said mammals as did you and neither you nor they specified "placental mammals" until now. Mammals are mammals. Placental mammals are placental mammals. OP did not ask "of mice, dogs, cattle, and elephants, which are most genetically different from humans?" - they acknowledged that there are mammals more different than the ones in their list and asked which those would be.

As far as genetic diversity, I cannot find a source that is consistent with your usage where you say things like "elephants are easily more genetically diverse than an other species in your list." This statement would seem to indicate more genetic variability among elephants, rather than distance between elephants and some other species. Genetic diversity is a population measure, describing either variation within a species or describing a population of species as in ecology. Genetic diversity is a measure of dispersion, not of distance.

For another example: This usage makes sense to me: "HOWEVER the Afrotheri are a big diverse group" - you are describing variation within a group, saying there is a high dispersion there. But: "which member of the Afrotheri is more diverse?" does not really make sense. You could maybe describe Afrotheri as more diverse than some other group; it would certainly be more diverse than any subgroup it contains, but an individual species cannot be diverse or more diverse unless you're describing variation within that species, which is not the meaning used in context.

@Pablo The gold standard these days for categorization is based on DNA, yes, but not necessarily by "similarity". Rather, since we understand generally how changes to the DNA occur (whether at a single base or larger level), it's possible to make inferences about shared ancestry based on changes that are shared or not shared by different relatives. You can't really do it with just two species, you need to take a more wholistic view. As M__ mentions, often this involves use of an outgroup to infer the ancestral state.

@BryanKrause thanks for the discussion but there is a significant technical gulf between us on taxonomy and population science, and leave it at that: the technical way concepts are worded is part the issue.

Can you give an example of the use of "genetic diversity" to mean "genetic distance" in taxonomy?

Look this is the last post, you are simply in error. "Genetic diversity" isn't the singular domain of population genetics and population genetics is first and foremost about allele frequency usually within a species complex. What you appear to be arguing is allele frequency is a singular function of genetic diversity and it isn't. This discussion is the genetics between species complexes. E.g. Nei's genetic diversity is a formal quantity based on allele frequency, but genetic diversity has a bigger context.

No, that is not my argument. My argument is that if you mean to say that two species are more genetically different, you should say they are different or distant, not "diverse". If you want to say that a group of species have lots of distance among them, you could describe them as "genetically diverse" just like you would individuals of a population. It does not make sense to write "elephants are easily more genetically diverse" in the context you have. You might say it if you meant to say a species of elephant has a lot of diversity or there is a lot of diversity between elephant species.

In phylogenetics, genetic distance is the quantitation of genetic diversity by modelling point mutations.

Do you mean the quantitation of genetic divergence?

The term "genetic divergence" (whatever that means) was not used at any point. This is increasingly looking like I am been trolled by a mod I have to politely ask you to desist.

I didn't say it was used, I am saying it is the correct phrase to use, instead of the one you are using, unless you're able to point me to some source to indicate that it is actually used in the field you claim to be from in the way you claim it is used. I understand that it feels like I'm being unnecessarily pedantic about this, but I think you are using terminology in quite an unusual way which is confusing for people trying to learn biology.

This is increasingly a troll, I don't teach undergraduate - but I wouldn't expect this kind of behaviour at that level. I am politely asking you to desist.

I guess I'll settle for Wikipedia references, I thought doing so might be seen as condescending, but if you're not familiar with the terms maybe it would help: https://en.wikipedia.org/wiki/Genetic_divergence https://en.wikipedia.org/wiki/Genetic_diversity

Here's the Frontiers definition - kids version https://kids.frontiersin.org/articles/10.3389/frym.2021.656168 . I didn't want to be condescending either. Frontiers has an impact factor

That source is using the diversity among a group of species definition, which I have referred to in each of my comments. It is not the way you are using the term incorrectly, which is to instead describe the distance/divergence between two species. You are using the wrong word.

We've been through this already - using allele frequency as the sole definition of genetic diversity and thats what you are saying ... and thats wrong

You've said that before, but I am not using allele frequency as the sole definition of genetic diversity.

Yes you are because the Wiki source is based on allele frequency calculations, as soon as you attempt to wrap numbers on the diversity - it's all allele frequencies. So whether it's a haplotype map, F-stasticics, HW, Nei's etc .... it's the frequency of allele they measure. Phylogenetics isn't based on allele frequency

I've several times acknowledged that genetic diversity is also used in e.g. ecology to describe dispersion in populations of species, not only for allele frequencies within species. What I have said several times is that it is not appropriate to say "elephants are easily more genetically diverse than an other species" when what you mean is "elephants are more genetically different/diverged/distance from humans". I have never said phylogenetics is based on allele frequency but thank you for the attempt to educate.

I've got to agree with @Bryan-Krause. It is simply incorrect to say, "elephants are easily more genetically diverse than an other species in your list," and intend to communicate that the genomes of elephants differ the most from humans compared to the other species. What that phrase does communicate is that, if one were to measure genetic diversity within elephants, and within humans, and within mice, etc., then the diversity measured within elephants is the highest.

Yes, one can talk about genetic diversity across species, and use a phylogeny to express that. That would be relevant for a sentence like, "Wow, there's a lot of diversity within this clade" (where the clade could be the whole phylogeny). But it's the wrong vocabulary to point to two taxa split deep in the tree and say that "these two are the most genetically diverse." As noted, one could say they are the most genetically divergent, or different, or distinct.

Yeah I accept that that specific phrase needs tightening (minor point), because it would get confused for infra-species diversity which wasn't its intention. The days when terminology from the English language was restricted to equations by Masatoshi Nei (who just died), are over.


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X-inactivation in ovaries
Background
In all eutherian (mammals excluding the marsupials), the female (who is $XX$ for the pair of sexual chromosomes) inactivates one of her $X$. This is called dosage compensation. This inactivation occurs at a given time during the development when randomly one $X$ is silenced. The daughters of this cell inherit the $X$-inactivation pattern epigenetically, which results in some part of a tissue having the maternal $X$ inactivated while others having the paternal $X$ inactivated (daughters of some other cell which silenced the paternal $X$). This process yield to the famous turtoiseshell coat in female cats.
Question
In short
Assuming X-inactivation occurred in the lineage of the oogonia/oocytes, when does the X-inactivation and X-reactivation occur in the lineage of the oocytes?
A bit developed
Are the X inactivated as well in primary oocytes? If not, is the $X$ inactivated in the secondary oocytes in a primary follicle? If not, did the diploid mother cells of the secondary oocytes have one $X$-inactivated? If yes, did all diploid mother cells of oocytes have the same $X$ inactivated (inactivation occurred relatively early in the development or is there an imprinting) or did the mother cells of oocytes differ in the $X$ they have inactivated (inactivation occurred relatively late in the development)

I'll post an elaborate answer in some time. Little occupied now

See these two papers:

Early Loss of Xist RNA Expression and Inactive X Chromosome Associated Chromatin Modification in Developing Primordial Germ Cells
X Chromosome Reactivation Initiates in Nascent Primordial Germ Cells in Mice

Basically it happens just before the meiosis.


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Where does the proton come in the reduction of NAD?
In our curriculum biology textbook the reduction of NAD+ is depicted as follows:
NAD+ + 2 H+ → NADH + H+
If this proton in the products was not present in the reactants, then where does it come from? Alternatively, if it does not take part in the reaction, then why is it depicted?

Can you reference the book? It's a bit weird, usually, NAD reduction is written simply like NAD+ + H+  >>  NADH, you don't need the extra proton. Having some more info from the book paragraph you have found this reaction may help.

In a very simple way the equation describes the reaction. NAD is reduced using 2 hydrogen atoms. The two hydrogen atoms can come from one reactant (lactic acid fermentation) or from two (in a reaction of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate; as shown in the figure below).

First of all, I will pick a particular example from glycolysis, catalyzed by glyceraldehyde-3-phosphate dehydrogenase.

Phosphate by its own has one hydrogen at cytosolic pH (because of the pKA). Thus in this reaction, there are two hydrogen atoms. One hydrogen atom is in the form of a hydride (a proton and two electrons) from the aldehyde group. This hydrogen atom is used to reduce NAD+ to NADH. A second hydrogen atom (in the form of a proton) comes from the phosphate. In the bisphosphoglycerate form, the proton dissociates from the phosphate group and is in solution.
The eventual fate of the electrons that were used to reduce NAD+ to NADH is the electron transport chain (in the mitochondria). In some cases, though, for example muscle cells in an anaerobic environment, or other species that don't have an electron transport chain, the electrons are used in fermentation of pyruvate to alcohol or lactic acid. When NADH donates its electrons in either case, it is then oxidized back to NAD+.

References:

Glycolysis
NAD
Lactic acid
fermentation
HPO4

Hi LDiago. I've edited your post to make it a little more readable, and added a little more explanation in a few parts. I hope you find it helpful! Please feel free to rollback if I've inadvertently changed the meaning, or you disagree with me on style.

A quick search on Wikipedia showed the same reaction you book is presenting.

In metabolism, the compound accepts or donates electrons in redox
reactions.[2] Such reactions (summarized in the formula below) involve
the removal of two hydrogen atoms from the reactant (R), in the form
of a hydride ion (H−), and a proton (H+). The proton is released into
solution, while the reductant RH2 is oxidized and NAD+ reduced to NADH
by transfer of the hydride to the nicotinamide ring.
RH2 + NAD+ → NADH + H+ + R

This should answer your question.


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Could Wobble Base Pairing ultimately yield an amino acid that was originally uncalled for or not expected?
How does the cell choose which amino acid to attach to tRNA when there is wobble base pairing involved (not the other way around)? Consider the example below.
For the purpose of this question I'm picking UGC, UGA and UGG codons (Cys, Stop and Trp aa's) so that the 3rd position of the codon really makes a difference (if it does).
I know there are other pairings out there but to keep it really simple for myself I derived the following tRNA anticodons to match the codons using these rules:
G pairs with C or U,
C pairs with G,
U pairs with A or G,
A pairs with U,
I pairs with A, U or C.
UGC: ACG or ACI anticodons
UGA: ACU or ACI anticodons
UGG: ACU or ACC anticodons
My question is (assuming I did my work correctly) if there are multiple possibilities for anticodons to match with each codon how would we know which amino acid will attach to which anticodon? Take for example the ACU anticodon that could potentially match with UGA or UGG codons which codes for STOP or Trp. Wouldn't there be a discrepancy/confusion on which to code for by the cell? Ultimately wouldn't this affect the peptide/protein synthesized?
NB I have edited the original question to clarify my problem, which I do not think is answered elsewhere.

Possible duplicate of Redundancy of the genetic code

Welcome to SE Biology. As you will see, your question has been answered before (by me, among others). You may also be interested in the situation in mitochondria where the wobble rules are different because of the different tRNA structures. See may answer here.

It may be irksome to post a detailed question and be told that it is answered elsewhere. However if you feel that it has not been answered, the solution is not to complain in the title, nor is it any way relevant to cast aspersions on answers to other questions. The latter course of action is likely to lead to the moderators deleting your question. People are trying to help without unnecessary duplication. What you should do is reply to the comment, in a comment, and expand your question as necessary. I have edited your question and will address your clarification in a second comment.

You ask “How does the cell choose which amino acid to attach to tRNA?” It sounds as if you are unfamiliar with the family of amino acyl tRNA-synthetase enzymes and their specificity for cognate tRNAs? If so, please read the section in Berg et al. on line. If this does not answer your problem, please explain why not.


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What does "Mutational Variance" mean?
Background
The concept of mutational variance can be found in many articles including this one for example. The mutational variance of a trait number $i$ can be found in the M-matrix in position $m_{ii}$ (in the diagonal). Elements of the off-diagonal represent mutation covariance. For example element at position $m_{ij}$ of the M-maitrx is the mutational covariance between traits $i$ and $j$. More info about the M (and G) matrix can be found here.
Question
What does "Mutational Variance" mean? What does it mean for a population to have a high or a low mutational variance?
Does "mutational variance" refers to:

Average effect of new mutations on fitness (mutational effect) (parameter $s$)
Variance in the effect of new mutations on fitness (variance in $s$)
Average effect of new mutations on phenotype
Variance in the effect of new mutations on phenotype
The increase in genetic variance ($V_G$) due to a new mutation
The increase in additive genetic variance ($V_A$) due to a new mutation
Genetic variance in the population at mutation-selection-drift equilibrium.
Is it a concept that is opposed to genetic canalization?
...

In Pigliucci (2004) (repeated in Hansen (2006)) the mutational variance is defined as being the new additive genetic variance entering in the population each generation due to mutations.
In consequence the mutational variance is not define at the level of the mutation in the sense that we do not care about how many mutations yield to this new genetic variance. So none of the suggestions of possible answers in the OP's question is correct.


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Rationale for two-components in feedback loop of circadian molecular clock
The circadian clock in humans and fruit flies involves a feedback loop in which the active components are protein heterodimers. This is illustrated for humans in the diagram below:

The nuclear proteins MBAL1 and CLOCK form a dimer which is a specific transcription factor for the genes of proteins PER and CRYS. The mRNAs for the later are transported to the cytoplasm for translation, where a PER/CRYS heterodimer is formed. This is transported to the nucleus (generally in a chemically modified form) where it inhibits the MBAL1/CLOCK dimer, and hence the transcription of the PER and CRYS genes.
The diagram above is take from Ko and Takashi (2006) and a summary of the process can be found in the Wikipedia entry for Circadian Clock.
I wish to know if there is any known reason or rationale for this feedback loop involving proteins that are made of two separate components, and whether simpler systems involving a single-component transcription feedback loop exist, for example in more primitive organisms.

Heterodimer of what? You need to provide more information about the process (preferably supported by a reference source) for your question to be intelligible.

In mice models, I speak of the heterodimerization of BMAL1-CLOCK and in fruit flies this is CLOCK-CYC. These are mentioned in the wikipedia article: https://en.wikipedia.org/wiki/Circadian_clock (scroll down to Mammalian Clocks and Insect Clocks section)

One question that is implicit here is whether complex biological feedback loops exist that do not have heterodimers. Heterodimerization is a fundamental design component of biological systems in cells. I don't have a reference but I'd be very surprised to find any complex cellular system that didn't involve the heterodimerization of protein components as a step!

As an example, the arabidopsis circadian clock involves a variety of distinct protein complexes (which at times are heterodimers), some of them homologous to animal models.

I think your question is valid, but the lack of response suggests that the problem could be presented more clearly. I have taken the liberty to do so. You can roll it back if you like or edit it further.


text:
Examples of mechanisms of metabolic trapping inside cells that create concentration gradient
I am looking for examples in biology in which a metabolite that can diffuse freely across a cell membrane (through passive diffusion), once inside, gets modified to a form that cannot diffuse back anymore. The metabolite, in this way, gets effectively trapped inside and this can lead to a concentration gradient inside vs. outside.
One such example is the one of glucose. Glucose can penetrate cells through facilitated diffusion. Once inside, it gets phosphorylated to G6P which cannot diffuse out anymore.
The phosphorylation is powered by ATP. At the end, thanks to this mechanism, one can have in principle [Gluc]_blood < [Gluc]_cell + [G6P]_cell.
However, I didn't find references measuring higher glucose concentration in the cytoplasm compared to the one in the blood. Do you know any?
Any additional example in which the same happens would be appreciated.

Welcome to SE Biology. Please finish reading the [Tour]. A point of clarification, are you asking for the concentration of free glucose within cells? There will be literally hundreds of papers from the 60s onwards with such values. Have you searched?

Concentration of free glucose + phosphorylated glucose inside the cell.
That value would be nice to have and to compare with the glucose concentration in the blood. I didn't find any paper measuring this value.


text:
What is the exact definition of the term 'trait'?
A trait is a characteristic shown by an organism.
For example a Tt plant would show the 'tallness' trait.
It seems to me that, by analogy, sickle cell anaemia (SCA) carriers should show the 'normal' trait, but I have found on various sites that SCA carriers are described as having the sickle cell trait because as carriers they can pass the mutated gene to their children.
This doesn't make sense to me, as showing a trait and passing it to the next generation are two different things. We do not say a Tt plant has the dwarfness trait just because it can pass it to the next generation.
So what is the exact definition of the term 'trait'?

Trait is used to mean alleles  multiple times, no?

I think you are interested in the difference between phenotype and genotype.

@David is there any official book for biological definitions just like we have IUPAC goldbook for definitions of chemistry?

@HarjotDhillon — In a word, no. Biochemists and Molecular Biologists have a joint Nomenclature Commission with IUPAC, which is available on a 20th century website the design of which is unbelievably awful. There are various specialist bodies for taxonomical nomenclature in various fields, but you won't find terms like 'trait' defined anywhere but textbooks. At least not to my knowledge. It's a bit of a moving target anyway, and convention emerges from the usage of the 'leaders' in the fields, without anyone trying to codify it.

I think the confusion stems from the word "trait" being used differently on the website you link, from how we use it in genetics.  From the website:

A trait is something unique about you, like your hair or eye color. Traits are passed down (inherited) from your parents. Genes carry information that makes a trait. People with sickle cell trait (SCT) have 1 sickle cell gene and 1 normal gene.
Having sickle cell trait is not the same as having sickle cell disease (SCD).
Sickle cell trait means you could pass sickle cell trait or disease to your children.

Thus, we see SCT, Sickle Cell Trait, is a specific condition someone can have, just like they could have SCD, sickle cell disease, or nothing at all.
I don't think the use of the word "trait" has much to do with how we use it in biology.  You are right that in biology, we usually use the word "trait" interchangeably with the word "phenotype" whereas in the website you link, it explains "Sickle Cell Trait" is the name of a heterozygous genotype for sickle cell.


text:
Are cytoplasm and collagen basic in nature?
Eosin is acidic in nature. Hematoxylin is basic in nature. What I have learnt about H and E staining is that the nucleus is blue in colour because it is acidic and takes up the basic dye, Hematoxylin. But I don’t understand why collagen and the cytoplasm appear pink? Is it because they are basic? Is collagen a basic protein which takes up eosin and appears pink? Is cytoplasm basic in nature? What am I missing?

Eosin generally stains anything with protein, and that includes the cytoplasm (full of dissolved protein) and collagen (made of protein).  It is also very nonspecific.  If you take a section or even live tissue/cells and put in eosin, almost everything will label to some extent.  When making H&E slides, they wash after staining to remove the less tightly bound dye, but even then almost all structures are labeled to some extent, with basic ones simply being brighter.

Hey Thanks a lot.


text:
If the shrimp is a decapod, why does it have 20 legs? (10 swimming + 10 walking legs)
Decapods like crabs have exactly 10 legs.

However, shrimps have 5 pairs of swimming legs and 5 pairs of walking legs. A total of 10 pairs. Why are they classified as decapods then?

Species are classified based on common ancestry. See https://en.m.wikipedia.org/wiki/Cladistics
Decapods aren't classified together because of the number of legs they have. That's where the order got its name, and it's one possible clue that they are related, but it's not why they are together.
Furthermore, swimmerets aren't legs. They're leg-like, but they aren't legs. Shrimp inherited the ten legs from the same common ancestor as other decapods, and they also share swimmerets with most other decapods, even crabs have them.


text:
Can elephants really paint?
I saw this youtube video of an elephant painting. (https://www.youtube.com/watch?v=foahTqz7On4&t=301s) There are others as well.
It looks completely real. However, like other people in the comments, I was also skeptical if someone was conditioning the elephant to paint, or if there was some trickery involved.
I'd like to know from a scientific perspective (i.e. via research or from some credible source) if elephants can actually paint things without being conditioned (someone shows them what to paint, then they recreate it) or trickery (someone has lines on the paper the elephant traces which are not visible to the camera).
Specifically, do elephants really have the creativity and mental capacity to paint things like flowers and elephants from their own imagination? Are they really that smart?

Can most  (excluding the possibility of a few genusies) humans paint without being conditioned?  Or is it just that with humans, we call the conditioning "art class"?  FTM I can't paint despite those elementary school art classes :-)

@jamesqf Any parent of a toddler can testify to the sheer enthusiasm of spontaneous artistic creativity that is often expressed by humans. The motor skills aren't great, however, and choice of media may often be disheartening to the adults...

@jakebeal: But how do the productions of toddlers splashing paint on paper (or other materials on any available surface) compare artistically with elephant painting?  (Always recognizing that in the modern world, "artists" can get remarkably high prices for splashing paint :-()

Interesting question! While it doesn't exactly address the topic of your question, I think the paper Is painting by elephants in zoos as enriching as we are led to believe? might have some insight.
I originally found this paper from the animal-made art wikipedia page, which states that:

The elephants draw the same painting each time and have learned to draw it line-for-line.

Although I couldn't find that claim in the paper they cited, it does seem like this is a highly structured activity (as opposed to a more free-form "art"). For example, from the above paper:

Painting involved following instructions from the keeper and performing the task in front of an audience. ... The brush was then handed to the elephant, which it then held with its trunk. Instruction was given by the keeper to the elephant when to start and stop painting, and when to give the brush to the keeper for colour changes. ...  Each session lasted between 2 and 5 min, and was a highly structured event. For example, when the elephant was not holding the paintbrush and awaiting the next instruction it was directed to rest its trunk tip on the ground.

There might be more information in this book, Cerebrum 2009: Emerging ideas in brain science, as it's cited a lot in the introduction, but it doesn't seem to be available online.
Overall, it doesn't seem like the elephants have much agency in what/how they paint. As the authors put it:

[T]he results indicated that elephants gain little enrichment from the activity of painting. Hence, the benefits of this activity appear to be limited to the aesthetic appeal of these paintings to the people viewing them.

Could and elephant paint from its own creativity? maybe but unlikely
Gorilla and chimps can paint creatively. elephants might be able to is allowed although studies on elephants in zoos show elephants do not have much desire to paint. elephants are not as visually oriented as apes, so creative painting may not hold enough attraction to do so, even if they could. But that is not what we are seeing in the video.
Is the elephant in the video painting creatively? No
The painting elephants are trained to paint line for line, stroke for stroke. the elephants in question always paint the same picture every time. the training to paint itself is not abusive, but the training to get the elephant to submit to training generally is abusive. Desmond Morris, a well known ethologist, (animal behavioral scientist) went to observe this personally and up close which requires special permission (link below). He noted that each animals always paints the same picture and the trainer is likely guiding the elephant with taps and tugs on the ear. so this is not a creative exercise but a trained response like a dancing bear or counting horse.
https://www.bbc.co.uk/sounds/play/p049jfky

In 1980 or so an elephant named Ruby exhibited some destructive behavioral problems. She was provided with finger paints and started to spontaneously generate art. It was abstract but once when a fire occurred within sight of her enclosure she created a painting which displayed colors like red and yellow -- it was suggested that the uniforms and color of the truck inspired this.
So the answer is yes - however, I do not think any elephant has yet to do actual drawings as seen by human-guided or memorized paintings -- but the fact that however produced such drawings can be made suggests that perhaps some elephant could independently make representational drawings.
In the wild, elephants have been observed making scratches in the dust and perhaps there is some utility in this -- maybe when a herd of elephants is embarking on a trek to find food or water they are communicating the route, maybe even discussing alternatives. Given that bees communicate via their dance paths to flowers or other food source (and this has been extensive documented) why is it impossible that elephants do something similar?