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Hardy-Weinberg Equilibrium Test Result for Merged Genotypes
I was curious if two populations are in Hardy-Weinberg Equilibrium (HWE), and if they are merged, then what happens? To find out, I considered populations from the 1000 genome project data. For example, at first, I considered the genotypes of the American (AMR) population from a specific SNPs and checked whether they were in HWE and found that they were. Then I selected the East Asian (EAS) population and found that the genotypes were also in HWE. However, when I merged the genotypes from both populations and checked HWE, I found that it was not in HWE. Surprisingly, when I added 50% of genotypes from each population, they were in HWE. So, I did it for different combinations, for example, 80% genotypes from the AMR population and 20% from the EAS population and vice versa, and found that they were also in HWE. I used the chi-squared goodness of fit test and the Haldane Exact test. The allele and genotype frequencies for each combination are different from the initial populations. What conclusion can I draw from my findings? Should I check to see if there are any assumptions about the test that are violated?

Welcome to Biology StackExchange! If I understand your question correctly: Imagine a limiting situation with two alleles and two populations, one of which only has one allele present ($p_1 = 1, q_1=0$) while the other has only the other allele present ($p_2=0, q_2=1$). Even if both of these populations are in HWE, when you merge them, they won't be ($p = 1/2, q=1/2$ but there are no heterozygotes).

Here are the allele frequencies and genotype frequencies: G T GG GT TT 0.408 0.592 0.184 0.447 0.369 → AMR Population || 0.651 0.349 0.427 0.448 0.125 → EAS Population || 0.550 0.450 0.327 0.447 0.226 → Combined all || 0.550 0.450 0.327 0.446 0.227 → 50% each combined || 0.471 0.529 0.247 0.447 0.306 → 80% AMR and 20% EAS || 0.614 0.386 0.390 0.448 0.162 → 80% EAS and 20% AMR @Domen

your initial question was: I was curious if two populations are in Hardy-Weinberg Equilibrium (HWE), and if they are merged, then what happens? I have given you an example which tells you that merging allele frequencies from two populations in HWE will generally result in a population not being in HWE.

Thank you very much! I get your point. My question is: how can I draw conclusions? Since different percentages of merging of genotypes result in HWE, except for all of them combined. Can I say something from the allele and genotype frequencies? Or do I need to take any further steps to reach the conclusions?

@statm I suggest that you look into the idea of statistical power. More extreme deviations from HWE will naturally be easier to detect by your test; "in equilibrium" is not a binary after all, every population is somewhere in a continuum of disequilibrium. I'd also suggest consulting prior attempts to test for HWE in stratified populations. I think that you can safely reach the trivial conclusion that well mixed populations are closer to HWE than stratified populations, but no more.

You may want to recheck your calculations. The fully combined and 50% combined groups should be the same, and I got G 0.52925, T 0.47075, GG 0.3055, GT 0.4475, TT 0.2470.

Why would you expect the result to be in HWE in the first place?

As @Domen points out, there is no expectation that adding two populations that are each in Hardy-Weinberg equilibrium will initially create a new population in HWE.
OP's procedure of combining different proportions of the initial populations, then checking for HWE, is essentially like asking how much of one population can be added to another before HWE is lost. This vaguely gets at the question of how different the two populations are to begin with, but doesn't provide any information on whether the assumptions underlying HWE are met.
A better function to ask about the initial difference between populations, and that can be calculated from the initial allele frequencies, is the fixation index, FST.
Incidentally, if the assumptions of HWE are still met after the two populations are merged, then after one generation of mating HWE will be reestablished across the whole population.

Well, the absence of migration is one of the assumptions of Hardy-Weinberg law. By merging the two populations you are basically simulating migration, violating the assumption, and thus (as @Domen and @Darlingtonia correctly pointed out) there is no reason why you should expect that the two populations are in HWE (https://www.nature.com/scitable/knowledge/library/the-hardy-weinberg-principle-13235724/).
The fact that you get different results when mixing different proportions may be due to different factors, such as (but not limited to):

Lower number of individuals obtained when mixing a fraction of each population may influence the power of the chi-square test. Seeing the numbers used in the chi-square test may help to understand.
The difference in frequencies between the two populations is small enough that only a total mixing brings to a significant deviation from equilibrium.
When you mix a large proportion of one population and a small proportion of the other, you likely get a final population which is sufficiently close to the first one, and thus does not significantly deviate from HWE.


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Is repeated exposure to near/mid/far infrared safe for skin and eyes?
I've been doing a lot of research into infrared saunas as they've risen in popularity. I've come across a fair amount of information about how harmful near infrared exposure can be to the eyes.
This study was done on rabbits, and doesn't differentiate between near/mid/far, but concludes that, "The protein of eye lens is very sensitive to IR radiation which is hazardous and may lead to cataract".
This research published by Berkeley does differentiate between near/mid/far and indicates that near poses the greatest risk to the eye.

"Near‐Infrared Exposure and Cataracts The most common eye disease
associated with near-infrared radiation is cataracts. Prolonged
exposure to IR radiation causes a gradual but irreversible opacity of
the lens. Other forms of damage to the eye from IR exposure include
scotoma, which is a loss of vision due to the damage to the retina.
Even low-level IR absorption can cause symptoms such as redness of the
eye, swelling, or hemorrhaging.
Cataracts caused by near‐infrared radiation have been noted
historically in glassblowers and furnace workers. Radiation between
800 and 1,200 nm is most likely responsible for temperature increases
in the lens itself because of its spectral‐absorption characteristics.
Visible wavelengths may also contribute to the problem, since the heat
absorbed by the iris could result in heat transfer to the lens.
Acute Skin, Cornea, and Iris Injury IR radiation below 3,000 nm will
penetrate into different depths of the cornea to varying degrees,
depending on the specific wavelength. The iris can absorb energy only
at wavelengths below approximately 1,300 nm.
IR thermal injury may have significant biological effects on the human
skin. The IR-A rays induce free radicals in the dermis and diminish
the skin’s antioxidant capacity, the main cause of premature skin
aging.
Both the skin and the cornea are opaque to wavelengths >1,400 nm.
Exposure to IR radiation in this region causes injury through thermal
mechanisms, with absorbed radiation being converted to heat."

But, it's hard to understand if this would translate to consistent usage of saunas that leverage near/mid/far infrared. In the case of the Berkeley research, it's looking mostly at workplace hazards (welding, etc.), which in many cases would require participants to have their eyes open and very close to the heat source. But if the issue is simply that infrared heat is penetrating and heating the cornea, it would seem that that could be an issue for saunas as well. It also seems to indicate that even far infrared would be damaging to the skin, when sauna companies are claiming the exact opposite to be true.
I find it quite alarming that sauna companies are touting near infrared as a "plus" when it sounds like most research points to it being harmful in the long run.
My question is this: does anyone know if far infrared is conclusively safe for the eyes and skin in repeated use in something like a sauna? Is near infrared really the risk? Or is how saunas are using it below some threshold of safety?

It would depend strongly on the intensity of the source. The cataracts for furnace/glassblowers are from high intensity sources in relatively close proximity - close enough to get splashed with liquid metal according to the historical documents.

https://en.m.wikipedia.org/wiki/The_dose_makes_the_poison

Forgot to add, our eyes are always exposed to IR while we are alive - our bodies are warm after all, and IR is the "heat" wavelengths of radiation. There is also ambient heat wherever we are.

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Why is sheep erythrocyte lysis considered as classical complement activation pathway, and rabbit as alternative one?
Any suggestions are highly appreciated.

Unfortunately I can not add "Complement" as a tag.

The sheep erythrocyte lysis you mention actually involves sensitised erythrocytes, i.e. erythrocytes already coated with antibodies. Antigen-antibody complexes are well-known for their activation of the classical complement pathway.
In fact, rabbit erythrocytes coated with antibodies also activate the classical complement pathway$^1$. Thus, sheep erythrocytes are not special in this regard.
The difference comes when we incubate only erythrocytes—devoid of any sensitising antibodies—with serum containing complement factors. In this situation, erythrocytes from the rabbit, but not those from the sheep, are lysed by alternate complement activation. Why is there such a difference?
Fearon and Austen$^2$ showed that this is due to a protective effect of the rabbit erythrocyte membrane on C3b. Normally, C3b is inhibited by factor I and  factor H in serum. This effect is lost with rabbit (but not sheep) erythrocytes, which explains the difference in complement-mediated lysis.

Journal articles cited:

Dijk HV, Rademaker PM, Willers JMN. Estimation of classical pathway of mouse complement activity by use of sensitized rabbit erythrocytes. Journal of Immunological Methods. 1980 Dec 22;39(3):257–268. https://doi.org/10.1016/0022-1759(80)90060-5
Fearon DT, Austen KF. Activation of the alternative complement pathway with rabbit erythrocytes by circumvention of the regulatory action of endogenous control proteins. Journal of Experimental Medicine. 1997 Jul 1;146(1):22–33. https://doi.org/10.1084/jem.146.1.22

That is a fantastic answer. Thank you Adhish Sethi.

@Andrew You're most welcome. :)

@Adhish, thank you for the answer.

The complement system is an innate immune response which has three pathways - as shown in the image below.
The breakdown of red blood cells assesses the functional capacity of the complement system. This experiment is titled: "Total complement activity", "CH50" or "CH100". Is this what you're referencing?
Hemolysis of sheep red blood cells occurs via the classical complement pathway.

More information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4360204/

thank you for your contribution.

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Stabbing muscles when flexed and when relaxed
Just a random question, would a sharp object pierce your muscle more(stabbed with the same amount of force) when the muscle is flexed or when relaxed?

I would say that it would depend largely on the muscle.

lets say any large muscle, abdominals, hamstrings, shoulder, etc @RoryM
Edit: or are you talking about the muscle density?

Depends on the stabbing force and how sharp the object is.

I suppose in theory the density of the tissue has increased during contraction if you stab in the middle so (preparing for a possible physics disaster) that would mean less penetration for constant force from an identical object

Well, if we look in very basic detail at how muscle contraction works within a myofibril of the sarcomere:

N.b. this isn't on a loop and only plays through seven times
The red lines represent actin filaments whilst the blue lines represent myosin filaments.  During muscle contraction the filaments move over each other:

As shown in the above diagrams the "more contracted" a muscle is then the smaller the size of the H zone (the area where there are just myosin filaments).
So if we consider a penetrating impact that went through a plethora of identically aligned sarcomeres (obviously this is not the case in nature) then we could presume that (et ceteris paribus) the object would not penetrate as deeply into a contracted muscle as it will hit more tissue on its route than in a relaxed muscle.

Thanks for a very detailed and clearly explained answer! Pity i didnt take Bio during high school...interesting stuff

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Significance of prostaglandins in semen?
I am trying to figure out how prostaglandins in the semen relate to the female reproductive tract.
More specifically,
How does prostaglandins in semen help the female reproductive tract increase the chance for fertilization?

Nevermind. While writing out the question I found the answer on wikipedia.
Prostaglandin type PGF2α will act on the FP receptor to initiate uterus contraction which will help propel sperm further into the reproductive tract.

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Function and process of TCTE-1 receptor
I was wondering if anybody knew of the function and process of the TCTE-1 receptor during the binding of a sperm with an egg. The only think I know of TCTE-1 is that it is a species-specific receptor.
I also know that it's removal will render homozygous males infertile. I know that researchers are experimenting with mice to study TCTE-1.

This is by far too long for a comment, so as an answer: I spend now quite a while using Pubmed and other search tools, to find more information. The most recent article I found over and over again was the one from Juneja and colleagues: "Sequence divergence within the sperm-specific polypeptide TCTE1 is correlated with species-specific differences in sperm binding to zona-intact eggs." (which you probably also found). This article has only been cited two times, which is a bad sign for an article making so important connections. My guess is that no further research in this area either happened or has at least not been published. So beyond this I am afraid that there is no other information available (I am happy to change this, if there is any other information available).


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3' or 5' DNA capping protein
Does anyone know of a protein/molecule that can be attached to one end of the DNAs temporarily ? eg. i would like to only to allow one strand of DNA be ligated to another DNA molecule to either it's 3' or 5' but not both. thanks

Could you explain what you're hoping to accomplish a bit more? Why wouldn't it be possible just to put RE sites at one end of your DNA and the correct end of the piece to be ligated, digest with the RE and then ligate the digest?

Alternatively, you could do fusion PCR/Polymerase Cycling Assembly: http://en.wikipedia.org/wiki/Polymerase_cycling_assembly . PCR up your fragments with additions to the primers complementary to the other piece you want to connect to, then combine the two pieces (now with short complementary regions) and do another PCR to make the full product.

Thanks A. Kennard for giving me the answer. you are right.


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Which organisms have the neuroanatomy Roger Penrose supposes play a role in consciousness?
In The Road to Reality, Roger Penrose suggests that certain brain structures might play a role in consciousness

Most particularly, lattice neuronal microtubules, as originally
  suggested by Stuart Hameroff but perhaps also other structures, like
  synaptic clathrins, whose structure closely resembles the c60
  molecules.

He supposes this would have to do with some sort of quantum coherence:

...the scheme would require some kind of large scale quantum coherence,
  acting broadly across considerable regions of the brain having
  features in common with high temperature superconductivity.

In general, which organisms have these structures? Are they common?

note that Penrose's theory for 'quantum coherence' playing a significant role in the brain is largely discredited.

i believe the structures mentioned here are just about in every neuron, fyi.  Artem is right though.

@ArtemKaznatcheev It's important to mention that Max Tegmark who rote paper on Penrose's work used his own model not the one proposed by Penrose and Hameroff.
Currently(2020) 6 predictions of the theory of 20 appeared to be true, other 14 are have not been discredited.

Microtubules are a structure in the cytoskeleton, they are rope like polymers that grow to a length of about 25 micrometers (25000 nm), and have an outer-diameter of around 25 nm. For comparison, the mean spacing between atoms is on the order of 0.1  to 0.2 nm; so the micro tubule really is micro: about 200 atoms across. In terms of quantum effects though, this is pretty big but not unreasonable. Researchers commonly use quantum dots to play with quantum effects, and these are typically spheres on the order of 10 to 50 atoms in diameter. Note, that we don't know how to couple 5000 quantum dots in one coherent chain (how many you would need to get the length of a microtubule).
So microtubules are small, but they are common! Microtubules are found in all dividing eukaryotic cells and in most differentiated cell types. In other words, that mosquito you just smacked and that philosophers always give as an example of something non-conscious is full of microtubules. This should raise some red flags, but we don't need to go into more detail of microtubules to discredit Penrose and Hammeroff. However, if you love cell biology, take a look at Desai & Mitchison (1997).
So microtubules are probably a bad basis, but why did Penrose want quantum effects in the brain? In The Emperor's New Mind, Penrose suggests consciousness is non-algorithmic and suggests that a magical quantum computer could do these non-algorithmic tasks. The reason I use 'magical' is because a real quantum computer is Turing-complete, if a classical computer cannon solve a problem then neither can a quantum one (of course, if a classical computer can solve a problem, then quantum one can as well and might be able to do it qualitatively faster). For a nice computer science debunking of this part of Penrose's argument take a look a Scott Aaronson's lecture notes.
Why did Hammeroff want quantum-ness? To avoid dualism in explaining consciousness. However, he has gone so far down the reductionist rabbit-hole that he popped out on the other side. He arrived at the same 'magic' we feared in dualism except now he called it 'quantum mechanics'.
The biggest irony of this approach is that Penrose was inspired in many ways by Schrodinger's beautiful take on life. Although Schrödinger does bring in quantum mechanics (both as a useful reduction and as an analogy) he uses completely different parts of it (he uses the discritization of energy levels, and specially avoids issues of the uncertainty principle and superposition of states that made him famous).  Schrödinger would completely disagree with Penrose and Hameroff::

[I]f we were organisms so sensitive that a single atom, or even a few atoms, could make a perceptible impression on our senses -- Heaves, what would life be like! To stress one point: an organism of that kind would most certainly not be capable of developing the kind of orderly thought which, after passing through a long sequence of earlier stages, ultimately results in forming, among many other ideas, the idea of an atom.

This response can be made precise through quantum decoherence (Tegmark, 2000) and there is little regard for the physical importance of quantum mechanics in the brain (Litt et al., 2006) although Hammeroff (2007) still defends it.

Nice summary but Schrödinger is wrong. Single, small molecules (few atoms) do make perceptible impressions on our senses, notably in smell and vision (where a single photon can trigger a perception).

@KonradRudolph I didn't want to imply that Schrodinger was right, just that he would disagree with Penrose. If the quote is misleading, the we can replace it by one from later on in What is Life?: "To the physicist I wish to emphasize that in my opinion, and contrary to the opinion upheld is some quarters, quantum indeterminacy plays no biologically relevant role" (emphasis from original text)

Fair enough, in particular since I happen to believe that Penrose is off his rockers here. That said (and unrelated to my first comment), I’m pretty sure that quantum indeterminacy does play a biologically relevant role. Otherwise catalytic effects of certain enzymes are hard to explain (e.g. electron transfer chain). From my limited understanding of quantum physics, these mechanisms rely on borrowing quantum particles, which works thanks to indeterminacy.

"mechanisms rely on borrowing quantum particles" made me shudder, but you are correct in spirit @KonradRudolph that quantum effects are important in chemistry. I will try to think of a way to remove the Shrodinger quote since it seems to make people uncomfortable (I just really like that quote :D).


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Is it safe to work with HeLa cells?
Hela cells are infected with HPV. So is it safe to work with them? What are the safety precautions?

Most guidelines for HeLa (and most cells of human origin) say they should be kept at a BSL2 level. For example, from a 2007 publication in Applied Biosafety:

Work with cell cultures from human or primate origin should generally be performed under BSL2 conditions. Containment level 1 may be considered if all manipulations occur in a Type II biosafety cabinet ...

--Animal Cell Cultures: Risk Assessment and Biosafety Recommendations
ATCC general guidelines recommend BSL2 containment for the broad category covering HeLa:

Biosafety Level 2

Cell lines that harbor mycoplasma or any other BSL 2 agent (See: NOTE)
Cell lines exposed to or transformed by a primate oncogenic virus
Primate cell lines that contain viruses
Cell lines carrying a part of certain viral genomes, even if whole virus is not released from the cell

--ATCC® ANIMAL CELL CULTURE GUIDE: tips and techniques for continuous cell lines
Their specific page for HeLa also recommends BSL2, with the note "[Cells contain human papilloma virus]".
That said, HeLa cells have been very widely used, including for decades before modern lab safety practices were agreed on, and I'm not aware of any actual problem ever arising (including such amazing practices as injecting live HeLa cells into convict "volunteers" to see if cancers would appear - They did not).
So the answer to the question is that it is safe to work with HeLa cells, but that proper BSL2 lab practices should be followed.


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Is it possible for an immune host to be reinfected and show symptom before swift recovery?
For example, let's say the pathogen is a virus, and the host was infected once but recovered purely on its own and thus retained a highly effective adapted immunity.
However, if we IV inject the the host with an overwhelming dose of virus, is it possible to infect some cells, cause some cell death before the immunity taking over and the host recovery? Is it possible to completely overwhelm the immune system and kill the host anyway?


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What is holding the immune system back to not attack human body cells?
There are plenty of loose proteins or other macromolecules free floating everywhere. Why wouldn't they be seized and presented to T cell to trigger an immune response? Does each of these molecules have a signature portion? Or do the presenter cells have some sort of friendly molecule database? Would a normal person's immune system ever possibly generate something like Tocilizumab, i.e. an antibody targeting a normal receptor in most cells?

What research have you done to try to find the answer to this question yourself? You are expected to do this before posting here. Have you searched for "self-tolerance" or similar terms or phrases?

The immune system of human body can keep human health from disease, but for many people, the immune system is the cause of disease. When the autoimmune system is in disorder, healthy cells and tissues will be killed as viruses, which will lead to a variety of immune system diseases.
Recently, scientists in the United States have discovered the genome that causes the disorder of the human immune system, which is equivalent to the "middle manager" of the immune system. This discovery is likely to bring new hope to the treatment of human immune system diseases, which has been published in the latest issue of nature.
Self defense system out of control immune cells "killing each other"
In the human immune system, a kind of immune cell named T cell is responsible for directly contacting and resisting the invading pathogen. Whether these cells can function normally is controlled by "regulatory T cells". Simply put, "regulatory T cells" are like a "double-edged sword", which can not only prevent T cells from attacking human body's own healthy cells indiscriminately, but when its regulation fails, it will cause immune cells to "kill each other" to normal cells, and its consequences usually include inducing type I diabetes, multiple sclerosis, lupus erythematosus and other immune system diseases.
Scientists have previously found that whether "regulatory T cells" can work normally is related to a major regulatory gene called Foxp3. If Foxp3 is dysfunctional, the human body will lack the active "regulatory T cells". But scientists don't know how Foxp3 controls "regulatory T cells.".
Richard young, a biologist at Whitehead Biomedical Research Institute of Massachusetts Institute of technology and Alexander Marson, a doctor of medicine, and other researchers recently discovered 30 genes directly regulated by Foxp3. It is by combining with these specific genes and regulating their activities that Foxp3 can complete the control of "regulatory T cells". If Foxp3 is the "boss" of the immune system, the 30 genes found in this study belong to the "middle manager".
Immune system diseases are related to the damage of "regulating T cells"
Researchers point out that ten years ago, it was found that the "regulatory T cells" in the human body are responsible for directing the immune system to resist foreign invasion, and the question is why the immune system that should protect health attacks its own cells. Now it has been found that there are gene defects in "regulating T cells" in the body with autoimmune disorder.
When "regulating T cells" cannot guarantee the normal operation of the immune system, the immune system begins to attack cells that should not be attacked. When the "regulatory T cells" were destroyed, several organs of mice developed serious immune system diseases. In some common human immune system diseases, such as multiple sclerosis, there is not no such "regulatory T cells", but there will be some dysfunction. In other words, "regulating T cells" failed to play its due role.
What is the problem of "regulating T cells"? "Studies have shown that when the immune system is disrupted, the activity of these genes is lower than normal. It is this reason that makes the activity of "regulatory T cells" decline, leading to its failure to work properly. Three years ago, scientists have found the main gene controlling "regulatory T cells", which is called Foxp3.
The researchers used DNA biochip technology to scan the complete genome of T cells and map the genes regulated by Foxp3. In the process, the researchers identified 702 Foxp3 binding sites. Until the discovery, the researchers admitted, they had no idea how Foxp3, the main regulator, dictated "regulating T cells.".
Anti rejection treatment for organ transplantation
The latest research shows that the "middle managers" of these 30 immune systems are not working properly. Because "regulatory T cells" are controlled by these specific genes, it can be said that most of the immune system diseases such as type I diabetes, lupus erythematosus, multiple sclerosis, rheumatoid arthritis and so on are determined by these genes.
The next step, the researchers say, is to determine how the 30 specific genes "dictate.". It has been found that these genes are closely related to each other and usually work together to control T cells, but the specific mechanism is still unknown. On the other hand, we should look for chemicals that can simulate the regulation function of Foxp3, the main regulator gene, in order to achieve effective therapeutic immunity.
In addition to the treatment of autoimmune diseases, this finding can also be used for anti rejection treatment in organ transplantation. When performing organ transplantation, once the patient's body rejects the transplanted organ, the operation will fail. Therefore, doctors usually use anti rejection drugs to temporarily inhibit or shut down the immune system.
At present, cyclosporine is mainly used to inhibit the immune system. It can inhibit a protein called activated T-cell nuclear factor (NFAT), which can also be controlled by Foxp3. If necessary, the researchers said, the 30 genes can also be used to "target the target", and the effect of inhibiting the immune system is more obvious.


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Does cartilage connect to other cartilage?
In the definition of a Ligament in Oxford states:

A short band of tough, flexible fibrous connective tissue which
  connects two bones or cartilages or holds together a joint.

the wording of "two" prior to bones or cartilages sounds like it could be bone to bone, cartilage to cartilage, and bone to cartilage.
Are all of these combinations correct? If so, is there a good example where each one can be seen for reference?

A ligament can connect two bones:

Picture 1: Knee joint ligaments (source: Wikipedia, Creative Commons license)
A ligament can connect two cartilages or a bone and a cartilage:

Picture 2: Larynx ligaments (source: Wikipedia, Creative Commons license)
Ligaments can also connect internal organs:

Picture 3: Ligaments connecting abdominal organs (source: Wikipedia, Creative Commons license)


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What type of white hard thing grows on lobster
I have no idea how to explain it. It looks like mini white volcanoes growing on a lobster shell.  Is it bacteria or parasite?

These are barnacles, which are interestingly related to lobsters. See the image for comparision (from here):

They have a mobile larval stadium, but once they mature, they attach to a hard surface. They can be found on ships, surfaces in harbours, on whales and obviously on lobster shells. See here and here for some more details.

ah, even more creepy in your up-close image!

The question also asked if they were parasitic - do they do any harm to the animal in question? Given that lobsters are food animals, would the lobster be safe to eat?

@nick012000: It's arguably a form of parasitism, since the barnacle gains (a surface to attach, and one that is usefully mobile for defence and food collection) whilst the lobster loses by having to carry the barnacles, and appears to have no benefit. But it is a surface contamination only, and AFAIK the types of barnacle pictured are harmless to us on outside of food, they can simply be ignored or removed. There is a different barnacle that has evolved to feed on the host directly - https://theconversation.com/the-crab-castrating-parasite-that-zombifies-its-prey-27200

There's a Disney movie waiting to be written about Larry Lobster and his frenemies Barry, Bill, Bud, and Barney Barnacle.


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Given an F, R pair of SSR primers of 20 bp, which is the active portion of each
I'm a math & physics person with a general understanding of PCR. For my question, consider this F, R pair of SSR primers:
TTGTCCGTTTCTTATACAAT
TCTTTTTAGGCAGATGTTAG
It is my understanding that if the 1st sequence is annealed with chromatin DNA from our specimen that a PCR product of about 260 will form with instances of the 2nd in the sample, using Beckman Coulter hardware. Likewise, annealing the 2nd will produce products with instances of the 1st in the sample.
I also have been instructed that only a portion of each primer is involved in composing the PCR products. If true, how do I determine what it is? In addition, a citable reference would be appreciated.
Thank you in advance.


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Muscle contraction and closing in of z line/disc
I have studied that during a contraction of myofibril, the globular heads of myosin attach to actin filaments and pull them towards the centre of the sarcomere pulling the z line/disc as well.
What I don't understand is that the z line must also in turn be connected to another sarcomere's actin filaments and they must also be getting pulled in the opposite direction by their myosin filaments. So how does the z line move in a particular direction?

What do you mean by particular direction? Do muscles ever move in a particular direction?

What I meant was that th he sacromeres contract individually and the z lines get pulled by 2 opposite forces. Then how does the I band get shortened? Is it not by moving of the z line towards the centre ( towards A band)?


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Why do we choose to use agar instead of agarose in various microbial applications?
When performing gel-electrophoresis we always use agarose. Is there a reason we can't perform it using Agar?
And in microbial culture Agar is commonly used as solidifying agent, could this be replaced with agarose.
I understand the difference in price, composition, and manufacturing but other than that how would it affect the result?

Welcome to the Biology Stack Exchange. Please visit the [help] for more information on this site and how it works. Please also note we have a homework requirement. You could help your question  by telling us what you have found out.

Agarose is indeed more expensive than agar because it is purified from agar, i.e. it is agar minus the agaropectin. Agaropectin is heterogeneous, and modified with acidic side-groups. The consequence of this is that it would interfere with the migration of nucleic acid in the gel.
Similarly, agarose is sometimes used for observing zones of inhibitions of growth or lysis plages of microorganisms caused some antimicrobials, because it interferes less with their diffusion than agar.


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What indoor plants or groups of plants are significant consumers of CO2?
I am experimenting with the goal to reduce CO2 ppm in a 4200 sqr ft (12 rooms) dwelling by either distributing more plants through the space, or using a hydroponic garden's air as a source in the dwelling for a CO2 filtering system.
Using plants that are high consumers of CO2 will provide ppm data measurements to influence which solution I take.
What plants or groups of plants should I consider?
Thank You!
Greg Messer

the type of plant might be less important than the growing conditions.

I would imagine there are other criteria that are equally as important as just CO2 consumption such how easy they are to grow and maintain and how much space they take up. And cost. I just used snake plants. Humans have pretty exhaustively gone through the list of what plants are suitable as houseplants.

What type of ventilation system is used in this dwelling? Is the CO2 mostly coming from the occupants, or are there combustion sources too?

Possibly one of the extremely fast growing aquatic plants such as Azolla might be an option. Plants in this genus are sometimes mentioned as carbon dioxide remediation mechanisms due to their extremely fast doubling times.
Anything else that shows high productivity (rate of carbon fixation/photosynthesis) might be an option. You would obviously need to tailor the environment to suit that high growth rate, as suggested by commenters.
I was surprised to read just now that plants apparently are (can be!) actually effective at indoor CO2 remediation. I had not thought that they were terribly effective. Though some of this is due to other associated organisms e.g. bacteria in potting soil.


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Help identifying this fossil
Found near alexandria mn

enter image description here

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. Pictures of the ends and sides would be helpful. Standard practice for photos like this would be to take them with the tape measure off to one side so that you don't obscure relevant details. Beside MN (Monaco? Mongolia? Myanmar? Montana?), what sort of rock did you find it in? Are you sure it is a fossil and not a random concretion?

It was in a bunch of random rock and black dirt and minnesota i will get more pictures it is def not concrete though

Ah - concretion is a type of rock caused by minerals joining particles of sand etc together. They can form some pretty odd shapes.


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Are facial 'cleansing' products 'effective' on human skin, and if so, what is their mechanism of action?
All major supermarkets and beauty stores stock some form of facial cleansing products. They come in the form of scrubs, gels, and lotions which vary in application (from in shower, to apply daily without rinsing). Many of these are not marketed towards clearing acne or other legitimate dermatological problems. The claims these products make tend to include: reduction of dry/oily skin, neutralizing skin PH levels, and clearing pores. I am unsure if any of these terms are reflective of a real problem, or if the products can even even help said issues.
Therefore, this is a three-part question:

Do facial cleansing products actually do what they claim?
If so, what is their mechanism of action (i.e., how do the ingredients work)?
If not, what do the ingredients in the product actually do to human skin?

Examples of such products and associated claims:

Deep Clean® Invigorating Foaming Scrub by Neutrogena
Dr. Alkaitis Organic Purifying Facial Cleanser
L'Occitane Aqua Reotier Gel Cleanser

Example ingredients from the Neutrogena product above:

Water, Glycerin, Sodium Laureth Sulfate, Cellulose, Lauryl Glucoside, Acrylates/C10-30 Alkyl Acrylate Crosspolymer, Microcrystalline Cellulose, Phenoxyethanol, Fragrance, Synthetic Wax, Methylparaben, Sodium Hydroxide, Menthol, Disodium EDTA, Polyquaternium-7, Sodium Benzotriazolyl Butylphenol Sulfonate, Ultramarines, Blue 1

This question is not looking to me to be much of a biology question - I see nothing that asks about biology. There are other sites like Skeptics.SE and maybe MedicalSciences.SE but be wary of each of their requirements for a good question.

This is a medical question (so for MedicalSciencesSE), but I encourage you to first try to find some info from some dermatological website, such as https://dermnetnz.org/ and include it into your question. You can also try to identify active ingredients, like Sodium Laureth Sulfate, and check how they work.

Welcome Michael. Sorry about the following rant, but I think this question should indeed be migrated as indicated above, but in its current form it cannot be, as it contains three quite independent questions, that are under-researched in my opinion. In other words, each respective question in itself might be too broad. I would advise you to go to Medical Sciences and post a new post over there and take a minute to familiarize yourself with their conventions.

I'm voting to close this question as off-topic because it should be migrated to MedSci.SE but cannot be in its current form as there are 3 questions that are very broad as stand-alones in themselves. This question needs work.

Thank you all, happy to have this closed and I will migrate to appropriate location.  Cheers again for your time. I will note comment regarding three questions, though I do feel that they are interlinked with the original. As I honestly know nothing, I can't really ask "how they work" if they don't work, right?

@Jan thank you for the link! Much appreciated.

You can elegantly merge all questions into one, for example: Are such cleansing products more beneficial for the skin health (reduction of dry/oily skin, neutralizing skin PH levels, clearing pores) than regular soap?

Do facial cleansing products actually do what they claim?

This dermatologist-tested cleansing gel formula lathers into a bubbly foam removing surface dirt, oil and makeup, while energizing exfoliators sweep away dead skin cells.

So essentially, they are claiming that it is a foaming soap.
Sodium Laureth Sulfate is a detergent, Lauryl glucoside is a surfactant, so it is a good bet that the product is effective as soap. There are a bunch of other compounds that modify how it forms films, so it probably also foams.
If so, what is their mechanism of action (i.e., how do the ingredients work)?
Similar to any other soap.  They make non-water soluble things on the surface of you skin (such as oil, make up, dead skin cells, etc) more water soluble so that it dissolves when you wash your face.
Some of the other you linked also have moisturizers, so they probably put another oil back in the place of the ones you removed to keep the skin from getting too dry.

I am unsure if any of these terms are reflective of a real problem, or if the products can even even help said issues.

Or do they work better than normal soap of comparable strength?  Probably not much, although having them labeled as use for your face is nice in that you have a reasonable idea that it won't be too harsh or irritating, whereas if you tried dish soap on your face that might not go so well.


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Can a Chihuahua and a Great Dane breed the "old fashioned way?"
I saw this vid:
https://youtu.be/eu2qe-FNtjg
And this question crossed my mind.  The dog in the video seems to be boxer sized... And I wonder if that strategy would work with something a little bigger....
Also, this is obvious, but let me clarify: 'I'm thinking about  a FEMALE Great Dane and a MALE Chihuahua. (The other way arround, we would get a Chihuahuaburger before anything even happened... And would be animal cruelty. ) Since they're the same species ( a dog, aka Canis lupus familiaris) that means they can make  viable offspring, rigth?

I'm not watching this video but yes, it is possible with artificial insemination or if you support the small dog during mating. Chihuahua and Great Dane might be a bit ambitious for the latter, though.

I don't think artificial insemination is very "old fashioned" ;) lol.  But thanks. What sort of support? like... putting the chihuahua on the Great Dane's back? (that's the way the chihuahua does it in the video, it jumps on top of the boxer, on it's own...)


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L-system rule for different plant types
I have coded an implementation of L-systems (Lindenmayer systems) and would like to use it to generate realistic looking trees. Is there a reference list that shows which rules are most appropriate for different types of trees? For instance, which rules are best for an oak tree, which are best for cherry trees, etc.?

I d search for procedural trees... i.e. https://amp.reddit.com/r/proceduralgeneration/comments/6mpthc/procedural_tree_generation_incl_code/

There are many good papers by Karl J. Niklas where he models tree growth. I'm not sure if he used L-systems in particular, but I'm sure his work can inform you about the 'rules'. You can find out more here and here.


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How do birds concentrate their urine?
I've read that birds have shorter loops of Henle in their kidneys, and their primary strategy of water conservation is expelling nitrogenous waste in the form of uric acid.

However, the nephrons of birds have loops of Henle that extend less far into the medulla than those of mammals. Thus, bird kidneys cannot concentrate urine to the high osmolarities achieved by mammalian kidneys. Although birds can produce hyper-osmotic urine, their main water conservation adaptation is having uric acid as the nitrogenous waste molecule. (Campbell Biology, 11th edition)

However, I still can't quite understand how uric acid could make birds excrete white paste-like urine with less water than mammalian urine. I know that uric acid is not very soluble in water, and birds reabsorb some water in the cloaca, but this still doesn't answer my question.

I don't know, but perhaps a better question is, "How do birds conserve water?" Their excrement is paste-like because it is both urine and fecal matter, and if you've ever owned fowl, you'll know that their production of excrement is... well, nearly prodigious.

First off, I think it's helpful to go backward a step and figure out why an animal might make and concentrate urine in the first place. There's no usefulness in itself to having concentrated urine, it's just waste. Rather, for mammals (which, being mammals, we have a bit of a bias of thinking about the world from a mammal's perspective), urine concentration is part of the solution to the problem of needing to get rid of nitrogenous wastes: humans, like other mammals, flush soluble nitrogenous wastes into our kidneys with a bunch of water. This strategy creates a new problem of water loss, and the mammalian solution to this new problem is to collect a lot of that excreted water back so we can get the waste flushed out.
I think that the paragraph you quote is taking the mammal-centric position a bit too far and therefore the ordering of the statements in this paragraph is a bit misleading. I'll rewrite it using most of the same words but a different order. Though the meaning is the same I think it'll be easier to understand:

Although birds can produce hyper-osmotic urine, bird kidneys cannot concentrate urine to the high osmolarities achieved by mammalian kidneys. That's because the nephrons of birds have loops of Henle that extend less far into the medulla than those of mammals. Instead, their main water conservation adaptation is having uric acid as the nitrogenous waste molecule which they can excrete as a solid rather than flushing with water.

I think "hyper-osmotic urine" misleadingly suggests "really really high solute concentrations" because of the prefix "hyper", but in this context "hyper" just means "greater than (blood/plasma)", it doesn't actually say anything about the degree.
Orosz, S. E., & Echols, M. S. (2020). The urinary and osmoregulatory systems of birds. Veterinary clinics: Exotic animal practice, 23(1), 1-19. mentions birds concentrating urine to 2-3 times plasma.
In contrast, "high osmolarities achieved by mammalian kidneys" seems to be using "high" relative not just to plasma but also to what birds can achieve.
Nawata, C. M., & Pannabecker, T. L. (2018). Mammalian urine concentration: a review of renal medullary architecture and membrane transporters. Journal of comparative physiology B, 188, 899-918. mentions urine concentrations in mammals relative to plasma in the range of 4-30x depending on species.

Back to worrying about the mammal-centric thinking: there is a causal implication in both the original and my edited version that is not warranted, which is that the anatomy of the loops of Henle is somehow determining the nitrogen excretion strategy that birds use. It's equally reasonable to presume that birds don't need long loops of Henle since they evolved an alternative excretion mechanism that makes it unnecessary to concentrate urine to a great degree.
The "trick" of that alternative excretion mechanism is using uric acid and excreting a paste. Because uric acid crystalizes and comes out of solution, it doesn't "count" toward osmolarity of the urine, it's excreted as a solid. Birds don't need to remove water to crystalize uric acid, and don't need to use water to flush it out at all, it falls out of solution on its own because it's not very soluble. You could add a bunch of extra water and it would still stay mostly solid rather than dissolving.
So back to your original question: how do birds concentrate their urine? Well, pretty much the same way we do as far as the kidney goes. They also pull some water back in through the cloaca before urine is released, similar to how mammals pull water in from stool in the large intestine. The important difference is not how birds concentrate their urine (because urine concentration isn't a goal/need in itself), but rather how birds excrete nitrogen waste. By not flushing soluble nitrogenous waste with water in the first place, they don't have as much urine to concentrate, so it's less important for them to be very efficient in doing so.

Having just read some papers on this, I agree with all of this. The main takeaway seems to be 'hyperosmotic relative to plasma', which is easy because of excretion of larger amounts of NaCl. Also, it seems there are other water conserving machanisms birds use that mammals don't, including in the cloaca. Interestingly, there are entire books devoted to just this topic of avian osmoregulation.

Thanks for your detailed answer! I would just like to ask how do birds reabsorb most of the water in the filtrate if they have shorter loops of Henle? If uric acid is not very soluble, and it does not count in determining osmolarity, would this mean that water would diffuse out of the nephron quicker, since the filtrate has higher water potential?

@Nibelung Are you looking for an answer for an assignment? Those questions are not bringing you closer to understanding.

No, I'm in high school and this is way deeper than what my teacher would give me. However, I would just like to know how bird kidneys reabsorb all that water in the filtrate. But I'm curious why are those questions useless?

@Nibelung Urine concentration isn't done for fun, it's done to avoid water loss specifically when you would otherwise need to use water to get rid of a lot of waste. Birds don't concentrate their urine any special way. They don't need to, because they don't need to flush a bunch of soluble nitrogenous wastes. They get rid of excess nitrogen by using a non-soluble, non-water-requiring method by converting it to a different chemical.

Unlike mammals, birds excretory matter is not liquid but a semi-solid matter which is concentrated uric acid (this is not to be confused with feces which is the dark solid matter). Their urinary system (consisting of kidneys, lower gastrointestinal tract and nasal/orbital salt glands) is somewhat different that can conserve water and produce hyperosmotic urine:

Unique aspects in the avian (urinary) system include the presence of loopless and looped nephrons, lack of the thin ascending limb of Henle's loop, a corticomedullary osmotic gradient primarily consisting of NaCl without contribution of urea, and significant postrenal modification of final urine. The countercurrent multiplier mechanism operates between the descending and ascending limbs of Henle via recycling of a single solute (NaCl) with no water accompaniment, forming an osmotic gradient along the medullary cone.
—Urine concentration and avian aquaporin water channels

Birds do not have any urinary bladder, so they don't store water anywhere. Instead they have aquaporins. In the absence of the bladder, the renal output enters the lower gastrointestinal tract, where it is significantly modified. Birds consume prey that is high in salt content or intake fluids high in salinity. So, they have functional salt glands that are capable of eliminating excess ions, usually sodium chloride, and in the process produce free water. Aquaporins come into the picture and facilitate transfer of water between cells, so they get absorbed and not get excluded as waste matter.
You may find more details of the avian urinary system and the osmoregulation process in the references below:

Nishimura H., Urine concentration and avian aquaporin water channels. Pflugers Arch. 2008 Jul;456(4):755-68. doi: 10.1007/s00424-008-0469-6
Yimu Yang, Hiroko Nishimura, Bird aquaporins: Molecular machinery for urine concentration, Biochimica et Biophysica Acta (BBA) - Biomembranes,
Volume 1863, Issue 10, 2021, DOI: 10.1016/j.bbamem.2021.183688
Eldon J. Braun, Chapter 12 - Osmoregulatory Systems of Birds, Sturkie's Avian Physiology (Sixth Edition), Academic Press, 2015, DOI: 10.1016/B978-0-12-407160-5.00012-9
https://avesbiology.com/bird_excretion.html


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Insect(Ant?) Species Identification - location: Singapore

I saw this arthropod (I am not sure if it's an insect) on November 11 at 10:57, at the Berlayer Creek Boardwalk in Singapore. The Berlayer Creek is a mangrove creek flowing towards the sea. This ant-like arthropod was jaw-locked with a weaver ant for 5 minutes or more, and I found them on the wooden partition that separated the bushes and trees from the boardwalk. Both the weaver ants and the unidentified animal is about 1.2 to 1.5 cm long (head to tip of abdomen)
Does anyone know what it is, and maybe even what was it doing?

Can you please tell much more information about this insect like no. Of legs , body structure, winged or not

I see three ants here: two seem to be of the same species (in red) and are somehow in a fight (usual ant business) with another, larger ant species (in blue):

All three have an ant-characteristic habitus:

a flattened head with large eyes and strong mandibles
long (elbowed) antenna and legs
a distinct thorax
a petiole (connects thorax and abdomen)
a distinct, segmented (and usually large) abdomen

... which you already correctly identified for two of them (the "weaver ants").


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Sequencing a PCR product with no band
I did a PCR that successfully showed the appropriate bands one time, but when I tried to re-do the same PCR just at a larger quantity to send for Sanger sequencing, very faint or no bands were seen. This same primer set has been used successfully for larger quantities before, it may be possible that the issue is in the gel. I cannot afford to run any more gels with this product, so my question is; how important is a visible band for Sanger sequencing? Will sequencing fail with a faint band?

How much did you scale up your reaction? How much do you usually scale up (2x, 5x, 10x)? Do you have any other way to measure DNA concentration reliably?

So for the functioning PCR reaction, the total volume was 10µl; 0.25µl each for forward and reverse primers, 2 µl of 5x premade mastermix (including the dNTPs, Taq polymerase, MgCl2, dye, etc), 5.5µl PCR grade water and 2µl DNA. The upgraded one was 25 µl, 0.5 each for the primers, 5µl of the mastermix, 17µl water and 2µl DNA. Do you think the DNA volume is a problem? It never caused issues before

As for the DNA concentration, we do have a nanodrop machine but it isn't exactly reliable

It looks like you're using the same amount of template DNA in your scaled up reaction as your smaller one ( 2µl), which essentially means it's at a lower starting concentration. Assuming the same number of cycles, you would ended up with the same amount of amplified product, just in a larger volume, which could be why the bands are faint in the larger one (though, that level of dilution shouldn't be enough to make a band disappear completely).

Not really responding to the issue but: agarose responds very well to remelting many times, if all I'm doing is looking for bands and not gel purifying, I used to reuse the same agarose to pour new gels dozens of times until it got really gross. Granted, this may not work so well for precast gels. My opinion: if you haven't evaluated it on a gel I'm not sure that it's a good idea to sequence.

Thanks, and while the template amount staying the same has not affected it before, I will try to increase it next time. And by not affording to test any more, I had meant I needed to retain a certain amount of the PCR product to send for sequencing, so I had no more left to run gels with. However, the remelting of gels sounds useful, how do you erase the previously added PCR samples from it?

@Nalonda understood. btw tagging with a "@" is necessary to notify us. Why can't you simply repeat the PCR with more template and use that? Are you out of template? As for remelting, once you remelt the DNA diffuses/degrades over time. Any particular band will still be brighter than background for visualization purposes. However the DNA doesn't get erased so you shouldn't purify from it! and it could contaminate e.g. your gel rig if post-pcr contam is a concern. You might consider having one gel rig for this and then a separate dedicated "clean" one.

@MaximilianPress Thanks, I just joined Stack Exchange so I didn't know. And also thanks for the gel tips! As for the PCR, I'm trying to keep the number of times I repeat the PCR to a minimum as I want to make sure there is enough of the other components left for a bigger project I have coming up. Anyway I have my answer now, so appreciate it!

In your original post you asked if the failure to detect the expected amplified product could be due to the gel.  What issue with an agarose gel would reduce the yield of a PCR product?


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Claim in article about why insects are attracted to light
In this article they are addressing the reason insects are attracted to light when they say

Heat radiation as an attractive component is refuted by the effect of LED lighting, which supplies negligible infrared radiation yet still entraps vast numbers of insects.

I don't see why attraction to LEDs shows they're not seeking heat. Could they for example be evolutionarily programmed to associate light with heat? So that even though they don't encounter heat near/on the LEDs they still "expect" to?

Do you have any reference to support your hypothesis? Bear in mind that the insects in the article are nocturnal. Until recently the only substantial light at night was the reflected light from the moon - not a lot of infra-red from that. How do you explain that the mechanism you propose might have evolved given the environment they evolved in?

@JiminyCricket.My example is only an attempt to provide a logical possibility that shows their conclusion doesn't follow from their premises.

Your right to question it, but it doesn't end there. There's a 2016 post here, the first answer might be of interest to you.

Then there's the idea that female moths are visually interesting at near-infra-red wavelengths which seems to have some support and there's: Physiological basis of phototaxis to near‑infrared light
in Nephotettix cincticeps which  suggests limited, but some possibility of (near) IR being visible to some insects.

Please be aware that this is a question and answer site, not a journal club for discussion of papers on external sites . Questions should be about biology and of general interest. Your simplistic criticism of a conclusion in a long and complex paper is not that. An appropriate question might be "How are insects attracted to light?". For this reason I am voting to close.

The BBC just has a layman's article on exactly this paper: https://www.bbc.com/future/article/20240215-why-insects-are-drawn-to-artificial-light-at-night

They're looking for and describing proximate relationships (see e.g. https://en.wikipedia.org/wiki/Proximate_and_ultimate_causation).
If the light isn't warm and insects still move towards it, that means they're not using heat to make the decision where to move. They're not saying anything about the ultimate underlying motives, just the immediate proximate mechanism.
Their alternative model is that it's based on orientation to the sky, by which insects point the top of their body (dorsal surface) toward light; if the sky is bright that would keep them oriented back-upward, but if it's a point source near the ground keeping their back towards the light causes them to fly in circles around the light:

Our guidance model demonstrates that this dorsal tilting is sufficient to create the seemingly erratic flight paths of insects near lights and is the most plausible model for why flying insects gather at artificial lights.

So, if you want to propose heat-seeking as a better hypothesis, you'd need to provide data that would explain why this dorsal facing tilt would make sense for an insect seeking heat.

Thank you Bryan!


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Why does 360 degree rotation not seemed to ever have evolved?
Of the designs of species that have evolved, I am curious why a 360 degree rotation, like a joint that can spin, does not seem to have evolved, for example wheels or a propeller.
Like, is there some reason we would expect evolution to not be able to discover those forms, or does it mean that it didn't evolve because it never was that advantageous? Owls can rotate their heads very far but not over and over in one direction. It's hard to imagine that wheels or propellers would not give you an advantage considering cars, helicopters, etc.
I think it's a puzzle because I never thought there was any form that evolution could not produce, and it's hard to believe it could not evolve in a way that was advantageous. But I think the second option is the better of the two. Maybe rotational joints are structurally weak?

Does this answer your question? Why do some bad traits evolve, and good ones don't?

It's tough connecting a blood supply to something like a wheel or propeller- it would basically need to be dead. How do you connect muscles?

Those are bad examples. Would you replace your legs with wheels? Cars are pretty useless without roads. Also, helicopters are really big for something that hovers. Look at how big hovering animals are compared to animals that can't hover: hummingbirds and insects.  They guzzle fuel. You can't find that much food in nature to survive and even if you could you wouldn't be able to consume it fast enough. Hummingbirds drink sugar and barely eat fast enough to not starve to death. At the sizes flying animals exist at wings are more efficient.

It has. Look up ATP synthase. Or flagella

Actually there are propeller like features called flagellum (3) evolved on many organisms like plants, animal sperms (4), bacteria (1) and flagellates (2). There are known only one macroscopic form of such features in bivalves and gastropods (5) but it is used for digestion not for locomotion.
One reason why we don't see it everywhere is thought to be evolutionary constraints which means that some feature might give very big advantage but the evolution to this final working "product" goes through "valley" where half developed feature is discarded by selection as less advantageous to competing features (6). In case of rotating features there are thought to be too many physiological and physical "valleys" like nutrient transfer, friction, power transmission (6,7,8).
Second big reason is using wheel on terrain has many disadvantages like bad maneuverability and going over obstacles (7). Propellers in water have efficiency up to 60% and in air 80% but fish tails and bird wings are in range of 96-98% (9). Also there are known that even in human civilizations like in Mexico have discarded wheel as way for locomotion (10).
References.

Bardy SL, Ng SY, Jarrell KF (February 2003). "Prokaryotic motility structures". Microbiology. 149 (Pt 2): 295–304. doi:10.1099/mic.0.25948-0. PMID 12624192.
Silflow CD, Lefebvre PA (December 2001). "Assembly and motility of eukaryotic cilia and flagella. Lessons from Chlamydomonas reinhardtii". Plant Physiology. 127 (4): 1500–7. doi:10.1104/pp.010807. PMC 1540183. PMID 11743094.
Jarrell K, ed. (2009). Pili and Flagella: Current Research and Future Trends. Caister Academic Press. ISBN 978-1-904455-48-6.
Malo AF, Gomendio M, Garde J, Lang-Lenton B, Soler AJ, Roldan ER (June 2006). "Sperm design and sperm function". Biology Letters. 2 (2): 246–9. doi:10.1098/rsbl.2006.0449. PMC 1618917.
Owen, Jennifer (1980). "Filter-feeding". Feeding Strategy. University of Chicago Press. p. 89. ISBN 978-0-226-64186-7.
Gould, Stephen Jay (1981). "Kingdoms Without Wheels". Natural History. 90 (3): 42–48. ISSN 0028-0712.
LaBarbera, Michael (March 1983). "Why the Wheels Won't Go". The American Naturalist. 121 (3): 395–408. doi:10.1086/284068. JSTOR 2461157. S2CID 84618349.
Dawkins, Richard (November 24, 1996). "Why Don't Animals Have Wheels?". Sunday Times. Archived from the original on February 21, 2007.
Diamond, Jared (April 14, 1983). "The Biology of the Wheel". Nature. 302 (5909): 572–573.
Gambino, Megan (June 17, 2009). "A Salute to the Wheel". Smithsonian. Archived from the original on June 26, 2017.

Another problem is both parts need to be made of living tissue, which means it needs to have a blood/nerve supply, but can't have any connection or it wont be able oto rotate.

@John - "Nutrient transfer" covers blood. The nerves involved in locomotion are mostly proximal and end at the neuromuscular junction. Of course pain and proprioception are important, too, pain as a warning and proprioception for the cooperation of the whole, but... could they be done away with for specific joints? Probably part of what the OP was asking.

blood without blood vessels only works if the wheels are very small. diffusion scaleing the bane of weird biology.

This very question has been asked a number of times before. Maybe an answer to why this is not superior to legs (or any other appendage) is in order.
Your head, arms and legs don't move through magic. They move because they are attached to other bones by ligaments, muscles and tendons. There are ligaments surrounding each joint holding it in place, and blood vessels feed these living tissues as well as the bones themselves. When joints are forced beyond their anatomical limits, ligaments tear, tendons tear or snap, sometimes muscles tear, and blood vessels rupture. (That's why even a mild ankle sprain results in swelling.)
The closest thing to full rotation of the arms is found in gibbons (picture these animals gracefully swinging through trees.) The range of motion of their arms is amazing, and occurs due to elongated tendons, significantly different shoulder bony anatomy, and greater forelimb muscle strength. But it is not, cannot, and will never be 360 degrees, nor is there a need for it: they simply change hands to achieve their forward movement. If they need to change directions (go back) they pivot/turn around, not swing backwards.
An owl's head can rotate an astounding 270 degrees in either direction. Deceased owls were studied at Johns Hopkins to determine how they can do so without keeling over.

If humans attempted to turn their heads as quickly or as far as owls do, artery linings would tear, causing blood clots to form and potentially leading to a stroke not to mention broken necks, explained study author Dr. Philippe Gailloud in a statement.

To understand the details, read the link. It's short and of interest. Still, it's not 360 degrees. This is true for any joint in the body.
Why? Because it's physiologically impossible. Full rotation would tear apart the very things necessary for any motion at all in living animals. So no wheels or propellers, please. At the very first 360° rotation, the joint would be rendered nonfunctional, which would very likely result in a much earlier death.
People with Ehlers-Danlos Syndrome have stretchier ligaments allowing more extremes of motion, but that comes with its own problems. So it's not "better".


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Is there any objective way to describe ethnicity?
Is there any objective way to describe ethnicity that does not rely on arbitrary sociocultural concepts like referring to racial constructs, modern nations like “Spanish”, or even continents like “European”, but instead just directly describes what traits/genes you have (skin color, facial structure, etc.)?

Please define ethnicity as you understand this relatively recent term, and explain how it differs from the term race, and is not a “socio-cultural concept” too. Examples are really needed if one is to attempt a biological (I assume this is what you mean by “objective”) definition.

Ethnicity is a sociocultural concept. A description of ethnicity without sociocultural concepts wouldn't be objective, it would be wrong.

Ethnicity is a spectrum, with phenotypic stereotypes and with legacy sub-species based on geographical boundaries, which are unacceptable to call subspecies because humans are not animals, sidespecies would work better, although even then... Before 1000 years ago, there were thousands of tribes in relative geographical isolation, even in Europe, and Africa, which didn't have major mixing with other tribes enough to make them similar, for example the Mbuti pygmies of the Congo Rainforest, previous to agriculture booms, almost the entire world was highly differentiated in that sense.

UN 1950 Declaration
As defined by the UN in 1950, 'race' refers to a biological concept while 'ethnicity' refers to a sociological concept. The same declaration said that the way people used the word 'race' was so out of line with biology facts, it would be better to stop using the word entirely:

To most people, a race is any group of people whom they choose to describe as a race. Thus, many national, religious, geographic, linguistic or cultural groups have, in such loose usage, been called “race”, when obviously Americans are not a race, nor are Englishmen, nor Frenchmen, nor any other national group... Because serious errors of this kind are habitually committed when the term "race" is used in popular parlance, it would be better when speaking of human races to drop the term "race" altogether and speak of ethnic groups. [Italics in the original]

Even that document is wrong however, in that it still proposes a definition of race could be rigorously defined, but we now know that is untrue.
Phenotypes
A phenotypic definition of race would determine if people were part of the same race using expressed traits. This basically amounts to phrenology, or the methods of phrenology applied to other traits, most notably skin color and intelligence. Even by 1950 most of these traits were shown to result from environment (e.g. nutrition, education) and not something inherent.
Genealogy
A genealogical definition of race would determine if people were part of the same race using family trees. In 2004 Nature published a study showing that the most recent common ancestor for all living human (the most recent person to shows up in every family tree) was probably from Eastern Asia and lived in ~50 AD. It further showed that the identical ancestors point, beyond which the family tree of everyone alive becomes identical, is ~2,100 BC. As the authors put it, "no matter the languages we speak or the colour of our skin, we share ancestors who planted rice on the banks of the Yangtze, who first domesticated horses on the steppes of the Ukraine, who hunted giant sloths in the forests of North and South America, and who laboured to build the Great Pyramid of Khufu."
Genetics
A genetic definition of race would determine if people were part of the same race using genetic similarities. The problem with this is that Africans are so much more genetically diverse than anyone else. One 2002 study even found the Africans have more in common with Eurasians than with each other. There has actually been a recent push to stop using race as a factor in genetic studies.
How should we understand race
The Stanford Encyclopedia of Philosophy as an article on race, which is a good place to start although it can get a little technical. It also has the section 'Race verses Ethnicity', which you would probably find interesting. Another interesting resource is The Price of Whiteness by Eric Goldstein, which describes how whether Jews were considered part of the White race changed in American multiple times, but always to the benefit of the upper classes.

Race and Ethnicity are not biological traits. They are both inherently sociocultural concepts. They often have biological components associated with them, and sometimes (not always) those biological features help to define a person's race or ethnicity (more commonly with race). But they always have a social/cultural component. And to be clear, if someone is of European or African decent, that is an objective statement about them, even if it's not the most descriptive biologically.
The more objective biological traits can always be studied or talked about in isolation, and then related back to the non-biological components based on their frequency or infrequency in those populations. This is common in public health research. For example, you could talk about specific allelic signatures that occur more commonly in members of the Greek diaspora, or the frequency of sickle cell disease in people whose ancestors came from sub-Saharan Africa.
My primary source is the cultural anthropologist that I'm marrying in a few months. When we met, she taught a university course on the subject of Race, Ethnicity, and Biology, so we had this discussion many times early on. This natgeo article also does a fair job of explaining it in general terms.

How can you answer a question in a scientific manner if you do not define the term that you are discussing? Citing an acquaintance as evidence compounds the unsatisfactory nature of this answer. Other defects are misinterpreting the question as about "biological traits" — a term that the poster does not use. Until the poster gives examples of what he means by ethnicity, it is better to ignore the question.

@David Thanks for your very useful feedback. If you think the question should be ignored due to incompleteness, you should vote to close and explain why in a comment so that others may be convinced to do the same.

I commented to the poster with a request for specific clarification, as is one of the stated purposes of comments. It is only when that is not forthcoming that I vote/ have voted to close, choosing as the reason “lacks detail or clarity” which requires no further comment on my part. As you had answered the question I felt it appropriate to point out that you too were discussing something without defining it, and that I felt your answer unsatisfactory for that reason. Again, I was asking for clarification but from you, and may downvote / may have downvoted on that basis.

Describing ethnicity can be a complex and multifaceted topic. It often involves elements such as cultural practices, language, religion, shared history, ancestry, and sometimes geographical or national origins. While ethnicity can include objective elements like genetic markers or historical data, it's often self-identified or identified by others based on a mix of subjective and objective criteria. There isn't a universally accepted objective method to describe ethnicity because it encompasses a wide range of factors that can vary in significance and interpretation across different contexts and societies.

ethnic classifications based on "objective" genetic data are themselves subjective. there are a lot of subjective decisions that go into how you do that work.

Like the poster, you do not define or give examples of what is meant by ethnicity, so  your post is futile. Please finish the [Tour] and the Help on answering questions. Your answer is just an expression of opinion with no evidence in its support. This is not appropriate for this scientific question and answer site.


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Using decoy proteins to treat viral illness
As a non-biologist, my understanding is SARS-CoV-2 uses it spike protein to latch on to the ACE2 receptor on cells in order to inject its genetic material into the cell.
Questions:

What would happen if you flooded a person with exogenous ACE2 proteins?
Would the virus attach to these decoy proteins and thereby save cells from being infected?
Would the injected proteins cause unwanted side effects?
Has this approach to treating viral infections been tried before?

Reference:
https://f1000research.com/articles/9-72

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users. In addition, if you are trying to "start a discussion" this isn't the site you're looking for. Finally, if you've read the linked paper you likely know whether these questions have answers and what they are as well as anyone here. Thanks!

I must admit your comment seems rather harsh. I don't have a biology background and included the paper as hopefully someone could use it to help me answer my questions (I was having trouble understanding it fully). My questions seem quite specific and don't see how I was inviting a discussion? Furthermore, prior to you commenting there was also an upvote.

A relevant article can be seen here.

SE Biology is a site primarily for questions about the mechanisms of biological processes that allow objective answers. Although I understand your concern about the coronavirus outbreak, your question is not about the biology of the virus but asks for comments on a proposal for treating the disease. Such questions about any disease are off-topic here. I suggest that you consult more appropriate reputable sources for such information, some of which are listed here.

This is indeed a reputable strategy (#1,2,4) for rapid response to novel pathogens.  See https://phys.org/news/2020-01-scientists-decoy-molecule-neutralizes-arenaviruses.html and the open access article it cites https://www.nature.com/articles/s41467-019-13924-6
In the case of coronavirus, however, there is an issue (your #3) in that ACE2 is an enzyme that catalyzes the breakdown of a circulating hormone, angiotensin II, which is responsible for maintaining high (or normal) blood pressure.  So the "bait" used would have to be at least somewhat altered from this.  You would probably have to take into account how it affected other protein interactions such as with integrin beta 1 ... (see articles like https://europepmc.org/article/MED/14754895 ) to avoid getting caught up in speculation, it makes sense that a neutralizing protein might be made from part of ACE2 just as a neutralizing monoclonal antibody could be made, but you still have to have something specific before you can test for safety and efficacy.

Thank you very much. This is very helpful!


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Do dragonflies smell nice?
We found this dragonfly husk in a box of files and grates. People don't rummage around there too often but its undamaged condition two or three weeks after we saw it alive is still remarkable. There's just that hole on the back just behind the head with the torso's hollow below it. It is about 10 cm long.
While picking off some motes, holding the tail with two fingers, I noticed the husk smells sweet, really just like musk. Though of two colleagues only one perceived the same, the other said it was just musTy.
Now I wonder, is it just an agreeable sort of decay going on, or do dead dragonflies usually smell like that? Do live ones?

Feel free to add any appropriate tags. Thanks.

Welcome Ariola. I doubt that anyone will have looked and documented this for us to know. Having said that the Victorian passion for collecting and cataloguing might have turned up something, but only an expert who has read species descriptions would note something like that in the literature. I'd suspect that there are other possible causes: bacterial/fungal decay smell, something else in the tool box like an oil or wood shavings, or possibly something like a mouse has passed through and left some urine/droppings.


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Unknown bacterial culture
I had taken a sample of bacteria from my toilet bowl and allowed it to grow on an agar plate. After 3 days, it now has a number of colonies and smells really bad. This was originally for my school science fair(next week) Now I am really scared that the culture may contain pathogenic bacteria. Is it safe to continue the culture or should I dispose it off?? Please help

If you need to show it to someone: clean your hands. Open a clean ziplock bag, place the petrie dish inside of it, and wash your hands again without touching anything else. Then seal the ziplock bag. It will be good for a couple of days this way. If you need more time, use photographs, or repeat the experiment, maintaining good hygiene throughout to avoid contaminating your sample. Don't bring the petrie dish into a public place without adequate isolation of the contents.

The project might benefit greatly if you could identify some of the microorganisms. A quick google search seems to indicate that some ways of identification are accessible to school students. For example this page lists a few methods like selective agar media. Perhaps your school or someone you know has a microscope?

Without the proper tests to identify the bacteria you have no method of identifying which species you have isolated and there is a chance that some of them are pathogens, especially as you have isolated from somewhere that is used for sanitation. There's a goodish chance that you haven't just isolated bacteria, but also yeast and other fungi.
Feces contains quite a range of bacteria, many species of which are opportunistic pathogens such as Escherichia coli (the famous "E. coli"), some strains of which are quite pathogenic. There are also species from genera like Shigella, Salmonella, Klebsiella, Clostridium and many others which are very common pathogens.
Handling these sorts of things is not necessarily dangerous with appropriate training and proper precautions (e.g. gloves, washing and sanitizing hands properly). If you decide to go ahead, make sure that you don't open the plate(s), to ensure that you can't spread the isolates around. If you do not have someone to advise on techniques and train you, you should not handle the samples!
You should discard the plate(s) in a biohazardous waste stream, do not just throw in the rubbish. Your school may be able to help with this.

Thanks for the answer. I have taped the lid of the agar plates and will be using gloves and a mask when handling them. The bacteria, or fungi will not have any effect on anybody if it the lids are not opened, right?

Not necessarily - the plates are designed so that there is airflow between the agar and the outside, so still a chance of liquid coming out. If you could seal them in a container or use clingfilm to seal the edges, that would be better.

Will ziploc bags be sufficient? Sorry for asking too many questions. I want to display the cultures but I also don't want them to harm anyone else.

Yes, Ziplocs would be perfect.

Oops, sorry, I didn't see this comment thread.


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How much oxygen does a brain consume?
I am not a biologist - my background is in quantitative sciences, and I am trying to answer a rather quantitative question:
How much oxygen does a brain consume?
This however raises many sub-questions of purely biological nature:

How is the brain supplied by oxygen? (My naive understanding is that lungs tie oxygen to hamoglobin, which is then carried by blood to cells, which then ingest the oxygen, converting it to ATF. Is this correct? Does this apply to neurons as well?)
How much energy a neuron or the whole brain consumes per unit time? (e.g., per hour, in energy units or oxygen content)

I will appreciate explanations in laymen terms or references to accessible literature.

https://www.dentinstitute.com/posts/lifestyle-tips/22-facts-about-the-brain-world-brain-day/ #16.please do a tiny bit of research before asking it here.

@trondhansen I've been doing research, and the link that you sent is a bit lightweight -  e.g., it says nothing about blood-brain barrier. Also, I need to see the numbers - e.g., how much energy does brain consume in Joules or kcals per hour?

As has been commented, the answers to some of the questions here can be found in the literature. The nutrients and oxygen reach all tissues by the circulatory system — i.e. in the blood. And the link supplied by @trondhansen suggests a litre of oxygen a day. (I wouldn’t know — I never studied physiology.) However, as regards energy, I supply the following from the biochemistry text, Berg et al.

Brain. Glucose is virtually the sole fuel for the human brain, except during prolonged starvation. The brain lacks fuel stores and hence requires a continuous supply of glucose. It consumes about 120 g daily, which corresponds to an energy input of about 420 kcal (1760 kJ), accounting for some 60% of the utilization of glucose by the whole body in the resting state.

Note the correct form of expression:

the brain  / consumes fuel / to generate energy / to perform ‘work’

Glucose is the fuel, ATP is the chemical energy currency, and the work performed (as the text makes clear) is for the main (60%–70%) to:

maintain the sodium/potassium ion membrane potential required for the transmission of the nerve impulses.

(I am afraid that’s about as layman’s terms as I do. It does say on the label that this site is for students of biology.)

Thank you for the explanations and for the reference (I have found a similar number - that brain consumes 20% of the total daily energy intake, which is about 2000 kcal.) Do I understand correctly that neurons receive both the sugars and the oxygen via the blood stream as raw materials, and convert them to ATP, just like any other type of cells?

Yes indeed. However cells are different in the way that the hormones of the fed and starved state affect the uptake of glucose through the cell membrane. This is done by transporter proteins. For tissues that can use other fuels in starvation, insulin is required by the transporters to prevent them using glucose, which is prioritized for the brain. The brain transporters are subtly different, in that they do not require glucose. The ATP generation is the same.

The project that I am working on actually presupposes using liposomes as a method for delivery of extra (Hb-bound) oxygen to the brain. From what I read, the liposomes are necessary for overcoming BBB (blood-brain barrier) which is inpenetrable for most drug-delivery methods. But it seems that this also raises the question of supplying additional sugars...

I don’t really know. I would doubt you could or would need to do that. Glucose uptake is usually a pull method in response to demand.


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Is Acetyl-CoA ever transported out of the cell, and in that case how?
Acetyl-CoA is sometimes formed as a result of protein katabolism. Certain cells (in the muscle for instance) can't use Acetyl-CoA to synthesize fatty acid. If there is no immediate need for energy, can the Acetyl-CoA then be exported out of the cell, so that it may be used for fatty acid synthesis in other tissues?
If so, how is this accomplished? I know Acetyl-CoA can be transported out of the mitochondria using the citrate shuttle, but how would it pass the cell membrane and get transported in the blood?


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How can the Na+-dependent Cl/HC03-pump pump several molecules against their gradient?
The molecular biology of the cell (6 ed) claims that:

"Another [antiporter] [...] is a $Na^+$-driven$Cl^--HCO_3$-exchanger
hat couples an influx of $Na^+$ to an efflux of $Cl^-$ and $H^+$. (so
that $NaCO_3$ comes in and HCl gets out)"

In the next paragraph, (regarding a transporter with an opposite direction) we can read that:

"The movement of $HCO_3$ in this case is normally out of the cell,
down its elecrochemical gradient, which decreases the pH of the
cytosol".

Meaning that intracellular concentrations of $HCO_3$ typically must be higher thatn extracellular concentrations. In addition, Khan academy (among other sources) tell us that the extracellular concentration of $Cl^-$ is higher than intracellular concentration.
This means that for the price of one $Na^+$, the pump is moving two molecules ($HCO_3$ and $Cl^-$) against their gradients. How is this possible?
Is the $Na^+$-gradient really so strong that it can power this simultanous unfavourable transport? Or are multiple $Na^+$ ions used? Have I misinperpreted the intracellular/extracellular concentrations of  $Cl^-$ and $HCO_3$?


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How do I find the derivation for the formula for total clearance?
In Rang & Dale (10 ed) on page 152, the formula for total clearance is given by:
$$Cl_{tot}=\frac{Q}{AUC_{0-\infty}}$$
$CL_{tot}=$total clearance, Q=initial does given, $AUC_{0-\infty}$ Area under the concentration/time curve from time 0 to infinity. No explanation for this formula is given, at least not as far as I can see, it's just stated as some kind of obvious fact. How do I arrive at this formula (i.e, where is the derivation?), is it given by some kind of elementary rule?
I did consider posting in math.stackexchange.com but they didn't have tags for pharmacology.

In the version of the textbook I have access to, it says "See Ch 8 and Birkett 2002" - have you looked there?

I found an explanation on my own (see below), but thanks for feedbak.

Previously on that same page it says that:
$$Cl_{tot}=\frac{X}{C_{SS}}$$
Where $Cl_{tot}$ is volume of plasma cleaned per unit of time, X is the amount of drug supplied per unit of time and $C_{SS}$ is the plasma contentration at the steady state. This formula is quite similar to the one in my question, although that concerns a single bolus dose, not a continuous supply of the drug.
The first thing I needed to do was to realize that this too describes a unit of time. More precisely, it describes the time between o and infinity. If $Cl_{tot}$ is interpreted as the volume of plasma cleared of that drug between 0 and infinity, the formulae are almost equivalent.
The only remaining stumbling block is whether or not $AUC_{0-\infty}$ can be said to be equal to $C_{SS}$. In a philosophical sense you can, since that "is" the total "sum of concentrations" which the body has gotten exposed to between 0 and infinity. We can make this even more similar to the formula for continuous drug administration by assuming that "sum of concentrations" could probably be spread out evenly over the entire timeline, giving us a mean steady state concentration (which would then hopefully yield the same result).
There might be some incorrect formalities somewhere but this is what made sense to me intuitively.


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Why do tumours need stem cells, when they can generate their own telomerase?
In the molecular biology of the cell (6th ed), it is stated that:

Some cancers seem to be organized in a similar way: they consist of
rare cancer stem cells capable of dividing indefinitly, toghether with
much lager numbers of dividing transit amplifying cells that are
derived from the ancer stem cells but haave a limited capacity for
self-renewal. These non-stem cells appear to constitute the great
majority of the cell population of some tumorus (p.1121).

Although in an earlier segment, however, we can read that:

Human cancer cells avoid replicative cell senescense in one of two
ways. They can maintain the activity of telomerase as they
proliferate, so that their telomeres do not shorten or become
uncapped, or they can evolve an alternate mechamism based on
homologous recombination (called ALT) for elongating their chromosome
ends. Regardless of strategy usedd, the result is that the cancer
cells continue to proliferate under conditions when normal cells would
stop (p.1100).

How do we interpret these two passages? Are some cancer cells incapable of lenghtening their telomeres, and is it these types of tumours that can't persist without cancer stem cells? Or are cancer stem cells beneficial in some other way to the tumour (such that a tumour stem cell might differentiate into several types of tumour cells, which might be suitable for different environments)?
I understand that having cancer stem cells that proliferate at a slower pace than regular cancer cells might be beneficial for withstanding things like chemotherapy. But what's being emphaphized is not their capacity for survival, but their greater ability at self renewal?

Be careful with thinking that tumors have wants and needs; these are descriptions of what happens, not statements of how things need to be.

Sure, I could have rephrased that in another way ("Why tumour cells which aren't stem cells have a limited capacity for self-renewal?"),

Isn't that a tautology?

This is like asking why there are multiple forms/mechanisms of dementia when "one would suffice".
To save this from being just a trivial comment, note that the mechanism of elongation differs between cancer types, likely depending on the types of cells involved:

Despite being present in a minority of cancers overall, the prevalence of ALT in cancers is not uniform, with cells of mesenchymal origin being more likely to rely on ALT for telomere elongation. Indeed, certain cancers, such as osteosarcomas and cancers of the central nervous system, have rates of ALT positivity approaching 90%, eluding to possible mechanistic reasons for ALT development. The most likely cause of this distribution is that, in contrast to cells of epithelial origin, cells of mesenchymal origin are more likely to have more stringently regulated telomerase expression, reducing the potential for telomerase-mediated telomere maintenance.

Are tumors cells vulnerable, as healthy stem cells, to DNA alteration?

My professor claims that cells go into senescence due to multiple reasons, and that many cells stop dividing after a set number of divisions, despite having ample telomeres and no appreciable DNA damage. He claimed that tumours (counterintuitively) often work in this very same way, so that cancer cells need to be able to differentiate back into cancer stem cells for the cycle to reset itself.
I'm not really qualified to determine who is right. I'll post this answer and let people vote for what's more reasonable.


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Can a macrophage differentiate back into a monocyte?
I know that monocytes differentiate into macrophages when they enter the tissues, but do macrophages stay in those same tissues for the remainder of their lifespan, or do they differentiate back into monocytes and re-enter the bloodstream at some point?

No, macrophages can not turn back into monocytes, usually once a monocyte travels around the bloodstream for 1-3 days, it then leaves the bloodstream and travel to a tissue where it will differentiate to a macrophage or dendritic cell. It undergoes a conformational change, this usually happens during inflammation as the macrophages travel over a chemical gradient, macrophages can still enter the bloodstream, however, they won't re-differentiate to a monocyte. So to answer your question directly, macrophages don't stay in the same tissue forever as their life span is pretty long(1-2 months) so most likely an inflammation will occur and force the macrophages to diffuse across the chemical gradient, but they usually patrol around the tissue area where they differentiated.
source: http://www.histology.leeds.ac.uk/blood/blood_wbc.php

This paper found dedifferentiation of macrophages back to monocytes
https://mbio.asm.org/content/10/5/e01743-19
"Bordetella Adenylate Cyclase Toxin Inhibits Monocyte-to-Macrophage Transition and Dedifferentiates Human Alveolar Macrophages into Monocyte-like Cells"
Jawid Nazir Ahmad, Jana Holubova, Oldrich Benada, Olga Kofronova, Ludek Stehlik, Martina Vasakova, Peter Sebo
mBio Sep 2019, 10 (5) e01743-19; DOI: 10.1
Found by searching with keywords macrophage dedifferentiation