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What is the actual mechanism of the birth control pill?
I've been trying to figure out through online sources (I don't own any medical textbooks) what the exact mechanism behind the birth control pill (henceforth "the pill") is, and I am often finding contradicting information. This surprises me, since so many women take hormonal birth control that what it does should be known and accessible to everyone.
The following is gathered from PBS and Harvard. As I understand it, the female menstrual cycle is controlled by several organs working in feedback loops: after menstruation, there is a low concentration of estrogen and progesterone in the bloodstream, impelling the hypothalamus-hypofysis to secrete FSH and LH. This stimulates the maturation of a single follicle in the ovaries. This follicle secretes estrogen, signalling to the hypothalamus-hypofysis duo to stop producing FSH and LH. With enough estrogen, a sudden burst of FSH and LH is secreted, causing ovulation. The rest of the cycle is high in progesterone, and by lack of implantation, progesterone production slows and we are back at menstruation.
The goal of the pill is to prevent ovulation (rather than prevent implantation) by playing into these feedback loops.

A first confusion is as follows: I know the pill contains estrogen, yet (as both sources attest to) it is supposedly the high levels of estrogen that induce the FSH/LH spike that triggers ovulation. So then, why wouldn't taking exogenous estrogen cause ovulation rather than preventing it? You are essentially replacing the follicle by a blister pack.

A second confusion is that FSH and LH are so often mentioned in the same breath (i.e., you'll see "FSH" and "LH" less than "FSH and LH") that it is unclear to me what their separate role is. On this ScienceDirect page, in the only exercept that mentions "CHC", it is mentioned that we should consider FSH and estrogen as one loop, and LH and progesterone. The former causes maturation of follicles, the latter causes ovulation (maturation of lutheal cells). This is the only place I have found this distinction, and I'm unsure if it is true; in any case, the above point of contention still applies, because as the pill also contains progesterone, taking exogenous progesterone would cause ovulation.
Besides, I am aware that there exist progesterone-only pills. I'm not sure if they use the same mechanism (this thread is too unclear), because if they do, I don't see the point of having the combined pill contain estrogen.

According to Healthy Women, it is actually the change in estrogen rather than a stable level which causes ovulation. (Rephrasing this as an engineer, the hypothalamus-hypofysis duo detects a high derivative rather than a high baseline in order to trigger the FSH/LH spike.) This seems to be confirmed by Cleveland Clinic in saying

"Chronic (long-term) estrogen exposure inhibits FSH release, whereas rising estrogen levels, which normally occur before ovulation, trigger your pituitary gland to increase levels of gonadotropins (FSH and LH)."

On the other hand, the Crash Course Biology video at 6:02 says in a pop-up that FSH and LH are inhibited by low estrogen but boosted by high estrogen. So, we have a third confusion: does the pill mechanism play on the hormone level, or its rate of change?

So far, I've hypothesised two possible pill mechanisms:

Pill keeps estrogen constant, which means the derivative is 0, so the FSH/LH spike isn't triggered (and their initial boost after menstruation is triggered due to GnRH from the hypothalamus which is secreted due to the drop in estrogen due to placebo pills, mimicking menstruation).
Placebo pills during menstruation cause very low estrogen. This causes GnRH, which causes FSH. Then the pill saturates the body with estrogen to make it seem like a follicle is growing (above a lower threshold), causing FSH to stop, yet a real follicle would keep increasing estrogen (above a higher threshold) to trigger the spike during ovulation.

I don't like either explanation. There should be a clear mechanism that disambiguates all of the above confusions and comports with all sourced cited above (assuming they're all correct), and comports with all the styles of pill (combined vs. progesterone-only).

+1 for the effort you've put into this post. Please understand there are more than two kinds of HBC; you can't make blanket statements/assumptions unless you specify exactly the pill you are referring to. Please edit your post to include the pill, by name at least, if that's all you have. Two additional nit-picky things: placebo cannot by definition have an active physiological effect - psychological, yes, and mind-body counts - and how the pill works is known and accessible, but requires some  preexisting understanding of endocrinology to really understand (as you've discovered.)

@anongoodnurse Glad to hear the mechanism is known. W.r.t. placebo pills, I guess I should have said "placebo pills give way to" rather than "cause", but indeed it is nuance that I'll gloss over. From your question, can I assume that there are multiple pill mechanisms? Note that I am not talking about HBC in general (e.g. progesterone-excreting IUDs), because that obviously involves multiple mechanisms. I am specifically talking about the pill. I have no knowledge of pill brands; AFAIK, there are two types (combined and progesterone-only). That's as far as I can specify. Does that work?

@Mew There is more variety than that; different doses of the progesterone-only pills work differently, and all of them have multiple mechanisms of action, not just one. It's a complex hormonal dance with multiple phases and interactions and delays and feedback, not something simple like antagonist drugs that primarily block a single receptor protein.

@BryanKrause Consider writing an answer sharing your knowledge, in that case.

The point is that without knowing to which pill you're referring, the "answer" will be w a a a a a a a a a a a a a a a a a a a a y too long, equivalent to a book on Reproductive Endocrinology. Edit to specify a specific pill or you'll not get an answer. Thanks.

@anongoodnurse I'm confused. Given that I don't know more than I have written, how would I have practical knowledge about pill brands? If you intended to ask me about the distinction made on this page (monophasic, biphasic, triphasic COC, and POP) then as my question already says, I am interested in knowing the difference between all those mechanisms. Sample your favourite brand from that page; presumably all monophasic COCs (e.g.) work the same at the level of analysis in my question.

Sorry, but anyone can google birth control pills and pick one. But as I said, I think you're expecting a course on reproductive endocrinology. That is not the role of any SE site.

The question appears to be over complicating what is a fairly straightforward mechanism of negative feedback characteristic of most endocrine function in the body, in this case, the effect that oestrogen in the usual or predominant form of oestradiol inhibits the release of FSH from the anterior pituitary required for follicle development and consequently ovulation.   By far the dominant effect of both exogenous oestrogens and progestogens -- the respective dosages of which are merely variations on the same general mechanism -- is this negative feedback on the release of gonadotropins from the anterior pituitary, thereby circumventing the natural interaction between the pituitary and its target organ.
To quote from 'Wikipedia' which is usually a good place to start such an inquiry;

Estrogen was originally included in oral contraceptives for better cycle control (to stabilize the endometrium and thereby reduce the incidence of breakthrough bleeding), but was also found to inhibit follicular development and help prevent ovulation. Estrogen negative feedback on the anterior pituitary greatly decreases the secretion of FSH, which inhibits follicular development and helps prevent ovulation.

That should resolve the 'first confusion'satisfactorily: that is, the follicular development induced by FSH has been inhibited by exogenous oestrogen, and ovulation cannot therefore occur.

Under normal circumstances, luteinizing hormone (LH) stimulates the theca cells of the ovarian follicle to produce androstenedione. The granulosa cells of the ovarian follicle then convert this androstenedione to estradiol. This conversion process is catalyzed by aromatase, an enzyme produced as a result of follicle-stimulating hormone (FSH) stimulation.

Progestogen negative feedback and the lack of estrogen positive feedback on LH secretion prevent a mid-cycle LH surge. Inhibition of follicular development and the absence of an LH surge prevent ovulation.

That should address the 'second confusion' and its proliferation into the 'third confusion' regarding the peculiarities of feedback, notwithstanding the anomaly that oestrogen positively feeds back on LH secretion.
The rest of that section of the article deals further with the influence of progestogens (progesterone) on cervical mucus and so on.
The relevant references cited are as usual noted at the end of the article.

Oh my, I missed the notification for this answer. I do follow the first quotation, which essentially matches my second hypothesised mechanism (it's the level of estrogen, not the rate of change, that inhibits FSH in the hypofysis; correct?). However, it doesn't answer the "first confusion", i.e. why the exogenous estrogen itself doesn't cause the FSH/LH spike. The second quotation essentially says that LH causes (is metabolised into?) estrogen catalysed by FSH, but nothing is said about LH's secretion nor about progesterone, so this doesn't really answer the "second confusion" either.

@mew.  You should read your question and my answer very carefully once again, and understand that the primary mechanism of effect is a NEGATIVE FEEDBACK on FSH/LH secretion by oestrogen, endogenous or exogenous, preventing follicle development in the ovary, and therefore making ovulation impossible, regardless of what happens in the mid-cycle: i.e. the effect you mention, that oestrogen also appears briefly to stimulate the release of those gonadotropins (in a mechanism about which I am ill-informed). It's all a lot simpler than you think, and more a medical question than biological.

Okay, let me give it a shot: you are saying that taking exogenous estrogen takes over for the follicle's estrogen production, hence shrinking the supply of LSH and LH faster than usual, keeping the follicle underdeveloped and hence even if the "surge" mechanism were to occur at a certain level of estrogen, no mature follicle would exist to be released. Is that what you are conveying? If yes, I still need an explanation on where progesterone comes in and how it is possible that progesterone-only pills exist if estrogen is what we intercept in the feedback loop.

@mew.  Correct. 'Negative feedback'.  Progesterone only pills function in essentially the same way, through this same typical negative feedback on the HT-Pituitary, to suppress the release of gonadotropins FSH and LH, both of which are necessary for follicular development and thus ovulation. The mid-cycle surge in LH said to trigger ovulation either doesn't occur or is ineffective in most cases. The follicle simply cannot mature. Progesterone also has other contraceptive effects on cervical mucus etc., but is usually prescribed in cases in which oestrogen is problematic.  FSH, LH: read wiki.


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Measures of animal intelligence
What is a good cross-species measure of intelligence?
I want to use this information to decide which animals to eat, so preferably it would have been measured for most commonly eaten animals.
I read about the Encephalization Quotient. Would EQ be a good choice?  Is there somewhere I can find a list of animals and their EQ?

The EQ is not a good measurement of animal intelligence. Note octopuses are highly intelligent but their nervous system is like an alien organism's. Also, note which animals are commonly eaten is country specific. Which country are you posting from?

@anongoodnurse I live in the United States

This might be opinion-based to some degree depending on how one defines intelligence. To get a reasonably reliable answer, I think you first need to define intelligence in your question. For myself (who also struggles with that question), I cannot bring myself to eat pork (even bacon), because they are highly intelligent and self aware. To me, to me, it's murder. I won't eat octopus. I'm glad dogs aren't on the menu in the US. It's not an easy question, but it's an honest one, and important.

We're getting a bit into philosophy, but you'd need to figure what counts as intelligence before that, and we're not yet sure what that is.
There's no singular measure for intelligence that you could really apply..

Have you tried the wiki on it It has a lot pf helpful information https://en.wikipedia.org/wiki/Encephalization_quotient

There isn't really a good answer, since we don't have a singular quantifiable measure of intelligence for humans, let alone other species.
Any human measures of intelligence might not apply properly to an animal, because it's based on either human behaviours, or specific human cultures/context. An animal that does not confirm to either might not complete the test as expected, or not recognise it as one at all.

Yeah intelligence is not a single thing so there is no single way to measure it. Even the most conservative definition of intelligence still has several separate aspects. Then you run into the sensory and manipulation limitations.

EQ or EZ can be helpful with several qualifiers.

you should account for differences among groups, birds for instance have smaller brains than mammals for what most would consider similar intelligence, bird brains have higher synaptic density than mammals likely due to weight constraints during evolution. the brain has evolved along sperate paths with different mass efficiencies. EQ gets less and less useful the further you get from mammals and primates. invertebrates in particular become very problematic since the brain is not extremally centralized like it is in vertebrates, so even estimating what is and is not the brain runs into issues.

Improvements have been done to EQ by using the only the parts of the brain responsible things we associate with intelligence, this helps account for drastic difference in sensory parts of the brain which affect overall brain size, but again this breaks down when you get away from mammals because the brains works differently in those groups. You also run into the issue that folding of the brain increases neuron density faster than mass so it can deflate EQ scores while making the animal more intelligent.

If you really want to estimate intelligence, then just like in humans,  behavior is your best metric, but this is not going to be a easy to research number. I have a similar issue to your conundrum and I won't eat anything that appears to understand the concept of death : elephants, great apes and some other primates, dolphins including orca and, grey parrots. I generally iffy on eating anything that has complex problem solving and tool use. I won't eat any primate at all for other reasons (disease). But this requires knowledge of animal behavior. You will never get a nice easy number to look at, intelligence is just too complex a thing.

If you lead a pig (pet or laboratory) to an area facing a mirror, if the pig sees an interesting object in the mirror, they will turn around and go to it without hesitation, i.e. they understand that a mirror is a trustworthy reflection of physical reality. Even dogs can't do that. I had a superintelligent dog that would watch TV with me, but he never figured out that it wasn't real. As he was a shepherd variety, if there were horses running, he'd try to nip at their fetlocks. I can't imagine eating dog, let alone pig.

There is no easy way to quantify intelligence because it's poorly defined. I would suggest narrowing your focus on measurable behaviour as a proxy for intelligence, and looking at the many behavioral research studies on commonly consumed animals.

Would you eat an animal that has social bonds?
Would you eat an animal that is able to be taught new skills?
Would you eat an animal that demonstrates problem solving?

There is good evidence that chickens, pigs, cows, sheep, fish, all form social bonds, can learn new skills, and solve novel problems. All of those things are a key part in survival and reproduction in many animal species.
You might find the mirror self-recognition test worth looking into, particularly as something that highlights the absurdity of trying to design a test across species.
Here's a list of animals by number of neurons which may help you on your quest - if you can find evidence that number of neurons is an adequate proxy to intelligence for your purposes. There is another on that page about number in the cerebrum. Not a lot of fish on there though.

source: Stack Exchange

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

sort: votes


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How to convert Kilo Units (KU) to mg?
Im searching for AChE (Acetylcholinesterase) and on sigma-aldrich it is showing 2 KU or 2000U/mg of protein and on MedChemExpress it is showing 50mg then how can we calcute how much will be the drug in the Sigma product

Would be easier to help if you provide the links to these pages. Sigma should also mention the actual quantity (ug) near where the price is. I assume that's what you are looking for?

There is no conversion from Units to mg. units are a measurement of enzyme activity, generally reported normalized to mass as units/mg

Have a look at the sigma product  - it should have the mass or the number of units. Simple conversion from mass to units using the provided info.

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


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How do i find and download targets of drugs which are in DrugBank?
Recently, I am focused on drugs and their interactions. But since I am new in this field, using experts experience would help me a lot. I have downloaded DrugBank xml file from DrugBank website and parsed the XML into dataFrames in python, and now i have drugs with their name and ID and etc. In a paper i read that we can make a similarity graph by comparing number of similar targets shared between drugs, but actually i don't know where and how i can download targets of drugs exists in DrugBank to compare their similarity. I appreciate answers that help me.


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How is an extreme insulin overdose counteracted
I just watched this comedy skit that went -
Trainee: I just gave him 10 of insulin
Doctor: 10 what?
Trainee: 10cc
Doctor: * look of terror *
As a diabetic myself I know that 10cc or 1000u is an insane amount of insulin to have in one go. A 10ml vial (1000u) would usually last me over 2 weeks.
1000u in one go would most certainly be fata (if untreated) whether the patient was diabetic or not. Although individual insulin sensitivity varies greatly, I, personally, know that I would need around 1500g of sugar/glucose to counter that much insulin which I would've thought just isn't possible. What I'm wondering is, is there some other way that, assuming you're already in a hospital, they could counteract, filter out, or otherwise manage such a severe overdose? Or is IV glucose the only option?
I know glucagon injections can be use to treat severe hypoglycaemia but from my research the average person would no have enough stored glycogen. Please tell me if I'm wrong.

I'm not sure what you're worried about. The doctor is right there. I assume the trainee didn't give 10cc sq (that's a big bolus, and certainly too big for an sq dose.) So one can assume it was given IV. IV insulin only lasts a few minutes. A liter of D5&W (1000 x.05 =50g glucose) wide open and the crisis is averted. It's not momentary hypoglycemia that causes the worst outcomes; it's prolonged hypoglycemia. (I know a resident who mistakenly ordered IV instead of sq insulin. Nothing happened.) It is used, though, to treat DKA.

SQ insulin lasts for hours, a few to a lot depending on the type. A hefty dose of sq insulin without po intake can be, and has been, lethal.

@anongoodnurse so what youre saying is IV insulin is metabolised very quickly and even an large dose would be easily fixed?

Say someone did manage a 10cc sq overdose. How would you manage that?

See long explanation above. Just a lot longer observation period.


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Why is There a Necessity for Two Rounds of Cell Division and Four Daughter Cells in Meiosis
Why does meiosis involve two rounds of cell division instead of stopping after meiosis I, where each daughter cell would have one chromosome randomly selected from each pair of homologous chromosomes? Theoretically, this could be achieved without DNA replication prior to meiosis I? Why do we need four daughter cells rather than two? Where in meiosis, effectively, one chromosome from each homologous pair goes into two of the four gametes, due to the chromosomes in meiosis I being composed of two sister chromatids. I am clearly oversimplifying the process and overlooking some important components.

In an attempt to answer my own question, I asked myself: whether the two daughter cells from meiosis II (I am referring to one pair that is produced from each parent cell), were identical. I realised I had forgotten to consider recombination. While it may be true that sister chromatids are identical copies of a chromosome created during DNA replication, crossing over during meiosis I can create genetic diversity between sister chromatids. Crossing over occurs between non-sister chromatids of homologous chromosomes. As a result, even though sister chromatids are separated during meiosis II, the daughter cells produced may not be genetically identical due to crossing over that occurred during meiosis I. The result I assume would look something like this. However, I realised recombination would still be possible, albeit with two unique gametes, rather than four.
If at any point I say anything incorrect feel free to point that out.

I saw a potential answer here, however, the answer is arranged in a way that is unclear and difficult to read for me.

If I understand correctly, your idea is to say, it would also be possible to start with unduplicated chromosomes (no S-Phase), perform crossing over to increase the genetic variety and then to distribute the single chromosomes into different cells - and now you want to know what's the difference to regular Meiosis and "why" it happens that way?
As you hopefully know, "why" questions are not really scientific. We cannot really know why something happened. We can only speculate that this could be a reason or provide an advantage for evolution. One explanation why it would be advantageous to have S-Phase before and use Meiosis 2 to reduce the chromosome number is (as explained in the question you cited) the following:

Crossovers (CO) play a huge and important role for generating gametes and is the basis of genetic diversity.
COs are generated by double-strand breaks (DSBs).
Most DSBs are not converted into COs and need repair through different mechanisms.
The sister chromatid helps as a template for that.
My speculation is that without a second sister chromatid during crossovers, the cell would simply die due to DNA damage.


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Is there such thing as "being aware of itself" at a cellular level, or is awareness only a multicellular thing?
It appears to me after a brief thought, that you need multiple cells to send and coordinate messages in order to have "self awareness". Basically, you need some sort of centralized brain it seems. But maybe I'm wrong there, jellyfish don't have centralized brains right? And are they considered self-aware?
What about individual cells, can a cell be considered "aware of itself"? If so, in what ways, if not, why not? I know the definition of awareness is probably ill-defined, but maybe you can pinpoint a definition and say why cells either are or are not in within that definition.
Any research in this line of thinking to link to?
I guess a related question is, if cells do not have self-awareness, is when/where in the evolutionary chain does self-awareness arise?
Trees and sponges (and algae mats for example) are networks of multiple cells, but do they have awareness of themselves? I don't know. So maybe only after a certain degree of centralized brain then self-awareness emerges? Like I would say any mammal is self-aware, maybe lizards and fish too? Anything with eyes, but maybe that is because they seem somewhat human.
But then ChatGPT and AI throw into the question what self-awareness can really be like :)

See https://en.wikipedia.org/wiki/Hard_problem_of_consciousness - It also seems you have a primarily philosophical question, rather than a biological one. People literally write entire books on this topic, as well, it does not seem to be scoped to something answerable in a StackExchange Q&A format.

I agree this is philosophical... biologically based (imo) but argued by philosophers. One measure of self awareness is recognition of self in the mirror (pigs can do this, dogs and cats can't) but blind people are self aware.


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How to quantify basic levels of samples in qPCR?
I do have to quantify the difference in basic levels of expression for a given gene in two types of tissues. There is no treatment, just basic levels.
Before I had a "control" sample that I taken as a "1", then a "treated" sample was calculated based on that control (its values were subtracted), therefore a fold change could be calculated between two types of tissue.
Now there's no fold change, just bare numbers, so I wonder how we suppose to quantify delta-deltaCT ? (what are these references?)

a hint - reference gene... You can easily find the original paper on the d-dCT method with a pubmed search.

if you mean the housekeeping gene - of course, I have it. That is how my delta CT is calculated.

yes, reference = housekeeping. In that case I don't think I understand what your question is. You either do a relative quantitation by d-dCT or an absolute using a standard curve. It looked to me like you were asking to how to do d-dCT.

correct. d-CT is calculated via housekeeping. But when it gets to d-dCT, this is the question. Maybe I just need to compare dCTs between two tissues? This will give me the "raw" number relatively to housekeeping gene.

d-dCT is calculated by comparing your treatment to the control - if you don't have a control then you need to look at your experimental set-up and ask yourself what are you actually looking at (what are you aiming to find out) and what might be an appropriate analysis. This isn't the site to ask those sorts of questions on - check with your supervisor or another student in your lab.


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Training AI models to identify the sex in some bird species
Through my limited knowledge and experience with parrots (especially African greys and quacker parrots), I came to notice that most often some species, in which the male and the female are highly similar, show some slight variations in the form of the beak or the head between the two sexes.
Consequently, I can't help but wonder whether the use of some CNN model could perhaps trace some underlying difference between the two sexes that may go unnoticed to the human eye.
Side note: on the context of the African grey there are some documented difference between the two sexes like the size of the eye, but even those are hard to interpret for the untrained individual. What matters most in my question is the practicality of this idea and the possibility of generalization on different species.

Welcome to the site! Specifically what is your question? This isn't a discussion forum, so if you're looking for "huh interesting idea I wonder how that would work" etc., take it to [chat]. You'll have to tell us what species you are looking at specifically, and what differences of beak form have been observed specifically. "I have observed" can't lead to a great objective answers. Please [edit] your question to include required detail. Thanks!


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How does a product form from a transition state in an enzyme despite the weak interactions being at its optimal
In the book Lehninger Principles of Biochemistry, there is a metal stick analogy to explain why an enzyme being compliment to its substrate would actually make a terrible enzyme.

If the enzyme is complimentary to the substrate, it will form many weak interactions, hence the enzyme-substrate (ES) complex is very stable, meaning it will require more energy to reach the transition state, so very few products are made

If the enzyme isn't entirely compliment to its substrate, it will form a few weak interactions (that allows it to bind to its substrate). This isn't its lowest energy state, as there are still more weak interactions that can occur. The weak interactions will mould the substrate into its transition state. This would mean that the transition state is the most stable state in this environment (I would assume). The thing that I am confused about is that if the transition state would be the most stable state, then why would it go on to form a product? Once the weak interactions mould the substrate, then energy would be released from the substrate, forming a transition state, therefore making the transition state have lower energy than the substrate, not higher, so the reaction profile in the final diagram doesn't really make sense to me. Is there anything that I am missing or not understanding?

I would really appreciate someone clearing up any confusion about this. Thanks.

I'd recommend starting from the diagrams here, since it seems like you understand them. Compare the 2nd and 3rd plots, and use them to explain to yourself why an enzyme that works like the 3rd plot is drawn is better than the 2nd in both the ES and transition states. Then reread the text and think about it as a comparison between those two diagrams rather than the imaginary other case you're thinking of.

I think I've got it now. The energy required to reach the transition state is lower because of 2 things:
-The ES complex is less stable in diagram 3 then diagram 2 (higher energy)
-Once the ES complex has formed, there are still more weak interactions that can occur which provide some energetic driving force towards the transition state, so require less energy to reach there.
Is this right?

That sounds accurate to me! I think it's worth keeping in mind that the "transition state" is energetically not very favorable: it's at the top of all of these charts. So, when describing "weak interactions (that) mould the substrate into its transition state", you're making the transition state more favorable than it would be without those interactions, not necessarily more favorable than a different, favorable state. If you have to jump over a rope, and someone else puts their hand on it to make it lower to the ground, there's still a rope to get over.


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Concentrating cell concentration after subsampling
I need some help with regards to a concentration correction. I am measuring how many cells detach from a rock vs sonication time. Becuase I start from a rock, I cannot make aliquots and measure independent samples. So I put my rock in 10 mL of PBS and and sonicat for 1 min and sampled 0.8 mL. With this sample I measure cell density using flow cytometry. I then placed the rock to sonicate for another 2 min (a cumulative time of 3 min of sonication) and subsampled 0.8 mLs again. I did this for a cumulative time of 30 min, with subsampling at 1, 3, 5, 10, 15 and 30 min. This means that I was left with 5.2 mL of sample after my final subsampling (0.8 mL per subsample * 6 = 4.8 mL; 10 mL - 4.8 mL = 5.2 mL).
I measured my cell density using Flow cytometry and was given a events/uL concentration. But I think that every time I am subsampling I am effectively increasing the concentration (events/uL) because my cells are being resuspended from the rock into an ever decreasing suspension. Is this correct or will the events/uL that the FCM is showing me the final concentration independent of this diminishing volume? If not, how do I correct for this to get a comparable events/uL?
Here is an example of the conctrations over time after a cumulative 10 min of sonication (i could not figure out how to insert a table, hence in picture format)

So the solution for this can be in two ways:

calculate the total number of events (evenst/uL * total volume of sample at time X) and then devide by the initial volume.

or perform a correction factor, by calculating the volume reduction factor (subsample volume / volume before subsampling) e.g. at 60 seconds: 0.08/10.
You then calculate the reciprocal of this. and multiply by events/uL

NB: In these calculations is not included the fact that cells are being removed in each step, and as such there is still some dilution happening.


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Does cooking kill all bacteria?
So I know that the general rules is that pathogen prone foods such as chicken shouldn't be consumed after 2 hours at room temperature. Cooking meat such as chicken is necesary as it kills the potentially harmful bacteria in th raw meat. What I do t understand is, if the cooking process kills the harmful bacteria, why would it still be not recommended to cook and eat chicken left at room temperature for longer than 2 hours? Would the process of cooking not still be able to kill the increased amount of bacteria?

There are (at least) two questions here, do you want to pick one and ask the other(s) in a separate thread. Remember, show your research when posting.

Heat-stable toxins.

It would kill the bacteria, but it wouldn't break down the toxic substances that the bacteria produced while they were digesting the chicken.
According to the WHO, the chicken must be maintained at 85⁰C for at least 5 minutes, so it is possible to cook it, but there's no real way to know for sure that all the toxins have been destroyed without reaching temperatures that outright destroys the chicken.
Since there's no way to perfectly know whether the chicken has been cooked long enough to destroy the toxins, without turning it to ash, it's better to avoid the risk in the first place, since a small amount remaining could lead to unpleasantness, and the temperatures would overcook the chicken (Poultry is considered cooked when its interior temperature reaches 74⁰C).


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Why is sport healthy if high metabolism decreases life expectancy?
There is something that appears as a contradiction to a newbie like me.

Sport is widely recognized as healthy and recommended by medical experts.

Metabolic rate is inversely correlated with lifespan.

To me, it makes sense that the more energy passes through your system, the more it gets damaged.
Sport goes against this desirable frugality, as it makes you consume more energy, which requires increasing your energy input to compensate (you eat more food). Also, growing a greater muscular mass increases the amount of energy needed for moving, for maintaining body temperature at rest; having more cells mean larger amounts of oxygen are needed, more DNA-copying errors are made, more free radicals are produced, etc.
At the same time, I've heard that sport is good because it lowers heartbeat at rest, it makes special immune-system agents enter cells more effectively, and other things...
I'm obviously missing something, but I'm just having a hard time understanding how something that increases the entropy of your system can be beneficial for your health in the long run.

I think you're drawing extremely broad and simplistic strokes to draw conclusion number 2 and ignoring certain implications by the reasoning in your largest paragraph For example, large animals have to produce more cells to get to the size they are yet tend to have longer lifespans. Also, your use of the term entropy seems to be a misapplication of the term. The reasoning 'To me, it makes sense that the more energy passes through your system, the more it gets damaged" is also incomplete because it ignores how if too little energy passes through your system, you promptly die.

@DKNguyen Although it is also worth pointing out that larger animals generally have specific anti-cancer adaptations that help them in that regard.
By comparison, you can't just blow up a regular animal, and expect it to fare quite as well. Larger dogs are at greater risk of cancer compared to smaller ones, for example.

having more cells mean larger amounts of oxygen are needed

Two things here. First is that that a large muscle usually comes from the individual cells becoming larger, not so much that there are more of them.
Second, is that exercise means that your body uses the oxygen more efficiently if it's fit (it's unclear whether this refers to it having a higher concentration of oxygen, or whether it is due to changes in metabolic processes).

more DNA-copying errors are made, more free radicals are produced, etc.

Although it's worth pointing that these happen anyway. Exercise doesn't really change much on that front, unless there's an injury.
Your body has protective mechanisms against these forms of damage, since they happen as part of regular metabolism. They don't just gradually accumulate throughout your lifetime.

I'm obviously missing something, but I'm just having a hard time understanding how something that increases the entropy of your system can be beneficial for your health in the long run.

It helps stave off other health conditions that would take you out first.
System entropy increasing isn't really that big of an issue anyway, since humans aren't a closed system. A warm bath also increases entropy (from heat), but certainly doesn't cause health issues, and hypothermia tends to be quite bad for you, even if it does the opposite.


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How does photosynthesis work exactly?
How does light reach the photoreceptors in plants? Does it need to travel through the plant or are the photoreceptors on the surface of the plant ?

I'd like to see that video. Can you please provide a link?

Quantum superposition has nothing whatever to do with time travel. You may have misunderstood what they were saying, or the video is tending towards the science-fiction end of things. Either way, it' doesn't sound like a good starting point for educating yourself about photosynthesis. As above, start with the Wikipedia article, then [edit] your question with what you need to ask.

@JiminyCricket  The title of the video is “we are from the future” and if it is true that the photons are put into a state of quantum superposition then technically it is like time travel, because all the possible realities where the photon should collide with other particles will collapse, & not occur, so rather than time travel it’s more like future assurance, all possible realities in which it does not reach its destination do not become actual therefor it has already reached its destination before it gets to it

@anongoodnurse https://youtu.be/15pOr1E6hvc

Thanks, @KeeganDavidson! That was interesting. I agree with Jiminy Cricket above; on the sci-fi spectrum. :)

The main thing about the video that is incorrect is the framing - the plants don't put the photon into quantum superposition and cause time travel of the information (nor are they near perfect efficiency)! It's a simple probabilistic function for the photo to reach a chlorophyll/photocentre. Yes, you could very weakly argue that "oooh we don't know where the photon is because it's quantum" which is sort of true, but it's much simpler than that. Lets imagine you had a million tiny ball bearings and a large board with lot of holes in it. Throw all the ball bearings at the board... cont

cont... Some hit and bounce off, a few go through the holes. The board is your leaf and the ball bearings are your photons. You must remember from basic atomic structure that atoms are mostly space - according to Dr Google, a Hydrogen atom is 99.9999...% space; if you could enlarge it to the size of the earth, the core proton would be about 200 m/600' (2 football fields long) across and the electrons circling around on the circumference of the earth. The forest analogy is more like running through the area of 37 football fields with 1 tree in the middle.

Scientific American has a helpful blurb, and here is part 1 and part 2 of a review about quantum effects in the light harvesting complex. It seems as though the chromophores in a complex can have quantum coherence, which does, indeed, lead to transfer of the photon energy from the harvesting complex to the reaction center with "nearly 100 percent efficiency."

The photoreceptors relevant to photosynthesis are the light-harvesting complexes. These are found embedded in the thylakoid membranes found within chloroplasts. To reach the thylakoid membranes, light from outside the plant must pass through the cell wall, cell membrane, cytoplasm, both membranes of the chloroplast, and some amount of chloroplast stroma. If the photosynthetic cell is not on the surface of the plant, the light would also need to pass through some number of intervening cells.


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How is axis formation in the mouse embryo determined?
I recently came across this MCQ question when revising for stem cell biology exam.
"How is axis formation in the mouse embryo determined?"
The 5 options are as follow:
A. By sperm entry point in the egg;
B. By the first cleavage division;
C. By the node;
D. By signals from the mother;
E. By signals from extra-embryonic tissues;
The information online points toward C, but my course material seems to suggest E.
Does anyone know which one is the correct answer, and provide an explanation?
Thank you very much in advance

It would be helpful to identify/quote/cite from "the information online" versus your "course material": what are each saying, and where do you see a conflict in your understanding? Note that this website is very uninterested in solving your multiple choice question. That's not a very useful task outside of the very specific context of you getting a point on an exam. However, if you have a question about understanding biology and can show your work towards answering that question, we'd love to help.


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Is there an ISO code for animal reproduction method?
Is there an ISO that can represent animals' reproduction method such as:
Oviparity, Ovoviviparous, Viviparous, and others?
Note: If the ISO term is not clear, here an example of an ISO: https://en.wikipedia.org/wiki/List_of_ISO_639-1_codes

I don't know the answer to your question, but aren't ISO standards relating to created things. I believe there are terms defined, but not a specific standard for something that occurs naturally. You can also do a site search in google for example type (without quotes): "oviparous site:iso.org" into your search bar.

From the ISO website https://www.iso.org/developing-standards.html: "ISO does not decide when to develop a new standard, but responds to a request from industry or other stakeholders such as consumer groups. Typically, an industry sector or group communicates the need for a standard to its national member who then contacts ISO." I can't think of anyone with both the financial incentive and resources to fund an effort to develop animal reproduction terminology.


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Can In Vivo Gene Therapy Cause allorecognition/Rejection?
Organ rejection from organ transplants is least common when donors and receivers are genetically related; As I understand it, this is because the antigens on the surface of the cells of the donated organ need to be unrecognizable as "foreign" ("allorecognition" in the case that the T cells mark the donor cells as foreign), requiring a genetic match in the major histocompatibility complex (MHC) on chromosome 6 (in humans). But from what I read, I couldn't determine whether 1) there were other histocompatibility genes outside the MHC, or 2) whether there needed to be an exact match between histocompatibility genes, or whether there was some proportion or threshold that would prevent rejection if met (or whether immune response against the organ is just proportional to the level of histocompatibility).
All of this is said the frame this question: Can localized (to a specific tissue or organ) gene therapy result in allorecognition? I imagine if those edits take place in the MHC, it could clearly cause allorecognition due to antigen difference, but are more histocompatibility genes sprinkled throughout the human genome? And even if there weren't, are there other genetic factors beyond antigen formation that can result in a genetically modified cell being rejected by pre-edit host T cells (aside from those modifications which stop the cell from functioning)


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Quantifying Hydrophobicity from amino acid sequence
fourth-year undergrad here so any help is super appreciated! Also this is not something I am working on for a grade, so pls don't think I am just looking for someone to do my homework lol!
In a gist, the project I am currently working on requires me to compare the same proteins involved in the Calvin cycle from both an extremophile and a mesophile. Specifically, I am supposed to figure out if the extremophile (which lives in the Arctic) protein's are more hydrophobic than the mesophile. I am expected just to use in sillico/bioinformatic techniques to figure this out
So far, all I have done is run the amino acid sequences through various hydrophobicity scales so each residue is given a ranking of hydrophobicity, then calculated an average from that. Obviously, this has a lot of flaws and is not proving to be very effective
If anyone has any ideas of programs or methodologies that could produce more accurate results I would be so grateful! I have been going in circles with this for a while now
Thank-you!

Please explain what flaws you think the method you are currently using has and what you mean by "is not proving to be very effective". Effective in what? Do you just mean you can't find any differences? And it hardly seems that "getting more accurate results" can be your problem — why would you think the measures of hydrophobicity are inaccurate? And are you just averaging values of amino acids for each protein, or plotting values graphically across a whole protein, as is possible?

Perhaps try to see if the protein is expected to be embedded in a membrane? See if hydrophobic parts are clustered, or if there is a signal sequence giving hints.

I believe that the standard hydrophobicity measure is protein GRAVY.
However, as David comments, I don't see any particular reason to expect that its estimates would deviate from what you find by other means, as it's just taking the average across the protein rather than considering any other aspects of structure:

Protein GRAVY returns the GRAVY (grand average of hydropathy) value for the protein sequences you enter. The GRAVY value is calculated by adding the hydropathy value for each residue and dividing by the length of the sequence (Kyte and Doolittle; 1982).

There are more recent, more elaborate methods that quantify different features of hydrophobicity, but I don't imagine that your professors are asking for these somewhat less readily interpretable measures.


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Increasing enzyme concentration does not increase product formation
I am cutting DNA strand 40 nt long with enzyme with single cleavage site in DNA. At the lowest concentration of enzyme I use, 50% of the substrate is cleaved, however, increasing enzyme concentration such as using twice or four times more has no affect in the product formation, meaning that I still see only 50% of the DNA substrate is cleaved. Reaction time and temperature is constant in all cases. What could be causing this phenomenon?


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Dark, long-legged spider with long mouthparts in front, long "pincers" in the back and very short 3rd pair of legs (northern Taiwan)
Just inside a doorway in northern Taiwan I found an interesting looking spider flat against the wall, pointed downward about 30 cm above the floor, sitting motionless.
Mostly dark but some patterns appear with the flash photo.
Everything is long; long mouth parts in front, long "pincers" in back, and long legs, except the 3rd pair from the front which were thinner and only about 20% of the front (longest) pair. See photo for an estimated scale bar - roughly 16 mm from mouthparts in front to "pincers" in back, over 80 mm toe-to-toe.
I assume it's just sitting there waiting for something delicious to walk by and eat, but why are the mouth parts and "pincers" so long and the 3rd leg pair so short? Are there specific activities or functions that can help explain these?
Does it always hunt like this or does it also build webs?

above: cropped, below: click for full size, the first uses a flash and is viewed from above-front, 2nd is with ambient light and top-down view.

From a browse through iNaturalist, I believe this is a member of the genus Hersilia also known as long-spinneretted bark spiders or two-tailed spiders. I have no idea which of the species this might be, but a Hersilia striata comes up as being present in Taiwan.
The characteristics are, unsurprisingly, the long spinnarets and long legs. I believe these will be largely ambush spiders similar to wolf spiders, using camouflage to hide and deceive prey.  I don't know if the long spinnarets play any role, nor the shortened legs.

It seems like you've got it narrowed down nicely, thanks!

I do a lot of walking and hiking - I come from northern latitudes so the much higher species diversity of Taiwan is a never ending source of discovery. I've been here 15 years and still on every long hike I photograph a new flower or two and several new insects I'd never seen before. I've seen many of these in the same general area, and always wondered if they were "really well reinforced egg cases". But I suppose it's captured, digesting prey, and those short 3rd legs and long spinnerets are just the right lengths to make these?

@uhoh yo might well be right there on the 3rd pair being the right length to fit the spinnerets. Still I wonder what the evolutionary pressure is to have such long ones.

I would venture a wild guess that it's to have a way to suddenly move forward very quickly to grab its prey without resorting to jumping and trying to land firmly on a new bit of tree without falling off. Need to find some video. If I were more adventurous I'd bring a few home, set up a tall terrarium with some vertical surfaces and a good camera and stock it with little crawly things and wait... but it seems a YouTube search is more likely.

This looks like the short 3rd set of legs are pulled under and forward and working with the mouth parts to hold prey https://youtu.be/u7VIHz9Dspc and this is just a nice, camouflaged specimen https://www.youtube.com/watch?v=OjnT-fzEV2E According to this they hunt by throwing silk, now I need to see it...

Interesting if they are web throwers - that would fit the extra long first and second pair of legs and the long spinnerets. Use the spinnerets to cast a web between all 4 pf the first 4 legs, then use these to spread and trap. The spinnerets wouldn't reach otherwise. The first two leg pairs might be too long for the mouthparts to reach and hold, so 3rd makes sense. The beauty of evolution in action! You'd need to see them at night to see the web casting, probably in a contrived set-up - that's how the doco crews do it.


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Why is scaffolding necessary in organ printing?
Most organ printing techniques seem to use a structural element for newly created cells to anchor themselves to, be it a biocompatible plastic or some natural material. Naively, I would assume that organs can be generated just the same as they are in an embryo, so why is scaffolding necessary? Here are my guesses:

The time taken to grow an organ to an adult size this way would take too long to be practical
Making the necessary germlines to emulate those formed in gastrulation is to difficult
Organs grown this way collapse into themselves without the exact environment present in an embryo (the pressure in an embryo could be necessary, or the formation of all organs concurrently allows each particular organ to maintain a solid boundary between itself and its neighbors)
Without scaffolding, organs printed in vitro would not generate the auxiliary structures necessary to be useful (nerve endings, blood vessel, etc.)

You can't extract the print a heart "code" from DNA, that's not how DNA or development works. Each organ develops according to a pattern influenced by all the other surrounding tissues. It's quite an intricate dance, with folds and migrations occurring at specific times. That's why you can't regrow lost digits or limbs, or replace damaged brain tissue: the connections those pieces make with the rest of the body are only possible during a specific time in development when all the correct cues and relationships are there.
In other words, to generate an organ the way it is generated in an embryo, you need a whole embryo. To generate one to an adult size that way, you need to grow a whole adult. Science fiction has used this as a plausible approach, but real society finds it problematic to grow people for the sole purpose of organ harvesting.
Read, for example, the Wikipedia article on heart development:

In the splanchnopleuric mesenchyme on either side of the neural plate, a horseshoe-shaped area develops as the cardiogenic region. This has formed from cardiac myoblasts and blood islands as forerunners of blood cells and vessels.[5] By day 19, an endocardial tube begins to develop in each side of this region. These two tubes grow and by the third week have converged towards each other to merge, using programmed cell death to form a single tube, the tubular heart.[6]
From splanchnopleuric mesenchyme, the cardiogenic region develops cranially and laterally to the neural plate. In this area, two separate angiogenic cell clusters form on either side and coalesce to form the endocardial tubes. As embryonic folding starts, the two endocardial tubes are pushed into the thoracic cavity, where they begin to fuse together, and this is completed at about 22 days.[7][2]

The only place you get a splanchnopleuric mesenchyme to start with is going to be a developing embryo. The heart is forming from different clusters of cells migrating and differentiating in a particular pattern.
Scaffolding is more of a trick. It gets you away from the organ-level patterning that shapes the entire structure and lets you deal with just the functional units: individual cell types like myocytes that behave sufficiently robotically that if you create approximately the right conditions they will settle in to do their job.


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AKT and chemoresistance in cancer
I would like to know your opinion about a paper on AKT-mediated chemoresistance and ion channels.
The idea is that the protein AKT is involved in chemoresistance by activating several downstream subcellular pathways like c-myc and p53.
Then, these two proteins may lead to the activation of ABC transporters like MDR1 and MRP5, two transporters involved in chemoresistance.
The paper has been published in arxiv: https://arxiv.org/abs/2307.07427
Thanks.


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How to access Target Data for PRS analysis on GWAS Dataset
I am working on conducting a PRS analyses on a GWAS Dataset that deals with the alzheimer's disease. The data is split into cases(Participants with the disease) and controls(participants without the disease) dataset. After this, I have performed Quality Control on this dataset. To calculate PRS analysis, I would need to have a target dataset that consists of genotypes that are typically formatted as PLINK binary files. How would I access these binary files and how do I access the target dataset from UKbiobank?
Cases Dataset

Controls Dataset

I have tried to access the dataset from the following link but to no avail:
https://biobank.ndph.ox.ac.uk/showcase/label.cgi?id=263
For reference, the dataset must be in this format:
https://drive.google.com/file/d/1uhJR_3sn7RA8U5iYQbcmTp6vFdQiF4F2/view?usp=sharing

Welcome to the Biology Stack. Please take a [tour] and visit the [help] for more information on this Stack and what we do here. You would be better off putting the required format in a code snippet box. You can do this by editing your question and using the preformatted text button on the tool bar - it looks like a pair of curly braces: {}. You might also find a better answer at our sister Bioinformatics site, but you should avoid cross-posting and request migration if you want to do this.

What do you mean by target dataset?

The page you link says the following:

Researchers must use the gfetch client (available from the Downloads section, instructions for use in Resource 668) to access the actual underlying genomic data or download them from the European Genome-phenome Archive (EGA).

Have you used the gfetch client? Do you still need to obtain the data or do you just need to convert it? It seems to be similar to the formats you've linked, e.g. BED/BIM/etc.


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Will a 5nm diameter uncharged object make it through the renal glomerular filtration apparatus in humans?
Will a 5nm diameter uncharged object make it through the glomerular filtration apparatus in humans? I think that it should as I have read that the smallest fenestrations are about 10-15nm in size and if the object is uncharged, I would think that it would be unaffected by the charge of the filtration apparatus. Any thoughts?


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How to generate pathway fingerprints of drugs?
I have studied a paper that constructs the pathway fingerprint of a drug, which has a vector of $0$ and $1$, and they compare the pathway fingerprint using a similarity measure to assess how similar the drugs are.
But I don't know where can I download pathways and how to generate their fingerprint vector to evaluate them. I checked KEGG website but could not find anything there to download. The paper can be downloaded from: https://pubmed.ncbi.nlm.nih.gov/22426982/
I really appreciate answers that can help me to solve the problem.
Update
Since i am not familiar with DrugBank and biology science, when I parsed the xml file of drugbank, I find a tag with name pathway . But i am not sure that do these elements show the pathway of drug or not? Is it possible to use them to construct the pathway fingerprint vector for drugs? what does <uniprot-id>P00734</uniprot-id> mean?
this is the content of pathway tag for Lepirudin:
<pathways>
    <pathway>
      <smpdb-id>SMP0000278</smpdb-id>
      <name>Lepirudin Action Pathway</name>
      <category>drug_action</category>
      <drugs>
        <drug>
          <drugbank-id>DB00001</drugbank-id>
          <name>Lepirudin</name>
        </drug>
        <drug>
          <drugbank-id>DB01022</drugbank-id>
          <name>Phylloquinone</name>
        </drug>
        <drug>
          <drugbank-id>DB01373</drugbank-id>
          <name>Calcium</name>
        </drug>
      </drugs>
      <enzymes>
        <uniprot-id>P00734</uniprot-id>
        <uniprot-id>P00748</uniprot-id>
        <uniprot-id>P02452</uniprot-id>
        <uniprot-id>P03952</uniprot-id>
        <uniprot-id>P03951</uniprot-id>
        <uniprot-id>P00740</uniprot-id>
        <uniprot-id>P00451</uniprot-id>
        <uniprot-id>P12259</uniprot-id>
        <uniprot-id>P00742</uniprot-id>
        <uniprot-id>P02671</uniprot-id>
        <uniprot-id>P02675</uniprot-id>
        <uniprot-id>P02679</uniprot-id>
        <uniprot-id>P00488</uniprot-id>
        <uniprot-id>P05160</uniprot-id>
        <uniprot-id>P00747</uniprot-id>
        <uniprot-id>P00750</uniprot-id>
        <uniprot-id>P08709</uniprot-id>
        <uniprot-id>P13726</uniprot-id>
        <uniprot-id>Q9BQB6</uniprot-id>
        <uniprot-id>P38435</uniprot-id>
      </enzymes>
    </pathway>
  </pathways>

```

I know nothing about drug databases, but am familiar with Kegg. As far as I can see from the paper (and I may be wrong) The drug target database would contain the names of enzymes, the activity of which is affected by drugs. So the problem would seem to be to identify so-called Kegg ‘pathways’ in which these target enzymes occur.
(I use the adjective “so-called” as Kegg pathways are not generally what a biochemist would regard as a pathway, but areas of metabolism. However this would not matter if all one is trying to do is find a correlation.)
The poster would seem, therefore, to need to download a list of enzymes for each Kegg pathway. At one time all the Kegg information was available free of charge (I downloaded a considerable amount — although not the enzymes — to construct a relational database). However now one needs to purchase a license to do this — presumably what the authors of the paper did — at a cost of over $1000 pa.
Unless one has grant funding or is independently wealthy, it would seem to be necessary to explore alternatives, such as MetaCyc (https://metacyc.org).
Postscript
The addendum from the poster shows the UniProt IDs for the targets of the drug. These can be converted to Kegg IDs using the conversion tool on the Kegg site (https://www.genome.jp/kegg/tool/conv_id.html). The XML tag entitled “pathway” is not equivalent to a Kegg metabolic pathway as such, although the example seems to consist of proteins involved in blood clotting. If my interpretation is correct, it would be irrelevant to the procedure I suggest. However the original paper is sufficiently vague that I cannot be sure.

Thanks for your reply and your information. I added a new update section to my question which shows a tag wit name pathway in xml file of drugbank. does show the desired pathway of the drug?

@Orca — I've added a PS. If I were you I'd email the authors of the paper.

thanks for the time you spent on my question. the answers did not solve my problem, but a appreciate it with upvote


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Very small, light and dark "insects" - Italy - Infestation, healthy problems? - Insect identification
I'm currently in a town near Savona, on the coast in north-west Italy.
We had a problem with pigeons, that create their nests in the space between the roof and the ceiling.
Now, from the tube of the kitchen hood, that passes through this space, fell down these little insects. I'm a bit concerned it might be ticks, or something that could possibly transmit something bad. We have hundreds of them.
What's the best solution to make them go away? Also, should we leave the house during they permanence? I'm sorry for the bad quality pictures but they are very very small (probably between 0,5 and 1 mm) and very fast, so it's difficult to take good pictures.
Thankful for your help.
Dropbox link with more images and better quality

study protections for your drains, like spike wires to stop birds landing, and search for options that decimate the animals in the drainpipes, like bleach, vinegar, whatever the specialists say, and pour it on the roof regularly to take the mites out of the roof.

What do you mean by "...Also, should we leave the house during they permanence?..." Do you mean: "Also, should we leave the house whilst they are there (the insects)" ?

I suspect these will be bird mites. These are a range of species from two genera (Ornithonyssus and Dermanyssus) that mainly infest birds, but can also cause infestations in humans, causing a condition known as Gamasoidosis. I don't know much about them, but a bit of googling tells me they are commonly seen when a colony of birds is removed from a building and they no longer have a host to live on, so spread out trying to find new hosts.
Adults are in the range of 1/2 to 1 mm long, so quite small. They cause non-specific itchy papules in humans, which are where they bite to suck blood. I think you should be able to kill them with common insecticides.
Getting professional pest control advice is a good idea as it seems infestations can be hard to get rid of because they can live off human and pet blood.


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How to Find Ticks for Research
I am an amateur researcher looking for castor bean ticks for a science project. Where could I procure them the easiest? I am located in southern California.

Why castor bean ticks specifically? There are lots of USA native species that might work in their place rather than getting one largely found in Europe.

We want Ixodes ricinus specifically because we are experimenting with their reaction to static electric fields and that interaction has only been shown with Ixodes ricinus so far.

Where do you live? How you obtain them most easily vs. most economically depends in part on where you live.

Near Los Angeles.

I'll assume (danger!) that your Ixodes behaves like most Ixodes do. The way "questing" ticks (e.g. Ixodes scapularis) are collected is to go where they are common and use a white flannel cloth attached to a pole, the ends of which are tied to a rope, then dragged behind oneself and checked periodically for ticks and collected if present. This works wonderfully for a variety of applications. If that mostly European tick isn't common near to where you live, then you'll have to buy them. Sorry I don't have a better suggestion.

I should add that the cloth should be weighted. Here's a link in case of interest. You might try exposing Ixodes scapularis to a static electric field; they aren't very different ticks, and are probably abundant somewhere not too distant from your location. Where I live (a hotspot for Lyme), I could probably find a hundred in a couple of hours or less this time of year.


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The Contradiction in Soy Production: Livestock Feed versus Human Consumption?
I'm not sure if this is the right place to ask this ecological question. I apologize for any inconvenience, and please let me know if it is.
There is a contradiction regarding soy production and its effects on the environment:

According to Our World in Data, more than three-quarters (77%) of global soy is used as feed for livestock, primarily for meat and dairy production. This means that only about one-fifth (23%) of soy is used for direct human consumption or other purposes.

The article also mentions that only 7% of soybeans are directly fed to livestock, while the remaining 70% is processed into soy cake, which is used as livestock feed. Soy cake is a by-product of soybean oil extraction and is classified based on its crude protein content.

Now, the question arises: what happens to the extracted soybean oil? Is it not used for human consumption? If it is used for human consumption, then humans are also directly responsible for 70% of soy consumption. Additionally, direct human consumption (including food and industrial uses) accounts for more than 24% of soy consumption.


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For wide trees such as Alerce Milenario, can't a longer core just be made (according to web sources the tree is too wide for standard corers)
The Alerce Milenario is only a candidate for the oldest tree. The verified oldest is a bristlecone pine. Trees like Giant Sequoia and Alerce grow both tall and wide, some others stay low to the ground but have massive trunk widths. Bristlecone pines do not grow that wide, they are more modest in size. This means that in the smaller trees complete cores can be taken. In the case of the Alerce Milenario, it's been commonly said that standard corers cannot reach the tree's centre so computer simulations were needed to extrapolate the age of the tree. But why not just make a longer corer? Why wouldn't that work? I haven't found any explanation for this.

It sounds like the centre of the tree is rotten so you can't get a meaningful complete core.

The dead wood is filled with tannins so it will not rot easily.

Rest assured that it will rot - otherwise the forest floor would be totally covered in branches and dead trunks would be standing everywhere. It's also possible that hitting the exact core is difficult, not because of length, but not knowing where it is exactly - trees don't grow as perfect cylinders, they shape themselves to dominant wind direction, ground slope etc. Cores also are fragile - they can break, and getting the rest out can be difficult. Without knowing the exact problem from the (unpublished) study in question, we can only make guesses as to the problem.


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Why can't your little finger move independently to your ring finger
If you attempt to curl either your little or ring finger, you will feel a noticeable about of pressure, then the finger you try to keep stationary ends up moving as well. What keeps the two from moving independently?

This question has been asked before here. Short answer is that they share muscles and nerves, which makes it difficult to move them separately.


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What is the relation between Transpiration and Physiological support in plants
According to my information,When transpiration increases, The amount of water lost from the plant's leaves increases.So,Shall i assume That the relation is inverse according to this condition,or shall i put in consideration that when transpiration increases , The amount of absorbed water increases to compensate the lost water so the relation is direct?

What do you think - what would be the result if water uptake did not compensate for water loss?

@bob1. I Think that no physiological support occurs.

Why do you think that? What would be the consequence for a leaf if it lost water and didn't replace it? A hint - what happens to a cut flower if you don't put it in water?

When transpiration increases, the rate at which water evaporates from the plant's leaves also increases. This creates a negative pressure (tension) in the xylem, which helps to pull water up from the roots to replace the lost water. So, in this case, there is a direct relationship between transpiration and water absorption, as increased transpiration can lead to increased water uptake from the soil to maintain the water balance within the plant.
However, an excessive transpiration, such as during hot and dry conditions, can lead to water stress on the plant. If the rate of transpiration becomes too high and the water uptake from the soil doesn't compensate for the water loss, it can lead to wilting or even damage. So, in this case the relationship could be considered somewhat indirect, as high transpiration could potentially lead to reduced water availability and stress on the plant.


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If Viruses use Host Proteins, why don't Immune Cells attack Host Cells?
The Wikipedia article for Viral Proteins contains the following line:

Thus, viruses do not code for many of their own viral proteins, and instead use the host cell's machinery to produce the viral proteins they require for replication

If the host-derived (i.e. not encoded by the virus) viral proteins are made following the hosts DNA, are those proteins still flagged as "viral" by cytotoxic T cells? If so, why don't they attack host cells that have those proteins when uninfected?
My guesses:

Those host-derived viral proteins are coded for by the host, but aren't usually produced during normal function
The proportion of host-derived viral peptides matters, with a lower proportion indicating normal cell function and a higher proportion indicates infection
The viral proteins are a mix of host proteins that, separately, are not recognized as viral, but when put together by virus instruction can form composite proteins whose peptides fragments are viral
I'm misunderstanding the quote, and what they meant was "Thus, viruses do not code for self-generation of many of their own viral proteins, and instead code to utilize the host cell's machinery to produce the viral proteins they require for replication"

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The phrase “viruses do not code for many of their own viral proteins” in this Wikipedia entry is an obvious oxymoron.
I echo what someone else said: “The beauty of Wikipedia is not that it is correct, but that it is correctable”. So I corrected it.
Unless it has been reverted (let battle commence) the first paragraph now reads as follows:

The term viral protein refers to both the products of the genome of a virus and any host proteins incorporated into the viral particle. Viral proteins are grouped according to their functions, and groups of viral proteins include structural proteins, nonstructural proteins, regulatory proteins, and accessory proteins. Viruses are non-living and do not have the means to reproduce on their own, instead depending on their host cell's machinery to do this. Thus, viruses do not code for most of the proteins required for their replication and the translation of their mRNA into viral proteins, but use proteins encoded by the host cell for this purpose.

To expand for this answer:

Many viruses rely on either the host-encoded DNA polymerase, RNA polymerase or both for replicating their genome, depending on their size and complexity
All viruses depend on the host-encoded machinery of protein synthesis (ribosomes, tRNA, aminoacyl-tRNA synthetases etc.) for the translation of the proteins encoded in their mRNAs (which in some RNA viruses are also their genomes)
Some viruses — especially those enclosed by lipid envelopes — may have host-encoded proteins included in their virions, whether by chance or to serve some function.

The immunity ‘problem’
There seems to be no problem to answer regarding the host’s immune response to viral particles, in any case. The immune response recognizes proteins that are ‘foreign’. Virus-encode proteins are foreign. Any host constituents of the virion are not. (This is the essence of the answer from @PrashantBharadwaj.)

I lack the permissions to delete the question, I have flagged it for moderator review. Regardless of whether it is deleted, I appreciate your answer and your Wikipedia correction

@Gumpf Since David's answer was useful to you, it probably makes more sense to let both your question and also David's answer stand, in case it's also helpful to someone else in the future.

@BryanKrause — Sure. Let it stand. I'll delete the PS.

The short answer is that what is attacked is usually what is recognized as foreign (other than exceptions as in autoimmune disorders). As any epitopes that belong to the host are usually protected from attack during immune cell training/selection.
So if viruses use host proteins, there is no reason to attack host proteins because of that.
Immune system only reacts to viral proteins that they have ready access to - such as the outer capsid or coat proteins - and these are not host derived.
I don't have any direct citations, but this article might be insightful -
Immune recognition of self and non-self explored in new study, from ScienceDaily
PS : I like the analogies in the comments below the question!


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Unknown insect in southern Kansas
My wife and I just moved to Southern Kansas and are still learning the local fauna could anyone please tell us what type of insect this is.

This is a male Metric Paper Wasp (Polistes metricus).
Bugguide is an an authoritative source for arthropods in North America and describes these as:

Very dark--abdomen is black... thorax dark reddish-brown with black
lines. Tibiae and tarsi are yellow (1). Males, like those of most
Polistes species (exception being P. annularis), have a yellow face,
while females have a reddish-brown face.

https://bugguide.net/node/view/60264
We see here that the abdomen, thorax and leg segment colours all match-up. The yellow seen at the top of the face is enough to separate it as a male.
Looking at iNaturalist for vespoid wasps in Kansas, we see that the most commonly observed wasp is this species.

Further, looking at the other species there in Kansas for similarly-coloured wasps, there are a few dark ones with reddish colouring but they would have red or yellow stripes in the abdomen, not all-black as this species has.
https://www.inaturalist.org/observations?place_id=25&taxon_id=48740&view=species
Bugguide has an extensive gallery of photos of this species, and I found one other with no wings:
https://bugguide.net/node/view/987823/bgimage
This is the only photo I found in the >1000 photos I browsed in Bugguide and iNaturalist of this species that shows a specimen with no wings. So it is probably not a natural occurrence for these wasps to lose their wings (like from some natural predator or mating or feasting ritual or anything) -  from the crumpled-look of the wings in the photo, my best guess is that these wings have been melted.


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Live cell imaging using confocal microscope - Question about the microscope settings and laser wavelength
I am doing some calcium imaging to measure calcium levels in HeLa cells. To do this I have expressed cameleon calcium indicator (YC3.60) in the cells and I am using confocal microscope Fluoview for the live imaging. I am having trouble to fully understand some settings about the microscope. As indicated on the picture settings below, I am using 440nm wavelength. However since the argon laser does not emit 440nm but 458nm I do not understand what does this 440nm stands for?
Also after performing the live cell imaging, I analyze the data ratiometically. Is is possible to tell from my confocal settings what would be the ratio of Channel2/Channel1 in nm? I suppose it is 530nm and 480 nm but I am not sure if this is correct.
I have read different papers using confocal microscope but it is not very clear to me since this is my first time using it.
I would appreciate it a lot if someone can help me with this.

Your best bet will be to ask the person who runs the facility - they will have an idea on the set up at your facility and what will work best for your needs.

I thought about that but for the moment I don't know yet someone I can ask there.


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What is the extent of the CSF system out of the brain?
Does it spread sideways from the spinal cord at all?
How far down does it go?
I've found a lot of information about the spinal cord itself but not about the central canal, and more specifically if it's all there is to CSF out of the brain, or if there are small canals exiting it.


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ddT-tailed TA cloning, and the fate of a double nicked plasmid in E. coli
In an undergraduate lab class on TA cloning, it was explained that ddNTPs are used as the substrate for terminal transferase when making the T overhangs of the vector. I was told this was to ensure that the overhang is only 1 bp long.
However, they also say that after the insert binds to the vector, the remaining 4 nicks are ligated. I was immediately confused, because due to the missing 3' hydroxyl groups (consequence of using ddNTP), a phosphodiester bond could not form in 2/4 of the nicks. I may be mistaken, but the oxygen from the 3' hydroxyl is integrated into the bond, so the nick cannot be ligated if it is just a 3' hydrogen. Some people said that ddNTP cannot be polymerised on, but can be ligated.
T.A. Holton and M.W.Graham, 1990 partially answered my question. They confirmed that 2/4 of the nicks cannot be ligated if ddNTP is used (see image).
I have several questions about this

Suppose the insert (striped) encoded a protein, can it be transcribed even if the nicks are there?
What would happen to the nicks during DNA replication?
Would the nicked plasmid be repaired somehow? Is there a mechanism that can recognize and fix the ddNTP nick?
This is a paper from 1990, does modern TA cloning (say, NEB T4 TA cloning protocl) still use ddNTP? If not, how do they assure that the overhang is only 1 bp long?

As for (1), I think perhaps in theory it can be transcribed, as the promoter side of the insert is not nicked, and RNA pol does not need to traverse a nick to access the insert. I suppose the polymerase would fall off the strand at the end?
As for (2), I would think that the whole plasmid would fall apart as the replication bubble spreads, unless the nick is repaired somehow prior.
Thanks in advance.

Image taken from figure 1 of T.A.Holton and M.W.Graham, 1990.
T.A.Holton and M.W.Graham, 1990, A simple and efficient method for direct cloning of PCR products using ddT-tailed vectors, Nucleic Acids Research, Vol. 19, No. 15

To answer question (4):
A-tailing can be done in multiple ways, including the way you described. See here for the most common protocols:
https://international.neb.com/applications/cloning-and-synthetic-biology/dna-end-modification/a-tailing
The way I usually do it is to incubate the insert (e.g. from PCR) with Taq-Polymerase, which will always create a single A-overhang. Simply incubate at 72°C for 30 minutes and you are done (no need for ddNTPs, dNTPs are sufficient). Then you can use pre-existing vectors with T-overhangs for a straightforward ligation.
For the other questions I'm not very sure, although when you perform the ligation and transform bacteria with it, there is probably some way they will repair it. The endproduct (after miniprep) will certainly be an intact plasmid.


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Can a crocodile crack open a turtle's shell?
To put the question more accurately I consider the Saltwater Crocodile, which has been measured to have a bite force of 16.4 kN and estimates of up to 34 kN in 6.7-meters long individuals.
For turtles I consider the following species:

Common land tortoise: Testudo graeca
Common terrapin: Mauremys rivulata
Green sea turtle: Chelonia mydas
Leatherback sea turtle: Dermochelys coriacea
Galapagos turtle: Chelonoidis nigra

Though not all species share the same geographical range as the saltwater crocodile they do represent different thicknesses and robustness of shells.
Note also that the giant extinct crocodylian Deinosuchus did crack open the shells of marine turtles, as it regularly preyed upon them. However, Deinosuchus' bite force is estimated up to 102 kN by Gregory Erickson.

Yes for everything but the Galapagos Its just to big and tall to get the shell to the back teeth that can do the crushing. sea turtle shells are not that strong, sharks which have a comparatively weak bite can bite through them.


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High value weed or plant that can replace the chemical treatment of pesticides and herbicides?
I'm working on a project that aims to replace (at least lower) the use of chemical pesticides and herbicides in farming with the use of high value weeds and plants that can naturally replace the chemical treatment.  So for example , if hedgerows (the edges of the field or the surrounding of a crop) made with high value weeds can be incorporated to fixate nitrogen, or to help the crop fight and resist a given disease, or maybe have a positive impact on the crop, etc...
My mission is : to build a database with high value weeds and plants, and their effects. For example the database should look like :

High value weed
effect

x
fixate nitrogen

y
help crop fight disease d

z
effect z

I'm looking for any already existing database, research or any resource that tackle something like this.
Note: I'm not an expert in farming , I'm just a data science student dealing with agriculture related problems. So please forgive my ignorance. I would be very happy to learn.

Your issue is not knowing proper terminology and using wrong terminology. Some search terms: cover crops, legumes, biological nitrification inhibitors, crop sequences, undersowing, ... You need to talk to a domain expert.


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Mitochondrial diseases inheritance
I've read information about mito genes inheritance but some parts are still obscure for me.
Here is the context:
Mother has a son that is affected by some mitochondrial disease and a healthy daughter. So I suppose that mother is carrier of the recessive mutated gene which she passed to him, right? Articles in the internet tell that mito genes are always inherited from a female (link), but some also tell that two carriers are needed in order to child be possibly affected ("How is mitochondrial disease inherited?" section). But this is controversy, isn't it?
My question is:
Can daughter be also a carrier of this mutated gene? If yes, what conditions should be met in order to her to create an affected child?
Can someone please explain me this?

We can't do personal medical advice here for you or your sister. We can, however, help you to understand mitochondrial inheritance. Please refer to the specific sources you're reading (rather than "articles in the internet"), and depersonalize your question a bit to ask about mitochondrial disease inheritance rather than your family so it can be acceptable here.

@BryanKrause I am not asking personal medical advises but about general inheritance mechanism. Here is one of the articles: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3757997/ "Mitochondrial Biology and Genetics" section. However, this specific one as far as I see doesn't tell about two carriers.

Actually you are asking for personal medical advice: whether your mother is a carrier is a personal medical advice question, whether your sister is a carrier and should be worried about possible children is a personal medical advice question.

You write in your question "Articles in the internet tell that mito genes are always inherited from a female" - you should have a specific source for this (rather than "articles in the internet"), and reference that source in your question (not a comment). "two carriers are needed in order to child be possibly affected" - you should have a specific source for this, and reference that source in your question. Referencing these sources will help answerers help you interpret what you're reading.

@BryanKrause I am working on it

Your second link is from a content farm website, effectively a scam for search engine traffic. Do not rely on websites like this for information.

@BryanKrause Ok, thank you. But what about the first one? It tells that mutated mitochondria number must be larger than some threshold in order to individual be affected. Is it easy for a newborn to pass this threshold when their mother already have some of these genes?


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Considering Two Genes, Are There Only Two Possible Outcomes for the Four Gametes Produced After Meiosis, Regardless of Independent Assortment?
Is it true that for a single meiotic event when considering only two genes, there are only two possible genetic outcomes among the four gametes produced, regardless of whether the two genes are found on the same homologous pair or on two different pairs?
To simplify my question I am disregarding recombination, but feel free to mention the importance and implications of recombination and other factors that I may be disregarding, in gamete formation.
To explain my thought process further, I will use an example. I think that if one daughter cell produced from meiosis I gets the alleles A and b for example, then the other daughter cell must get the alleles a and B, because each gene only has two alleles, one of which is given to each daughter cell in meiosis I. Thus, 50% of the gametes will be the same as one another, again this happens only theoretically, when considering only two genes and disregarding recombination. In this case, two gametes will have the alleles Ab and the other two will have the alleles aB, irrespective of whether the two genes are found on the same homologous pair or on two different pairs. Of course my example is only considering two alleles. Below is an image which illustrates my thinking:

I take it each band represents an allele and the colour of the band represents the gene. I think the image is overcomplicating my question, but it does seems to be consistent with my above simplified description.
I think when people say there are four unique gametes resulting from meiosis e.g., Ab, AB, aB and ab, when considering two genes and assuming independent assortment, they need to be more specific and emphasise that there are four possible gametes per meiotic division, or maybe more depending on whether recombination is considered. Now, that I think of it there are probably more than four possible gametes if you add recombination to the mix.
Regardless of independent assortment, I take it that the result of the meiotic division will actually be two genetically unique gametes, if you disregard recombination and only consider two genes. However, the number of possible unique gametes will be greater.
In summary, I think we need to specify whether we are talking about the observed number of genetically unique gametes resulting from one meiotic event or the possible number of genetically unique gametes, which could be observed given more than one meiotic division, and obviously we need to specify how many genes we are considering in order to determine the genetic uniqueness of the gamete. Lastly, we need to state whether we are assuming recombination or not.
Again, I am assuming everything in I have written based on what I have learned so I may be wrong at any point, I am just a Biology student at University.
To add to my confusion, I assume there are actually two possibilities for the specific combination of alleles found on each chromosome, when two genes are found on the same homologous pair. But these possibilities only express themselves at the individual level, rather than at the 'meiotic event' level. For example, if two genes are found on the same homologous pair, one individual may have the alleles Ab on one homologous chromosome and aB on the other homologous chromosome, whereas the other individual may have the alleles AB on one homologous chromosome and Ab on the other homologous chromosome. However, there is only one possibility for the gametes produced from each meiotic division for each individual. So, in this case, considering only individuals with these two specific genes on the same homologous pair of chromosomes, the gametes produced will be different between individuals for the two genes, whereas the gametes produced for individuals that have these two genes on different homologous pairs can be different between independent meiotic events.
My last inquisition is on how one would calculate the probability of a specific allelic composition for a gamete, with the correct interpretation. If two genes are found on different homologous chromosomes and if we disregard recombination, I assume there is a 50% chance that 50% of the gametes will be Ab and 50% will be aB or 50% will be AB or ab? Is this the correct interpretation?
Apologies for the length of this question!

Yes, correct. But there are many cells to begin with, not just 1, meaning that all 4 end-combinations will be present. Importantly, crossing-over is not a rare optional event, but a necessity with control mechanisms.

I am surprised because to me most of what I said was 'logical' assumptions and I suspect more of the later. Thank you.

A "single meiotic event" would include both meiosis I and meiosis II. So, if you start with an AaBb mother cell prior to any phase of meiosis, then observe one of the resulting final daughter cells, you would have an equal probability (25%) of finding AB, Ab, aB, or ab.
The line of reasoning from OP is only relevant after meiosis I has occurred, and in the absence of recombination. At that point the two intermediary daughter cells have either the genotypes AB and ab (the left side of the figure), or Ab and aB (the right side). From that point the possibilities of the final daughter cells are indeed limited, so if one knew the outcome of meiosis I, they would know the set of genotypes held by the four final daughter cells.
One would also know—again, in the absence of recombination—that a single AaBb mother cell will produce four daughter cells that contain only two possible genotypes among them (but not which genotypes they will be). However, this would only be useful in very narrow circumstances because, first, recombination is integral to meiosis, and second, usually there's a population of mother cells to consider. (And third, it doesn't seem like very useful information in the first place.)
As other comments point out, recombination is not a rare event. When recombination is considered, it is indeed possible to get all four genotypes among the daughter cells

Thank you so much for clarifying Darlingtonia! While the information is certainly not practical, it is very useful to know and helps in understanding the theoretical basis of human knowledge on the subject, especially for a student like me. I came to these conclusions independently because teachers would always 'breeze' past this stuff. Now my understanding is more thorough and I can utilise this. Furthermore, now I understand the mechanisms of recombination, rather than just the implications. Thank you for providing an excellent answer!


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What animal makes these sounds?
An animal near where I live in Austria is making these sounds. I'm thinking it is in distress, but I can't find it. Can anyone tell me what it is?
It goes quiet when you get close, but responds heavily to a cat meowing. The environment is a residential area with many rather large gardens. I haven't heard it make any noise after sundown, only throughout the day, morning til evening. There is a small stream nearby, but no larger bodies of water.
https://whyp.it/tracks/116934/unknown-animal?token=bqQEa

Welcome to the Biology Stack. Can you please edit your question with a couple of details: What sort of environment are you in (rural, urban, semi-rural)?, are there any bodies of water nearby - rivers, lakes, streams etc?, and what time of day does this happen?

@bob1 Thank you for the guidance, I have added more details.

Sounds like a kitten in distress to me. Maybe an abandoned one or if it's at particular times, maybe when it's mother leaves. I am not sure enough. Somebody please confirm.


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Bi-phenyl degradation pathway in lignin
I am studying lignin - and really like the bi-phenyl degradation pathway of DDVA by SYK-6, as shown below

But I can't find any literature on whether this pathway transfers from the dimer to the oligomeric lignin.
Do you think this pathway translates to oligomeric degradation of the 5-5' bond in lignin?


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What reproductive advantage do superhydrophobic spores bring?
Clubmoss plants produce spores that are superhydrophobic, meaning they will not mix with water. When you drop water on top of a whole bunch of these spores, the water will form tiny water droplets on top of the spore powder instead of being absorbed by it. You can see an example of this in this video. The spore powder is also known as lycopodium powder and is used in fire shows and magic tricks.
To my knowledge clubmoss is the only plantspecies that produces superhydrophobic spores. This made me wonder what the reproductive or evolutionary advantage of a superhydrophobic seed or spore could be.
I personally think the superhydrophobic layer could protect the spores from being digested when the clubmoss plant is eaten by a herbivore. The superhydrophobic layer could also prevent the spores from sinking when they fall into water like a river, instead they would stick to the surface. A river could help disperse the spores accross a larger area pretty easily. Eventually the spores would drift to the shore again where they could settle and become new clubmoss plants.
What do you think the reproductive advantage could be?

Water encourages pathogens and is generally detrimental to long term conservation of seeds, actually, nearly all commercial seeds have a lower shelf life in a humid environment, and are generally packed in wax or foil paper.

This paper seems to agree with you; It says that the spores of the clubmoss plant are likely hydrophobic to spread more easily.

This is also a part of the secret of the well-known Lycopodium powders: the clubmoss-spores (diameter ca 30 μm) are weakly hydrophobic, but as powder, they exhibit remarkable functionalities. Many spores—even of aquatic organisms such as the spores of Isoetes or fungi, or myxomycetes [80] are hydrophobic for dispersal purpose.

[80]
(citation from the paper)
Hoppe T, Schwippert WW. 2014 Hydrophobicity of myxomycete spores: an undescribed aspect of spore ornamentation. Mycosphere 5, 601–606. Crossref, ISI, Google Scholar
Additionally, this article believes spores are hydrophobic to protect against environmental factors.

When spores are carried over a long distance, survival is compromised by exposure to diverse abiotic stressors, such as drought, extreme temperatures, and ultraviolet (UV) radiation [12, 13]. Thus, fitness can be estimated using not only developmental parameters but also spore properties that influence dispersal efficiency in different media and resistance to stressors.

Most filamentous fungi disperse through airborne spores that can be transferred by wind over a long distance [11, 14]. For this reason, fungal spores usually remain dry and hydrophobic [15].

(citations from the article)
[11]
Wyatt TT, Wosten HA, Dijksterhuis J. Fungal spores for dispersion in space and time. Adv Appl Microbiol. 2013;85:43–91.
[12]
Fuller KK, Ringelberg CS, Loros JJ, Dunlap JC. The fungal pathogen Aspergillus fumigatus regulates growth, metabolism, and stress resistance in response to light. mBio. 2013;4.
[13]
Norros V, Karhu E, Norden J, Vahatalo AV, Ovaskainen O. Spore sensitivity to sunlight and freezing can restrict dispersal in wood-decay fungi. Ecol Evol. 2015;5:3312–26.
[14]
Roper M, Seminara A, Bandi MM, Cobb A, Dillard HR, Pringle A. Dispersal of fungal spores on a cooperatively generated wind. Proc Natl Acad Sci USA. 2010;107:17474–9.
[15]
Aimanianda V, Bayry J, Bozza S, Kniemeyer O, Perruccio K, Elluru SR, et al. Surface hydrophobin prevents immune recognition of airborne fungal spores. Nature. 2009;460:1117–21.


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Phonotaxis and Preference
(Am I losing my mind?) I could have sworn there was solid research indicating that phonotaxis evidence for preferences (during ex situ experiments) was "held up" by en situ experiments...(by this I mean lab experiments were replicated in wild populations).
Does anyone have, ideally, a peer reviewed article (honestly even a thesis will do at this point) showing that preferences among animals for certain other individuals (shown via phonotaxis) have some sort of real world, in-habitat related replication? Surely there is some reason/real world application as to why we do so many phonotaxis experiments in ecology. (Phototaxis is fine too by the way). What am I missing here? Anyway even something tangential could help me so please don't hesitate to reply to this. Thank you so much in advance.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929774/, https://www.sciencedirect.com/science/article/abs/pii/S0003347206003939, https://www.journals.uchicago.edu/doi/full/10.1086/501376, etc. Depending on what you mean, of course- some of this is wild populations and some of it is field experiments, not totally sure what you're going for. I found this stuff by literally googling "phonotaxis field experiments" and "phonotaxis wild population". Possibly more details would help to see why the abundant studies that I find aren't what you want.