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Are probabilities of mutations symmetric?
For the premise of this quiestion let's assume that there is an allele A and an allele B. The allele A has a probability P to mutate into the allele B in the given timeframe.
Is it also true that the allele B has the probability P to mutate into the allele A?

The short answer is no, there is heterogeneity in the rate at which different nucleotides mutate into one another. This is generally a property of their differing chemistries (although I'm not an expert on this). Therefore, it doesn't really make sense to talk of alleles being $p$ or  $q$ like we do in most of population genetics, because the actual nucleotide (whether it's A, C, G or T does make a difference).
This is important in fields like phylogenetics, where people construct substitution matrices which describes the rate at which one base in a sequence changes to another nucleotide. Currently, it's possible to estimate the matrix parameters from empirically data relatively easily.
For example, in one of the earliest and most simple models, Kimura (1980) introduced a matrix which had two parameters - one for the mutation rate of transition substitutions (A/C -> G/T, more likely) and one for the rate of transversions (A/G -> T/C, less likely). Later methods got progressively more complex, which account for e.g. the different amino/keto properties of different nucleotides. Felsenstein's model (1981) accounted for the equilibrium frequency of the target nucleotide. These substitution values are also allowed to vary across time as well within a phylogenetic tree (e.g. Yang 1994).

References

Kimura, Motoo. "A simple method for estimating evolutionary rates of base substitutions through comparative studies of nucleotide sequences." Journal of molecular evolution 16.2 (1980): 111-120.
Felsenstein, Joseph. "Evolutionary trees from DNA sequences: a maximum likelihood approach." Journal of molecular evolution 17.6 (1981): 368-376.
APA
Yang, Ziheng. "Maximum likelihood phylogenetic estimation from DNA sequences with variable rates over sites: approximate methods." Journal of Molecular evolution 39.3 (1994): 306-314.


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ID Request: What is this frog? Eastern Long Island, NY USA mixed hardwood forest
Apologies for the potato quality photos, but can anyone ID this frog?
My son found a few frogs living under a porch at my father's house, which is situated in a mixed hardwood forested area of eastern Long Island, NY. I say "living" because he sees them sitting just at the edge of the low porch every day for a while now.

It is hard to tell exactly from the photos, but given the location and time of year, it is either a juvenile green frog (Rana clamitans) or juvenile bull frog (Rana catesbeiana).

Would a juvenile bull frog be in an upland setting? I know there are bull frogs in the pond about 300m away, but I'd always thought of them staying in the pond.

Yes, they disburse quite far away from their natal ponds as juveniles, often into impermanent water sources, before settling in a permanent waterbody as adults.

Then I think bull frog is likely the answer

source: Stack Exchange

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

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Does acuity of a re-mapped region of cortex depend on the need of the animal to resolve between two closely related stimuli?
From my informal research so far, I've learned that cortical magnification is evident in at least the visual cortex and the somatosensory cortex.
My question is the following:
If there were a hypothetical experiment to be done where the one area of the cortex, say the visual cortex, were to be re-mapped to a different sensory modality like touch, would the acuity or "resolving power" of the re-mapped region depend on the extent to which the animal needed to distinguish between closely related touch stimuli? In other words, has anyone tried an experiment that results in a re-mapped and magnified cortical portion in one go?

Interesting question. I doubt an experiment like this would survive an Institutional Review Board (IRB) review, though, so my guess would be that this hasn't been tried (if it is possible from a surgical perspective).

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


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Why don't snails run out of slime?
I understand that land-snail-slime and slug-slime are made of mucus.

Externally, one kind of mucus is produced by the foot of the gastropod
and is usually used for crawling on.
https://en.wikipedia.org/wiki/Snail_slime

Travelling on a trail of mucus seems very expensive. How do snails manage to replace it so abundantly without ever running out? Do they ever run out - if so, what happens to them?

Cool info here: https://www.google.com/search?q=mucus+slug+dry+weight&oq=mucus+slug+dry+weight

Why don't you run out of mucus when you have a bad cold?

@jamesqf  If a human produced mucus in the same proportion to body size as a snail, they would dry out within minutes. Also a lot of mucus from a cold gets swallowed and so is recycled.


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Are diplobacillus physically connected?
I know that a diplobacillus is a bacillus bacteria that has a buddy 'attached' to it.
What I haven't been able to determine is exactly how is it 'attached'? Are their cell membranes fused - are they even touching? If they aren't fused, what keeps them together? Also, does this make diplobacillus a multi cellular organism because there are multiple cells in this organism?

I couldn't find anything about diplobacilli, but I did find some information on Streptococcus pneumoniae, which has been extensively studied. S pneumoniae (R6 strain) normally occurs as diplococci. Electron micrographs—see here and here—show that the two cocci of a pair share a portion of cell wall. This is a result of incomplete separation during cell division. Also, mutations in peptidoglycan-hydrolysing enzymes have been shown to produce longer chains of cocci.
Presumably, something similar holds for diplobacilli.
Calling these bacteria 'multicellular' might be inappropriate, because multicellularity implies at least some division of labour: the cells perform different functions in a cooperative manner. Diplobacilli (such as Moraxella lacunata) or diplococci have not been shown to have such a division of labour, as far as I know.


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Consequences of abnormal blood pressure unrelated to cardiac output?
A question from Kaplan's MCAT Biology Review asks:

In bacterial sepsis (overwhelming bloodstream infection), a number of capillary beds throughout the body open simultaneously. What effect would this have on the blood pressure? Besides the risk of infection, why might sepsis be dangerous for the heart?

The answer is:

Opening up more capillary beds (which are in parallel) will decrease the overall resistance of the circuit. The cardiac output will therefore increase in an attempt to maintain constant blood pressure. This is a risk to the heart because the increased demand on the heart can eventually tire it, leading to a heart attack or a precipitous drop in blood pressure.

I had always viewed blood pressure as a means to achieve appropriate blood flow, and a system with lower resistance would simply operate with lower pressure (via Ohm's Law). However, the answer implies that maintaining normal blood pressure is a goal in itself, such that the body would naturally raise cardiac output to dangerous levels in order to maintain it.
Can someone help explain:

Does blood pressure play a role in blood circulation that makes it more important than just a means towards appropriate cardiac output?

What are health consequences of abnormal blood pressure unrelated to cardiac output from a biochemical perspective? If I search for "abnormal blood pressure" I'll get broad symptoms like "dizziness" that don't explain its effect on different tissues that cause the symptoms.

For the second part of your question, I suggest you use better search terms. E.g., 'pathophysiology of hypertension' gets much better results than 'abnormal blood pressure'.

Blood pressure, as you noted, is just a means to an end: the flow of blood through tissues. The trouble is, many of the body's regulatory systems use blood pressure (rather than flow) as an index of cardiovascular status. A key example is the baroreceptor system, which senses changes in blood pressure and tries to correct them by effects on the heart, blood vessels and kidneys.
In sepsis with decreased blood pressure, baroreceptor firing increases in an attempt to increase cardiac output $^1$. This increased demand on the heart can be counterproductive and cause the heart to fail. But this phenomenon is not unique to sepsis. There are many other conditions where a hyperdynamic circulation leads to heart failure: such as anaemia, thyrotoxicosis and thiamine deficiency $^2$.
All of these examples highlight a basic principle in pathophysiology: adaptations can sometimes turn maladaptive.
Note: The effects of sepsis on the cardiovascular system are complex and go beyond vasodilation. For more details, you could read a textbook of pathophysiology/medicine. Or go through any of the review articles on this topic, such as the one by Lelubre & Vincent $^3$.

References:

Gattinoni L, Carlesso E. Supporting hemodynamics: what should we target? What treatments should we use? Crit Care [Internet]. 2013 Mar 12 [cited 2020 Aug 24]:17(Suppl 1):Article S4 [8 p.]. Available from: https://ccforum.biomedcentral.com/articles/10.1186/cc11502
Mehta PA, Dubrey SW. High output heart failure. QJM. 2009 Apr;102(4):235–41. https://doi.org/10.1093/qjmed/hcn147
Lelubre C, Vincent J. Mechanisms and treatment of organ failure in sepsis. Nat Rev Nephrol. 2018;147(7):417–27. https://doi.org/10.1038/s41581-018-0005-7


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RT-PCR: Not seeing how it can measure mRNA expression levels
From my understanding, in RT-PCR we start off with an mRNA molecule, use the enzyme reverse transcriptase to create a cDNA copy (hence creating a double-stranded mRNA / cDNA hybrid), degrade the mRNA, and finally create a complementary strand to the cDNA with a DNA polymerase. If we're ultimately creating DNA and it's being duplicated at each cycle, how are we able to deduce the original quantity of mRNA in our sample? It seems like we would need to combine it with some other method, but a lot of sources I'm seeing seem to imply that RT-PCR alone is enough to "quantify" the amount of mRNA in a sample. Any thoughts on this are welcome

There might be a confusion of terminology. There is real-time quantitative PCR, which can sometimes be called RT-PCR. There is also reverse-transcriptase PCR, which is also confusingly called RT-PCR. To try to reduce confusion, real-time quantitative PCR is also called RT-qPCR or qPCR.
What you describe in your question is the reverse-transcriptase type of PCR. This is used for amplification, not quantification, of starting material.
QPCR or quantitative PCR, on the other hand, uses fluorescent dyes to measure the amount of amplified gene product. Standards provide a baseline measure of how much genetic material you should expect to see over time, at each PCR cycle, for a given amount of measured fluorescence. Measuring fluorescence of your own sample over time, and comparing it against the standard, gives you an estimate of what you started with, initially.

I just wanted to elaborate on the previous answer regarding the confusion between real-time (quantitative) and reverse-transcription(RT) PCR. RT-qPCR refers to real-time quantitative PCR, but some organizations refrain from any reference to quantitation (because it's really only semi-quantitative), instead using the nomenclature rRT-PCR (reverse transcription real-time PCR, I guess). In either case, this technique is theoretically capable of quantification of mRNA copies using the appropriate assay design and standards.
The general principle is that, after the cDNA is reverse transcribed from RNA, it is amplified similar to a normal PCR reaction. This can be accomplished in a single reaction with master mix containing both the reverse transcription and qPCR reagents, or in two separate reactions, by first performing an RT first, and then a standard qPCR on the resulting cDNA. The all in one method requires fewer reagents and less hands on time, but it can be difficult to optimize both reactions at the same time.
Here's a good primer on qPCR assay design. As stated in the previous answer, the quantification comes from some measure of fluorescence related to the amount of amplification product present. In an optimized reaction, the number of amplicons should double with each cycle, allowing for quantification based on how many cycles it occur before a specified fluorescence threshold is reached by each reaction well. Intercalating dyes like SyberGreen quantify total DNA present, whereas fluorescent probes are more specific to your gene of interest. Because it's only semi-quantitative, a standard dilution series of known concentration is included on each plate and used for quantification. The standards should be of the same material and sequence as your gene of interest (DNA or RNA) and should be diluted into a range of concentrations that will likely include the concentration in your experimental samples. You also need to be careful about the possibility of degredation of your standards, as the quality of your quantification is entirely dependent on the quality of your standards.
An alternative approach is to quantify a gene of interest relative to some reference gene that is constituatively expressed at the same level regardless of the experimental sample. This method (sometimes called the delta-delta Ct method) eliminates the need for running a standard curve, but requires additional reactions or multiplexing, in addition to identifying a stable reference gene with primers and possibly probes that will work under the same thermocycling conditions as your gene of interest.
A third option is absolute quantification via digital PCR (dPCR). One issue with qPCR in general is that, even when running samples in duplicate or triplicate, it can be hard to confidently resolve differences in quantification smaller than about 3-fold. Enter absolute quantification. dPCR works by dividing up the reaction into tens of thousands of nano-liter sized compartments, such that each compartment may or may not contain an actual copy of your gene of interest. Fluorescence is only used at the end of the reaction to determine whether each compartment has amplified or not (hence digital, each compartment is a 1 or a 0). Quantification is calculated by determining the ratio of positive to negative compartments and comparing to a Poisson distribution for discrete probability distrubutions. It can have much finer resolution than qPCR, supposedly capable of reliably detecting a 1.2-fold difference in concentrations, with the trade-off that it has less dynamic range with reduced confidence in quantification estimates near the top and bottom of that range. Plus the entire system is usually much more expensive at just about every level (equipment, reagents, and consumables). But with most gene expression assays, you really need to ask yourself if a 1.2-fold change in transcript level is even going to be meaningful in your biological system.


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The Proofreading Function of Coronavirus Polymerases
I have heard that the Coronavirus family have a proofreading and editing function in their polymerase enzymes which can recognize and excise mutations. This is obviously disastrous for the population of infected individuals. Is this true, and if so, would it be possible to knock out the proofreading and editing subunit selectively so that the mutational burden would progressively increase in the viral population ?  Could this then lead to something like Muller's Ratchet and dampen the virulence in the population or would there still be a mechanism to remove the mutated viruses from the population and retain the virulence over time?

Welcome to SE Biology. Please finish reading the [tour] and check the help on writing good questions. You will find that you are expected to research a topic for an answer before posting, ask one question at a time, and make sure that questions relate to problems in biology. If your question is whether coronavirus polymerases proofread and edit, then that is one question. If not, you need to cite references that it is so. That would leave a question that is not a question but a suggestion for an anti-viral strategy, which is off-topic here.

Not an answer but the keywords are exonuclease and nsp14. You could look up how lopinavir and remdesivir work and how ribavirin does not work.


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Where can I find a cannabinoids profile of hemp strains?
For my web article, I need to find out the content of individual cannabinoids in hemp strains, specifically for Kompolti, Carmagnola and Purple Haze. I mean the content of all the components, not just THC and CBD.
Do you know of any website that provides this information?
Thank you for answer


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How the vaccine based on "non replicating viral vector" is produced?
As I understand, this kind of vaccine is a virus that can infect the cell, start synthesis of  proteins encoded by its genome, but cannot finish the replication cycle till the proper end. It can have extra genes in its genome, encoding proteins that cause the wanted immunity to develop. Some important vaccines against COVID-19 are based on this approach.
The question is, how such an "incomplete virus" could be produced in large amounts? It would be logical to assume that it was replicating during the manufacturing process, but then why does it cannot any longer? The only hint I found is the usage of the "helper virus" that infects the same cell, so the "incomplete virus" can borrow some parts from the healthy "coworker". However this raises another question: the helper virus obviously replicates also itself, and how to discard it later without inactivating the "non replicating" one? It would just cause infection without any use if not discarded.
I have done some search over web and article databases but was not able to find a short and clear explanation of this method. The main focus of the works I found is always somewhere else. I understand that exact technology may be secret, but it is likely at least remotely based on some research work anyway.
How is a "non replicating vector" replicated to produce enough of it, for making a vaccine out of it?

Complementing cell line (or complementary cell line) is a cell line which has been genetically modified to produce proteins necesary for non-replicating virus replication. It is designed to express exactly the genes which had been deleted from virus to render it non-replicating. The non-replicating viral vector can replicate only in complementing cell line and not in other cells.

I have learned this in a lecture. I have tried to find some comprehensive reference for this answer but found only use cases.

do you have any other good sources for "complementing cells lines? I upvoted your answer. By the way, does a Adenovirus vector for covid-19 vaccine carry the spike protein - as an experienced user would you think that's a good question to publish? How can Adenovirus be replicated in vitro without "expression" of the implanted mRNA for the spke protein? It should carry it.

@Peter Bernhard Sorry only sources would be what I would google. I wouldn't call myself experienced user and I try to stay out of judging questions. You can ask the question but be careful to not conflate expression of protein with virion packaging. The host cell expresses and contains a lot of different proteins. Only specific proteins assemble into 3D structure to form a virion.

Thank you. Good yo said "expression of protein", now up above "expression of genes" seems better in formulation. However, this  improves ma understanding - the "cell line" as a helper adds the proteins, not the genes (correct me if I am wrong, please) that are necessary for a virus to still be an intact virus, for the purposes of vaccination, to be specific. So, "packaging" seems to be very illuminating: maybe packaging genes have been deleted, and the helper cell lines add that stuff, to build viruses that last their life time only.


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Is this a carpenter bee?
This bee visits our balcony every day multiple times, but only for a brief time, making it hard to take a good picture:

Here's another picture, I finally got lucky so I'm adding it to the question:

It does not look like a typical honeybee. It does not make noise as bumblebees do. It also looks a lot like it's really the same creature every day. It always comes and leaves on the exact same path. The face looks a lot like carpenter bee, but I also couldn't find one like this on the internet.
This is in central Europe.


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how long would oxidation of ammonia solution to nitrates take?
A hot topic among amateur chemists is making nitric acid from ammonia. While not as useful, im interested in making nitrate salts from ammonia as well.
A simple idea is to just infect ammonia solution with soil bacteria and add some fresh grass as source of other necessary nutrients for bacteria. If kept at optimal temperature, how long can i except the process of forming ammonium nitrate to take?

Hi, maybe tell us how far you got and where your research got stuck. A lead can be to search for COMMOX (COMplete AMMonia OXidiser), they do the whole process from ammonia to nitrate.

haven't started the experiment yet, i just wanted to know whether it would take days, week, or months


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What determines whether a reaction using ATP produces ADP or AMP?
Most reactions using ATP seem to involve:
ATP → ADP + Pi
but in some the reaction is
ATP → AMP + PPi
followed by hydrolysis of the pyrophosphate:
PPi → 2Pi
Is there any principle that determines which ATP-requiring reactions generate ADP and which generate AMP? And is there any reason why the generation of inorganic phosphate does not proceed as follows?
ATP → ADP + Pi
ADP → AMP + Pi

I have edited your question to remove some of the false assertion it contains (e.g. "hydrolyze the pyrophosphate for additional energy") and focus purely on the essential point of whether a reaction generates ADP or AMP. I have also changed the style. Asking how to memorize something is not, I think, a valid question here — asking whether there is a principle behind something is.

Summary
It is the nature of the biochemical reaction that determines whether a reaction of ATP involves hydrolysis of the β- or γ- phosphoanhydride bond. If a part of the ATP molecule is incorporated into one of the products, the choice of bond to be cleaved emerges from the chemistry of the reaction. If the hydrolysis (with a negative free energy change, ΔG) is being coupled to a reaction with a positive ΔG, hydrolysis of single (γ-) phosphoanhydride bond usually suffices, with the production of ADP and Pi. If the free-energy of hydrolysis of the phosphoanhydride bond is being ‘transferred’ to another molecule in order to ‘activate’ it for a specialized group-transfer role (often in the synthesis of macromolecules) two bonds are often broken: the first (β-) transfers the free energy with the production of pyrophosphate, whereas the second (now in the pyrophosphate) is hydrolysed non-productively (free energy lost as heat) to ensure that the overall reaction is irreversible.
Energy considerations in reactions involving ATP
I have discussed some of this at greater length in an answer to another question, however it is important to clarify this at the outset. In considering biological reactions, it is usual to adopt a thermodynamic approach in which the thermodynamical (Gibbs) Free Energy change (ΔG) of the reaction is considered. This is because, to quote from Berg et al.:

A reaction can occur spontaneously only if ΔG is negative.
A system is at equilibrium and no net change can take place if ΔG is zero.
A reaction cannot occur spontaneously if ΔG is positive. An input of
free energy is required to drive such a reaction.

The literature provides values of the standard free energy changes, ΔGo, for reactions, i.e. the values obtained under conditions in which the concentration of all reactants and products are set at the same concentration. The actual free energy change, ΔG, depends on the concentration of reactants and products (mass action effects).
The hydrolysis of the β- and γ- phosphoanhydride bonds of ATP both have a high negative values of ΔGo of ca. –45 and –30 kJ per mol, respectively†.
Use of ATP to drive unfavourable reactions
In many cases the hydrolysis of ATP is coupled to an energetically unfavourable reaction (one with a +ve ΔGo) so that the coupled reaction has overall negative free energy change and hence the energetically favourable reaction can take place:
A → B                    ΔG =  20 kJ/mol (unfavourable)
ATP → ADP + Pi           ΔG = –30 kJ/mol (favourable)
A + ATP → B + ADP + Pi   ΔG = –10 kJ/mol (favourable)

In this hypothetical example, 20 kJ/mol of the free energy of hydrolysis of ATP is used to convert A to B, the other 10 kJ/mol is lost as heat, but makes the reaction essentially irreversible. The energy of hydrolysis of only a single phosphoanhydride bond is sufficient for this, and is achieved by the hydrolysis of the γ bond with the production of ADP. (Hydrolysis of the β bond would ‘loose’ the second bond in pyrophosphate, where its hydrolysis cannot be used productively.) An example is the conversion of pyruvate to oxaloacetate in gluconeogenesis, in which energy is required to form a carbon–carbon bond:
CH3COCOO– + HCO3– + ATP → COO–CH2COCOO– + ADP + Pi
Incorporation of ATP into products
In some cases there is not only hydrolysis of a phosphoanhydride bond, but a chemical component of ATP is incorporated into one of the products. In this case the actual chemical reaction determines which bond is hydrolysed.
In the first type of reaction a phosphate group is incorporated into the product, in which case this will obviously be the γ-phosphate and ADP will be generated. A simple example of this is the hexokinase reaction:
Glucose + ATP  → Glucose 6-P + ADP
The reaction is essentially irreversible as the energy of the hexose phosphate bond is much less than that of the phosphoanhydride bond.
In the second type of reaction the AMP component of ATP (or similar molecules) is incorporated into one of the products, so that the other product must be pyrophosphate. The obvious example is the RNA polymerase reaction, which for our purposes can be represented as:
------ribose-3′OH + ATP → ------ribose--3′O-PO2-O-5′-Adenosine + PPi
ATP and ‘activation’ reactions: rationale for pyrophosphate
In certain reactions of ATP the energy of a  phosphoanhydride bond is being used to created a bond of similar free energy of hydrolysis, which can itself be used subsequently to activate other reactions. In this case the reaction may involve little of no free energy change, so that it would appear to be easily reversible. In many such cases the β phosphoanhydride bond is cleaved, generating pyrophosphate. The rationale for this is that the pyrophosphate is then converted to phosphate in a reaction catalysed by pyrophosphatases, which has a high negative DG and is hence essentially irreversible because the free energy of hydrolysis of the phosphoanhydride bond in pyrophosphate is lost as heat.
A + ATP → B + AMP + PPi     ΔG = 0 kJ/mol (reversible)
PPi → 2 Pi                  ΔG = –33 kJ/mol (irreversible)

The examples often given to explain this are the nucleic acid polymerase reactions, but, although this applies also to them, the nature of their reaction necessitates the generation of pyrophosphate. To some extent this is the case with most other activation reactions, but it may be clearer to consider one in which the component of ATP is incorporated as a temporary intermediate, rather than as a component of the end product. Such a reaction is amino acid activation for protein synthesis:
amino acid + ATP → aminoacyl-AMP + PPi
aminoacyl-AMP + tRNA → aminoacyl-tRNA + AMP
The ‘activation’ is the formation of bond with a high free energy of hydrolysis in the aminoacyl-AMP from the β phosphoanhydride bond. This is then used to drive the reaction forming a bond between the amino acid and the tRNA. The generation of pyrophosphate ensures the effective irreversibility of this key step in protein biosynthesis.
†Possible role of differences of free energy of hydrolysis
The fact that the standard free energy of hydrolysis of the β phosphoanhydride bond is greater than that of the γ phosphoanhydride bond may also be relevant in some cases, as @user1136 has argued in his answer to this question.

DNA polymerase uses this form of the reaction NTP -> NMP + PPi which is followed by a rapid degradation of pyrophosphate for a very important reason. It makes the reaction irreversible (or quasi irreversible). The backward reaction is (practically) impossible because in order for it to take place, multiple compounds must simultaneously reunite in the catalytic site of the enzyme and multiple non-spontaneous processes must occur simultaneously. So, in the case of the DNA polymerase, an important consideration is the irreversibility of the reaction. On the other hand, if your primary goal is to harvest energy (e.g. metabolism), you can catalyze the reaction through a suite of potentially reversible steps.

I agree with you that the hydrolysis of pyrophosphate makes the reaction irreversible, but your explanation of this in the following sentence does not make sense. A reaction is irreversible because of the free energy change. What is this reaction with multiple components you mention. And what do you mean by "harvesting energy"? ATP is "metabolic energy". It's not used to harvest it, surely.


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What causes motor laterality/ side dominance?
I would like to understand what leads up to motor laterality, or side dominance of motor skills.
I made this assumption that it depends on neuroplasticity and the side in which one first learns the motor skill; whereas the more you practice, the more you strengthen that side. I appreciate your time and patience. Thank you; can't wait to discuss.

I think this question is overly broad in scope. There is abundant literature on the various causes of handedness: genetic, epigenetic and environmental. The following might serve as an introduction: https://www.nature.com/articles/s41598-018-37423-8.

I found this article on forced right-handedness; can I get your opinion on if it supports my assumption, @Adhish? Thank you for your help! https://blog.cognifit.com/ambidextrous-brain/

The available evidence (and the article you shared) suggest that training does play a role. So your assumption is correct to an extent. But inherited factors are important too.

Ah, Thank you! Just one more question, if you don't mind me asking: What "category" of factors would training/practice fall under? Physical factors? My apologies; I'm very new to this field. Thank you for your patience, @Adhish.


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Does the corpus callosum have a significant relationship with motor memories/ muscle memories?
With the corpus callosum located in the cerebrum, and motor memories having a closer relationship to the cerebellum (which I'm not quite sure about), is there a significant relationship between the corpus callosum and motor memories? Do motor memories process in one hemisphere and are then shared with the other- if so, how? Thank you so much for your time and patience!

Almost all parts of the brain have a relationship, but what deems a neuronal relationship significant? Maybe this will help (pay-wall): https://onlinelibrary-wiley-com.ezproxy2.acu.edu.au/doi/abs/10.1002/cne.902470303

@Andrew thank you for sharing! However, I don't have a user account with ACU . Can anyone sign up or just students? Cheers!

Apologies, try this link: https://pubmed.ncbi.nlm.nih.gov/3722441/

@Andrew got it, thank you so much!

This study tests the time it takes for patients with damaged corpus callosums to perform intermanual transfer motor tasks.
Patients drew a meaningless figure with one hand, then did it again with the other hand (And vice versa). Thus performing intermanual transfer.

All three patients displayed a significant benefit for transfer from the dominant to the non-dominant hand but not vice versa during proximal motor activity.

...the proximal transfer behavior was found to be similar for all patients in the healthy group.

From these results, a relationship exsists.


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Why most small organisms seem not to be interested in any organic matter which has all moisture removed?
On the first glance, it seems that most small organisms do not exhibit any interest in consuming any live or dead organic matter if it is completely dehydrated. Regardless if the food consists of protein, fats or carbohydrates, or any mixture of them, it appears to me that removing water makes bacteria, mould or even insects not consider it food.
Here I consider organic matter which can last for years without being subject to decay by small live organisms:

ghee, made from butter by boiling off all water, lasts for a year or more
freeze-dried food, which still can have 0.5% to 3% moisture, but can last 20 years
honey, supposedly can last forever

While the humble homo sapiens will happily put freeze dried milk in his mouth, most small organisms seem not to have any interest in organic matter with ultra-low moisture:

bacteria
mould
and to a certain extent even insects

For example I noticed ants will quickly gather around any drop of fat used in cooking, which has moisture and other impurities, but will ignore clean, dry ghee.
Why is moisture removal such an universal protection against small organisms and where exactly is the boundary between organisms which can't consume dry matter and the ones which can? Are there any known microorganisms which will consume completely dry organic matter?

Just a hypothesis: a lot of these small organisms who are not interested in completely dehydrated "food" would also be ones who don't explicitly drink water (at least, not enough). Pretty much all organisms need water to live, they also lose water to the environment via urination, perspiration, or other pathways. For organisms that don't explicitly drink water, their major source of water would come from the food. So if the food doesn't contain enough water, they don't bother.

For microorganisms, the lack of water in the food may inhibit their ability to even break down the food, mechanically (too hard) or chemically (lack of solvent to facilitate chemical reactions).

TL;DR
If it doesn't last forever this is some organisms consuming it. It is a matter of ecological niches, what are the requirements (humidity, temperature, etc.) to live and reproduce
I believe we should separate the discussion in two: small organisms and microrganises
Microorganisms
Microorganisms that consume our food need to get there, either they got there from the air or they are already there. Other vectors can be insects, animals, water and soil but since this discussion is about food and we tend to keep our food protected from those vectors I'm going to ignore them.
Most of the microorganisms of interest (Bacteria, Archaea, Fungi & Oomycetes) exist in air as spores. This are analog to seeds, they are alive but inactive and need to arrive to a good environment to sprout. Spores can survive for many years, even millions of years("Revival and identification of bacterial spores in 25- to 40-million-year-old Dominican amber". Science. 268 (5213): 1060–1064.). This survival mechanisme includes dehydration and therefore rehydration is necessary for sprouting.
In addition some of these (mainly oomycetes) need free-water to live & reproduce while others require some levels of moisture.
Dehydrated organic material tends to be hygroscopic. Thus if the non-spore form of the microorganism lands on it the organism will probably loose water and die.
Microorganisms, like every organism, have niches they occupy. One of the characteristics of these niches is the temperature. Freeze-drying includes freezing which lowers the temperature below the survival temperature of many microorganisms and preserves the food. Microorganisms that grow in low temperatures grow slower so it will take more time for us to notice their presence. They still require water so the combination of freezing and dehydration provides a good protection.
Honey has a antibacterial activity in it preventing growth of microorganisms. In addition honey contains a lot of sugar and other molecules making it hypertonic to most microorganisms causing them to loose water if they land on it. Also his high viscosity prevents the free movement of microorganisms.
Small organismes
Many small organismes still need water to live and reproduce (like nematodes)
Insects are highly specified to their environment and food intake. They might not be able to consume dehydrated food.
In addition, as mentioned in the comments by Kal

a lot of these small organisms who are not interested in completely dehydrated "food" would also be ones who
don't explicitly drink water (at least, not enough).[...] For organisms that
don't explicitly drink water, their major source of water would come
from the food. So if the food doesn't contain enough water, they don't
bother.

Ants and other insects do eat dehydrated organic material like seeds, but it still has around %10 moisture
Oil is not hydrated but liquid, since it is oil and not water


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Why do mammals rarely have eyespots?
An eyespot is a marking to mimic the eyes. Many examples of eyespots can be found in fish, reptiles (including birds), and insects. Recently Radford 2020 has shown that artificial eyespots can reduce predations in cattle. However, apart from cats (tigers and servals), mammals, especially herbivores, rarely have this trait.
Why does mammals rarely have eyespots?

does this answer your question https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont

A lot of mammals do have eyespots. Specifically "mid-guild" predators such as raccoons, coatimundis, ringtails, foxes, raccoon dogs, many opossums, skunks, red pandas, civets, etc. It's thought to be an anti-predator defense, with the eyespots or face mask being places further back on the head. A predator might mistake these eyespots for its actual eyes, and because they're placed further back they create the optical illusion that the animal's head belongs to a much larger animal than it actually does.

This is a photo of the gray four-eyed opossum (Philander opossum). It's called "four-eyed" because of the two eye spots it has just above it's eyes. It's thought that the position of these spots mimics the position of the eyes on a much larger predator, so if a predator like a raccoon or a coyote sees the opossum they'll mistake it for a much larger predator and they'll leave it alone.


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How would one track a mineral nutrient in a plant in order to determine if the nutrient has been remobilized?
Before abscission, senescence of a plant’s structural components that contain mineral nutrients (E.g. Magnesium, Potassium...) are re-mobilized from the senescent tissue and used in other plant tissue for anabolic activities.
How could an experiment to demonstrate this?
I was told that a radioisotope method would work. We can detect the presence of the radioactive particle in one part at a time-point, but how would we know whether it is the very same particle that shows up elsewhere after abscission?

You can't do it on a single-molecule level, but I'm in agreement with whoever told you to use radioisotopes. As to it being the same molecules, I would suspect that under most growing circumstances your plant isn't going to be exposed to neutron radiation or uptake radioisotopes from the environment to any significant degree., so the radioactive molecules would be the same ones you started with.

This looks like it was a homework question. Was it?

Magnesium isotopes would allow you to track the movement of magnesium.
Injection of the radioisotope 28Mg (half-life of 20.915 hours) into senescent cells may allow you to observe the direct effect of magnesium movement from senescent cells to other cells. If abscission were to occur, you could check abscised plant tissue. If you wanted to check if anabolism was also occurring, this may take more thought.
This is assuming senescents and abscission in the plant model takes under ~20 hours. Which I think is unlikely, however there are plenty of other 'mineral nutrient' and magnesium radioisotopes available.
Note
Radioactive isotopes have the ability to emit radiation allowing them to be imaged. This is great when they are inorganic molecules, because plant tissue is (mostly) organic. These variables allow imaging to be highly effective at particular emissions.
A similar approach was done here (Pay-wall(another here with-out paywall)).  However these studies added another step 'fractionation'. This may be a helpful idea, fractionation is a separation process to measure the abundance of Magnesium (they refer to it as Magnesium Purification). This is another reason to use an isotope, instead of imaging it may be useful for purification.

I suspect injection into already-senescent tissue is too late in the process to answer the OP's question.  Perhaps a much earlier injection of a longer-lived isotope, then periodic testing over time to see if migration of the isotope occurs only/mostly with the onset of senescence.

There are a variety of methods for visualizing elements in plants. Here is a review discussing various such methods.

As suggested by other answers, radioisotopes are one such means (works in vivo?).
One may also use X-ray spectroscopy: "With x-ray fluorescence-based approaches, elements are detected based upon their characteristic fluorescent x-rays. These fluorescent x-rays are generated by passing the specimen through a focused beam of high-energy x-rays (XFM), electrons (SEM- and TEM-EDS), or protons (PIXE)."
Various electron microscopy methods, sometimes in combination with X-ray or radiography methods.
Fluorescent tagging of elements with high-affinity fluorophores (works in vivo?).
X-ray fluorescence microscopy (XFM).
etc., go look at the paper.

Here is a helpful graphic summarizing strengths and weaknesses of various approaches:

If you are interested in non-destructive sampling for tracking over time, there are several methods available from that list.


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What's the name of this green fruit with little pikes fallen from a city tree on the pavement?
What's the name of this green fruit with little pikes fallen from a tree on Paris (France) pavement ?

Seems horse chestnut.

It would be very  helpful to know the location of the photo (city, country).

Also something idea of the size.

Its 100% a euro or an indian conker tree species.

Welcome to Biology.SE! Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible) — in this case clear pictures of the leaves and bark of the tree; and 2) an estimate of the size of the tree and the fruit. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site, which differs from the SE sites that you are more familiar with. Thanks!

It is horse chestnut it is very common to plant chestnut trees in public parks and a lot of people do have them around their property and by the side of many roads.
What you have in your picture is the fruit and the leaves on the ground confirms that this is horse chestnut.
Source https://en.wikipedia.org/wiki/Aesculus_hippocastanum
The nut is poisonus and the toxin can cause loss of coordination and tremors in horses if they eat the nuts.
Touching or handling the nuts do not cause any adverse effect to humans they are only dangerous to humans if they are eaten.
Horse chestnut contains alcaloid saponins and glucosides that have a toxic effect on mamals.


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Why unripe, very young coconut fruits spoil in days, but the ones picked medium mature can keep months?
Coconut fruits can be collected at various stages of maturity.
Coconuts which are collected just when the flesh starts forming (about 5-6 months on-palm age), so they have very thin or almost no flesh, mostly just coconut water, they will spoil within just a few days in ambient temperature 30°C (86°F). Coconut water from such a fruit which stayed (in a n intact coconut) just a few days will start to taste off, and give stomach cramps.
As coconut mature on the palm, about 7-8 months of on-palm age, they grow more flesh and the flesh is becoming more firm, but not completely firm yet, while the outside of the coconut still remains more or less the same as the very young ones. Such coconuts will keep without spoiling much longer at the same temperature 30°C (86°F), provided the shell is intact, no cracks. Such coconuts are still considered young. I am not talking about fully mature coconuts, when the meat is completely hard and the outer shell starts to turn brown - this happens after about 10 months of on-palm age.
What biochemical difference is in the coconut water that prevent the medium-young (7-8 month) coconuts from spoiling as fast as the very young-picked ones?


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Does double stranded RNA (dsRNA) exist in eukaryotic cells?
I know it sounds like a stupid question. Obviously, tRNAs and rRNAs, for example, form loops and could therefore be considered as dsRNAs... but are they really considered as such?
Are there examples of RNAs, in eukaryotic cells, that could be considered exclusively as dsRNAs, or are dsRNAs considered as unique to certain viruses?
Thanks in advance for your help. I couldn't find a clear answer to that question in my textbooks and on the internet, so I hope you can help.

Yes, dsRNAs are present in eukaryotic cells and regulate various biological processes.
These nucleic acids are also present in the nucleus and regulate mitosis. Altering this nucleic acid could even lead to cell death.
(Reference: https://pubmed.ncbi.nlm.nih.gov/25504323/)

I attached the image of a research article as Peter Bernhard can't access this article. And I tried to add the whole article but couldn't do that because of size issues. I will remove this image because of copyright issues. I Will keep this in mind from now onwards. Thank you David.

I will keep it very very short and simple.
dsRNA is very critical in regulation of gene expression at translational level.
In our system we have specific miRNA (micro RNA) that are somewhat complementary to a specific  mRNA and miRNA-mRNA binding forms a double stranded molecule that is degraded by our system at a cellular level. So in a way it controls the translation of mRNA(s).
Further reading about miRNA-
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6085463/

Sure about  "at translational level" if it's mRNA being degraded - that doesn't make it "at transcriptional level"?

No. Transcriptional level would mean it interferes with DNA.

@PeterBernhard miRNAs bind mRNA and block ribosomes from tranlating it. So it is at a translational level.


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Why humans didn't evolve to safely consume rotten food?
I'm not a biology person at all so please forgive me if my question is silly.
I was just wondering that why didn't evolution cause us to digest, without issues  decomposed food?

What evolutionary advantage would that give us? "Rotten" by definition means that some or all of the usable nutrients have decomposed, so what is the point?

Well imo animals eat half decomposed things.

I understand that is what spices were originally used for ; to mask bad flavors in food that is "turning" ( bad).

There's really no "why" answer here, any more than you can say "why" cows eat grass, or blue whales eat krill.  Evolution doesn't have a purpose or goal.  The only answer is "because our ancestors survived without eating rotten food".

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4519257/ it doesnt give us a significant survival advantage... food rots very fast in some climates, but while fruit and leaves are alive, the are very abundant.

You could argue that we have the ability to eat certain "rotten" foods, those that have fermented.

Yes, there are animals called carrion eaters that will preferentially consume rotting food, because they have either enzymes or commensal microbiota that aid in digesting it and obtaining energy/nutrients from it. However, we and most other animals don't have that ability because of biochemical trade-offs.

@Bryan Krause: Then there's cheese.  Or various sauces made from rotten fish, from Roman garum & liquamen to southeast Asian things like the Vietnamese nuoc mam.

@jamesqf I believe those are also fermented (besides cheese).

Food is considered "rotten" when it has a large population of micororganisms like bacteria and fungus eating it. Some of these microorganisms have evolved to produce toxins that harm animals that would otherwise eat the food. Animals could evolve to tolerate these toxins, and some have. However, bacteria have a large advantage over animals in an evolutionary arms race due to their short generation time and large population number. So competing with bacteria over carrion is a specialized niche, avoiding it has been selected for in most animal lineages.


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What kind of caterpillars are these?
My niece found some caterpillars that we can't identify. Anyone know what these are? They were found in Massachusetts. The look kind of like Luna Moth caterpillars to me, but I'm not sure.

These are "the big kind" of caterpillars! :-)

Most likely it is Polymopheus moth caterpillar, known as Antheraea polyphemus  from the giant moth family.

yellow-green, and the setae become relatively less prominent with each molt. The translucent yellowish-green to green, full-grown (fifth instar) caterpillars are 60 to 75 mm in length. They have yellow mid-segmental lines that run from the sub-dorsal scoli (setae-bearing, wart-like bumps) touching the spiracles and to the lateral scoli on abdominal segments 2 to 7.

Reference

The species is widespread in continental North America, with local populations found throughout subarctic Canada and the United States. The caterpillar can eat 86,000 times its weight at emergence in a little less than two months.

Reference

The adult wingspan is 10 to 15 cm (approximately 4 to 6 inches). The upper surface of the wings is various shades of reddish brown, gray, light brown or yellow-brown with transparent eyespots.

Reference

Adult male moth

Adult female moth

These ones don't appear to have any setae at all, would the latter stage instars lose them completely?

@asgallant 'Older instars are yellow-green, and the setae become relatively less prominent with each molt. ' reference

Yes, I read that. I'm asking if "less prominent" could mean "not visible at all".


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Can anyone identify this microorganism?
I was examining some rainwater from my backyard in Richmond, VA, and found this microorganism. I took some pictures of it at 400x and 1000x (see below). The microorganism is attached to some moss and appears to be using it as an anchor while hunting/feeding. While feeding, it stretches out and searches for food, and once it catches something, it snaps back into itself. I also got some pictures of the microorganism while resting.

I'm not sure what this is and would appreciate any input. Thanks!

They seem to be rotifers, the fuzzy (supposedly rotating) mouthparts are part of what convinces me. The behavior you mentioned of latching on the moss with their 'tails' is also a characteristic behavior of rotifers. They are also able to retract their bodies just as you mentioned.
Here are some images of rotifers that might support the argument.

I am least certain about the last image but I am making the assumption for now that it is either some variety of circular/retracted rotifer or a completely different kind of microorganism.
Stay curios!

by a moment I thought you were Joe Hanson. LOL


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How much percent of image does our eyes focus at any instant?
I learned in highschool that even thought we have a wide view, we only observe a tiny fraction of that view through our eyes. So at any instant we are not really looking at all the objects infront of us, this is why we need to individually focus at each object at a time.
Question: What is the % of view that is in focus at any instant of time compared to the full view we observe thorough our eyes?

What you learned in high school isn't exactly true (or is misremembered). Human eyes get visual input across about 120 degrees of visual angle, and some herbivore mammals see near 360 degrees total between their two eyes.
However, the resolution is not constant. The fovea is an area of high-density receptors in the retina. When you look at something specific, you are directing light from that area of the visual field to the fovea. The fovea is limited to about 2 degrees of visual angle.
Additionally, your attention is often limited to a small section of the visual field. When viewing a scene, your eyes will naturally make saccades to bring various points into high acuity vision to get a good sense of the entire scene, but you are still seeing all the surrounding area, even if you aren't paying much attention to it. Importantly, you are still sensitive to surprising stimuli (especially those that are high-contrast or moving) in those areas that might cause you to redirect your attention, otherwise you would be very easy to sneak up on.

yes its the 2 degrees of visual angle that i remember now. So still a small fraction around 1/60th area of the whole view is in focus at any one time. You mentioned that the "attention" is limited to small section of visual field, can we say that its limited to 1/60th of the visual field? So to say some entity is in attention is in the fovea as we are focusing on it?

@gfdsal It's roughly spherical so more like 2^2/120^2. For attention it's a bit complicated and there are no sharp boundaries, but you could say it's on a similar spatial scale.

note the rest of the eye is still used but it is more to detect change (usually movement) , once something changes your attention and focus move to that point. you focus is constantly moving around to what you think is important, so although you only get a god image of about 2% your brain can reconstruct a much larger image.

To be precise, I think the answer (and the question) are mixing focus and resolution. For example, a myopic eye wouldn't focus the image, regardless of the fovea resolution. Focus would depend on the quality of the lens, not the sensor.

@jinawee Did you notice I didn't use the word focus at all? OP used that word, but it is clear from context that they are referring to the target of gaze (which is also what a properly working eye focuses on), rather than the specific processes that go on in focusing.


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Why don't the female lions in a pride help their male lion to protect their children from other males?
I watched a dozen of videos taping the fights between male lions; none of them involve female lions assisting in the fight. It is also known that the male lion who take-over the pride will kill all the under-age lions.
Why don't the female lions help their male lion such that their offspring won't be eliminated?
From an evolutionary perspective, the female lions will surely fight for their children as raising a new child is costly. Though they will most likely not fight to death. Even if a lioness does not have any child yet, her older sisters might already have a child so help defending the entire pride is the optimal strategy. In this case, the younger sister might only contribute half of their strength comparing the older sister, as the child is only her nephew and not her direct offspring.

if they don't fight they just have offspring with the new proven more successful male instead of propping up a weak male. lets the males fight and take the winner.

@John Good point!

Alright, after watching a few more documentaries, here is what I found:
Lionesses do try to expel nomadic males, even if the male lion is not in presence.  On the other hand, I am still yet to find a single video taping the male and females collaborating to expel the invading lions.
When invading a pride's territory, the nomadic brothers will usually not attack first, even if there is only one "lion-king" in the pride. The nomadic brothers might think that the females will help the lion-king to protect the territory; otherwise the brothers will just simply attack as it is a 2 to 1 odd.
The nomadic brothers will usually disrupt the pride's food-supply first. As the pride usually have many cubs to feed, it consumes much more food than the nomadic brothers, and the lion-king is then forced to launch his attack first.
The fight between male lions are usually not lethal possibly due to male lions' body structure. Most of time the nomadic brothers are expelled, but sometimes the lion-king is wounded or expelled from his own territory.
After being wounded, the lion-king cannot protect his cubs. The nomadic brothers then start to find and kill the cubs. The females do sometimes try to protect their cubs, but their attacks can only lightly wound the male lions as males are well-protected by their hairs. In contrary, the males can one-hit the youngsters.
Cubs close to 2-year-old do try to run away and the females do sometimes help them by providing them food, even if the females seem to be obedient to the new dominating males. In this video the lioness even decide to run away from the original territory to raise-up her children and half-children: https://www.youtube.com/watch?v=eMgPf83uDec.
After all cubs are killed or expelled, the females lose the motivation to fight against the invaders, and the new pride is formed.

Interesting summary! What do you mean with 2 to 1 odd?

@KaPy3141 For example, the invading nomadic brothers are two male lions, while the defending pride only has one adult male lion. Even if it is a 2:1 odd, the invader will not directly attack the pride.

Oh I get it, thanks!

This looks like it could become a good answer, but answers are expected to include supporting references (primary literature is best) — links to videos are not sufficient (and are also unstable). Without that support, your answer is indistinguishable from opinion and thus inappropriate for this site. This is a good example of how to format references. ——— Please take the [tour] and consult the [help] pages for additional advice on [answer] and [ask] effectively on this site.

Usurpers and attackers would be useful vocab here. I didn't understand WHY the lionesses don't affront the challengers. just the outline of what they do.

" The male lions as males are well-protected by their hairs." I think that's the key information here, presumably the females are scared of the males because of their size and added protection. It's a good question, I hope someone can theorize why 2v1 fights are preferred over 2v7 to protect cubs. perhaps 2v7 encirclement can result in fights to the death because the adult females die, and 1 adult female is more valuable than a cub to the population.

@LifeInTheTrees Dear Trees, I agree with your terminologies. I directly copied and pasted the terminologies from those famous documentaries.

The prides mostly comprise at least 10 individuals, up to 40 and 1-3 alpha males. The average pride, both in Kruger NP and the Serengeti, consists of 13 members. In Kruger, the average composition of 14 prides totalling 181 lions was 1.7 adult males, 4.5 adult females, 3.8 sub-adults, and 2.8 cubs (including yearlings).
In larger prides, it is rare for the whole pride to be together, but individuals or small groups, typically of three-five members will scatter throughout the pride’s territory for days or weeks at a time, especially in dry environments or times where the number of prey are in small supply.
The mortality rate for the mature males is about 4/1 when they wander in between territories, and when they mount a challenge, it's often as a group of three or four bruising males.
There can be fights of a 270kilo alpha vs 2-3 challengers of 200-250kg, and the question suggests "shouldn't 2vs7 and 3vs8 lion fights happen? to protect the cubs?", including 100-150 kilo females. The females have a very vulnerable neck so a 7v3 serious fight could easily end in the death of 2-3 lions, weak hunts and hunger. That is why they are probably scared to mount a defense.
Animals tend to avoid potentially mortal fights, and the territorial fights are too life-threatening and vicious for the females to risk getting involved in. Prides usually have two alpha males so the strategy of challenges is very dynamic. It's best to find someone who has read a book about social organization of lions.

I’m watching one right now on Disney plus and I was literally wondering the same thing as you until it showed that two out of a pack of 5 male lions initiated a fight and to protect her daughter she charged and fought one of them which inspired the other females and they all started to fight. They don’t show much of the other lion fighting thr prides male but I can assume they did.

I've seen a video or two where the lioness will fight a male to protect the cubs.
And another thing, when a nomadic male or males take over a pride by force, it isn't considered a new pride being formed, it's actual meaning is the pride have new resident males.
Remember a pride is a pride without any males being part of it. Prides are so,
consisting of females only, the males that are there are residents of any said pride. So a pride of lions is so without a male unless they are male cubs of the lionesses within a pride.

And another thing, you all can watch every video ever made but until you go out into the bush and spend 35+ years observing Lions your answers are just guesses


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Role of epigenetics in evolution and transmission of defects caused by drugs
In a documentary, they were saying that epigenetics changes caused by the environment in an individual can be transferred to the following generations. I have some questions on that:

How many generations are affected by an epigenetic change? can this be permanent?

Can drugs cause epigenetics changes in the current population that are visible in the following generations in the form of disease and birth defects?

Do epigenetic play any role in evolution? For example, is it possible that an epigenetic change becomes a permanent genetic change after a certain number of generations?

You may not be aware that you have stepped into a minefield. The term epigenetics has been subject to considerable hype (I would be interested to know what documentary you watched and what precisely was claimed), phenomena in insects extrapolated to humans, and association confused with causation. In order to separate fact from fiction here, one needs to be able to understand the basic science. Do you have the background to understand this article, for example.

Generally speaking, epigenetic modifications are not inherited as they are reset during embryogenesis. However, subsequent epigenetic modifications can be acquired during the period of pregnancy, which as a mechanism depends on the epigenetic state before the reset and on the physiological conditions of the mother including nutrition, health, stress, etc.. Obviously drug-intake years before pregnancy can still affect the mothers health-state.
Answering your first question: Epigenetic modifications generally cannot be directly passed, but indirect effects could theoretically pass through multiple generations without hard limit.

A major barrier to transgenerational epigenetic inheritance is germline reprogramming, during which histone variants and their modifications, as well as small RNAs and DNA methylation, are all reset. In mammals reprogramming occurs both in the germline and in the zygote immediately after fertilization. (Source: Heard & Martienssen 2014 doi: 10.1016/j.cell.2014.02.045)

2: The great potato famine is said to still have epigenetic effects, generations later. 3.: Epigenetic changes cannot directly "become permanent" as genetic changes, although hypothetically speaking, epigenetic states can lead to viability of certain mutations that would otherwise be lethal and can therefore in theory influence evolution.

"Epigenetic modifications cannot be directly passed" seems to be a bit of a controversial statement, as far as I know (as is the converse, that they can be directly passed), especially for humans. If you want to make that claim, it needs a reputable citation to back it up.

I agree, I added a source. Sorry! What I meant is that modifications are at first removed but then partly could be restored later. So it's not "direct". Given question 3 implies that the OP is no biologist, I didn't want to unnecessarily complicate things.

I think it would be helpful to be more specific about what "epigenetic modifications/changes" are. People tend to fixate on methylation/histones, but there are perfectly good epigenetic circuits set up that are based only on transcription factors/protein components. The heritability of the different kinds, that's a different question.

Much better. Thanks! The word "generally" adds a lot, too. I've made some edits to include the author names and made the DOI a link.

Epigenetic changes can only be passed directly onto the next generation when they occur in the cells that proliferate into the gametic cells (ovum and sperm cells).
There is some research with rat models that show the inheritance of epigenetic changes over several generations, so it´s possible.
(an example for cocaine-addiction: https://www.nature.com/articles/nn.3280)
The main protein family that participate in epigenetic regulation are the histone deacetylases (HDACs) and the histone acetyltransferases (HATs), which can modify proteins that bind to the DNA and thus control the expression and activity of genes, and these proteins can be influenced by environmental changes.
(Several types of cancer are thought to be caused/affected by the activity of HDACs that shut down tumor suppressor genes, and there are many medical studies focusing on chemotherapeutically inhibiting their function in cancer patients.)
This paper can give you a good overview: https://pubmed.ncbi.nlm.nih.gov/11420732/

Question 1: how many generations.
In one of the first description of transgenerational epigenetic inheritance, before any of the mechanisms were worked out, Woltereck found (my translation, caveat emptor) that he could find influences on both children and grandchildren of starvation in Daphnia (Figure 1).

Figure 1. Daphnia head morphology response to starvation. Left: control animal (fed normally, parents and grandparents fed normally). Right: successive generations of descendants of starved animals. 1. Gen: child, 2. Gen: grandchild, 3. Gen: great-grandchild.
How common such epigenetic changes are is a huge subject of debate. Nutrition appears to be the big one- see also the Barker hypothesis in humans, especially in re: the Dutch Hunger Winter.
Question 2: don't know.
Question 3:
It's a thorny question! Woltereck and similar people were already arguing about whether these observations might be evidence for Lamarckian inheritance, e.g. inheritance of acquired characteristics. We've pretty much gotten rid of Lamarckian inheritance in favor of vanilla Darwinian inheritance via DNA, but people still argue about it, as e.g. here.


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What types of cells HPV can infect?
I am wondering if there is any new information on which cells HPV is able to infect. Is it still limited  to squamous cells or are there other cells such as columnar cells it is able to infect?


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Are self pollinated plants genetically different?
Gametes in pollen grain are formed during meiosis in the anther. And meiosis produces genetically different gametes. When the pollens grains are carried to the stigma to fertilise the egg cell of the different/same flower from the same plant, doesn't it produce genetically different flowers even though it is self pollinating because of the variation in gametes?

Yes, it does.
In Meiosis there is genetic recombination (by recombinase) in the Meiosis-1. So even though it is self pollination, there is significant genetic variation.
Still for higher degree of variation cross pollination is exhibited.
It should be noted that cross pollination has greater evolutionary significance.
Few plants exhibit self-incompatibility to supress self pollination (in monoecious flowers/plants).


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What is the animal in Nosferatu movie?
I was watching Nosferatu, and this dog-like animal appeared, with very curious stripes. I was wondering if this is clearly a specific animal, and which one it is, or if it's too mixed up and low resolution to tell. You can see in this video, at 11:43 and 12:22 (close up) to 12:33.
https://www.youtube.com/watch?v=PH7L4V-3VxA&t=703
Sorry about my lack of a more scientific research, but I couldn't be farther from being a biologist. This is all I got: from the stripes, it immediately brought to my mind a Thylacine (which is what caught my attention), but even though it would not me an anacronism (it was extinct in 1936, the movie is from 1922), the movie is European (filmed in Germany, Slovakia and Romenia) and the story happens in Europe too, so it wouldn't make sense to be a Thylacine (not to mention that in 1922, you wouldn't find them right around the corner ;) ). Further investigation confirmed the already almost obvious, the stripes are too in the front in their body to be a Thylacine. My second thought, from the apparent big head and the way it moves (hips lowered), it resembled a hyena to me. But it doesn't seem to have ears big enough, they also wouldn't make sense in context of the movie, and hyenas usually have spots instead of stripes. A quick search showed me that there are striped hyenas, and from pictures it looks kind of similar, but the snout doesn't seem to match. Also, they don't occur in Europe, according to Wikipedia.
So at this point I'm in doubt if it's a striped hyena (that doesn't seem to make sense to me), another real animal that I don't know, or if it's a fictional creature, some animal "modified" specifically for the movie (painted, extra/less fur, artificial modifications in height, body size, ear size, etc). Although that also doesn't make sense.
Any pointers appreciated, sorry if this should belong in scifi or another SE.

It looks like a natural Hyena to me. But you can look into the possibility of "Wild dogs".

definitely a hyena. MSB they could have footage from other movies or even zoos, recycling footage is a age old practice. Notice it is never seen with anything else in the same shot. likely B-roll. Just look at the second shot where it stands up in profile, very easy to identify.

@John Early vampire movies are famous for misplaced wildlife. The 1931 Dracula movie famously depicted a wild armadillo in Transylvania.

It's a striped hyena, it is relatively rare/endangered these days. Hyenas are closer to cats/felines than to dogs. They are in the suborder Feliformia.
https://en.wikipedia.org/wiki/Striped_hyena
some images here

Did they occur in Europe in the past?

The range used to be at least up to lebanon and Georgia/Armena, So there's chances that they were in western europe a few thousand years ago. Elephants used to live in egypt, north africa and turkey only until roman times too.

there was a cave hyena in europe until about 8000 years ago.


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PDB id to protein environment ph
How can one find the information of a protein environment ph from its PDB id?
Can one assume the ph to be the same as its cellular location?

I know that ENSEMBL, PDB and the Human Atlas give known locations for many proteins at different levels of certainty, but such data is far from complete. Also experimental indication of a proteins localization does not prove the absence at other locations. Dependent on your scientific questions it might still be valid to theoretically look into specific scenarios of a proteins localization and to assume a certain pH of that sub-cellular context. SO to answer your question: Higher pH-resolution than the hypothesized cellular sub-localization is unrealistic, and the justification of the assumption of localization depends on your specific plan.

So can one assume that a protein https://www.uniprot.org/uniprot/O96693 located in the apicoplast will function at that ph (the one of the apicoplast)?

I am not saying that it is correct to make that assumption, but that high-resolution pH estimates seem unrealistic to me, as you clearly don't have enough information, as you wouldn't ask the question if you did. For me your assumption of taking the pH of the known compartment seems to be the least problematic one, out of all options. Only you can make that call in the end.


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Clarification for the anatomical terminology of the cerebellum
I've been trying to find descriptions for some of the fissures found on the inferior surface of the cerebellum, and so far the only source I've been able to find that provides an adequate description is Gray's anatomy (1918, 20th edition):

The prepyramidal fissure crosses the vermis between the uvula in front and the pyramid behind, then curves forward between the tonsil and the biventral lobe, to join the postnodular fissure.
The postpyramidal fissure passes across the vermis between the pyramid and the tuber vermis, and, in the hemispheres, courses behind the tonsil and biventral lobules, and then along the lateral border of the
biventral lobule to the postnodular sulcus; in the hemisphere it forms the anterior boundary of the inferior semilunar lobule.

So, that would make these fissures the following ones:

(the blue one being the postpyramidal fissure, and the red one being the prepyramidal fissure)
However, I checked a few atlases:

(here, 2 and 2' are the postpyramidal fissure and 4 is the prepyramidal fissure)
And on radiologykey, the descriptions it gives for these fissures is the following:

The postpyramidal (secondary) fissure separates the pyramis/biventral lobule above from the uvula/tonsils below
the prepyramidal fissure separates the tuber above from the pyramis below.

It seems like Gray's anatomy has the names swapped or something, is that the case? If so, that means I can still use these descriptions but just swap the names.
And is the secondary fissure the same as the retrotonsilar fissure/postpyramidal fissure?


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Mammary gland development and lactation
I was reading on mammary gland development, and I found this (1):

As a girl approaches her teen years, the first visible signs of breast development begin. When the ovaries start to produce and release (secrete) estrogen, fat in the connective tissue starts to collect. This causes the breasts to enlarge. The duct system also starts to grow.

Wikipedia has an article about the duct system(2):

The development of the mammary gland occurs mainly after birth. During puberty, tubule formation is coupled with branching morphogenesis which establishes the basic arboreal network of ducts emanating from the nipple.

It goes on to say, developmentally, mammary gland epithelium is constantly produced and maintained by rare epithelial cells.

By the pubertal stage, the mammary ducts have invaded to the end of the mammary fat pad. At this point, the terminal end buds become less proliferative and decrease in size. Side branches form from the primary ducts and begin to fill the mammary fat pad.

In the end, I understood that the mammary alveoli (containing milk) are not formed during this. During pregnancy, the ductal systems undergo rapid proliferation and form alveolar structures within the branches to be used for milk production.
And from where is the milk produced? (Just for some more detail)

After delivery, lactation occurs within the mammary gland; lactation involves the secretion of milk by the luminal cells in the alveoli. Contraction of the myoepithelial cells surrounding the alveoli will cause the milk to be ejected through the ducts and into the nipple for the nursing infant.

Three questions:
An interesting case is one of neonatal milk.(3)

It is thought to be caused by a combination of the effects of maternal hormones before birth, prolactin, and growth hormone passed through breastfeeding and the postnatal pituitary and thyroid hormone surge in the infant.

The article doesn't mention anything about developement of mammary alveoli, though. How does that happen, then?

I know milk formation primary requires prolactin, oxytocin and indirectly, estrogen.(4) So does this process wait till pregnancy?(If yes, then the lobes and branches are devoid of any lumen, and they remain empty until pregnancy, which seems skeptical to me.)

Can lactation occur without alveoli formation?

1-
www.hopkinsmedicine.org/health/conditions-and-diseases/normal-breast-development-and-changes%3famp=true
2- https://en.m.wikipedia.org/wiki/Mammary_gland
3- https://en.m.wikipedia.org/wiki/Witch%27s_milk#:~:text=Breast%20milk%20production%20occurs%20in,not%20by%20prematurely%20born%20infants.
4- https://www.ncbi.nlm.nih.gov/books/NBK148970/#:~:text=Hormonal%20control%20of%20milk%20production,indirectly%20in%20lactation%20(2).

You take a long time to ask your questions, and should really restrict yourself to one. But am I to understand that all three relate specifically to the phenomenon of lactation in the neonate and what you want to know about the cells responsible for this? Or are you asking also about the general development and role of alveoli in the pregnant female?

I sure do, but I want the question to reflect what I understand as well- that takes time to write. The questions were related, so I clubbed them and added a bounty; I'll make sure to not repeat this, thanks. Only the first question relates to the neonate.

There is a comprehensive 2012 review of the development of the mammary gland by Macias and Hinck which covers the poster’s question(s). I shall try to summarize the points they make regarding the development of alveoli and their role in milk secretion, ‘borrowing’ two of their illustrations to do so.
Development of mammary gland and role of hormones

At birth there is a rudimentary system consisting of a few rudimentary ductal system.

Until puberty this system grows along with the rest of the organism, under the same hormonal influences that affect other tissues.

At puberty oestrogen — in concert with growth hormone and insulin-like growth factor — accelerates the growth of this ductal system, and its branching is subsequently stimulated by progesterone.

It is only in pregnancy that alveoli form, with a continued requirement for progesterone (perhaps partially indirect) and a specific requirement for a prolactin — which is secreted both from pituitary and — as a different molecule, placental lactogen — from the placenta. The alveoli express the genes for the synthesis of specific milk proteins such as casein, α-lactalbumin and β-lactoglobulin.

[Lactating Mammary Gland: Alveolar cells shown in pink (nuclei blue and milk droplets white) with surrounding adipose tissue yellow]
Oxytocin does not affect the development of the mammary gland (as is made clear in the reference cited by the poster). After parturition it is released from the pituitary in response to the nervous stimulus of suckling and causes the myoepithelial cells around the alveoli to contract causing ejection of the milk.
It should be mentioned that the alveolar cells apoptose on weaning, being replaced by adipocytes. However new alveolar can develop from undifferentiated epithelial cells during a subsequent pregnancy.
Regarding the poster’s specific questions
Q1 The article doesn’t mention anything about development of mammary alveoli, though. How does that happen, then?
A1 The development of the mammary alveoli occurs during pregnancy, under the influence of prolactin/placental lactogen and progesterone.
Q2 I know milk formation primary requires prolactin, oxytocin and indirectly, oestrogen.(4) So does this process wait till pregnancy?(If yes, then the lobes and branches are devoid of any lumen, and they remain empty until pregnancy, which seems skeptical to me.)
A2 The poster’s statements are not completely accurate. Milk formation does not require oestrogen, and oxytocin only affects it in so far as failure to remove milk causes involution. The ducts are indeed devoid of the alveolar lumen until pregnancy, and return to this state on weaning. It is not clear why you are sceptical that this is so. The mammary gland development after puberty prepares the ductal network, but alveolar cells only arise when they are required. Pregnancy is quite long enough for them to develop.
Q3 Can lactation occur without alveoli formation?
A3 I would think not, although the situation regarding neonatal milk secretion (witch’s milk) is unclear because of the obvious ethical barriers to its study in humans. The increase in breast nodule size is suggestive of development. So my opinion is primarily based on argument. The formation of milk requires cells with a specific pattern of gene expression, i.e. of milk proteins and metabolic enzymes that are required for fat formation. It also needs a structure and organization that allows the milk to be secreted into a duct. That is what an alveolus is. Therefore I would imagine that in these circumstances the rudimentary mammary ducts of a new-born infant develop alveoli under maternal hormonal influence.
Postscript
This is a topic I worked on for my doctorate, but have not had contact with for many, many years. It was interesting reading the review — how the technology has changed! I also find it curious that the review makes no mention of corticosterone, as one of the earliest systems for observing alveolar development in vitro was in explants of mammary gland from pregnant mice cultured in defined medium with insulin, prolactin and corticosterone. Perhaps the corticosterone was mimicking what is now known to be the effect of progesterone in vivo.


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Insect crawling Identification

What kind of insect is this, and is this venomous, or dangerous? Don't need full species name just common name will do, color is red. Grandma always warned me of this, they usually are seen in monsoon season during heavy rains. They coil upwhen disturb .
Location: Country: India, lower himalayas
Google Map :Exact location
A miniature version of this also exist in my area don't have pic though.

Given the shape and the number of legs. That most definitely is not an insect. An insect has exactly 6 legs. No more, no less.
That critter in your picture is some kind of millipede (“a thousand feet”; not literally a thousand, of course; https://en.m.wikipedia.org/wiki/Millipede), not to be confused with a centipede (“a hundred feet”; also not literally a hundred).
Millepedes are mostly harmless to humans. They eat things like dead plant matter or fungi. They sometimes also eat seedlings so they can be considered pests in gardens.
And given the colour, that’s possibly a rusty millipede (https://en.m.wikipedia.org/wiki/Trigoniulus_corallinus). They have a very wide distribution around the Indo-Malayan region. Although there seems to be no recorded observation of it on iNaturalist around your region (https://www.inaturalist.org/observations?place_id=9248&taxon_id=123010).


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Is this a deathstalker?
I caught a scorpion in my house and wondering if it is a deathstalker? This was caught in Central Asia Northern Tajikistan.

No, it is not a "Deathstalker". The members of the Genus Leiurus are what are commonly referred to as the "Deathstalkers". I do not like using vernacular or common names as they can be too broad in iverlap for multiple species and so to avoid confusion and for clarity utilize Genus and where can be determined species and subspecies. The scorpion you found appears to be a member of the Genus Mesobuthus. While superficially similiar to Leiurus sp., the pedipalps in Mesobuthus are shorter and more bulbous...among several other features.
In 2018 there was a good paper on Mesobuthids in that region. A quick google scholar search should provide you sites for the paper to be viewed at.

Revision of the Mesobuthus caucasicus Complex from Central Asia, with Descriptions of Six New Species (Scorpiones: Buthidae)

I am not that familiar with types or some terminologies you specified in your answer. Is it a deathstalker?

@Dilshod No.  Deathstalkers are members of the Leiurus genus (as RCampbell says), which is a different genus from Mesobuthus

Dilshod, sorry for any confusion. I shy away from use of common names as many times they are apied to multiple species or multiple Genera. I posted with the Genus of the scorpion you found so you could further investigate avenues of identification for Mesobuthids of your region.

@RCampbell, your answer would be improved by editing the question to include the useful information in these comments.  @Punintended seems to provide a good direct answer, so maybe add something like thisNo. Deathstalkers are members of the Leiurus genus. I shy away from using common names as many times they are applied to multiple species or multiple Genera.


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

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

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

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

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


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Can someone help to identify this insect?
I found a few of these insects around my house, and I'm curious what insect it is.

Seen mid-August in Singapore
At least several mm but lest than 1 cm long
Seen walking slowly. I can't be sure but don't think it can fly
No sound noticed

For species identification questions it's necessary to include as much information as you can. Can you mention at least roughly your location on Earth? Also, can you estimate the approximate size of this insect? 1mm? 1 cm? What about behavior; was it flying, or walking, moving quickly or slowly? Did it make any noise? Thanks!

Singapore, less than 1cm, walking slowly, dont think it can fly, no noise. Appreciate your help thank you


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Term for a prey animal's recognition that something potentially threatening is looking at it?
On my daily walks I frequently see individual or small groups of cattle egrets. At first I would try to photograph them but they would fly away. This vexed me because they ignored everyone else walking by as well as bicycles or loud vehicles in areas where there were roads.
I took it personally until I realized it wasn't me or my clothes, but the act of looking at them and taking an interest in them that spooked them.
This even happened at distances approaching 100 meters in open spaces, so I am not sure they could resolve my eyes and determine if my gaze was fixed on them. However, a few non-scientific tests suggested that they seemed to get nervous when I turned my head and looked at them, even though I kept moving. But even if I didn't look at them but instead continued to look forward, simply stopping and standing in place to take out my phone to snap a photo was enough to trigger them to fly away.
Question: Is there a term for this phenomenon in birds or other animals, not the flying away or fleeing part, but the recognition that something or someone potentially threatening is looking at them and/or may have taken an interest in them? Are there separate terms for responses to motion and responses to a gaze based on eyes or perceived face orientation?
Note: I have noticed a similar phenomenon with Malayan Night Herons as shown in What kind of big bird is this seen walking around Taipei? The individuals I see are more acclimated to people, but I still have to act at least disinterested when photographing them.

I have heard this from a professional bird photographer. As I remember she only looked at birds through the camera viewfinder  when ever feasible.

I have noted this phenomenon as well, exactly as you describe, with the Great Blue Herons in my area (and, notably, only with them.) It seems to derive from a combination of variation in gate and gaze, as the herons are perfectly content to ignore me standing or walking or running, but go into an alert posture whenever I alter speed or turn to look at them. However, a steady gaze does not perturb them, even at close range. As you say, acting indifferent is key, but this can be done, with practice, with one's face in any orientation.

@kheironiscus Thanks for your feedback! Based on this I'll do some more "experimentation".

"Gaze" is the typical term for the direction something is looking, including head/neck and eye position. Gaze detection, gaze following, and gaze perception are used in the literature; there might be other combinations with the term "gaze", as well, I see lots of results with a more general gaze+predator search.
These are all more general terms than the specific use by prey animals, particularly in social gaze: being able to figure out what others around you are looking at, but they are to some extent the same sort of ability.

This is exactly the kind of help I'm looking for, and now I can do further reading. Thanks!


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What type of factor is practice of motor skills?
I recently asked a question about the cause of motor laterality: What causes motor laterality/ side dominance?
I understand that there can be genetic factors, epigenetic factors, or environmental factors. But in terms of continuous practice of motor skills, what type of factor will that be? Physical factors? Thank you!

Hopefully someone will post an answer to your linked question as well!

@uhoh Hope so! So far I've only been conversing in the comments, as you've probably seen.  •-•


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Can someone help me identify this Ficus plant?
I have a bonsai with me which I grew from a seedling germinated in my backyard. It's been with me for the last 5-6 years. I definitely know its a Ficus, but I am not able to identify which species it belongs to. I have provided pictures of the specimen below:

I need to know if its F.virens (white fig) or F.ingens (Red leaf ficus). This specimen is from Kerala, INDIA.

There are up to 900 different species within the Ficus genus... you might want to add in some more detail e.g. location, measurements, the shape of different sections of the plants (which can be done by taking more photos of different parts through different perspectives). Also, keep in mind that, without genetic testing, it may be difficult for most people to identify which exact species this is with the absolute certainty.

This is a Ficus Bonsai, size and shape wont be natural. However its from Kerala India


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How do the biophysics of how cerebrospinal fluid mechanically protects the brain work?
The two mechanisms I've seen mentioned are the cerebrospinal fluid (CSF) acting as a hydraulic cushion or shock absorber, and how CSF creates a micro-gravity environment through buoyancy.
I have very little understanding of the former, but I do have a vague idea about the latter: since the brain is submerged in a fluid (the densities of the brain and CSF are also similar I think), it experiences a buoyant force upwards that counteracts the force of gravity on the brain, therefore decreasing its "effective weight" from around 1400g to about 50g. How does this help precisely? The explanation I've seen that I could understand is that it makes it so that the brain isn't pressed up against the base of the skull due to gravity, and so that it doesn't get deformed under its own weight. This buoyancy also helps the various structures attached to the brain, like nerve roots and blood vessels, hold it up and support it. Wikipedia also says that it allows the brain to maintain its density without being impaired by its own weight, which would cut off blood supply and kill neurons in the lower sections without CSF. This explanation is plausible but I'm not sure if it's the entire story.
There's also this bit from "Neuroscience in Medicine" that says the decrease in effective weight decreases injury by reducing brain momentum in response to stresses/strains inflicted on the head. How does that work? I'm not super familiar with the physics of buoyancy, I just know the basics. I don't understand how it reduces momentum during movement.
I couldn't find anything that went into the physics of the whole hydraulic cushion thing, so an explanation for that would be great.

This is a cool question! Here's another way to understand the "momentum" part: A function of CSF that comes from its physical properties as fluid is to protect the brain from the damage that would result from a sudden movement of the skull. Any rapid acceleration/deceleration of the head has the potential to injure the delicate contents contained within.
The CSF helps reduce the potential damage in such an event by acting as a cushion and a shock absorber.(https://www.ncbi.nlm.nih.gov/books/NBK470578/)

@Bipasha thanks! So essentially, “reducing momentum” is more or less the just saying the same thing as “it acts as a hydraulic cushion”. That makes things simpler.


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Does the harvesting time of broccoli sprouts change their glucoraphanin content and sulforaphane formation capacity?
Does anybody know if the harvesting time affects glucoraphanin content and sulforaphane formation of broccoli sprouts? Do they also get affected by light exposure or lack of it?

Welcome to SE biology. This review looks like it has information on at least the light exposure aspect of your question - it might be worth checking it out https://bit.ly/3gkoqPZ

Thank you for the article. In case, someone else is also interested in this topic, here is the link https://orgprints.org/11395/1/11395.pdf to another study in which researchers compared glucosinolate profiles of different B. oleracea sprouts. To my surprise, the researchers found that red cabbage sprouts contained about twice as must glucoraphanin as broccoli sprouts.


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Beetle Identification / able to retract its head

I can't find any identification of this beetle online. The closest guess I got to it is "Hister beetle" but the rough surfaces on its shell make me think otherwise.
The most common behavior is that when feeling threatened, it plays dead for some time. It retract its head, and then covers it with its 2 front limbs, which make it look like a piece of wood or a tree seed.
Here's a video showing its movement
https://www.youtube.com/watch?v=cSjQ_8vbYw4
Philippines, Southeast Asia.
under tropical savanna climate

Welcome to Biology.SE! For identification questions please [edit] your post to include the location (e.g. country and region — the more specific the better) where you observed this creature. The location can be an essential clue for identifications. ——— If possible clear, closeup photos of the creature from multiple angles would also be helpful. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Edit: Based on Arthur J Frost's comment, Trox Beetles more likely resemble it in movement and behavior. So it's probably more like a member of Trogidae beetle family.

Um, no.  I'm not completely sure, but the Scarab family Trogidae (the Skin Beetles) looks more likely to me (see here for photos of some North American species; the family is worldwide).

You're right. I saw some videos about it on youtube which greatly resemble the movement, including the behavior of playing dead, retracting its head(not sure if it's the right term) and covering it with their front limbs. Though this is probably just one of the types under it, since one video shows it's able to produce sound when playing dead, but this one is not.


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Identification of a lifeform
There's a video I found on Facebook and I'm unable to figure out what the creature featured happens to be.
Adding images that have been taken from the video itself, apologies in advance since they're not high qualify images.

Can anybody shed any light on what it is?
The video was shot near Ratan Babu Ghat which is situated along the bank of Hooghly river, Kolkata, West Bengal, India. Here to be precise.

This is a polyclad flatworm.

Here is a video of notoplana vitrea moving similarly to the one in the video that you linked:
https://www.asturnatura.com/especie/notoplana-vitrea.html
Here is a gallery of polyclad flatworms observed in India:
https://inaturalist.ca/observations?place_id=6681&subview=grid&taxon_id=52318
A number of the images in this gallery look similar to the one in your video, but very few of them are identified beyond this order taxon of polyclad flatworm.