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Does active transport go only against concentration gradient?
Does active transport go only against concentration gradient? Is there any scenario that active transport moves molecules from high to low?

I'd parse this into two sub-questions for yourself. 1) What would the benefit be of using active transport to move something down a concentration gradient? 2) If you artificially or pathologically or experimentally changed concentrations such that something that would ordinarily be moved up a concentration gradient is now moved down, would that interfere with an active transport system already in place?

These questions are the exactly why I'd ask this question. Some of the textbooks and my teacher said the active transport is not always against concentration gradient. I don't think that's right too. An example introduced by my teacher was the active transport was done by small intestine cells from low to high after eating dinner.

If you include the quotes from the textbooks in your question it would significantly help.

If the molecule to be transported has a ionic charge, then the change in free energy is not only due to the concentration gradient, but also on the membrane potential (Vm) and molecule charge (z).
If the electrical free energy necessary to move the molecule surpass the free energy released by the chemical gradient, then an active transport is necessary.

Does active transport go only against concentration gradient? Is there
any scenario that active transport moves molecules from high to low?

What's active transport?
Have you considered the ion transport mechanism of gastric pump?

There are two types of Active transporters. 1) Primary Active Transport is generally energy driven by ATP Hydrolysis. 2) The other category of active transporters do not rely on ATP directly.
One:
The primary term refers to transport mechanisms that are directly coupled to the consumption of metabolic energy ATP.
Thus "pumps" encompasses all transporters capable of thermodynamically uphill transport (so-called active transport). Let's consider a couple popular active transporters (ion pumps) of the cell membrane that are directly fueled by ATP.
Within ion pumps itself there are those active transporters that pumps ion against a concentration gradient e.g. H+,K+-ATPase (gastric proton pump) where high concentration of H+ is actively transported across the appical membrane of parietal cells towards the low concentration of H+ of gastric lumen. Gastric pump maintains a 1H+:1K+ ion stoichiometry, yielding overall electroneutral ion pumping mechanism and cycel. This is a type of active transport mechanism that is specific to a particular physiological task such as digestion.
Then a more popular ion pump of the same family, Na+,K+-ATPase which actively transports ions (3Na+:2K+) across an electrochemical gradient (a combined concentration gradient and an electrical gradients) in basolateral membrane by pumping Na+ from cell interior (cytosol) to cell exterior in exchange for K+ from cell exterior to interior where cytol has high [Na+] concentration and extracellular is high in [K+]. The electrochemical gradient is necessary for the pump's ion pumping activity and infact gradient is maintained by the underlying concentration and asymmetric selective substrate ions (Na+, K+) stoichiometry (3:2). Na+K+-ATPase's active transport is at work in all cells of the body (not just human).
Primary active transporters, such as Ion pumps do infact pumps ion across high to low concentration (concentration gradient). Have you considered H+K+-ATPase?
Two:
The second type of active transporters depend on the electrochemical gradients of other ions as an energy source. They are usually called ion exchangers. These active transporters are able to carry more than one ion up its electrochemical gradient and at the same time taking another ion (most often Na+) down its gradient. e.g. the Na+/Ca2+ exchanger that shares Ca2+ with the PMCA Ca2+ pump.The exchanger keeps intracellular Ca2+ concentrations low. The Na+/H+ exchanger regulate intracellular pH, in this case by acting directly on the concentration of H+.
Such that It is not quite just to simply to characterize that 'all' active transport mechanisms are 'only' based on concentration gradients alone. Further, just because a molecule (substrate) to be actively transported by a transporter, is an ion, it does not engage in a concentration gradient. There are transporters such as P-Type 4 ATPases which are evolved to actively transport phospholipids as substrates that are not cations/ions.
I am not going to contaminate the answer by introducing passive transporters such as ion channels which are crucial to the co-existence and function of the ion regulation of the cells. e.g. ion channels produce electrical signals by diffusing down substrate ions across electrochemical gradients (again a combination of ion concentration and signaling. That means ionic currents depend on the electrochemical gradient across the cell membrane (of some type). In the case of nerve cells, such an electrochemical non-equilibrium is crucial. Diffusion will continue until this gradient has been eliminated. Imagine, with ongoing electrical signaling and ion diffusion, if there's no reserves to constantly replace these ions, these necessary ion concentrations would reach a zero, so is the nerve signaling.


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Why don't all plants grow like weeds?
I'm well aware of the Gardening/Horticultural approach of "a weed is any plant that you don't want in its current location".
But I think most people would agree that there's a more useful interpretation of "weed" that relates to its growth.
I would say that weeds are the plants that would be extremely easy to introduce if you wanted to them in a particular place, and extremely hard to remove if you didn't want them.
Common properties that I can think of, of the top of my head, for such plants include:

quickly growing.
quickly reproducing.
self-seeding.
re-growing from roots even if the above-ground plant is removed.
not particularly sensitive to ground conditions.

Question:
Why don't all plants exhibit these behaviours?
It feels relatively "obvious" that the plants that exhibit these behaviours should be able to out-compete plants that don't, since they reproduce faster and are more resilient.
And yet the slightest glance outside demonstrates a wide variety of plants that I think would trivial die if I attempted to attack / damage them.
What gives?

Crops have been bred to have certain characteristics like quantity and quality of yield. Often that breeding process has made them less competitive because they don't spend most of their resources on reproduction but on yield.

every advantage has a disadvantage.
self seeding means less genetic diversity, fast growing also means more energy requirements  and even a structurally weaker plant, fast reproducing means tiny sieeds so individual seeds have a very small chance of survival. Biology is all about cost vs benefit, there is no such thing as universal advantage.
regrowing is actually something all plants can do provided they have enough resources, this is one way humans replicate crops. Weeds are often more sensitive to ground conditions, and don't do well in places where humans have not cleared and irrigated the land. weeds are often pioneer species good at taking over open land, one effective way to deal with weeds is to plant a cover crop because weeds can't actually compete well when there is already healthy grass. Many crops on the otherhand are being grown in sub-optimal conditions, in climate/soil other than the the one they evolved for while weeds tend to be native plants already adapted for the local conditions.

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Is “Oxygen-Starvation” during exercise a real phenomen?
Cross-Posted from Physical Exercise, as I suspect this Q is a bit more bio-science focussed than is appropriate for that StackExchange

I play hockey (field hockey) at a slightly-below-elite level. I train (but don't play) with players who play in the UK National Prem.
I, and other players I play with, and coaches I've trained under, have always talked about us and our brains being "oxygen-starved", when you're playing beyond your fitness level. (Especially common during pre-season when everyone's unusually un-fit :D )
What we mean by this in terms of external observable actions is that, when we get very tired we stop making good decisions, and our fine motor control drops - we chose bad passes, we take people on when we wouldn't normally do so when not tired, our hand-eye cooridnation drops so that we can no longer execute skills as well, etc. etc. etc.
Certainly the effect exist - those actions are clearly observable.
But is there truly a physiological effect behind it, and if so, is that effect truly about oxygen levels in the brain?
If one were able to install an O2 sensor in one of major arteries leading to the brain, would you be able to see actual drops in O2 levels, when someone is reaching a point of combined aerobic and anaerobic exhaustion (hockey is a heavy mix of both forms of activity, like many team sports)

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Lifetime of clothes moths
Cross-posting, as I'm not at all sure which StackExchange this belongs in. Very happy to move / delete where I've chosen poorly, and a better SE can be recommended.

Question:
Can anyone advise on how long clothes moths eggs can last unhatched, and how long the larvae would then be able to survive without any natural fibre food.

I'm currently trying to deal with a clothes moth infestation, and your site has been invaluable.
Are you able to advise how long the larvae can survive without any available food?
We've removed the carpet and soft-furnishings from a room, and thoroughly hoovered, but there are nooks and crannys (especially around the skirting boards), which I suspect still have eggs in. I've thoroughly removed any fibres left from the carpet, so my plan is to leave the room for 10 days to ensure any remaining live eggs have hatched into larvae (which then have nothing to eat, and then ... X? ... days to ensure that those larvae have all died.
Are you able to advise what X should be?
We're under the impression that the larvae can ONLY eat natural fibres, so they can't eat, e.g. artificial foam underlay or cardboard boxes & books. Even if those are the only things around them, they can't consume those and will thus starve.

If you are dealing with a real clothes moth, your natural plant fibers should be safe, they can digest only keratin, which translates to hair and feathers.


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Will moth larvae pupate in response to food deprivation
Context: Trying to exterminate a clothes moth infestation.

Supposing you have a room with clothes moths, or rather, with clothes moth eggs and larvae.
Suppose then, that you remove all of the soft furnishings, all of the clothes, all of the carpet, and you thoroughly clean and vaccuum to remove as much dust and hair as possible.
Would one predict that the remaining larvae would then immediately pupate into moths, in response to this food deprivation?
I know that lots of plants will suddenly flower or fruit if they perceive that they are at risk of dying, in order to reproduce before they die. I believe the moths are essentially just a reproductive phase of the moth, so I'd be unsurprised if they did pupate.
On the other hand, I imagine pupation takes a lot of energy and food reserves (not to mention needing material for the cocoon), so I can imagine that they might be unable to do this?
Which way do it go?
Will moth larvae pupate in response to food deprivation

Specific reason for the question is that, a week after we pulled up the carpets, we've started seeing more and more moths in those rooms. Trying to work out if this is "expected" or not :(

Not officially an expert, but I have been watching clothes moths for years and haven't noticed any small ones, so dont expect early pupation. I would expect small pupae to give small moths (like with houseflies). I do see the hormone traps reduce population, but only with lots of them (2 per small room).


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Competitive inhibition - Similarity between substrate and inhibitor
I have this question -
Q. Competitive inhibitor which binds to the enzyme (a) has structural similarity with the product (b) is chemically similar to the substrate (c) has physical structure similar to the substrate (d) both option (b) and (c)
I'm confused between options (c) and (d). I looked up the answer and it said option (c). But say, for example, malonate [inhibitor] and succinate [substrate] for the enzyme succinic
dehydrogenase, inhibitor and substrate are chemically similar as well :

Image source - https://www.toppr.com/ask/en-bh/question/the-activity-of-succinate-dehydrogenase-is-inhibited-by/
Kindly explain the answer to this question.

You've found an example where they are chemically similar; that doesn't mean this holds for all cases. A lemon is a sour fruit, that doesn't mean all fruit is sour.

MCQs are educational poison, as this example illustrates. Option (a) refers to “structural similarity with the product“, whereas (c) refers to “a physical structure similar to the substrate”. What is the difference between “structural similarity with” and “a physical structure similar to”? None that is apparent to me. So the question is designed to trick the student, not to see if he understands what a competitive inhibitor is. This is completely unforgivable. If I want to know if a student knows how a competitive inhibitor works, I ask him. If I’m employed to teach him I mark his answer.

@BryanKrause I've just been introduced to this topic so I guess my knowledge is pretty limited, I looked up the internet too but couldn't find anything. It would be a great help if you could give me an example where the substrate and competitive inhibitor are NOT chemically similar. Thanks:)

@ApogeePoint Tubocurarine at nicotinic acetylcholine receptors? Bicuculline for GABA receptors? Though at some point it depends on what you mean by "chemically similar" since this is a very non-specific, qualitative description. I'd very much agree with David on this that it's better to understand what competitive inhibition is than to learn answers to MCQs like this one.

I also think the MCQ is simply wrong/misleading, as it's only necessary for competitive inhibitors to interfere directly with binding; it need not fit in exactly the same way as the normal substrate. But, for the concept it's trying to teach, it's only really important to recognize that concept. If you continue in biology education you'll learn that almost everything you learn has an exception.

@BryanKrause Okay, now I've learnt that substrate and inhibitor need not necessarily be chemically similar. But my textbook has this - When the inhibitor closely resembles the substrate in its molecular structure and inhibits the activity of the enzyme, it is known as a competitive inhibitor. By molecular structure isn't it referring to chemical similarity?
Textbook link - https://ncert.nic.in/textbook.php?kebo1=9-19 (Page 117, 1st paragraph)

@ApogeePoint Looks to me like just a bad textbook. Yeah, usually when an inhibitor has those characteristics (closely resembles the substrate in it's molecular structure) it's a competitive inhibitor. But that's not the definition of competitive inhibition. Unfortunately, and this is the worst part, it also doesn't actually help you understand what competitive inhibition is to describe it that way. Competitive inhibition describes a relationship between the inhibitor and the substrate, where it's possible to overcome the antagonism by increasing the concentration of substrate...

...that's the competitive part: competition between the antagonist and the substrate/ligand. Physically, that occurs because they're binding in the same place on the target molecule, so if you have more substrate then the inhibitor can't bind, and vice-versa. Binding in the same place means they have to "fit" in the same place, so often that means the antagonist is similar to the ligand, but it doesn't have to be.

But, your textbook doesn't really make that connection, because it tells the story backwards and mixes up the logic in the process.

@BryanKrause I finally got your point! Certain molecules can act as competitive inhibitors, competing for the active site of an enzyme even if they do NOT possess a similar chemical structure as the substrate.
I read this article - https://www.sciencedirect.com/topics/medicine-and-dentistry/competitive-inhibition
And the textbook…yes some parts are messed up! Still thanks a lot for clearing my concepts.

@BryanKrause One last question please, if the target site of the competitive inhibitor and substrate is the same then, they should have similar chemical interactions with the active site to bind and that would mean chemical similarity. So how do these competitive inhibitors manage to compete and bind at the same active site if they are different from the substrate chemically? Is there any mechanism for that?

State of the art is a "transition state mimicry". Make the MCQ even more ridiculous.

Like others commenting, I am not impressed with this question's answers even as multiple-choice questions go. Depending on how the question is interpreted, all 4 could be argued to be correct.
But only C is always true for a competitive inhibitor.  The others are true for some competitive inhibitors, but not all.
What characterizes competitive inhibition (rather than non-competitive and uncompetitive inhibition) is binding at the active site of the enzyme.  Nothing else need be true. An inhibitor that binds the active site regardless of how or why it binds there is considered a competitive inhibitor.  The other two types of inhibition rely on binding to allosteric sites (binding sites other than the active site) that affect catalysis typically by altering the tertiary or quaternary structure of the enzyme.
An enzyme's active site is characterized by its shape (the space it occupies and does not occupy), and which amino acid functional groups project into that site in order to chemically interact with substrates as a part of the mechanism by which catalysis occurs.
In order to bind to the active site, the inhibitor may but does not have to interact with the amino acid site chains involved in catalysis.  But they all must be capable of fitting into the site well enough to stick there, typically through multiple low strength interactions such as Van der Waals forces.  Which means the molecule must have a shape that resembles the substrate enough to fit in its place. It must have "physical structure similar to the substrate" enough to do so. Occupancy of the site prevents the substrate from fitting into the site at all and/or interacting with mechanistically important amino acid side chains. Simple capacity to interact with mechanistically important amino acid side chains is not enough if it doesn't fit into the pocket of the active site as well.
And since the core definition of a competitive inhibitor is binding to the active site and nothing else, similar physical structure is the critical factor that must always be present.  Thus, C is the answer.
But there are issues that can confuse making other answers seem correct even to someone who has a reasonably good understanding of competitive inhibition. First, for enzymes catalysing reactions reversibly (such as carbonic anhydrase which can either take CO2 and water and produce bicarbonate and hydrogen ions or take bicarbonate and hydrogen ions and produce CO2 and water), the products can be substrates so one could argue A is also correct.  They probably discount it because the product of the forward reaction is the substrate of the reverse.  Statement A about competitive inhibitors could only be considered true for reversible reactions, whereas statement C is always true for both reversible and nonreversible catalysts.
Second, as you observed, the primary way an inhibitor has "physical structure similar to the substrate" is because it is chemically similar to the substrate.  But this is not the only way.  In your example consider the case where one carboxyl group (COOH) of the succinate is replaced by a nitro group (NO2). The geometry and size of the nitro group is quite similar to the carboxyl group.  Thus the physical structure is also quite similar despite the chemistry being dissimilar.  3-nitropropanoate inhibits this enzyme by binding at the active site and thus would be a competitive inhibitor of the enzyme.

So the reason C is the best answer is because it is the only statement that must always be true for an inhibitor to bind at an enzyme's active site.

In point of fact, option "C" is not always true for a competitive inhibitor.  A competitive inhibitor does not need to resemble the substrate at all in any respect, nor does an inhibitor need to bind to the active site for (reversible) inhibition to display a competitive pattern: an allosteric inhibitor (one that binds to a site other than the active site) can display competitive kinetics.  This point is very well discussed in Segel (Model 5).

Segel's famous diagram (Segel, (not Segal), p102) is also reproduced here (where Model 5 of Segel is labelled Model e). As a corollary to the above comment: binding of an inhibitor at the active site does not necessarily mean that the kinetics are competitive.  The binding of I to the active site may not prevent but only impair the binding of S to the active site: an inhibitory ESI complex may form with both E and I bound at the active site.

Model 5 was initially proposed by Changeux.  See here: "Models proposed by myself
in 1961 for the feedback inh of L‑Thr deaminase by L‑Ile. Model 1,
named ‘overlapping’, describes the classic model of competitive inhib
by mutual exclusion through steric hindrance of a common site. ...
the substrate and inhibitor compete for the same site on the protein. In
model 2, named ‘no-overlapping’, the binding-sites for the substrate and
inhibitor are topographically distinct and the interaction between them is
indirect or ‘allosteric’."

In addition, an Uncompetitive (or anti-competitive) inhibitor may bind at the active site.  One model for UC inhibition is where I binds to the ES complex. For a two-substrate enzyme (where UC inhibition is common) this could  be at the active site for the second substrate, in which case the inhibition pattern might be UC with respect to substrate 1 but competitive with respect to substrate 2, assuming (in the simplest case) an ordered addition of substrates to form a ternary complex

user338907, who I suspect to be a physical biochemist, further illustrates the original multiple choice problem's poor quality.  His comments also illustrate the difference between understanding something on an intro to biology level and an expert in the field level.  I freely admit that I am not at the field expert level, my undergrad degree is in biochem, but my graduate degree is in molecular biology... meaning I am neither a particularly good biochemist nor a particularly good geneticist (as the joke goes). The more one knows, the more one knows the exceptions from classical cases.

Enzyme inhibition at its base is about kinetics not chemical and physcial similarities. The different types of enzyme inhibitors produce different patterns on a Lineweaver-Burke plots, graphs of the reciprocal of the substrate concentration on the x-axis and is the reciprocal of the reaction velocity on the y-axis. This is how the types were defined. Increase in slope, decrease in x-intercept, no change in y-intercept = competitive inhibition. But that doesn't answer the question asked, why are they saying C is the answer re: chemical vs physical similarity with no kinetics discussed at all.

At the intro level, competive inhibition is described from the "classic model" as Segal calls in in the referenced figure.  And the question as asked references only it: substrate and inhibitor competing for the same site.  So that is how I answered it.  I was aware mechanisms 2, 3, and 4 in the referenced figure were also possible.  But it doesn't help with the answer, nor do the difference between binding at exactly the same site and very close adjacent ones.  I was not aware of #5, which is a major deviation from classic models which is probably why it was not covered in my classwork.

Likewise, I mentioned other inhibition types in their classic cases and in a cursory manner just as contrast to competitive inhibition.  So going into detail about examples of uncompetitive inhibition limited to enzymes with 2 substrates with independent active sites, while more strtictly accurate, would not have been very helpful.  And to get ahead of one other issue. 3-nitropropianoate is not actually a competitive inhibitor because it is not reversible.  It is a 'suicide inhibitor' that binds irrevocably to the active site.  Competitive inhibition, kinetically must be reversible.  But in

ways pertinent to the question, it acts like a competitive inhibitor and would be one is its binding to the enzyme was reversible.  Like other parts of my answer, I simplified.  And while there are those who would argue that such simplification is always wrong, I suspect most of them have not tried to explain something to people at varying levels of experience.  Especially when constrained by trying to answer why one of 4 poorly written answers to a poorly written question written by someone else is best.  And in such as way so as not to confuse and make things even more complicated.


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Insect decline and CO2 concentration
In the UK, where I live, for several years we have had cold dry springs which seems to delay appearance of insects. So irratic weather could cause species to emerge out of sync with their food species and that is an example of how climate change could lead to decline. But insect decline is occurring globally and not all areas have the same factors that could contribute like use of pesticides, habitat destruction etc.
One factor that is more global is the increase of CO2. Could it be that because insects rely on diffusion through tracheae to respire they are more affected, at part of their life cycle, by increased CO2? you might not think that the concentration of atmospheric CO2 at 470ppm and a 47% increase since pre-industrial era would be enough to make a difference but has anyone done the experiments to check?

Interesting idea - what did your searches of the literature tell you?

First question: is there a way to dissociate this from pesticide use? second question: is there a way to dissociate this from temperature? e.g. recent studies consider both of these to be major contributors to recent declines https://beyondpesticides.org/dailynewsblog/2022/05/climate-change-and-industrial-agriculture-are-supercharging-the-insect-apocalypse/

@bob1 I dont have access to journals but I found no mention of it in general web seach

Looks from your reference that CO2 concentration might not be significant


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Does the smoke produced by tobacco affect mitosis in vegetables (plant cells)?
There is a plethora of literature and research studies on the effects of tobacco on the human body and other animals.
I am interested in knowing whether the rate of mitosis in plants is affected by the smoke produced by burning tobacco (e.g. a vegetable under study would be put in a chamber filled with tobacco smoke).

Just a word of caution: there is no such thing as "mitosis speed" without careful consideration of meaning. Plants are composed of a lot of differentiated cell types. Some in the soil, others above ground, some internal, others external, some compose growth cones at the shoot/root tips, others simply structural and inert. Some cells are old, young, in sexually or asexually reproducing specimens, some cells would exhibit readily easier exposure to a 'general smoke' experiment than others. Both biotic and abiotic factors are known to affect cell division, but the particularities matter.

You can ingest tobacco as inhaled smoke and observe heightened co-incidence of lung cancer, but that doesn't mean that all cells may experience "faster mitosis" or shorter cell cycles as a result of tumor growth (uncontrolled cell proliferation). Nor for that matter "slower mitosis" or longer cell cycles (as a result of toxicity, hypoxia or indirect effects). Also, beware of false attribution fallacies: smoke (particulate matter in the air, like soot) is NOT carbon monoxide, but we consider it part and parcel of smoking, which isn't smoke per se. Remember to think about Qs carefully!


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Is it true that all spiders are venomous?
This is a factoid I heard as a kid at some point, probably on a playground somewhere, and just accepted without question in the way that children do:

All spiders are venomous, but most of them aren't venomous enough to harm humans.

(I'm pretty sure the wording used was actually "poisonous", because the distinction between venom and poison is a little too technical for a nine-year-old, but I understood it at the time to mean what I now know is called "venomous".)
Is this true? Are all spiders venomous? Or is this just one of those made-up "facts" that circulates playgrounds and campsites?

If threre are herbivorous spiders, then no, not all spiders have venom.

@anongoodnurse I have never heard of herbivorous spiders. Are there some? That also doesn't mean they don't have venom for self-defense or just vestigially, either.

There is an herbivorous spider, yes, Bagheera kiplingi. It may have been too subtle, but my point was, you should have researched this a bit before posting.
We get a lot of "I heard..." questions here, which is rarely a reliable source.

@anongoodnurse I did look it up, but the state of search engines right now means it's hard to find anything, especially anything debunking common misconceptions and playground rumors (you're more likely to get some LLM arguing that they're true).

Um... I don't believe you're correct. I'll leave it at that.

Try (not for herbivorous spiders): Uloboridae.

@anongoodnurse Bear in mind that I'm an electrical engineer, not a biologist or zoologist or anything, and I almost certainly don't know the right terms to make a search engine give me actual scientific articles and not "10 cool facts about spiders you won't believe" repeated a million times. Yes, I'm exaggerating, but it's hard to find information that's actually reliable these days.

https://s3.amazonaws.com/scschoolfiles/552/non_venomous_spiders.pdf

@NilayGhosh Beware of the information in  your link, it states they are non-venomous, but that is incorrect in absolutely every case listed there. They may have venom insignificant to most humans, but that's a different thing.

@anongoodnurse: B. kiplingi aren't 100% herbivorous, though, and will sometimes hunt e.g. ant larvae. I couldn't confirm with a quick Google search whether they have venom, but it seems that most jumping spiders (Salticidae) do and use it as a key part of their hunting method, so there's a decent chance that B. kiplingi have also retained the trait.

I would add that the venom of many (most?) spiders is technically dangerous indeed to humans, but because it is administered in such a small dose, it is not efficient. Also, while all spiders can bite, most of them won’t bite humans (except in rare cases of extreme self-defence), as they “know” their fangs are not long enough to pierce the skin. (In Québec, no spiders are harmful to humans, although we are starting to see some Latrodectus mactans—the (in)famous black widow spider.)

@IlmariKaronen - I've read that the way they 'eat' ant larvae has never been explained. However, that wasn't really my point. I guess subtlety is not my forte. I had (erroneously) assumed all spiders were venomous as they prey on animals.

@PierrePaquette Is it true that many spiders' fangs are too short to pierce human skin? That's another thing I heard on playground rumors (usually in the form of "(whatever spider species they just saw) is the most poisonous spider but it's harmless to humans because its fangs are too short"; I expect the "most poisonous spider" part is wrong, but I'd never realized the "fangs are too short" part was actually true. (The spider in question in that rumor was usually the daddy longlegs in my experience, which I know isn't even a spider.)

@Hearth: I would almost say that most spider’s fangs are too short, as there are multiple species of very small spiders—those I find in my apartment rarely exceed 2–3 mm in body length (when measuring a spider, only its body length is considered). Those definitely have fangs that are too short to pierce human skin! Even a black widow’s fangs are only about 1 mm in length: long enough to pierce skin, but it would rather run away than bite someone! (This does NOT mean you should try to manipulate them!) Only larger spiders have fangs that are long enough to pierce human skin.

@Hearth There are three different kinds of creatures that are called "daddy longlegs".  One of the three is a spider.

Note that "factoid" means something that looks like a fact but isn't, which in this case is indeed accurate.

@OrangeDog https://www.merriam-webster.com/dictionary/factoid both "an invented fact believed to be true because it appears in print" and "a briefly stated and usually trivial fact" are definitions.

I searched Google for "non-venomous spiders".
The first result that came up was Uloboridae (Wikipedia):

Uloboridae is a family of non-venomous spiders, known as cribellate orb weavers or hackled orb weavers. Their lack of venom glands is a secondarily evolved trait. Instead, they wrap their prey thoroughly in silk, cover it in regurgitated digestive enzymes, and then ingest the liquified body.

However, non-venomous spiders are atypical, and it is true that most spiders that humans don't consider harmful are still venomous to their prey; the playground statement is a reasonable approximation.

I don't know why this got a downvote; it definitely answers the question. Have an upvote. It didn't occur to me to use that specific search term; I just tried "all spiders poisonous", "is it true that all spiders are poisonous", and so on--which didn't turn up any useful results.

@Hearth Which makes sense, because being poisonous is not the same as being venomous. Venom is injected, poison is ingested or touched, so for example Pitohui dichrous is poisonous but not venomous, while Acharia stimulea is venomous but not poisonous, despite physical contact being the hazard for in both cases.

@AustinHemmelgarn I didn't really realize that "venomous" would be the correct term until I was typing up the question here, yeah. It's not a distinction that comes up often when working as an engineer!

You know, after this description I have decided that I actually prefer the venomous spiders ;-).

Considering that all spiders inject digestive acids into a prey, the method and speed of the venom is debatable. Here's an interesting spitting spider: https://www.youtube.com/watch?v=vUUm2OCMCzY they catch their prey by spitting a fluid that congeals on contact into a venomous and sticky mass. The fluid contains both venom and spider silk in liquid form, though it is produced in venom glands in the chelicerae. The venom-laced silk both immobilizes and envenoms prey such as silverfish.  https://en.wikipedia.org/wiki/Spitting_spider found in America.


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What causes metallic tastes when you receive electric shocks
Whenever I receive small electric charges (most often by, e.g. touching the jack of a plugged in charging cable, or the casing of a charging Apple device), I experience a very distinctive taste in my mouth.
I'm relatively certain that the taste is what is termed "a metallic taste", and some brief googling suggests that this is a common experience when receiving an electric shock.
What is going on, biochemically, in this experience?

FWIW, it's the same sensory experience that I associate with a sudden physical danger shock, such as times when I've been standing on a branch that then broke (I was holding another branch, so was fine, but had a huge fear/adrenaline rush, plus that same metallic taste).
Are they linked experiences at all?

I think adding more support for your metallic taste sensation would add a lot of body to the question. As of now you seem to be asking the community to explain an anecdotal personal observation. Sensation and perception are subjective phenomena and personal anecdotes are not a very solid basis for a scientific question. I can list a quite a few sensations I have repeatedly perceived under various circumstances, yet I hardly find them to be solid enough to raise a question about.


text:
Length at which a branch 'branches'?

An image from this question (and originally from Karl Niklas' computer model) has prompted the following question:
The branches in this tree divide with increasing frequency as we progress from the bottom of the tree. This clearly makes sense from the perspective of light absorption efficiency and is a phenomenon I have often observed in real trees. The model in question created trees for optimal light favourability, stability and reproductive ability (in this case just light favourability). What other factors affect the length at which a branch splits or produces an offshoot? How does this initial sprouting determine the 'final' shape of the tree's branches.
DISCLAIMER: appreciate that perhaps this question is too broad - my initial interest in the specific subject was from a more mathematical standpoint (I am a physicist). I am simply seeking a more biological/complete explanation to the phenomena.


text:
Is it a trichoderma?
I have got some fungi on a polypore. Can it be a trichoderma?

It certainly could be, given how prevalent they are, but fungi are nearly impossible to identify visually like this. You need to look at its microscopic structure, run various biochemical assays, and ultimately do sequencing, just like with bacteria.

There are fungal morphologists but they do require microscopes.  some penecilia also have this color... they are also very common... :)

The green colour is darker than I see with fresh Trichoderma infections. It looks like an old infection. My experience limited to growth on coffee grounds and cocopeat.


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What is the biological advantage of bilaterity?
I was wondering why there were so many bilateral species (under the bilateria clade) in comparison with the cnidaria clade. I have two or so questions:

Am I (or are we) unaware of the diversity and population of the cnidaria clade, so I can't say that bilaterity seems to be prefered by the natural selection?
Is bilaterity an advantage only on earth and not in water (where I think most of the cnidaria clade is (jellyfishes)).
If the answer to the last question is true, why is bilaterity an advantage on earth and less an advantage in water, and why is the contrary true for "unilaterality" (I don't know what is the word to describes the cnidaria clade).

Thanks!

Welcome to Biology.SE! Interesting question and I look forward to seeing what answers you get, but unfortunately I suspect it may not be answerable. ——— Jellies have radial symmetry.  ——— You may want to take the time to check out the [tour] and then the help pages starting with [Ask] effectively questions on this site. Thanks!

keep in mind cnidaria are bilaterally symmetrical, they are just symmetrical in other ways as well. Then you have sea cucumbers which may have evolved bilateral symmetry twice independently.

Bilateria, as a clade (all animals, excluding sponges, cnidaria, comb-jellies, and placozoans) is monophyletic, and as such, originated from a single species that was bilaterally symmetrical. Sometimes the explanation for a particular trait involves ancestry, and if an innovation is advantageous, it tends to spread. Along with this group came advances in the central nervous system, and digestive systems. It is advantageous to put senses up front, in the head, with the mouth. Having a tube-like digestive system, with a mouth at one end, a gut in the middle, and an anus at the other end, turned out to be efficient. Cnidaria (and other non-bilaterians) are not nearly as diverse as bilaterians, and most bilaterians are marine. So the bilateral advantage holds both in water, and on land.


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Does Cholestyramine (CSM) raise Tyramine levels?
This is a layman's question.
Will ingesting Cholestyramine (CSM, the resin, in powdered form to be specific) raise tyramine levels?
I am asking because Cholestyramine clearly has "tyramine" in its name, so i don't understand the chemistry behind all this and/or how this interacts with the body.
Thank you.

I'm not sure why "tyramine" is in the name "cholestyramine", but the molecular structure of tyramine is not present as part of the molecular structure of cholestyramine. Specifically, in tyramine the amino group is on the beta-carbon from the ring, and in cholestyramine the ammonium group is on the alpha-carbon (note the different number of points between the ring and the nitrogen in the line structures provided). I find it highly doubtful any reasonable metabolic reactions by the body could generate tyramine from cholestyramine.
Cholestyramine molecular structure
Tyramine molecular structure


text:
Which functions of skin cells have scientists been able to revert 30 years?
According to this article Scientists discover new method to reverse ageing in human skill cells by 30 years (and several others from 2022-2024)

"Researchers said they have been able to partly restore the function
of older cells, as well as renew the biological age."

Which functions of skin cells have scientists been able to revert 30 years?

You'll notice the telomeres were not lengthened by the process.

The original scientific article >accessible here< mentions rejuvenation of cell attributes such as displaying a 30 year-younger transcriptome, statement reached through comparing to a reference data set. So such rewind of the cellular biological clock by around 30 years is then established according to molecular measures. The functional analyses involved properties such as wound healing simulation experiments (in vitro migration speed) commonly associated and displayed by skin cells.
Due to technical advances that allow researchers to measure age-related biological changes in human cells and through their method based on the Nobel Prize-winning technique to make stem cells, using a shorter-timed version (13 instead of 50 day exposure), these researchers were able to reset ageing indicators in genes associated with diseases and restore cells to a more youthful state, regaining their specialised function to an improved potential, and overall reversing ageing as the gradual decline in cellular functions, which is normally considered irreversible at "senescence" state.
The aspiration would be to identify genes that rejuvenate without a full reprogramming or erasing cellular memory identity, and specifically target those to reduce the effects of ageing, an approach that holds promise for valuable discoveries in the therapeutic horizon.
For a complementary and holistic view perhaps, an alternative article from a lay magazine (with elaborate text and without typos unlike the one cited by OP) can be accessed >here<.

did you say one of the properties they restore was being able to heal like younger cells? Or did I get that wrong?

yes - experimentalists test "wound healing" simulated on a petri dish with a layer of cells deliberately scratched and then cell movement monitored over time by camera captures (in incubating conditions), tracking how long it takes for the cells to migrate and seal the gap, the speed is the factor compared.


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Does anyone know what kind of bug is this?
i found these tiny little bugs today all over my windowsill, the walls around the window, and on my chargers in the plugin near the window. they’re like microscopic i can’t even see them. i used a spider and ants spray to kill them, it’s all i had for now. i’ve also been cleaning and wiping my walls down but there’s still a few left. i’m scared they’ll all come back again by tomorrow. does anyone know what they are and how i can get rid of them?

Welcome ca.bus. Could you tell us where in the world you are, what if anything is visible that they might view as a food source. Looks to me like a type of thrip instar, but more info needed, and ID isn't easy anyhow. A close-up picture from on top and another from the side would help if you can get them. Use the [edit] facility to add detail.

Likely related (but awaiting better picture to confirm) : https://biology.stackexchange.com/a/85321/16866

any shipping plans? (asking for a friend)

This is a mite: it has eight short legs and only one body part (in comparison to spiders, which have two body parts). No idea which order or even species though.
Here is an article about indoor mites - maybe "yours" is among them - with some recommendations to manage them.


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Identification of Bone like subject found on Beach in santa cruz ca
I found this at the Beach in Santa Cruz California, it is about 2 inches long and at its widest it is about 1.5 inches wide and it weighs 3 grams, and I'm not sure what it is, Google Image search suggests a dehydrated ducks Foot, it looks more like a fin from a fish or something or at least part of one. Does anyone have any ideas of what it could be? (All images are of the same subject)


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Living in Singapore, what’s this bug? Found an identical one in my house on the floor

Hi! I’m living in Singapore (Southeast Asia). Found a small brown bug with a prominent dark stripe on its back like the pictured one, about the size of half a grain of rice. It was wandering around on my living room floor and I have no idea where it came from. I live in a high floor apartment.

This is a beetle. They typically have hard wings (so-called elytra) that distinguish them from many other insect groups. Globally, there are almost 200 described beetle families with more than 300,000 species - so, I can't even tell the family, sorry. But most likely, it was in your appartment accidentally.


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Does Plasmodium affect the female Anopheles mosquito?
I was studying the life cycle of Plasmodium, and I read that the infectious form (sporozoites) is what causes malaria in humans. I also read that this form resides in the salivary glands of the female Anopheles(carrirer of Plasmodium). My question is that if the sporozoites reside in the salivary glands, do they affect the mosquito itself? Or, in general, do the pathogens attack, or affect the disease vectors in any way?

tl;dr yes, Plasmodium does appear to interact with its mosquito vectors — many species of mosquito have reduced fitness when infected with plasmodia due to the cost of mounting an immune response (this implies that they would lose even more fitness if they didn't mount an immune response ...). However, mosquito species that are frequently infected in the wild appear to have evolved tolerance, so they incur less fitness cost (there is even a positive correlation between infection intensity and fitness in some cases (for not-fully-understood reasons).
From Shaw et al 2022:

Numerous studies using rodent model species have detected a fitness cost of infection to mosquito fecundity [26–29], fertility [27,28], and survival [30], most likely due to the considerable investment by the infected female in immune responses (Box 1). When Anopheles stephensi or An. gambiae were infected with Plasmodium yoelii nigeriensis, there was a reduction in fecundity of 21–41% [26–28], but with no significant correlation between egg numbers and oocyst loads [26,28]. The reduction in fecundity was due to apoptosis of follicular epithelium cells, promoting resorption of ovarian follicles in infected females [31,32]. The density independence between
egg and oocyst numbers suggests an all-or-nothing cost to activation of the mosquito immune system preventing significant egg investment [33,34]. An. stephensi also showed reduced survival when infected with a number of rodent malaria parasite species [26,35–37]. Compared with uninfected controls, mortality rates were significantly higher when mosquitoes were infected
with P. berghei or with P. yoelii nigeriensis, while infections with P. chabaudi reduced median survival (with parasite strain- and experiment-dependent effects).

On the other hand, a meta-analysis on 11 published studies found that in infections involving
P. falciparum and its natural mosquito vectors – An. gambiae, Anopheles funestus, and An. stephensi – no costs to survival were detected [38]. Similarly, in recent studies, An. gambiae and An. stephensi females infected with P. falciparum developed the same number of eggs as
their uninfected sisters [39]. In An. gambiae, an unexpected positive correlation existed between paired egg and oocyst numbers from individual infected mosquitoes, with females that invest more in reproduction supporting higher infection intensities [40].  ...

Shaw, W. Robert, Perrine Marcenac, and Flaminia Catteruccia. “Plasmodium Development in Anopheles: A Tale of Shared Resources.” Trends in Parasitology 38, no. 2 (February 2022): 124–35. https://doi.org/10.1016/j.pt.2021.08.009.

It does not because it causes no structural damage to mosquito in either stage i.e while penetrating into endolymph via gut and also while penetrating the salivary gland since there is complimentary protein ligand (on surface of gut and on surface of salivary gland) which facilitates its entry without causing any harm, on the other hand some research even goes to the extent that it's mutually beneficial since it enhances the smelling capacity of mosquito thus their relationship is advantageous hence sustained in nature over the course of evolution.
https://phys.org/news/2021-11-mosquitoes-mutual-symbiotic-relationship-malaria-causing.html
https://www.pnas.org/doi/10.1073/pnas.241491198


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How to include multiple DNAs into a crystal structure
I have a crystal structure (PDB 3OS1)that shows the interaction of PFV intasome with a substate DNA. I would like to replace the existing DNA in the intasome as well in the substrate with a longer sequences. What is the easiest way to do it. Thank you.

Welcome to Biology.SE! We encourage you to do some research on your own and then ask questions informed by what you have learned (ideally with references to reliable sources). You are also more likely to need to get a positive response if you provide more detail and background about what your are trying to accomplish — I'm not clear on whether you are trying manipulate actual crystals or a structure file. ——— Please also take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site and then edit your question accordingly. Thanks!

Could you clarify? Why do you expect the protein to have the same structure with a different substrate DNA? And even if it is a reasonable assumption, you are going to have to edit the coordinates of the existing bases with those for different ones. Furthermore how do you imagine you can model additional bases? Your request for “the easiest way” to do it suggests you don’t realize what is involved. Do you?


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What is health?
I was studying human health and diseases in a book and first it defined general health as: “The overall complete physical, social, and mental well being.” It further went to say that health is being efficient, devoid of negative thoughts, etc.
The word complete is throwing me off, here. Isn't that the definition of an 'ideal' health that is impossible to achieve?
To some extent, we can have complete physical well being, but that is not the case for mental and social well being. We are humans, and it's in our nature to have negative thoughts and things like that, and that makes us human. But, that means that the definition of the health I read isn't true. How would you define health?
(Or,it might just be me who's overthinking all this.)

Complete here means "considering all these attributes together" rather than independently. Complete doesn't mean ideal, health is a spectrum.

That's not a good definition of health, even though it is used. One can be in good health, poor health, excellent health, average health, good physical health but poor mental health, the opposite, etc. There may be people in perfect health, and many people might claim to be in perfect health, but I'm very skeptical it exists and I've never seen a physician's report state that someone was in perfect health unless "perfect health" was clearly defined before hand (e.g. Air Force fighter pilots have very specific requirements, including height.)

Then, instead of defining health as perfection, or "completeness" in all the aspects, which are practically unobtainable, wouldn't it better if we defined health as a 'balance' between all those things?

Health is one of those things we don't have a good single definition for, health is contextual kinda like species.

The sentence does not indicate unobtainable perfection, you are inventing this. Just remove the word complete from the sentence and it still means the same thing, the word is just there to make clear that it involves all those things.

So the book invokes individuals with low levels of psychopathology and negative thought. They have very high scores in psychometric health tests.
Yes most of us have average symptom levels of mental disorder, and there are those with very high and very low levels of mental disorder.

This refers to health strategies:

Psychology used to be associated mostly with illness, maladaptive practices and negative thoughts, so in 1998 the term positive psychology became popular.
Mental health can be defined by positive or negative outlook, self-belief, judgement, good sleep, efficient organization, mental energy.
Negative views of the past, of oneself, of others, of society, sometimes nightmares, bad daydreams, and poor logical processing.
It is possible for someone in very good mental health to have very few of those types of negative thoughts.
Positive psychology and the absence of negative thoughts can be measured using various psychometric instruments and assessments:
Positive and Negative Affect Schedule (PANAS): A questionnaire measures both positive and negative affect, capturing the presence of positive emotions (e.g., joy, enthusiasm) and the absence of negative emotions (e.g., fear, sadness).
Satisfaction with Life Scale (SWLS): This scale assesses an individual's overall life satisfaction, reflecting their cognitive evaluation of their life as a whole.
Flourishing Scale (FS)
Resilience Scale (RS)
Self-Esteem Scale
Positive Psychotherapy Inventory (PPTI)
I have heard people described as being "almost completely devoid of complexes", i.e. they are very rare and fortunate to have a can do attitude about everything, social confidence and no particular secrets or conflicts with themselves.

It would be cool to be the human on the left. To clarify what you questioned: Those who are especially well-balanced may not be very wise or performant in other psychometric scores for knowledge or life skills, for example, it just means that they sleep well, wake up feeling good and ready for the day, don't worry much, enjoy their lifestyle, feel socially confident and optimistic to achieve what they want, they enjoy a lot of things in life, have few subjects that they find embarassing or complexing, deal with challenges well, have few bad memories or social hangups, are very satisfied with themselves, and enjoy themselves... The other end of the scale is often people with trauma, they have mood-swings, depression, possibly agression or argumentative cycles, out of control thoughts patterns which torment them, negative views of society, family, contemplate suicide, often dwelling on memories, have nightmares at night, bad sleep, strong ego, judgement... Most of use are somewhere in between those two extremes. The scientific way to measure it is psychometric tests.


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How does mitochondrial uncoupling enhance performance in muscle cells?
As far aas I understand, in mitochondria, the citric acid cycle breaks down fatty acid or glucose to produce NADH and FADH2, which are then utilized by Complexes I through IV to generate a proton gradient in the intermembrane space. This gradient powers ATP synthase to ultimately generate ATP for the cell.
Uncoupling refers to alternative ways of decreasing the proton gradient without involving ATP synthase, such as through transmembrane fatty acids or Uncoupling Proteins (UCPs).
On the one hand, I recall learning that uncoupling is considered a disease condition since it disrupts the 'pull-effect' where an increased need for ATP essentially drives the entire reaction chain from the back, and because it generally dissipates energy into non-productive work. For instance, a textbook I recently read stated that ketones promote uncoupling in cardiac muscle cells, which is detrimental for obese individuals as the heart's performance capacity is impaired due to efficiency loss.
On the other hand, it is widely accepted nowadays that physical activity leads to significant mitochondrial uncoupling. This is surprising to me since one would assume that during a biologically relevant process, such as the adaptation of a muscle to movement, the adaptation would typically be 'beneficial'. Multiple authors write sentences like 'this optimizes the mitochondria's ability to synthesize ATP.'
It is evident that mitochondria deal better with a high nutrient supply when uncoupled, as fewer superoxides and peroxides are produced. But during physical exertion, an excess supply of nutrients is probably not the main issue?
I'm looking for insights to guide my understanding. How could the uncoupling of the electron transport chain I-IV from ATP synthase potentially enhance the performance capability of mitochondria and by this means the performance capability of skeletal muscle cells?

Skeletal muscles have multiple systems that increase the rate of energy generation in response to faster energy consumption during excercise.

System
Rate
Sustainability

Phosphagen
highest
10-15s

Glycogen-lactic-acid

30-40s

Aerobic
lowest
indefinite

The phosphagen system represents the immediate source of ATP, it is relied on for power surges. ATP itself and phosphocreatine, which can donate its phosphate radical to ADP, form this system.
When muscle activity is prolonged, the other two systems come into play. Which of the two being predominant depends on the intensity of the activity (rate of ATP utilisation).

The glycogen-lactic-acid system is used for strenuous excercise because it generates ATP faster than the aerobic system. It involves glycogenolysis, glycolysis and homolactic fermentation. Glycogenolysis is the breakdown of glycogen to glucose. Glycolysis is glucose oxidation into pyruvic acid by oxidative coenzymes with production of ATP (substrate-level phosphorylation). In homolactic fermentation, which happens under anaerobic conditions (oxygen insufficiency), instead of the reduced coenzymes (byproducts of glycolysis) being oxidised by the ETC in the mitochonderia, pyruvic acid acts as the final hydrogen acceptor to oxidise them so they can be used for another cycle of glycolysis. This produces lactic acid which is a strong acid that causes fatigue as will be explained later. Krebs' cycle is not part of the glycogen-lactic-acid system because there is no pyruvic acid to oxidatively decarboxylate into the acetyl moiety of acetyl-CoA (active acetate).

The aerobic system involves glycogenolysis, glycolysis, Krebs' cycle and the ETC. The Kreb cycle substrate is the active acetate radical that is oxidatively decarboxylated completely by oxidative coenzymes, with substrate-level phosphorylation. The ETC requires oxygen supply since oxygen is the final electron acceptor that drives the movement of hydrogen from the reduced coenzymes and its splitting to electrons and protons. (Oxygen is the second most electronegative element in the periodic table.) The movement of electrons (redox reactions) generates energy that is used to pump protons in the matrix across the inner mitochonderial membrane into the intermembrane space. This pumping continues until a proton back-pressure (proton motive force or proton gradient) is established. Once established, ATP synthase inhibits further proton pumping and stops the activity of the ETC. The pumped protons then diffuse through ATP synthase (chemiosmosis) and the energy that was used to pump them before is now used to phosphorylate ADP to ATP (oxidative phosphorylation). ATP synthase is sometimes also called complex V though it doesn't transport electrons, only facilitates proton diffusion. ATP synthase is activated by high ADP concentration in the matrix which discharges the proton back-pressure and consequently activates the ETC. ADP is produced from ATP hydrolysis and increases at low energy states when energy consumption is faster than energy production. The aerobic system is thus relied on for moderate-intensity prolonged excercise where oxygen consumption by the ETC is balanced by oxygen supply and where the long metabolic pathway still provides ATP at a sufficient rate. The reduction of oxygen by electrons can form either

water if the electrons are sufficient $\ce{O2 + 4e- + 4H+ \to 2H2O}$ (The protons are taken up from the matrix).
superoxide ion if the electrons are insufficient to form water $\ce{O2 + e- \to [O2]-}$.

Superoxide ions form hydrogen peroxide $\ce{2[O2]-  + 2H+ \to H2O2 + O2}$. Hydrogen peroxide, as with all ROS, has a high affinity to electrons and pulls them from other compounds damaging them, to combine with the electrons and with protons forming water $\ce{H2O2 + 2e- + 2H+ \to 2H2O}$. This causes peroxidation (oxidative damage) to lipids, proteins and DNA. Cells therefore have to split hydrogen peroxide to water and oxygen $\ce{2H2O2 \to 2H2O + O2}$ by catalase enzyme. Hydrogen peroxide can also be useful for the same reason. It is used by immunity cells to kill pathogens by damaging their cell membranes, which are made up of phopholipids, causing their lysis.
The muscle burns through the phosphagen system first and then operates through the aerobic system indefinitely, as long as there is sufficient oxygen and glucose supply. Any extra energy needed in a short amount of time is supplied by the glycogen-lactic-acid system. However, the latter limits activity time (causes fatigue) as will be explained later.

Muscles are divided into fascicles which are groups of muscle fibers (cells). Following are the most important organelles in a muscle fiber.

A sarcolemma (plasmalemma)
A sarcoplasm (cytoplasm)
Many mitochonderia
Multiple nuclei
Many sarcoendoplasmic reticula (smooth endoplasmic reticula) that surround the most important organelles, myofibrils
Many myofibrils

Myofibrils are formed of many myofilaments (actin and myosin) organized into contractile (motor) units known as sarcomeres.

Muscles contract when a threshold electrical stimulus depolarises the sarcolemma resulting in an action potential that propagates to T-tubules. At the T-tubules, the reversal of relative charge accross the membrane changes the shape of dihydropyridine receptors so they now allow for the influx of $\ce{Ca^{2+}}$. Consequently, ryanodine receptors on the terminal cisternae of sarcoendoplasmic reticula open and more $\ce{Ca^{2+}}$ diffuse into the sarcoplasm ($\ce{Ca^{2+}}$-induced $\ce{Ca^{2+}}$ release). This increases sarcoplasmic $\ce{Ca^{2+}}$ concentration. $\ce{Ca^{2+}}$ binds to troponin which changes shape. Since troponin is bound to tropomyosin, changing the shape of the former displaces the latter. Tropomyosin consequently exposes myosin-binding sites on actin so myosin can now bind, bend, detach and get back to original conformation to repeat the process (cross-bridge cycling) until $\ce{Ca^{2+}}$ is actively pumped back to where it came from causing tropomyosin to block active sites and relaxation. The magnitude of the response of the muscle to stimulation (whether acetylcholine or depolarisation can elicit an action potential) depends on

strength of the stimulus (amount of acetylcholine or change in membrane potential).
duration of the stimulus (time for which acetylcholine or charge persist).
frequency of stimulation or rise of stimulus intensity (since acetylcholine and charge accumulate).

Muscle fatigue as we know it can be attributed to different mechanisms that happen at different stations.

Neural (central) fatigue
Metabolic (peripheral) fatigue

Neural fatigue happens because the muscle stops listening, specifically because the frequency of electric stimulation is not high enough to maintain contraction. It can happen because of exhaustion of neurotransmitter (acetylcholine) stores for example. That is to say, the rate of release and breakdown of acetylcholine by acetylcholinesterase is greater than the rate of its formation and packaging into vesicles. Neural fatigue is what limits activity time in well-trained athletes. It's not associated with pain. Athletes work on increasing the capacity of their neurons to keep firing at a high frequency by training.
Metabolic fatigue on the other hand happens because the muscle gives up, specifically because of

$\ce{Ca^{2+}}$ not doing its job being too little or ineffective.
substrate shortage.

Lactic acid, being highly acidic, dissociates readily into protons and lactate. The protons, having the same charge as $\ce{Ca^{2+}}$, displace it decreasing the sensitivity of the muscle to $\ce{Ca^{2+}}$. The binding of protons can also deform proteins by breaking the bonds that form their secondary, tertiary and quaternary structures. Amino acid radical groups pick up the surplus of positive charge and the interactions between them change. Thus, lactic acid causes inhibition of active $\ce{Ca^{2+}}$ pumping outside the sarcoplasm by deforming pumps, so high $\ce{Ca^{2+}}$ concentration is maintained allowing for more forceful contraction. However, it's a matter of time until the insensitivity becomes too much. Lactic acid (which would have been an active acetate inside mitochonderia in the aerobic system) also causes hydrolytic damage to myofilaments. Any damage to a muscle is called microtrauma. Repetitive strain on myofilaments, connective tissue, tendons and bones by lengthening (eccentric contraction) can also cause microtrauma. Microtrauma results in inflammation and muscle soreness. Muscle soreness (pain) aims to stop the physical activity which can cause more microtrauma to the muscle. Muscles can adapt to metabolic fatigue and microtrauma by increasing

substrate stores (glycogen)
$\ce{Ca^{2+}}$ stores (sarcoendoplasmic reticula)
number of myofibrils (hypertrophy)
number of connective tissue fibers, to increase stiffness
diameter of nerve fiber, to increase speed of conduction
amount of glycolytic enzymes

as seen in pale (also known as type II or fast-twitch) muscle fibers, to decrease the likelihood of reinjury.

Thus, muscles don't necessarily need the ETC to generate energy and in fact, rely on the fermentation pathway for faster and more forceful activities because of its higher rate of ATP production despite its fatiguing effects which they can adapt to.

Now, we can look at the effects of uncoupling. Uncouplers work on the aerobic pathway by uncoupling oxidation from phosphorylation; they make it possible for oxidation to take place without phosphorylation. They cause proton discharge through the inner mitochonderial membrane before the threshold back-pressure required for protons to flow through ATP synthase is established. As a result, the energy from proton diffusion across the membrane is released as heat instead. This mechanism is utilized for example in brown adipose tissue where thermogenin transmembrane protein (uncoupling protein 1) causes rising of body temperature (to maintain body temperature in cold environments) and fat loss by metabolising fatty acids in stored fat which enter Krebs' cycle as acetyl groups and the resulting reduced coenzymes are oxidised by the ETC, with no oxidative phosphorylation. That's why this type of adipose tissue is more vascular relative to white adipose tissue; to maintain the high rate of oxidation which requires oxygen. The increase in heat can

decrease viscosity of myofilaments so they slide more easily over each other.
increase enzyme activity since more enzyme-substrate complexes form as enzymes and substrates move faster with greater chances to collide which increases the rate of ATP formation and utilisation.
relax blood vessel smooth muscles resulting in vasodilatation and increased blood flow, with consequent increases in oxygen supply and lactic acid removal during excercise. Whether lactic acid causes fatigue depends on the difference between the rate of its production and the rate of its flushing during activity. At rest, the remaining lactic acid is flushed or oxidised locally. We maintain the vasodilatation and high ventillation rate at rest, to oxidise the remaining lactic acid and myoglobin and form ATP by the ETC to rephosphorylate creatine to phosphocreatine (oxygen debt). The flushed lactic acid is mostly reoxidised into pyruvic acid then glucose in the liver by reversal of glycolysis, also known as gluconeogenesis (Cori cycle). The remaining lactic acid is reoxidized locally to pyruvic acid which enters Krebs' cycle instead, but the majority is flushed. The increased blood supply also helps in healing from microtrauma at rest which ultimately stops soreness. Cold, on the other hand, treats soreness directly by decreasing blood flow carrying inflammatory cells that cause pain by secreting cytokines.

Besides increasing temperature, uncoupling causes

faster flow of electrons through the ETC since the sufficient proton back-pressure is never established so ATP synthase doesn't inhibit pumping of protons and electron transfer (electron transfer is continuous). As a result, oxygen is reduced rapidly to water instead of being reduced merely to hydrogen peroxide that can cause damage if catalase is saturated and can't split the excess to water and oxygen.

Wow! What did you do? That's 1/2 a textbook! 1000s kudos! Great job! I really appreciate your effort!

Thank you. I truly appreciate your nice words. It just so happens I am studying biochemistry and physiology. So I thought why not try writing a logical, comprehensive, self-contained answer that makes total sense to make sure I understand what I am learning that can also be my reference since it integrates everything. My former answer also didn't address peroxidation so I had to fix it.


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I need help identifying a bug
Basically this tiny bug plopped on top of my laptop keyboard. And as much as I disdained bugs, this one didn't look like anything I've ever seen. It had something that resembled bits of a dandelion on its back, and its body seemed like half a moth/ whatever insect. After closer inspection, I thought it was just a dying moth, the thing on its back being clipped wings and its body cut in half... but when i tried to shove it off the keyboard with my pen, it jumped about a hundred times its width onto my wall - instantly. Tried to get a second picture but it jumped again/disappeared... no idea where it went, or what it was... Here's the picture I took, and a quick sketch of what it looked like.

What's your location?

This looks like an immature passionvine hopper (Scolypopa australis).  They are informally known as fluffy bums.

Source: http://ketenewplymouth.peoplesnetworknz.info/friends_of_te_henui/images/show/1486-nymphs-fluffy-bums-scolypopa-australis
This is am image of the adult stage from the Encyclopedia of Life site:

More information can be found at the Encyclopedia of Life link above.  It appears that their distribution may be only in Australia and New Zealand and I'm not sure where this photo was taken so take this information into consideration.

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


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What type of movement is "spontaneous movement" if it isnt reflex movement and it isnt purposive movement?
According to Spontaneous and induced fetal activity

Spontaneous motor activity of the foetus depends significantly ot the
  foetal age; during the period between the 12th and 16th week it was
  recorded in 94.4%

By spontaneous, correct me if I wrong, I understand non reflexive movement and by induced I understand reflexive movement, since

A reflexive reaction or movement occurs immediately in response to
  something that happens.

But also, according to this other article Fetal movement

purposive movement begins at about 18 weeks, gradually replacing
  reflex movements

If "spontaneous movement" it isnt reflexive movement since it isnt an automatic reaction to something, and it isnt purposive movement, what is it exactly, and what does it generate it?

Although I can't read the original article in Czech, from their abstract it is clear that all they mean in differentiating spontaneous versus induced movement is whether the experimenter manipulated the uterus to induce a movement. Movements they observe could still be reflexive, they make no distinction of the type of movement (and do not intend do) except indicating whether the movement was purposefully caused by the experimenter.

There are several articles like that one, how about this one, it seems to say spontaneous movements at week 10-21 are movements generated by the fetus itself: https://www.karger.com/Article/Pdf/293158  "Fetal movements (FM) may be spontaneous, originating in the fetus itself, or evoked, caused by external stimuli. The FM in 21 normal twin pregnancies at 10 and 21 weeks of gestation were studied. The percentage rate of evoked FM which occur simultaneously in both twins was 4.96% of all observed FM. The rate of the spontaneous FM which occur independently in each fetus was 95.04% of all FM"


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What's the evolutionary purpose of having hearts?
According to this
New understanding of heart evolution

Humans, like other warm-blooded animals, expend a lot of energy and need a lot of oxygen. Our four-chambered hearts make this possible. It gives us an evolutionary advantage: We're able to roam, hunt and hide even in the cold of night, or the chill of winter.

But in the other hand, there are heartless JellyFish of 2.3 meters with up to 70-150 tentacles per one of each 8 lobes of up to 37 meters in lenght. Lion's mane JellyFish
Having humans spending a lot of their energies in moving limbs, even though I understand JellyFish move in another environment, I'm having a hard time believing moving our limbs spend more energy than moving 70-150 tentacles per one of each 8 lobes of up to 37 meters in lenght.
What's the evolutionary purpose of having hearts? Is it for animals with it to be able to expend more energy or is there any other reason for it?

Perhaps the currents help move those tentacles... water is approx 1000 times as dense...

Evolution has no purpose. BTW, bacteria also move and they don't even need nervous system for doing so.

Have you tried looking up the energetics of movement for vertebrates?  ——— Note also that a jelly doesn't need a heart to transport oxygen to its tissues since it is very thin and absorbs oxygen from the water.  This makes the comparison to the energetics of a jelly completely irrelevant!

There are very important advantages (not purposes) of having heart.
Animals that have heart are more agile and can be much larger than others. That is because they can move nutrients, gases and waste products faster and efficiently between parts of the body. Without heart and circulatory system, all the necessary material must be moved inside the body through diffusion which isn't efficient especially at longer distances and fast.
All of the largest animals that live and had lived on earth have heart. An animal which doesn't have heart can be large and can be very long, but will be thin to get a very large surface area which will increase the efficiency of diffusion between the body and the environment.
On terms of advantages that they provide, having a heart (and circulatory system) is better than not having one, having closed circulatory system is better than having open circulatory system.


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Is the medium which transmits the electrical impulse through the heart different to a nerve?
According to Nerve

A nerve is an enclosed, cable-like bundle of nerve fibres called axons

Being an Axon

An axon (from Greek ἄξων áxōn, axis), or nerve fiber, is a long, slender projection of a nerve cell, or neuron, in vertebrates, that typically conducts electrical impulses known as action potentials

In the other hand,
Electrical Conduction System of the heart

The electrical conduction system of the heart transmits signals generated usually by the sinoatrial node to cause contraction of the heart muscle.

The conduction system consists of specialised heart muscle cells
Is this conduction system consisted of cells (which I assume also transmits electrical signals through axons) different in nature to nerves?


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When does the brain stem appear in humans?
This article states:

Once the neural tube closes, at around week 6 or week 7 of pregnancy,
  it curves and bulges into three sections, commonly known as the
  forebrain, midbrain and hindbrain. Just to the rear of the hindbrain
  sits the part that will soon turn into your baby's spinal cord. Soon,
  these areas bubble into those five different regions of the brain that
  we're most familiar with: the cerebrum, cerebellum, brain stem,
  pituitary gland and the hypothalamus.

How "soon" after 6 - 7 weeks is this soon the article talks about? When does the brain stem appear in humans?
Fetal Brain Development


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Is sexual desire stronger in men than women?
Usually in popular culture it's considered men sexual desire is stronger than women. This seems to be congruent with the availability of sexual related items for men and women, such as magazines, movies, and more. Trying to understand if there is a biological connection to this, I found these paragraphs in some articles.

Estrogen, progesterone, and testosterone are hormones that affect a
  woman’s sexual desire and functioning.
When it comes to sexual desire, the most influential hormone is
  testosterone. Though it’s often considered a male hormone,
  testosterone — like estrogen– is present in both men and women, though
  the proportions differ between the sexes.

Hormones affecting sexual desire
and

On average, in adult males, levels of testosterone are about 7 to 8
  times as great as in adult females.[7] As the metabolism of
  testosterone in males is more pronounced, the daily production is
  about 20 times greater in men

Testoterone
Is this greater production of testoterone in men related to a stronger sexual desire? Is there any research studying this, or studying differences between male and women sexual desire intensity in general?

Some of the work of Bob Trivers makes some sense to me. He talks about parental investment https://en.wikipedia.org/wiki/Parental_investment.
The "investment" of a man could be as little as paying for dinner, followed by a few minutes of sexual pleasure, and then he is free to go. The woman's investment for the same thing is the risk of pregnancy (or cryptic STD). Pregnancy is difficult, and before modern medicine, was one of the most common ways to die for women. Then she must feed a helpless infant with her own body, and tend to its needs for the next 15 years. We have social structures for the man to stick around and contribute. But these are not biological differences. The man can leave. The woman cannot. She bears virtually all the risks of sexual behavior. Of course, sexual desires vary by individuals, likely in a bell-curve that overlaps (I anticipate some PC doofus pointing out that some women have strong desires, and some men don't). But I would not be surprised at all, given the biological differences in risks and investments between men and women, that the peak of these overlapping distributions is higher for men than women. Also, evolutionary fitness is defined by the number of offspring an individual can produce. A man's strategy is fundamentally different than a woman's. A man who has 1000 sexual partners is likely to leave more surviving offspring than a man who marries the woman he loves, and stays faithful. A woman with 1000 sexual partners would not be able to have hundreds of children, and would likely put her health at risk.

You are saying as if the only result of sex pertinent to evolution is getting pregnant or an STD. Women have menstrual cycles with concealed ovulation which allows them to be sexually active almost all the time. They can have sex during pregnancy. These kinds of non-reproductive sex can help to keep the man around and have more resources and better-protected children. So women may have evolved to have less desire for new partners but not lower overall sex drive. Or not. It just hard to reason without actually measuring it.

I did not say that this was the only explanation, but it seems to fit many observations across a wide range of animals. Yes, hard to measure. However, what do your observations tell you? How common do husbands complain that their wives want "it" too often, relative to the other way around?


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Is there a definition of species where Lions and Tigers are the same species?
According to Species concepts

There are at least 26 recognized species concepts

And according to Why are lions and tigers considered different species (not sure how reliable this source is though, but I've seen exactly the same answer in another website)

The reason tigers and lions are different species is because of different behaviours, different habitats, different social hierarchies, and they each have their own subset of genes that they share within their species (like the genes for stripped fur or for manes).

Now, I'm not sure about "social hierarchies" (which I'm sure it's a fuzzy concept) , but there are different breeds of dogs with different behaviors, living in different habitats, and there has to be differences in genes in different breeds, since even in humans populations there are 1% of differences in genes and according to other sources more.  Then my question is, since Tigers and Lions are closed to each other to the point they can produce offsprings, is there any of those 26 definitions of species where lions and tigers are the same species?

The concept this would fit under would be the "Biological Species Concept."
Concerning this concept, the Evolution site for Berkeley says "members of populations that actually or potentially interbreed in nature..." constitute a species. By this definition, since lions and tigers can (and do) interbreed, they would be considered the same species under this concept.
EDIT: As Bryan pointed out, though, lions and tigers do not breed outside of captivity. NatGeo and Britannica both second this. With this, then, the Biological Species Concept would not be viable.
EDIT2: With the above in mind, there don’t seem to be many options.
Mate-Recognition: This idea posits that organisms who “recognize one another as potential mates” (Wikipedia, “Species”) make up a species. By this, it could be argued lions and tigers are the same species, but I would be hesitant for this to be the concept, for the same reasons against the Biological Species Concept (not occurring in nature).
Ecological: Using this definition, a species is made up “of organisms adapted to a particular... niche, in the environment” (Wikipedia). Again, this is very fuzzy, as I wouldn’t define them in the same niche (though this might depend on how specific you get).
Conclusion: These seem to be the most likely, though that’s a very loose term. I couldn’t find any others that would fit nearly as well. I would say the answer is “no”, but I don’t think I found all of the concepts.

I think one could question this. Although lion-tiger hybrids are viable, occasions where those hybrids have been able to reproduce themselves are quite rare, and they can be effectively considered sterile. They also only interbreed in captivity.

@Bryan Good point. Thanks for that!

Your quote...

The reason tigers and lions are different species is because of different behaviours, different habitats, different social hierarchies...

...is not entirely correct: lions (Panthera leo) and tigers (Panthera tigris) overlaped geographically in the past, since Panthera leo was common from western Europe to southeastern Asia. On top of that, if you consider that Panthera atrox is actually Panthera leo (which is the view of some paleonthologists), you can even add America to the list.
Until today there are (very few) lions in India (photo: Wikipedia):

And, despite that geographic overlapping, lions and tigers do not breed, so we can clearly rule out Mayr's BSC.


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What is this toad suffering from? Myiasis or chytridiomycosis?
I found this toad on Aug. 29th at this location: position on osm

I think it is a bufo bufo, approx. 10 cm long. The nostrils seemed to be completely filled with a grey matter and from the activity of the floor of the mouth it apparently tried to breathe againgst this obstruction. It probably had enough oxygen via its skin though.
I tried to remove the obstruction using a blade of grass but this seemed to produce some pain as the toad closed its eyes on contact, so I stopped. The skin looked fairly normal and the toad was able to walk away after a while.
I can think of two causes for this condition.

Batrachochytrium dendrobatidis infestation
Lucilia bufonivora larvae

I could not see properly, if there were any larvae or unhatched eggs inside the nostrils, but as the rest of the skin seemed unharmed I assume the latter.
Is my assumption valid or is there even a third possibility?

It is a female Bufo Bufo and you are right, there are toad fly (Lucilia bufonivora) larvae/eggs inside her nostrills. These flies lay their eggs inside toads' nostrills (specifically on Bufo Bufos) and the larvae start eating them. Sadly this disease ends up by the death of toad. They slowly eat nostrills, then mouth, eyes, and all the head.
Here's a photo of a male bufo bufo, without a head. Someone found it walking around at this situation. https://i.sstatic.net/I6twl.jpg

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


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How does a ribosome gather tRNAs at a fast enough rate for Translation?
There are many animations of the ribosome in action, and all I have seen show the correct tRNA neatly entering the ribosome and its amino acid being added to the growing protein chain. My question is this: is it really possible that mere brownian motion and diffusion are responsible for getting the right tRNA out of 20 possible types to that point? Presumably that would require tRNAs of every type arriving and most being rejected until the right one meets its codon and is used. Not only that, you would expect orders of magnitude more tRNAs to be arriving at almost the right place but being the wrong way round or hitting the wrong place on the ribosome.
Has anyone in the field ever done any calculations using dynamics equations, along with the known volume of cytoplasm and tRNAs to see if this is even feasible?

I think it has something to do with the cytoskeleton. https://www.nature.com/articles/nrm2818

Forget any animations you have seen — they are irrelevant. But the fact is translation happens at a particular rate. That's chemistry. What else do you suggest? Magic?

@user237650 — Certainly the cellular environment may increase the concentration of components, but the fact remains you can do it in the test tube with purified components.

Please look up the definition of Brownian (names after Brown) Motion. You will find it refers to macroscopic particles, not the molecules that cause it.

And why do you think it matters if there are 20 times as many collisions that cannot be productive as those that can? It would only matter if it competed with the potentionally productive collisions, which it is unlikely to do at the concentrations in the cell. The need for collision of molecules in the right orientation for reaction is a standard feature of chemistry. Catalytic or binding protein in biochemistry often work by facilitating the correct interaction by binding to others. Transfer RNA is brought to the proteins ribosome A-site by elongation factors.

The answer is simply due to the random walk of the amino acids. Over small volumes, this process is incredibly quick and is also responsible for nucleotide delivery to polymerases as well proteins searching for their substrates, in fact, only a few enzymes/proteins are limited by the rates of random walk motion. I'm sure there are lots of papers which discuss the rates of trna movement in the cell, but this is the first one that I found: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2727733/
(You are completely right about competing tRNAs and the orientation of the tRNA entering the ribosome, all of these factors are taken into account in calculations. Ribosome animations are also a massive oversimplification, they illustrate certain points well but they are by no means accurate, they are useful for reaching purposes!)

I have upvoted your answer as you provide a useful reference, but please edit it to remove the reference to diffusion. Diffusion is the movement of molecules down a concentration gradient. The motion of molecules in general (and in this context) is random (stochastic) motion resulting from their kinetic energy. Hence its temperature dependence. You might also mention the existence of elongation factors which have an affinity for the A-site on the ribosome.

Hi David, I think I would disagree with you on that, diffusion is a stochastic process and the paper both mentions this and states several times that the method of transport is diffusion.

I think you misunderstand my point. The basic movement of molecules that allows their collision and reaction is not due to diffusion but to their kinetic energy. The poster is asking a chemical question and seems not to understand that. Molecular diffusion can, of course, occur in addition to this when there is difference in concentration between the point at which there is an accumulation of molecules and that at which they react. The random component of this is in addition to the effect of concentration difference.

Thanks for the answers. I should say I am not a biologist or a chemist but a mechanical engineer by training but now I run an animation company. As per my original question I am somewhat frustrated by the way molecular biology animations always show proteins and other molecules involved in transcription/translation floating around as though they have agency and the ability to 'swim' where they are required. As the replies have asserted, this is not the way it works - I just wonder if there's a way of conveying something more accurate in an animation.. I will have to experiment


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Chromosome size without heterochromatin
Im doing different analysis of the human chromosomes and diffent loci, however when using different databases, the heterochromatin structures are not part of the human genomes. I know that heterochromatin is a more dense structure within the DNA and stained differently and are not part of the different reference genomes.
However all the information regarding the human chromosome sizes, I can find all includes the heterochromatin regions.
So i would like to know, is there anywhere i can find the length of the human chromosomes without the heterochromatin structures?
Thanks for your time and help.

There are a couple of caveats that need to be addressed before answering this question:

We don't know all of the regions in the human genome that can be heterochromatic. In some cases large chunks of heterochromatin are simply missing from the genome assembly. For a somewhat outdated but still informative review of the topic see here.
Which regions are heterochromatic differs from cell to cell. For example, I would recommend reading about the differences between constitutive and facultative heterochromatin at wikipedia.
Heterochromatic regions of the genome are very important biologically and not taking them into account could be a mistake, though it depends on your motivations.

The human genome project initially estimated that 92% of their original genome build is euchromatic, 2.85 Gbp total. However that original genome build has been substantially updated. That estimate is close enough for many purposes, probably. But we've learned a lot about genome structure and biology since that time.
We do have a lot of data that is highly correlated with what we think of as heterochromatin. The UCSC human genome browser has a lot of information about chromatin modifications (I would look at the ENCODE analysis section here). In principle you can make educated guesses about regions of heterochromatin based on chromatin modifications. This will be somewhat noisy, and you will have to make decisions about which cell types are relevant, as they will have somewhat different regions.
For more information about which chromatin modifications might be relevant, you might start looking here. You will likely need to analyze some data yourself to find a more precise answer.


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Population structure and SNP's in Linkage Disequilibrium
I am reading about population structure and how you could as an example use plink to analyze a set of SNPs for individuals in a vcf file to identify a given population structure.
I know that LD can be influenced by inbreeding, selection and genetic drift amongst others.
But for a given population, where the individuals who are not inbred, couldn't Linkage Disequilibrium also be used to identify population strucutre for the individuals present within a vcf file.?
So my question is, when would you use independently associated SNPs? when would you use SNPs in LD? or would you always simply prune those SNPs who are in LD?
Thanks for your time and help.

The answer hinges on a crucial distinction, which the difference between linkage and linkage disequilibrium.

linkage (physical linkage) is a measure of closeness on a chromosome between two loci. You can measure it in centiMorgans.
linkage disequilibrium (LD) is when genetic variants at two loci show a pattern of statistical non-independence. You can measure it using a correlation coefficient, or related statistics.

Linkage causes LD, but many other phenomena also cause LD, including (yes) common ancestry, selection, or even meiotic issues. There is no requirement that loci in LD be on the same chromosome.
To get at your question, yes, you could use LD to infer population structure or selection (examples linked), or other things.
Pruning SNPs in LD is used when you are making a strong assumption about the absence of LD. For example, using many SNPs in LD can lead to inflated estimates of heritability. This is because SNPs in LD are not independent observations, most obviously in the case of physical linkage. There is no point in observing 2 SNPs that are right next to each other in QTL mapping, for instance.
You would not want to prune SNPs in LD when you are doing any kind of haplotype-based inference, as just one example.
LD is a signal like any other, the question is whether you are interested in the non-independence of SNPs, or assuming the independence of SNPs.


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chromosome 19 and recombination
Im doing a project with structural variation created by recombination within the human genome during spermatogenesis, where im especially examining intrachromatid homolog recombination.
I find that chromosome 19 is less prone to recombine and form strutural variation. I know that chromosome 19 has a high gene density and have a high amount of linked genes, so a low CentiMorgan unit. But some articles, states that chromosome 19 contains duplicated regions, which i would assume would be prone to recombine with intrachromatid recombination.
So my question is, from an evolutionary perspective, does anyone know any articles, which might describe why chr 19 is less likely to recombine. if chromosome 19 have a higher amount of life essential genes, or is it simply the high density between the repeats which affects the recombination (so sort of like heterchromatin structures).
I've looked and cannot find any results to support that chromosome 19 are "more different" when compared to other autosomes. As an example chromosome 1 has a higher CentiMorgan unit and are thus more likely to recombine, so "it" handles structural variations better, but it still contains important genes.
Thanks for your help.


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Meiotic recombination hotspots
Im trying to find a proper and general file with chromosomal coordinates for meiotic recombination hotspots.
I know that ucsc hgtables, has a table with recombination regions and their recombination rate. However these regions are all 1Mb, and several articles states that these hotspots regions are more local with a regional length of 2Kb.
https://genome.ucsc.edu/cgi-bin/hgTables?hgsid=782680683_Cxp9zzjwgsql7P0T81FFyATyTNOl&clade=mammal&org=&db=hg19&hgta_group=map&hgta_track=recombRate&hgta_table=recombRate&hgta_regionType=range&position=&hgta_outputType=primaryTable&hgta_outFileName=
Do any of you know of a file or database containing the chromosome coordinates for humans which have been identified as a recombination hotspots?
Thanks a lot for your time and help.