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Does terminology for changes in membrane potential refer to additive or multiplicative change?
Is the membrane potential just the number of mV, or is it to what extent it differs from 0?
For example: If the mV goes from -40 to -60, can you say that:

The membrane potential decreases, because the number of mV decreases (from -40 to -60)
or
The membrane potential increases, because the difference to 0 increases (from 40 to 60)?

Note to others: this question appears to be about terminology rather than the biophysics behind the membrane potential.
When the terms "increase" and "decrease" are used relative to membrane potential, they refer to additive changes in potential, not to multiplicative change or effects on absolute value. The standard is to relate the potential inside to the potential outside of a cell (so a negative potential means the inside is more negative than the outside; potentials in biology are always relative, just like in physics).
Therefore, a membrane potential decrease means that the value of the potential becomes more negative, and a membrane potential increase means the value of the potential becomes more positive. The changes on the absolute value of the potential depend only on where you start from.
Other terms that are more clear to use are hyperpolarization and depolarization, where hyperpolarization always refers to the membrane potential becoming more negative than rest, and depolarization refers to the membrane potential becoming more positive than rest. Repolarization is also used, particularly in the context of action potentials, to refer to voltage changes in the direction of hyperpolarization when the cell is currently depolarized.


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What is this small tissue structure found in kidney?
It's covered with white adipose tissue and it is smooth with reddish brown colour. HE dyed with dimensions 3 cm long and 1 cm wide. I'm guessing that this is a rare thing because I already checked pubmed etc. On the right is a closer picture of the tissue.

Voted to close because this sounds like a homework question - I don't think there would be another reason to ask this question unless you are a student - if you clarify otherwise I would consider retracting my vote. We aren't here to do your homework for you, I'm guessing if this was given as an assignment then part of your lesson was on this structure specifically.

You added that it is rare - what if it is actually very very normal? (where did you get the images from?)

Could you add a pointer?

@SanjuktaGhosh It's the whole structure. The entire pink-tinted area on the top picture. (it's actually quite obvious I just don't want to give the OP the answer if this is homework...)

I can't find anything abnormal. Had a histology course recently so I'm curious if there's something I can't spot. @BryanKrause

@SanjuktaGhosh That's because it's not abnormal.

It's the whole structure and this is not a homework. I saw this on webmicroscope and got really interested. I have been looking kidney histology articles and books and I have hard time figuring out what are these since i'm not studying medicine. Smooth structure made me think it could be multilocular cyst but i'm not sure and the sice of these is huge in kidneys.

Ok...hint: it's a gland. (and it's very normal to have these particular glands on your kidneys..)

@BryanKrause this is interesting. Suprarenal? aldosterone, cortisol etc...

Okey so they must be adrenal glands then. Why did I even think that these would have something to do with diseases...

@KatariinaJ. Bingo. If it makes you feel better, your description at the start was so spot on I assumed it was from a textbook question. If you read about adrenal glands they are often described precisely as being found under adipose tissue on top of the kidneys. The best identifying feature besides the location is the clear separation of tissue type into adrenal cortex and medulla, which are also quite distinct in function.

Thank you for helping me figure out this one with hints. This made me learn a lot. I was assuming way too many things.

@BryanKrause Please post an answer!

@canadianer Done. I like these IDs better than species IDs, those are too hard for me :-P

@BryanKrause Thanks +1. I do too. Wish there were more of them

This is a slice of an adrenal gland:

Source (Creative Commons Attribution-Noncommercial-Share Alike 3.0 License): http://histology.medicine.umich.edu/resources/endocrine-system
These glands sit on top of the kidneys, typically under adipose tissue (which can also be seen in both your image and the image I included here). The most identifying feature of the adrenal gland is its clear separation into two parts: the outer "cortex" and inner "medulla", as labeled on the image.
The two parts have different endocrine functions: the cortex primarily produces steroid hormones, like aldosterone and cortisol, whereas the medulla makes catecholamines epinephrine and norepinephrine (also called adrenaline and noradrenaline). I believe the inset in your image is of the medulla.

source: Stack Exchange

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Can some prokaryotic cells be larger than eukaryotic cells?
Can the sizes overlap in some bacterial species? My science teacher claims so. My research says the opposite. Can someone confirm?

You should really unaccept the answer by Radek Martinez and change it to Remi.b's answer. The former is both unhelpful and simply not correct, while the latter gives specific examples of its point.

Prasinophytes are the smallest known eukaryotes. They are around 0.5 µm in diameter.
Thiomargarita namibiensis is the largest known prokaryote. They are around 100-300 µm in diameter.
So, yes some prokaryotes are much larger (up to about 500 times larger) than some eukaryotes.

To add to it, Pandoravirus, a virus, is about 1 µm by 0.5 µm. So not only can some prokaryotes be larger than some eukaryotes, some viruses are larger than some eukaryotes.

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Why is thrombin time longer than prothrombin time?
Thrombin time (TT) and prothrombin time (PT) are two different clinical measures of blood plasma coagulation.
Both clotting tests end with the conversion of fibrinogen to fibrin; however, the TT skips directly to this conversion by adding thrombin reagent, while PT involves the entire extrinsic pathway. Despite the fact that PT involves the same clotting steps as TT plus several others, the normal range for TT is slightly longer than the normal range for PT.
Why is the normal range for TT longer than the normal range for PT when the former skips several clotting steps? Without background information about the normal ranges, it seems much more logical for the prothrombin clotting test to take longer.

I think the close votes here are a bit premature - this question could be improved a bit but it is actually an excellent question.


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When to use fixed effects vs random effects models?
I had previously read some on this topic and my understanding was that a fixed-effect model is when you are sampling an entire population, for example, a school district, a school, or a village. And a random-effects model would be used when taking from any of the populations a sample where the goal of the random-effects model would be to estimate the population. I am reading Successful hunting increases testosterone and cortisol in a subsistence population and the authors describe:

Individuals were modelled as random effects to control for
non-independence of multiple specimens collected from the same
participant.

I am not understanding this that well and am asking for further explanation, please. While on the one hand, it seems because the entire population (viz. the village) was not sampled we would use the random-effects model.

Is there some reason you aren't asking this on [Statistics.SE]? If not, I recommend you move the non-biology questions to that site and delete them from this one; NB: please do not crosspost. ——— Please also post each question separately — this helps you get answers to each question and makes those answers much easier to find for future users. Please see the [tour] and consult the [help] starting with [ask] for details.

@Tyersome IMO this is a good fit for the site. It's contextualising a statistical question in terms of biology - the biology is key to the question.

There are too many questions here; I've removed the additional questions, but you can ask them separately.

For the quoted text, the mixed vs. fixed has nothing to do with sampling the entire population vs. a subset but rather with multiple samples per individual. This makes the samples non-independent, so a mixed model is necessary. The question is better answered here: https://stats.stackexchange.com/questions/4700/what-is-the-difference-between-fixed-effect-random-effect-and-mixed-effect-mode

While I am a biologist by trade, not a statistician, I still do a fair bit of statistical modeling. It seems like you were taught a flawed, or at least incomplete understanding of mixed effects modeling. While your experimental design is what determines whether an effect is fixed or random (at least it should be), the description you gave doesn't really match with how they are used (at least in my experience with modeling). I'll try to break that statement down a bit just based on what you wrote in the question.

... my understanding was that a fixed-effect model is when you are sampling an entire population, for example, a school district, a school, or a village. And a random-effects model would be used when taking from any of the populations a sample where the goal of the random-effects model would be to estimate the population.

First, you don't need to sample the entire population to measure a fixed effect. If you surveyed 10% of the people in a village at random, you still model your response variable as a fixed effect for that village. But, say instead you sampled 10% of the household units in a village, sampling each person within each household once. There are likely to be various environmental or genetic factors that are shared within a household that vary between different households. Because of that non-independence, each set of household samples can be thought of as it's own sub-population of samples that aren't truly independent from one another. So you would include a random effect term for households in your model, to account for those variations. But the actual response variable (or variables) of interest would still be modeled as fixed effects.
The same goes for the example in the paper. Even if the entire population had been sampled, each individual has their own unique set of genes and metabolic processes that can vary from person to person, so those repeated measures are not independent from one another. Modeling individuals as random effects allows you to see how your variables of interest are related at a population level without being confounded by those little difference between people.
This is one reason that cross-sectional study designs, where each subject is sampled only once, can be limited when it comes to generating generalizable inferences about a larger population. Without those longitudinal samples, it's not possible to account for any of that inter-individual variation in your models.
Mixed models can get pretty complex pretty easily with more comprehensive sampling efforts and study designs. Say you have longitudinal samples collected from multiple households across multiple villages. Now you have to consider how all of those confounding variables (village, household, individual) are related to one another and design statistical models in which each of those terms are appropriately nested to properly account for random effects.
For some more reading, I think this chapter from Applied Statistics for Experimental Biology by Jeffrey Walker does a pretty good job of explaining mixed how models work with some good examples of how they are constructed for different scenarios.

I think the confusion OP has about "sampling the whole population" should be about sampling the levels of factor, rather than the population. Generally, you use fixed effects when your data include all the levels of a factor (for example: Smokers and Non-Smokers cover everyone; smoking/non is a fixed effect), and random effects when they don't (for example, you sampled students in Paris, London, and Berlin; city is a random effect). However, that's not a comprehensive explanation of the difference, just a superficial guideline. It's certainly important for OP to learn more before using this.

(...cont) If you are "sampling each person within each household once" you don't need any random effects for the household - your error by household is wrapped up in your overall error term. However, if you sampled multiple people in each household, you may want a random effect of household to account for the part of the error that is shared among people in a household. It's only necessary when you have multiple observations there.

(...cont) Same thing at the village level: if you're sampling multiple villages, you'd probably have village as a random effect, not a fixed effect, if those villages are somewhat arbitrarily selected from all the possible villages in the world or in a country or whatever. If, however, you want to compare Springfield to Shelbyville as a research question, you'd model village as a fixed effect: you haven't chosen those villages randomly in that case, you've selected them specifically as part of your research question.

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Why are the posterior and anterior inferior temporal cortex called area TEO and area TE respectively?
I don't understand why you would call them that. How did these names originate/where did these names come from?

Was able to add some more information on the "TE" terminology after you accepted the answer, just a FYI if you are interested.

Thanks I see now, it's a lot clearer now that I know it has no meaning.

These are very old names for primate cortical areas, originally from the anatomist Constantin von Economo and also used by von Bonin and Bailey (1947) (where the TEO region name seems to originate).
Like Brodmann areas these regions were defined by cytoarchitecture well before most functions were determined.
I discovered another work that I can access from 1935, Rose (1935) that is quite helpful for the TE terminology. From Rose it is clear that von Economo labeled areas in the temporal lobe TA, TB, TC, etc. up to TH. So they seem to be simply "temporal"+letters of the alphabet. Rose refers to "Area temporalis propria" as area TE, comprised of Brodmann areas 21 and 20; Rose calls Brodmann 21 "TE1" and Brodmann 20 "TE2" which are separated based on the size of layer 3 pyramidal cells.
As far as the TEO terminology, Boussaoud et al (1991) write:

In their study of  the cytoarchitecture of  macaque cortex, von Bonin and Bailey ('47) labeled this region with a question mark on their section drawings but showed a photomicrograph through the region that they labeled  “TEO.”

This is the best evidence I can find that the TEO name a) originated with von Bonin and Bailey, and b) that the further origin or meaning of the name is unclear; it's just a label on a photomicrograph that wasn't even used in the drawings by those authors who instead used a ?. I suspect further authors preferred the TEO terminology rather than confusingly referring to "area ?" and yet they felt like giving credit to von Bonin and Bailey for their work on the macaque cortex.
It's unclear to me whether TEO is meant to be an acronym; "temporal" is part of the name, but whether O stands for a word (perhaps occipital, as it is toward the occipital lobe?) or if it is actually the number 0, or a non-English word (possibly German or Latin?). However, when more modern neuroscientists refer to area TE and area TEO, they are simply intending to refer to "area TE and area TEO in the von Economo/von Bonin & Bailey terminology."
Other terminology, such as referring to posterior or anterior inferior temporal cortex, may seem more descriptive but there isn't anything inherently wrong with referring to the older names as long as people know what area you refer to. TE and TEO are clear, short names that have been used for decades, whereas inventing a new acronym like PIT or AIT would be unfamiliar at this point.
References
Boussaoud, D., Desimone, R., & Ungerleider, L. G. (1991). Visual topography of area TEO in the macaque. Journal of Comparative Neurology, 306(4), 554-575.
Rose, M. (1935). Cytoarchitektonik und Myeloarchitektonik der Großhirnrinde. Handbuch der Neurologie, 1, 588-778.
von Bonin, G., & Bailey, P. (1947). The neocortex of Macaca mulatta.(Illinois Monogr. med. Sci., 5, No. 4.).
von Economo, C. F., & Koskinas, G. N. (1925). Die cytoarchitektonik der hirnrinde des erwachsenen menschen. J. Springer.

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Do blood cells immediately die after leaving the body?
I am wondering, do blood cells die right after they leave the body?

Reasonable question, but it could use some clarification re: what you mean by "die".

Hi C. Jordan, wlecome to Bio.SE. What research did you do to try to answer this question on your own? We ask that all question askers on Bio.SE try to answer their own questions and then ask questions only about specific details they cannot find an answer to or that they do not understand. Please update this question with evidence of such prior research, and please be mindful of this as you continue to interact with this community. thanks!

@theforestecologist I was looking up on a website about refrigerating blood samples, but got varying results.

No. If they did, blood transfusions wouldn't be possible (or they would require some sort of direct body-to-body system).
Red cells collected can be stored under refrigeration for over a month. See for example the description of what happens to donated blood from the Red Cross. Platelets don't last quite as long, but they also survive for some time in the right conditions. Of course, some cells die during storage, but there is no instantaneous die-off once cells leave the body.

+1, though this is perhaps a philosophical question

Blood cells do not die immediately because they still have some amount of nutrients in them that they can use until it finishes.
They only die when they lose their source of nutrients after using up all that is in them.
Cells in blood still have access to nutrients due the presence of plasma which helps keep them alive for while.
Put in a fridge(4-18°C), the temperature slows their rate of metabolism allows which further extends their lifespan. But can die of heat shock if frozen and thawed.
You can read more on it in;
Effect of Blood Storage on Complete Biochemistry
Effect of Specimen Collection and Storage on Blood...
The pathophysiology and consequences of red blood cell storage
Red blood cell storage time and transfusion: current practice, concerns and future perspectives

Please provide support for your answer. Cite at least one reputable source that backs up your claim. Thanks


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What is the meaning of a 1,4 bond between sugars?
I don't know how to express my question. I want to know what are bonds like 1.4 bond between molecules. I've read somewhere like the amylase enzyme can break 1.4 bond. I want to know what are these bonds and what are their benefits and where  can I find more info about them?

Amylase breaks the bond between two sugar molecules in a chain (the chain is called starch).
The type of bond is called a glycosidic bond which is just a covalent bond between sugar molecules.
The "1.4" bond you are talking about is normally written "1,4" or "1-4"; you could interpret it as "1 to 4" because it is referring to a bond involving the first and fourth carbons of the sugar (they aren't bonded directly, there is an oxygen in between); they are just numbered that way so that (bio)chemists can talk about the molecule - see this other Q&A from Chemistry about the numbering of the carbons of glucose.


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Does the modern synthesis theory of evolution deny that acquired characteristics can be inherited?
The following is an wikipedia article on Lamarckism.
https://en.wikipedia.org/wiki/Lamarckism

According to Ernst Mayr, any Lamarckian theory involving the inheritance of acquired characters has been refuted as "DNA does not directly participate in the making of the phenotype and that the phenotype, in turn, does not control the composition of the DNA."[75] Peter J. Bowler has written that although many early scientists took Lamarckism seriously, it was discredited by genetics in the early twentieth century.
The evolutionary biologist T. Ryan Gregory contends that epigenetic inheritance should not be considered Lamarckian.

It seems to me that the assertion that acquired characteristics can be inherited was denied by the modern synthesis theory of evolution.
Is this true?
If yes, what is the reason of the denial?

Where did you hear it?

Answered before searching the site. Might be a duplicate of    http://biology.stackexchange.com/q/884/19650

@Chris Please read my new edit to the question.

Generally, yes, this is not part of theory of evolution as it is generally accepted by most of the scientific community.
For a trait to be subject to natural selection over several generations, it needs to have heritability, meaning it needs to show up in offspring (or their offspring). Generally, what is called an "acquired trait" does not fit that criterion. What's passed on is the genetic material of the parents and that doesn't change when the parent acquires these traits.
For example, bonsai trees are kept small by environmental conditions, as such, their height could be called an acquired trait. Their offspring does not naturally grow as a bonsai tree. Giraffes did not grow longer necks because they stretched them, but because those giraffe ancestors with longer necks (which just happens randomly through mutation - you have varying neck lengths in a population) could reach food more easily and could survive when those with shorter necks didn't. The giraffe example is a classic one that was proposed by Jean-Baptiste Lamarck, whose theory of evolution (called Lamarckism) was superceded by Darwin's.
There are traits where acquired versus genetic traits are hard to differentiate - while a good athlete does not have children who are athletic because their parent did sports, they are often also good athletes. For one thing, the parent might be genetically "suited" for sports and has passed these genes on. Another reason is that they will probably train their children and want them to become more athletic.
I know of one example where something that could be called an acquired trait is passed on to offspring - methylation patterns. Those are modifications of the genetic material that happen during an organism's lifespan and aren't modifications of the actual genetic code - they can be passed on to offspring. Since these patterns influence gene expression, they have an effect on the offspring. However, that's usually not what people mean when they talk about acquired traits.
Lamarckian inheritance

It's worth pointing out that popular conceptions of epigenetic inheritance (methylation patterns) are wildly out of line with the actual science.  Popular media have spread the notion that epigenetic change is much more powerful, long-lasting, and widespread than it actually is; in reality epigenetic inheritance is rare in general, typically has little impact, and even when it does occur generally fades before it can impact evolution significantly.  People who read popular science often believe that Lamarckian evolution has been supported, a view that isn't supported by the actual evidence.

What about the hologenome theory?
The hologenome theory of evolution contains Lamarckian aspects within a Darwinian framework.
http://www.ncbi.nlm.nih.gov/pubmed/19573132


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Herd immunity without vaccines? (corona question)
Obviously there is herd immunity against many viruses such as measles because of vaccines.
Can we say that there is herd immunity against any particular virus even though people are not getting vaccinated, and what virus would that be?
Do you typically get herd immunity without vaccines against viruses without vaccines or do the viruses just linger around and infect fewer people because many have already become immune after catching the virus and developing anti-bodies?
What is "normal" virus behaviour?

Can you please not substancially edit a question after it has been answered to bascially add another question to it? Please open a new question instead.

This is not just a corona related question, this is true for each disease which is can be transmitted easily and which builds up a lasting immunity.
Herd immunity per se means that a large proportion of a given population is immune to a given disease, either because of vaccination or because the population went through the disease, survived it and built up lasting immunity. This means that even when this disease comes around again, it will only infect few people who have no immunity, but will not spread through the population. This can be seen in the figure below (from here), which implies vaccination, but works as well with getting the disease.

The first case is what happens right now with SARS-CoV-2, it is a new disease to which no one has immunity, so everybody who gets in contact will get the disease (either more or less severe).
If no vaccine would be available, this infection would go on, until a big enough proportion of the population has gone through the infection, developed immunity and thus stops the spread (go to the third part of the figure). At this point a big pandemie would stop.
However, this strategy has one problem: People who are coming into the population (newborns for example) who have no immunity are susceptible for the disease. This ensures low level infection rates and will make sure that the disease will stay in the population, but mostly not noticable. Over time the number of not immune people will rise until there are enough of them to feed another big breakout.
As @bryankrause pointed out, in the past getting to the point to reach herd immunity (at least partly) for diseases like smallpox or measles and to maintain it, cost a lot of lifes.
This is exactly what can be seen in the number of measles cases before the introduction of the vaccine in 1967. Before vaccination every 18 - 24 months enough people without immunity where present, causing another wave of cases. After introducing the vaccination this pattern changes and case numbers went down drastically. See the figure (from reference 1) for illustration. This figure uses data from the US, but you see similar pattern in the rest of the world.

For some more information have a look at reference 2.
Reference:

Evolution of measles elimination strategies in the United States.
Vaccination and herd immunity: what more do we know?

Might be worth pointing out that for previous diseases in which herd immunity was present in parts of the human population, like smallpox and measles, there was a substantial cost in deaths to get to and maintain that point.

@BryanKrause Good point, I will add it.

"this infection would go on, until a big enough proportion of the population has gone through the infection, developed immunity and thus stops the spread" This assumes the vaccine, or rather the immune system, gives immunity. Influenza for example, develops unrecognisable antigens faster than our population can develop immunity, hence an individual can get the flu many times. How does that fit in with this model of herd immunity?

@James It still fits. After the mutation of the flu you don't have the same virus anymore that run through it before. There is immunity against the old virus (either from vaccination or the infection itself) but there is none to the new one. Thus we get a lot of infections until we cross the threshold in the population and reach herd immunity. Luckily we only see real pandemic flu viruses rarely, with the last one 2009 being an exceptionally mild one.

Herd immunity is not a steady state. There are always new babies born, adding susceptible persons to the population. So even in the case that there is neither immunity waning nor antigen drift in pathogen, herd immunity goes away over time, and a new wave of infections becomes eventually possible and happens sooner or later.
In order to keep herd immunity (as in the case of measles) you will have to vaccinate the children.


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What factors allow some species to outcompete species formed by the local environment and become invasive?
If an invasive species is introduced to a new environment, why can they outcompete local species in the same nische, if they specifically evolved in this local environment and are adapted to it, whereas the invasive species would have evolved in a similar, but not identical environment?
What factors determine wether a new species will become invasive or nor be able to survive in the new environment, and can we predict that beforehand?
What does this mean for future space exploration? Lets say, we find life on mars and bring it back (or accidentally bring it back with the sample return mission), what are the chances that it could survive on earth, and what is the probability it could pose a threat to native life?

one of the best examples about  invasive species is iceland,it once had forrests covering large parts of the country and then sheep was introduced,you can read a bit about it here: https://www.skogur.is/en/forestry/forestry-in-a-treeless-land/history-of-forests-in-iceland

Interesting! Thank you very much :)

In this case, the competitive advantage of sheep is obviously that they are useful to humans. But that is quite a special case. I am more interested in the general case. What determines if a species is well adapted, and why are local species not even better adapted to the local environment?

You are right, most species cannot invade most new environments, they have to be specially adapted to the new environment. For example, a jungle frog can't invade a desert; it'll dry out and die.
You are also right that a newly introduced (invasive) species is (almost) always going be less adapted for the new environment than the local species already living there.
So why can introduced species out-compete the locals despite not being as well adapted?
-->Most of the scientific evidence seems to point to a lack of predators in the new area for the invading species.
-->This can make some sense if you think about the power dynamic between predator and prey.  If predator and prey have been living together and evolved to have relatively equal hiding and hunting ability, then they can coexist.  But if a prey and predator have never encountered each other, it's possible there'll be a power imbalance.  Perhaps, the predator is really good at hunting the new prey, or maybe the prey is really good at avoiding the predator.  If the prey is invincible, then it becomes an invasive species in the predator's habitat.  If the predator is invincible, it becomes an invasive species in the prey's habitat.
I love that you're thinking about space, but science can only really answer testable questions. -- Mars Aliens -- aren't really testable right now.
That said, probably the Mars aliens would win since their incompatible chemistry would be to their benefit.  If we assume the aliens are made of weird chemicals that nothing on Earth has evolved to digest, then we wouldn't be able to eat them and derive energy, so they probably wouldn't have any predators at all.  But why would they be able to eat us? Well, just like astronauts on Mars could live off the ice we find at Mars' poles, probably the Mars aliens would be able to find something similar, some of their chemicals here on Earth that they can still use for themselves to take over.
--> But I don't think they'd be eating us humans any time soon! :)

Oh, I was thinking about Bacteria from Mars (either by bringing back soil, or even naturally, through Panspermia). The predator-prey relationship is certainly interesting! Would it be correct to say that invasive species usually do well in environments, if those environments themselves have undergone radical changes recently (for example, certain predator species dying out, recent changes in climate, ...)?

Because what confuses me: If there is an obvious niesche, like animals that can kill turtles on an island, where before, they had no natural predator, why did no other animal evolve to fill that niesche? Is it just a question of time? (iE would there have been canivorous dodos hunting other dodos if we had left them alone for another couple million years? Or are environments like that stable without outside interference?)

And since you mentioned predictability: Is there any way to quantify what environments are "at risk" of invasive species surviving there, vs environments, where most introduced species would not pose a threat? Is there a way to quantify if a specific species would pose a threat to a local ecosystem if it was introduced there?

I don't know too much about the evidence on recently disturbed environments, but it is well studied by ecologists worried about human disturbance,  I'm sure you can find lot's of information about it.  Maybe even post it here as answer afterwards.  I remember hearing about it once in class, and I think it depends how the environment is disturbed,  some disturbances open up new niches, while others just destroy the environment, lol.

re 2nd comment: no! environments are not stable without outside involvement.  Look up the experiments on trying to establish a mars or moon style colony prototype here on earth.  they can't do it because inside the locked away biomes, nature does it's thing and the ecology comes crashing out of balance.  Also look at the rabbit fox/wolf simulation experiments where they show the expected predator/prey boom bust cycles.  all that said, yes, I do expect eventually we would see dodos evolve to eat other dodos. and then once that new animal evolves, new parasites would evolve to parasitise it...

re 3rd comment: yeah, definitely investigate the literature for all that,  I don't know much, but I think it's well studied.


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What is the water and fat composition of the human brain?
Everywhere I look online says the brain is about 60% fat. But when it comes to water, I see numbers like 70-75%. One webpage even makes both those claims back to back! That doesn't make any sense. So what is it, really?

Can you provide citations (e.g., links) to the competing claims?

Whenever you see a percentage, you should think "Percentage of what?".  Not doing this is usually at the root of the trouble people get into with percentages.
The water and fat percentages mentioned in the question are certainly not percentages of the same thing.  The sources of the figures should make clear what the percentage is of, but non-scientific writing quite often fails to do this.
In the paper "Lipid composition of the normal human brain", there is a table giving percentages of water and lipids (fats), and at the bottom of the table it says:

All values, except water, are expressed as a percentage of dry weight.

This is a common approach, as, for example in this table from a textbook the lipid percentages are also given as percent of dry weight. This is convenient because water is such a large part of most organisms, and also dry weight is what is usually measured in the laboratory.
Thus the water percentages you are seeing are presumably percentages of total weight, and the fat percentages are percentage of dry weight.  You can convert the latter to percent of total weight by multiplying by the dry percentage of the brain, which is what is left when you subtract the water percentage from 100%.
Thus, assuming say 73% of total brain weight is water, the 60% fat figure would translate to about 16% of total brain weight is fat.

mgkrebbs is totally right. It's standard in biology to evaporate the water to get the wet/dry weight, and then to see for the rest. This study is old so it may lack accuracy:

Please give a citation for the source of this table.

The reference is: JS O'Brien and EL Sampson. Lipid composition of the normal human brain: gray matter, white matter, and myelin. J Lipid Res. 1965 Oct;6(4):537-44.

The reference to what? Answers on StackExchange must be self-contained; it's very good to provide references, but also important to include the information that is referenced.


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Can an epileptic seizure start in the spinal cord?
My understanding of an epileptic seizure is caused by "invalid electrical signaling" in the brain. Can these start from the spinal cord  (outside the brain) and move into the brain and cause an epileptical seizure? (sorry for not using the right terms)

Can you clarify what you mean by "outside the brain"?

can you provide example of place "outside the brain"? is it leg/spinal cord? Space 2 feet away? I am serious

Yes, spinal cord


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Can insects or mosquitoes be astonished(shocked)?
Can insects like mosquitoes get astonished by sudden happenings?
Background
I missed hitting a mosquito on a wall with great force. However even though I missed hitting it, it was dead.
So I wonder if insects can reach death or at least astonished by sudden happening, or lead to something like cardiac arrest.
Hope it isn't a noob question :)

+1 for the title. By the way, astonished is maybe too strong a word, but I guess that you could have its monocle fall out of surprise and maybe spill a drop or two of tea on the armchair. :-)

Have you considered alternative explanations? Seems like simpler explanations include: you hit the mosquito but didn't realize it (because it was not trapped between the wall and your hand), or that you caused a sufficient air pressure wave to damage the wings of the mosquito. They are relatively delicate, after all.

@BryanKrause Thanks, that could be. However I am curious about this question (Insects' abilities to get shocked)

I originally thought there was no way anyone had studied this - it felt like one of those questions we get here a lot where people seem to assume "scientists know (almost) everything" - but I decided to give a check anyways.
Short answer
There is in fact evidence that some insects could be scared to death. However, the process is a bit less dramatic than the one you suggest.
I didn't see much on mosquitoes specifically, but your question seems to allow extrapolation from other insects.
Longer answer
I found at least one paper, McCauley, et al. 2011, that studied whether the mere presence of a predator could cause fatal reactions, in this case in dragonflies. There are several others that show more generic stress-induced responses.
McCauley, et al. exposed dragonfly larvae to predators (either fish or a larger dragonfly) who were unable to actually eat the larvae because the larvae were contained within a 'cage' within a larger aquarium.
The larvae exposed to either predator type had substantially more mortality, and only about 30% as many survived to adulthood. This is not precisely insects being startled to death, but rather they propose that the chronic stress of predator exposure caused their growth to be impaired. An alternative explanation is that the larvae exposed to predators simply spent too little time eating to obtain enough nutrition, but they argue in their discussion that this is not likely to be the only cause in the case of the dragonfly predators, because unlike the fish those predators did not reduce their foraging behavior.
There are many other papers that talk about "non-consumptive mortality" more generally but these often include causes of death such as succumbing to injury from failed/incomplete predation, energetic expenditures, etc (Siepielski et al., 2014; Veselý et al., 2017) - few others actually use a highly controlled environment to prevent physical contact between predator and prey like in McCauley. Other studies do show that exposure to increased stress levels causes changes in gene expression and impacts on the immune system in insects (De Block & Stoks, 2008; Slos & Stoks, 2008).
On the point of mosquitoes, I did find one paper that showed reduced lifespan duration in adult mosquitoes exposed to increased predation as larvae (Bellamy & Alto, 2018) - again not exactly what you were looking for in terms of an acute event, but still somewhat related.
In summary
I think an important takeaway is that insects, like vertebrates, can be susceptible to stress.

References
Bellamy, S. K., & Alto, B. W. (2018). Mosquito responses to trait-and density-mediated interactions of predation. Oecologia, 1-11.
De Block, M., & Stoks, R. (2008). Compensatory growth and oxidative stress in a damselfly. Proceedings of the Royal Society of London B: Biological Sciences, 275(1636), 781-785.
McCauley, S. J., Rowe, L., & Fortin, M. J. (2011). The deadly effects of “nonlethal” predators. Ecology, 92(11), 2043-2048.
Siepielski, A. M., Wang, J., & Prince, G. (2014). NONCONSUMPTIVE PREDATOR‐DRIVEN MORTALITY CAUSES NATURAL SELECTION ON PREY. Evolution, 68(3), 696-704.
Slos, S., & Stoks, R. (2008). Predation risk induces stress proteins and reduces antioxidant defense. Functional Ecology, 22(4), 637-642.
Veselý, L., Boukal, D. S., Buřič, M., Kozák, P., Kouba, A., & Sentis, A. (2017). Effects of prey density, temperature and predator diversity on nonconsumptive predator-driven mortality in a freshwater food web. Scientific reports, 7(1), 18075.

Great Answer, but sad.. At which taxanomical level should we stop messing with being's lives?


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What would be the fate of protein made from D-amino acids after ingestion by humans?
There are some natural peptides made of D-amino acids, rather than the L-amino acids normally found in nature. It is now possible to chemically synthesize artificial proteins made of D-amino acids.
If such proteins were ingested by individuals, how would they be metabolized and what consequences would they have?

Please read the help on what questions are acceptable on Biology before posting: "You should only ask practical, answerable questions based on actual problems that you face. "

I believe my question meets those guidelines. To follow on from the statement you quoted, "Chatty, open-ended questions diminish the usefulness of our site and push other questions off the front page.", and that is not the sort of question that I'm asking. I'm asking what the scientific understanding of what the effects of ingesting biological material composed of opposite-chirality amino acids would be. Since the properties of those chemicals are (presumably) well understood, the effects of eating said organic matter should be answerable.

Questions about alien planets are not on topic here. Also questions to which you have applied no effort yourself, assuming that you are a 'student' of biology. If you want to ask this question you need to think about the biochemistry involved. For example you could ask "Do the digestive proteases (trypsin, chymotrypsin, pepsin hydrolyse peptides made up of D-amino acids) and on from there to the next stage in digestion, assuming they do. Until you reformulate your question in such terms I hold by my opinion.

I'm a computer programmer, I don't know anything about biology past high-school tier other than random bits of trivia. It's not my expertise; that's why I'm asking a question. If I already knew the answer I wouldn't have to ask, would I? Asking questions so that people who are experts in that field can answer them is literally the entire purpose of Stack Exchange.

I'm sorry Nick, but the first line of the Tour states "Biology Stack Exchange is a question and answer site for biology researchers, academics, and students." If I went onto Stack Overflow (as I do sometimes) and asked what a "for" loop was I wouldn't last two minutes. Indeed, if I have asked far more sophisticated questions that people regarded as too basic. And the problem of asking on a specialist SE is that you get specilized answers, that you likely wouldn't understand, or at least wouldn't be able to assess for correctness. (There's no code to run to check if it works for you.)

"If I went onto Stack Overflow (as I do sometimes) and asked what a "for" loop was I wouldn't last two minutes." I'd give you an answer for that. Probably upvote your question, too, for showing interest. I don't see why you can't do the same for me. And I tried posting this on the scifi stack exchange, and they closed it for being off-topic, so I don't have anywhere else to post it. I don't care if I can't assess the answers for correctness, since that's what the upvote/downvote process is for anyway.

OK, I'll edit your question and give you an answer.

One aspect of the basic biochemistry needed to approach this question is the fact that the enzymes that catalyse cellular reactions show various levels of specificity towards their substrates (reactants), including stereo-specificity. This is illustrated below (an ill-favoured thing, but mine own). The first example shows that the specificity of proteases may depend on the general chemical or physical nature of the substrate. The second shows the how stereospecificity works.

The enzymes that are relevant here are proteases, which are responsible for breaking down proteins to their constituent amino acids, which are then absorbed by the gut, and then the enzymes that would normally catabolize (break down) or metabolize (convert to other compounds) those amino acids. It is well known that the specificity of the enzymes is such that, even if the proteins were broken down to D-amino acids, these could not be used for protein synthesis.
I am not an expert in this area (‘for’ loops are more my sort of thing) but I found some pertinent references in a recent paper on D-amino acid analogues of peptides. To quote from the introduction to that paper:

A useful consequence of this is that (D)-proteins are highly resistant to degradation and have low immunogenicity (7). The fundamental change in backbone–side-chain connectivity and geometry means they are not recognized as proteins by many (L)-proteins—including proteases. Consequently, (D)-proteins are reported to have greatly increased gut, blood plasma, and intracellular half-lives (8). Better cell penetration has also been reported in some cases (9, 10).

The references are:

Uppalapati M, et al. (2016) A potent D-protein antagonist of VEGF-A is nonimmunogenic, metabolically stable, and longer-circulating in vivo. ACS Chem Biol 11:1058–1065.
Rabideau AE, Pentelute BL (2015) A D-amino acid at the N-terminus of a protein abrogates its degradation by the N-end rule pathway. ACS Cent Sci 1:423–430.
Nickl CK, et al. (2010) (D)-Amino acid analogues of DT-2 as highly selective and superior inhibitors of cGMP-dependent protein kinase Ialpha. Biochim Biophys Acta 1804:524–532.
Brugidou J, Legrand C, Méry J, Rabié A (1995) The retro-inverso form of a homeobox-derived short peptide is rapidly internalised by cultured neurones: A new basis for an efficient intracellular delivery system. Biochem Biophys Res Commun 214:685–693.

So it would appear that the D-amino acid proteins are less likely to be metabolized and thus would be less likely to be useful as food. I do not understand why they would have low immunogenicity, but if this is the case it seems unlikely that they would cause allergic reactions.

Could you please add an explanation about why L-amino acid could not be used to artificially synthetize proteins?

@totalMongot — Of course they can, but that is not the question.

Yes that's not the question, but I asked because the OP said that in his question: "There are some natural peptides made of D-amino acids, rather than the L-amino acids normally found in nature. It is now possible to chemically synthesize artificial proteins made of D-amino acids."

@totalMongot I think you misinterpret what the poster wrote — certainly the state of chemical synthesis of peptides from amino acids. This was first achieved at the beginning of the 20th century, led to the synthesis of peptide hormones by the 1950s, and was made much more efficient by the introduction of the solid support  methodology for which Merrifield received the Nobel prize in 1984. My mailbox is full of offers from companies that do this. Naturally L-amino acids were used, but D-amino acids will react similarly. That’s the point of needing to explain enzyme specificity towards L.


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Do electric eels produce current as they just move about, and how/why?
https://www.youtube.com/watch?v=y9wktSQdyaE
This video demonstrates how an electric eel can supposedly produce up to 800 watts, and power a Christmas tree, which is very topical (a late Merry Christmas to the Biology community!). The video, sadly, is not very detailed as to how this works.
I was under the impression that electrical discharge was a conscious action on the part of the eel, rather than a natural state for it. But, apparently, the electric eel generates electricity "whenever it moves," as the video's narrator put it? Do electric eels produce electricity subconsciously, just by moving? Surely, though the host lists off the 800 watts of power, it's not constantly producing 800 watts, either?
How do the fish's electrocytes work in this instance, where just lazing about is powering the Christmas tree?

You are right - the 800 Watts are not constantly produced:
There are three types of electrical discharge: (i) low voltage (ii) high voltage doublets or triplets and (iii) high voltage high frequency.
(i) low voltage allows the animal to orient itself in its environment [b].
(ii) high voltage doublets or triplets are used for hunting: By discharging a high voltage doublet or triplet the electric eel induces involuntary twitching in the prey animal. Since this twitching is producing a weak electric field, this allows the electric eel to locate its prey. See Figure 3 of [b].
(iii) high voltage high frequency is used to incapacitate the prey. It's about 400Hz at up to 600V [b]. Wikipedia [c] states that these electric eel can produce about 1Amp of current. That's in the region of 800Watts the narrator is speaking of. Edit2: The pulse duration is about 1ms [e]. With a frequency of 400-500Hz this leads to a surprisingly high ~50% dutycycle. The ability to keep the frequency stable depends on the age (=length) of your eel: The older the eel, the more stable the inter-pulse interval.

Caption: Fig3 from https://doi.org/10.3389/fnint.2019.00023, red=50cm, green=75cm, blue=115cm length of eel
In Figure 5 of [a] you can see that the electrical eel is able capture prey in ~5 sec. During these 5 seconds the electric eel is pretty much constantly producing high voltage discharges. These could be used to light a Christmas tree.
To summarize: Yes - electric eels are very much in control of when and how they discharge. This can be quite clearly seen (or rather heard) in [d] which is  Supplementary Movie 8 from [a]
[a] https://www.nature.com/articles/ncomms9638
[b] https://s3.amazonaws.com/vu-wp0/wp-content/uploads/sites/182/2015/11/Science.pdf
[c] https://en.wikipedia.org/wiki/Electric_eel
[d] https://static-content.springer.com/esm/art%3A10.1038%2Fncomms9638/MediaObjects/41467_2015_BFncomms9638_MOESM559_ESM.mov
[e] https://www.frontiersin.org/articles/10.3389/fnint.2019.00023/full

Comments are not for extended discussion; this conversation has been moved to chat.

I wish I could bookmark this answer and upvote it again. Great work, dtadres!

@Johnny you can bookmark your own question just below the up/downvote buttons.


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Does electrotonic spread/conduction occur in saltatory conduction?
Even as textbooks, and almost all web pages I've seen so far, explain electrotonic spread/conduction as the passive current flow along an axon, they do so with continuous conduction only. Apart from myelin sheaths which enwrap axons leaving only the Nodes of Ranvier exposed, and of course, the energy requirement and speed of conduction differences, I can't see how else continuous conduction differs from saltatory.
My question then is why electrotonic spread is never mentioned in saltatory conduction.

Generally textbooks take the following pedagogical flow in basic neurophysiology:
Ions flow, so voltage changes propagate
This is the "electrotonic part". The key concept is that if you add some ions or change the voltage of one part of a neuron, adjacent areas will also change in voltage as current flows 'passively'. The further away you go, the longer it takes the signal to arrive and the smaller it will be as the charge spreads out.
A more advanced course might also talk about the sources of those charges, like sensory receptors or neurotransmitter action, and might talk about the ways that polarizing pulses integrate over space and time. Or these may be saved for later.
(side note: in reality, neurons aren't all that passive, there are lots of conductance changes occurring even in this supposedly "electrotonic" scheme, but the electrotonic equations tend to work pretty well, and in a simplified experimental system they are sufficient. Biology is almost always too complex to try to include everything at once)
Action potentials
The key concepts here are that if the voltage changes enough, it stops being possible to think about just the passive flow, you now have to think closely about voltage-gated channels that create a positive feedback loop response to voltage. Above threshold, voltage-gated channels cause sufficient depolarization that adjacent areas of the membrane are also depolarized beyond threshold, and we call this propagating signal an action potential.
At this point, you are supposed to remember and understand that what is driving this active response is still a somewhat "passive" flow of charge that you understood from the "electrotonic" part of the course. That part is the physics and is always present, you can't get rid of it. However, you're in a new scheme where you can't use the electrotonic equations to understand what happens anymore.
Saltatory conduction
Myelination and saltatory conduction comes next. In this section, you're supposed to be thinking about the way action potentials spread, but to add one extra little wrinkle. What if, instead of transmitting piecemeal to the next adjacent segment of membrane, axons were more insulated? In this scenario, the flow of charges will extend much further. You should still be applying the concepts you learned in the "electrotonic" part, though: if you add some ions/change the voltage of one part of the neuron, adjacent areas will also change in voltage as current flows. The further away you go, the longer it takes the signal to arrive and the smaller it will be as the charge spreads out.
Therefore, even though insulation lets the signal travel further, it still decreases in amplitude over long distance, and you need to "boost" the signal again. That's where nodes of Ranvier come in.
Back to your specific question...
"Does electrotonic spread/conduction occur in saltatory conduction?" - No, but not because the "physics" part is different: saltatory conduction is necessarily active (involves voltage-gated channels), not electrotonic, even though all the electrotonic principles still apply.
The "electrotonic" part of the lesson contains important concepts that you are supposed to remember and carry through the other sections, even if it's not discussed explicitly. I think making that active/passive distinction is possibly a bit misleading, but the concepts you are supposed to grab from the electrotonic section in terms of the physics of how charge/voltage moves around in a neuron applies to everything.
Additionally, you should gather that the nodes of Ranvier are spaced in order to conduct action potentials. These are big voltage changes. Smaller voltage changes that are subthreshold will of course also travel down the axon (this is the physics part - nothing stops physics!), but if they aren't strong enough to open voltage gated channels at the next node of Ranvier then the voltage change isn't of any consequence and just decays with distance. If it was strong enough, then by definition it is superthreshold rather than subthreshold, and we are talking about an action potential.

All the content in this answer is material like you would find in a basic undergraduate neuroscience textbook. The ones I usually recommend are Purves or Kandel.

Ok. Since the passive current actually flows, why don't we say electrotonic potential is a propagated response? Because of its reduction in amplitude as it moves?

@Chemo-Mike Yes, it's "propagated" locally in the cell (so you will observe spatial summation of potentials at different nearby dendrites), but not propagated down the axon so cannot typically influence other cells.


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Features of phosphatase
I was wondering if you would be able to help me with discovering what the main regulatory feature of a phosphatase is. I understand many have separate catalytic and regulatory subunits, however, so do kinases so I feel that there is a different answer that I am not understanding. Thank you,

Your question is a bit unclear. What do you mean by feature?

there are LOTS of different phosphatases - and LOTS of different regulatory   mechanisms - this is too unclear of a question

I answered assuming the OP was unclear about the difference between phosphatases and kinases, based on the statement "I understand many have separate catalytic and regulatory subunits, however, so do kinases" - that seems to suggest that the OP thought kinases and phosphatases did the same thing and that OP was looking for how they differed from a regulatory standpoint.

@AlwaysConfused I'm not familiar with the specifics of the catalytic activity anymore, and you may very well be correct, but from a regulatory perspective the modified protein doesn't much care about the extra water. :) But importantly: phosphorylase and phosphatase are not the same at all, and phosphorylase does not cleave phosphate, so I think you have a typo in the comment since it seems clear you are meaning to talk about phosphatase.

@WYSIWYG. firstly: a. that is a trick question... features are defined according to the object definitions in a given standard, and definitions of the past may be obsolete, for example a feature may be a field in a .gff3 file, or a .gff2 file, or see this example glossary, in accordance with the EnsEMBL database schema: https://www.vectorbase.org/glossary; b. how do you maintain so many posts, are you a bot?

Kinases phosphorylate, or add a phosphate group.
Phosphatases remove a phosphate group.
Beyond that, the concepts for regulating them are the same, though the precise factors of course are different.


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Human Evolution Chromosome 2: Fusion or Break?
I have a question regarding Chromosome 2.  I've heard that there is evidence that the Human Chromosome 2 is a fusion between the two ancestral chromosomes 2a and 2b, but could it be possible that it is the other way around?  That is, could it be possible that what we call chromosome 2 in the last common ancestor between humans and other great apes could have broken in some offspring of this ancestor and preserved the broken copy in their descendants. Meanwhile other descendants of this ancestor kept an intact chromosome?  Can someone please point me to evidence/papers that ruled out this possibility?  I'd like to hear why they thought it was a chromosome fusion and not a chromosome break, especially with an incomplete archeological record available.

I've heard that there is evidence that the Human Chromosome 2 is a fusion between the two chimp chromosomes 2a and 2b -- a small but important correction: human's didn't evolve from chimps, so human chromosomes cannot be derived from chimp chromosomes. It is more correct to say that chromosome 2 is hypothesized to have formed by a fusion of two ancestral chromosomes after the divergence of the "human" lineage from the most recent common ancestor of humans and other primates.

Related: Evolutionarily speaking, why do humans have 46 chromosomes.  There is very good evidence that human chromosome 2 is the result of a telomere-to-telomere fusion of two ancestral chromosomes (ref is here)

The way you answer these sorts of questions is by looking at other, further relatives because that gives you more hints about what the "ancestral" trait is.
Since other apes (gorillas, orangutans) also have the separate "2a" and "2b" chromosomes (see, e.g., Fan et al 2002), we can conclude that the common ancestor to all of the great apes had separate 2a/2b chromosomes. That makes humans the outlier, and therefore suggests the fusion occurred somewhere between the most recent common ancestor of chimps and humans and modern humans.
The alternative would have to be that the ancestor had a single "chromosome 2", and then separately in every other great ape lineage that chromosome broke in the same place. That is effectively impossible to have occurred in the same way like that by chance.
I've annotated the cladogram from the Wikipedia page on great apes to show how this works:

If the great ape ancestor has separate 2a/2b, then one fusion event is required to explain why humans differ from the others (top diagram).
If, however, the great ape ancestor has a single chromosome 2, which then broke to make 2a/2b in chimps, that's a perfectly reasonable hypothesis if you just look at the chimpanzee/human branch. However, when you also consider gorillas and orangutans that have separate 2a/2b, that would mean that the ancestral chromosome 2 would have had to break at least 3 separate times in 3 separate lineages in the same place. That doesn't make much sense.
Fan, Y., Linardopoulou, E., Friedman, C., Williams, E., & Trask, B. J. (2002). Genomic structure and evolution of the ancestral chromosome fusion site in 2q13–2q14. 1 and paralogous regions on other human chromosomes. Genome research, 12(11), 1651-1662.

there is also structural evidence in the chromosome itself, chromosome 2 has telomere like sequence in its center and a second inactive centromere. those only make sense if the it was to different chromosomes in the past. https://en.wikipedia.org/wiki/Chromosome_2

It's important to emphasize, I think, that the unfavorability of the "break" hypothesis arises not merely from the pattern of occurrence in contemporary apes and humans alone, but from that pattern together with the fine details of their past evolutionary relationships. If it were the case that all non-human apes shared their own common ancestor after the one for both them and human apes, only one break would be required, even were the distribution at the leaves identical. But because Hominina splits off where it does, instead of before the first fork in the diagram, 3 breaks are required.


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Is this trial that reversed aging in humans worth taking seriously?
In September 2019 Fahy et al. published results from the TRIIM (Thymus Regeneration, Immunorestoration, and Insulin Mitigation) trial. Their stated goals were to investigate whether they could restore the immune systems in eight healthy older men (ages 51 - 65) using a combination of recombinant human growth hormone, dehydroepiandrosterone and metformin. While they achieved impressive on-paper results partially restoring the thymus, the most impressive result came from their epigenetic measurement of aging of subjects in the trial.
Fahy et al. had successfully reversed aging in their subjects according to four epigenetic measures of aging. The effect size was large: each measure indicated an average gain of over 2 years after 1 year of treatment.
In other words, if hypothetically a subject was 60 years old at the beginning of the trial, both chronologically and epigenetically, then by the end of the year they would be 61 years old chronologically but less than 59 years old epigenetically.
Of the epigenetic measures of aging, GrimAge is thought to be the best available predictor of lifespan. From the paper introducing GrimAge,

Using large scale validation data from thousands of individuals, we demonstrate that DNAm GrimAge stands out among existing epigenetic clocks in terms of its predictive ability for time-to-death, time-to-coronary heart disease, time-to-cancer, its strong relationship with computed tomography data for fatty liver/excess visceral fat, and age-at-menopause.

Fahy et al. demonstrated a mean age reversal of 2.16 years after 1 year of treatment according to the GrimAge measurement (see Table 1 in the paper).
Fahy is reportedly spearheading a new trial, called TRIIM-X (see this part of his recent TEDx talk). He hopes to investigate the effects of a modified version of the same treatment with the benefits of a larger trial and a more diverse set of participants.
The skeptical side of me has a question:

Is a reversal of the epigenetic clock good evidence that aging was reversed, or is there a good theoretical reason to think that you can reverse the epigenetic clock without reversing “true” aging and thus increasing lifespan?

SE questions need to be targeted and should be a single question rather than a collection of questions. I've edited out your second question to help you adhere to this rule, and also because I think that second question is going to be a pretty broad/chatty/opinion-based one.

Also would like to see the results of a longer study checking for increased cancer and autoimmune disease rates. Testing the blood for increased autoimmune activity would be nice too.


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Why use embryonic neurons to study protein knockouts/mutants in long term potentiation?
Just wondering if anyone had some ideas about the question in the title. I'm just wondering why some papers use embryonic cultures of specific brain regions for neurones to test the effects of knockouts/mutations on synaptic plasticity (for example, long term potentiation, LTP) instead of adult cultures?
Many thanks

Could you edit your question to include a definition for LTP?

@Michael_A I think adding a definition for LTP to the question isn't necessary for the OP, but I made a clarifying edit that LTP is a type of synaptic plasticity and added a link to wikipedia for anyone who is unsure. These edits are pending. I also previously spelled out the abbreviations in OP, and it looks like that edit was accepted just after your comment.

@BryanKrause,  nice. My request was a nudge to help keep this interesting question as accessible as possible.

Some suggestions, there may be more:
1) The knockout may not be viable to adulthood (the animals die). Perhaps heterozygotes are viable, but to test the full knockout you need a homozygote.
2) Even if the knockout is viable to adulthood, the brain may develop adaptations to the knockout that aren't specific to the knockout itself: up- or down-regulation of certain channels, for example.
3) Plasticity is upregulated in developing brains compared to adult brains, so the effects may be more pronounced in the young tissue.
4) Younger tissue cultures better - you can keep cells alive longer, more easily.
Also good to note is that undifferentiated stem cells tend to be "neuron-default" - that is, if you just culture embryonic stem cells and you don't do anything special to them, they will tend to generate neuron-like cells. In the adult, neurons are always going to be alongside other types of cells: glia, vascular tissue, etc.


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Connectivity Relation between axon terminal synapses and dendrites
With regards to the synapses between axon terminals and dendrites, what is the relation between a given neuron's axon terminals and its neighbouring neurons' dendrites?

Does each axon synapse on only a single dendritic spine from another neuron, whereby all other connections that axon makes are with distinct neurons, or
Can multiple axon terminals from a given neuron end up connecting to a single neuron via multiple dendritic spines?

@BryanKrause am seeing you are both a neuroscientist, and programmer. Mind if we connect separately about neurons and AI? :-)

Cleaned up the comments and wrote a formal answer. I generally check the Biology.SE chat: https://chat.stackexchange.com/rooms/1997/the-biosphere every day or two, and will respond to pings there. I'm okay answering some questions there outside the StackExchange Q&A format, but won't necessarily commit to having any long conversations. If there are some specific things you'd like to ask about or you're looking for some direction I'm happy to help with what I can.

Synapses are pretty much one-to-one
Here's some EM pictures of synapses, from Wikimedia commons:

You should gather from these images that these are super organized structures. There's a dense, dense gathering of cellular machinery at the synapse that creates a dark electron-dense region shown by the arrows. There's no room for more than one cell to be directly involved in this area, it's one membrane closely coupled with another membrane. It's as if you put the palms of your two hands together.
Some neuromodulators (and sometimes traditional neurotransmitters) are not released synaptically, though, and are just dumped into the extracellular space from where they diffuse in to the cleft or bind outside the synaptic region.
There can be multiple connections between two given cells
Though a synapse is a one-to-one connection, axons make multiple synaptic contacts as do dendrites. Though this can mean that cells receive and send input to 1000s of different cells, it's also very common for there to be multiple individual synapses between two specific cells.
For some examples, Tamas et al 1997 looked at synapses made from inhibitory interneurons to excitatory cells in visual cortex:

All presynaptic cells established multiple synaptic junctions on their postsynaptic
target cells. A basket cell innervated a pyramidal cell via fifteen release sites; the numbers of synapses formed by three dendrite-targeting cells on pyramidal cells were seventeen and eight respectively, and three on a spiny stellate cell; the interaction between a double bouquet cell and a postsynaptic pyramidal cell was mediated by ten synaptic junctions.

Note in this paragraph they are literally talking about 5 specific pairs of cells, where they trace both cells in EM. This is an exhausting process. The presynaptic cells were one basket cell, three dendrite-targeting cells, and one double bouquet cell. The post-synaptic cells were all pyramidal cells except one was a spiny stellate cell. In the five pairs they found 15, 17, 8, 3, and 10 connections. Of course they could have missed some, too.

Tamas, G., Buhl, E. H., & Somogyi, P. (1997). Fast IPSPs elicited via multiple synaptic release sites by different types of GABAergic neurone in the cat visual cortex. The Journal of physiology, 500(3), 715-738.


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Why do some viruses cease being a problem even though no vaccine or cure is found?
No vaccine or cure has been found for SARS-CoV or MERS-CoV yet the world is not too concerned about them. How can it be? Did all people who had those viruses die or do viruses just randomly decide to stop being infectious at some point?

Infections spread in a population when the number of new infections caused by an infected person is greater than or equal to 1.
If each infected person spreads the virus to less than 1 person, eventually no one will be infected, without a need for any sort of cure. Of course, the longer a deadly infectious disease spreads in a population, the more people will die during this process. Ideally you want to get the number of transmissions as close to zero as possible as quickly as possible.
SARS and MERS are each a bit different, but share some similar characteristics. Compared to COVID-19 caused by SARS-CoV-2, both are more severe in a larger fraction of the people infected (note: all three viruses are closely related betacoronaviruses). This made it easier for public health officials to identify and isolate infected individuals.
The MERS virus is really not gone at all: it lives on in animal reservoirs, like camels (so it is primarily only a concern in places where those reservoirs live). Cases continue to occur sporadically. However, MERS is usually not that transmissible between people, having a natural transmission rate that is already less than 1: that means that most people who get it get it directly from an animal, and don't continue to spread it to others besides occasional infection of individuals with close-contact, like a family member. There have been exceptions where isolated incidents involved substantial human-to-human transmission. Some of these incidents were associated with "super-spreaders": particular individuals who got infected and spread the virus to way more people than the average. See https://wwwnc.cdc.gov/eid/article/26/2/19-0697_article for more.
SARS caused by the original SARS-CoV virus indeed seems to be gone, with no cases reported since 2004. The elimination of SARS from the human population occurred via controlling the human-to-human spread through isolation and contact tracing. See https://apps.who.int/iris/handle/10665/70863 for a report on the epidemic and how cases and spread in different locations were handled.
Viruses don't have any agency: they can't decide to do anything. However, humans can, and our best response to outbreaks of novel diseases is to trace the spread and try to limit transmission as much as possible.

Good answer. It at first puzzled me how a disease with R0<1 could spread in the first place, since on average, the case count won't be continuously increasing. But that's just an average, it's still possible for patient zero to spread it to several other people, some of whom will then spread it again, with the final result being an outbreak, but one that has a quickly and naturally decreasing case count. It's the super-spreader events you mention that cause sporadic (but not ongoing) problems, and those are by definition rare given the low R0 of those diseases.

@NuclearWang Yeah, it's particularly interesting that mutations don't seem to be a factor in the different rates of spread among MERS cases. Well, at least not mutations in the virus. Instead, it's particular people that just dump a lot of virus to the environment they share with other people, especially when they are sick and in a healthcare setting. The CDC report I linked has more on this.

To belabor the obvious, if you get a disease from camels, it's not going to be a problem for people who never come into contact with camels.  It's basically the same reason why many tropical diseases aren't a major problem outside the tropics: they have vectors (usually insects) that don't tolerate cold.

Are we sure that viruses have no agency?

@personjerry Yes.

@personjerry viruses have as much of an agenda as rocks, or grass. They don't live, they are the biological equivalent of snippets of computer code. Those snippets that happen to be packaged in a way that they get injected, and that also happen to cause the cell to create more replicas, those are what we call a "virus"; snippets without these properties exist but we don't even notice them, let alone give them a name.

Nice answer! I wonder about one thing: as SARS and MERS are both more severe in a larger fraction of the people infected, could SARS-CoV-2 (going through it or being vaccinated) pandemic positively impact our resistance to these two?

Bryan Krause's answer addresses the reasons pertinent to SARS and MERS. If you meant those two as examples but are interested in the title question more generally, I can note an additional mechanism. This is herd immunity, which fits the bill in that it can occur when "no vaccine or cure is found" and when it is neither the case that "all people who had those viruses die" nor "viruses just randomly decide to stop being infectious". After a significant fraction of the population has been infected and recovered, herd immunity can bring a virus with $R_0 > 1$ to an effective rate $R < 1$ if those that are recovered are immune to reinfection and this immunity lasts for long enough.

And considering the title more broadly,
We learn to live with them, manage the infections, and consider a significant death toll or other related injuries as "normal".
For example, a measles vaccine was only developed in the 1960s. Before that, it was just known as one of the diseases children would usually get when they were young, because the virus was endemic in the population. On average, 2.6 million people a year died of measles globally, and that was just expected. (For comparison, that's now down to 122,000 by the way, and most of them are in extremely poor countries who either can't afford the vaccine or can't reach clinics.)
For an alternative case, the rate of congenital disabilities or birth defects in children was simply accepted as what it was - something which just happened without any cause. It was not until 1941 that the connection was made to rubella (German measles) causing up to two-thirds of all birth defects. Before that point, we didn't know that this wasn't "normal".
And currently of course we still have no solid vaccine for flu. The vaccines we do have are relatively effective and certainly do reduce the impact, but they are not effective to the same extent as, say, the MMR vaccines. As a result, we still have thousands of people dying of flu every year, and currently that is "normal". Maybe one day we'll crack it, but until then we'll just expect people to continue catching it, doctors and hospitals to continue treating it, and some people to die from it.

One more effect: a pathogen that is both deadly and highly contagious either triggers strong response (when we talk about humans, human pets, cattle, etc) or simply wipes out the population it infects (and disappears with it).
This creates a strong selection pressure over the pathogen. In order to successfully spread, it either becomes less deadly, or less contagious, or both. The generations of the pathogens change quickly and mutation rate is usually high, so the pathogen (given time and groups of hosts to infect) will react to the selection pressure.
The groups, once survived the less-deadly version of the pathogen are at advantage - they are most probably immune also to the original. The pathogen is also at advantage - it gets less organizational reaction (quarantines, vaccines, etc) and more hosts to infect (because survived hosts reproduce and the new hosts are not immune).
p.s. a second-order of the same effect is the pathogen becoming less dangerous only to minors of the host. We all know a lot of examples.


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Is there a convention regarding the use of forward vs reverse DNA strand to represent DNA sequence?
I see in this paper the notation IL-1A C[-889]T which suggests that for this gene, the reference allele is C and the variant is T.
However, when I look up the same gene on dbSNP, it says the alleles are G>A / G>C / G>T.
I noticed for a number of other genes I looked up in the same paper, G becomes C and vice-versa, T becomes A and vice-versa. Is it because of different conventions regarding which DNA strand is used to represent DNA sequence (forward vs reverse)?

"Genetic code" refers to the translation from three-nucleotide codons to amino acids. A change in genetic code would be changing the amino acid that is associated with some triplet.

The first is with respect to the transcriptional unit of the IL-1A gene. For example the "-" indicates that it is upstream of transcription start site.
The second is with respect to the GRCh38 build of the reference human genome, which has a defined orientation.
I don't have access to the paper that you link, but the NCBI annotation for the gene indicates that it is on the reverse strand of the reference genome sequence.
That would seem to indicate that the two annotation methods are concordant, if somewhat confusing. One refers to a position's distance from the start of the gene, one refers to a position's distance from the start of the reference chromosome. Those will necessarily diverge in the reference allele for genes transcribed on the reverse strand.
If you are interested in analyzing the behavior of a specific gene, the transcriptional unit is obviously the relevant level of analysis (for example, predicting translated protein sequence). However, if you are interested in defining global genomic coordinates (for example, mapping sequencing reads), the reference genome become the relevant level of analysis. So each is useful for different purposes.
So, in brief, the answer to your question is yes.

When you say "those will necessarily diverge" do you mean the reference allele will always obey the base pairing rules - like here C for the reference human genome and G when reading from the transcriptional unit ?

@Youcha Assuming that I understand correctly, then yes. C will only ever base pair with G (or at least that's a foundational assumption of how we represent genomes on computers)


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Animal species anatomy
https://en.wikipedia.org/wiki/Animal
Do all animal species have two lungs and two kidneys similar to human beings?

You made this completely unreadable with your edits, which seem to be completely unexplained links. The question itself is very underresearched, but adding random links does not help that. You are fortunate that someone gave you an answer anyways.

I just saw your edit, it completely changes your question and makes it much more vague and hard to give a specific answer to. Even just "do you feel" makes the question opinion-based and thus inappropriate for the site. Do you want information, or a debate? For a debate, try reddit. For information, put more thought into what info you really want and which question could best elicit it (for example "do all animals have 2 lungs and 2 kidneys" was clearly not a good question for the info you really wanted). As @BryanKrause said, looking for the answer yourself could also help focus the question.

The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure. Please see our homework policy for more information. In this case, merely looking at the Wiki articles for lung and kidney would give you the answer.

No.
Lungs are a feature of tetrapods (land vertebrates) and some lungfish. Many fish have swim bladders, which are thought to be homologous to lungs (they evolved from the same ancestral structure) but are not lungs, and I don't think they come in pairs anyway. Some other air-breathing organisms evolved air-breathing structures that also get called "lungs" but they are not related to human lungs, like spider "book lungs", and those don't necessarily come in pairs either (for example, spiders can have apparently one to four such lungs).
Kidneys are an organ specific to vertebrates.
It's worth noting that even the concept of having "two X" is specific to bilaterians, which is animals that show left-right symmetry. That includes all your vertebrates and insects and worms and squids and such, but it does not include animals like jellyfish, sponges or corals. You also have animals that are in the bilaterian family, and do have left-right symmetry in some life stages, but don't in others, like starfish and sea urchins.

Thanks. Can you please give the references of the medical books, encyclopaedia, medical dictionaries, medical journals, Wikipedia etc where this information is cited?

@PrashantAkerkar You are asking for far too much effort for the amount of effort you have put in for your own question. What is the motivation here? The answerer here has provided plenty of reasonable evidence against the idea that every animal has 2 lungs and 2 kidneys. We don't need medical texts about arthropods and fish because there is very little medical interest in those animals.

@PrashantAkerkar dude I did, look at the links.

This is an excellent answer to a really lousy question. However, in the future, I would suggest not answering very low quality, unresearched questions like these. From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.


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Do plants refix some of the carbon dioxide in the Calvin cycle that they produce through cellular respiration?
Plants do cellular respiration and release CO2 into the air, but does the plant also use some of this CO2 to do the Calvin cycle? Or does all the CO2 required for the Calvin cycle come in through the stomata?

Gases like CO2 move quite freely in biological systems, approximating the laws of diffusion (note: there are of course some exceptions, especially underwater, as well as with proteins that assist in bulk transport of CO2 like hemoglobin).
If you were to measure the net amount of CO2 coming into the stomata, it would indeed approximate the net CO2 use by the plant. From this, you could make a claim like "the CO2 a plant needs comes in through the stomata": this is true for the net, and that's usually what's most important to a biologist.
However, if you want to get picky about what really happens at a molecular level, the flux of CO2 coming through the stomata is not the same as the net: no one is keeping track of the individual gas molecules, they just float around back and forth. The only reason there is a net flow at all is due to a concentration gradient: because the plant uses some CO2, there is less inside than outside. When molecules move around randomly, that means that a few more end up coming inside than are leaving. When we talk about net diffusion we are talking about the averages of many many molecules over time.
Included in that random motion are not just the CO2 molecules present inside and outside the plant, but also those that the plant is producing through cellular respiration. By chance, certainly, some of these molecules could end up back in the Calvin cycle. Some could even exit through the stomata and come back in (my intuition is that this is quite improbable for an individual molecule but I haven't done the math...the important concept is that it's all one "pool").
If you really wanted to know, you could set up a Monte Carlo simulation (or use differential equations) and calculate probabilities of all sorts of event sequences for individual molecules. You could also tilt the scales a bit if you, say, put the equivalent of a 'plastic bag' over a leaf, either physically or in a model: if there's a limited amount of CO2 in the "outside" space it would be much more likely for individual molecules to be "reused".
From a biologists' perspective, though, and especially for ubiquitous, freely moving molecules like CO2, it's usually only important to think about net flow.

Great answer — thanks for fixing the egregious mistake I introduced into the title!

@tyersome Haha no problem. Shh don't tell anyone but I edited my answer before the time edits register to fix the place I referred to CO2 as an "ion" - maybe a bit too much neuroscience for me. Happens to us all sometimes :)


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What causes rashes to appear in specific parts of the body without a site specific trigger?
Why do rashes appear randomly at highly specific locations (and not others), without location specific triggers? Like, if it's a systemic issue, then it should be distributed to other areas on the body too.

It appeared on the back of my right hand, and nowhere else, and then died down. I've had similar rashes in the past where they appear without any obvious trigger, on a highly specific location and nowhere else, then disappear spontaneously after a few hours.
I'm curious what, in theory, can possibly cause this observation. If I have sensitive skin, they should not be localized like this.
I'm not asking for medical advice, just curious as to how exactly this even happens.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular note that personal medical questions are not appropriate for this site. Saying it isn't personal is not enough when the text of your question contradicts you! This also seems likely to generate opinions rather than facts (also against site guidelines). Finally, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

I've pared your question down a bit but it could still use some prior research to improve it. Keep the personal anecdotes out of it.


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Why do larger diameter myelinated axons have greater conduction velocities than small diameter myelinated axons?
A canonical statement I have frequently read is that "large diameter axons conduct action potentials at faster velocities than small diameter axons". After recently learning the effect of increased capacitance on the cell membrane (namely, that more charge is required for depolarization to occur...Are large cell bodies of neurons harder to depolarize than small cell bodies of neurons?), I find this canon to be rather confusing.
I have attached a picture to make my question clearer:
In the above picture, both neurons have the same myelin spacing. So, my question is why should the action potential in Axon B traverse the distance X1 to X2 more quickly than in Axon A. Shouldn't the increased capacitance of Axon B (due to its increased diameter) increase the time it takes for the action potential to travel between the two points?

Why should the action potential in Axon B traverse the distance X1 to X2 more quickly than in Axon A?
The larger the diameter of the axon, the less the longitudinal resistance, so the current can propagate along the axon more easily.
Shouldn't the increased capacitance of Axon B (due to its increased diameter) increase the time it takes for the action potential to travel between the two points?
Both, the capacitance and the number of ion channels increase quadratically whit the diameter. So the increase in capacitance is compensated by an increase in total ionic current.
Wiki cable therory


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How does SARS-CoV-2 spread from cell to cell in the lung?
This virus exits the cell using exocytosis after assembling golgi vesicles which contain the virus by fusing with the cell membrane.
In the case of infected pneumocytes, I imagine that the virus could then exit into the alveolus and infect other pneumocytes using again the interaction of the S protein with ACE2 or it could exit into the blood and spread to other pneumocytes in a 'miliary' fashion like TB.
Is either or both the main mechanism of spread in the lung?
Does lymphatic spread play any role?

I'm voting to close this question as off-topic because it was cross-posted to MedicalSciences.SE. In the future, please choose a single site to submit your question to. Cross-posting is rude.