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Is there a program that demonstrates overall fitness will increase in a population overtime?
Of course this will not always be the case with environmental factors, but generally speaking. I'm searching for a program that shows evolution works from a statistical standpoint.

Which theory of evolution requires fitness to increase in populations over time to "work"?

Look into Richard Lenski's long-term experimental evolution work. In addition to more than 60,000 generations of E. coli evolution with numerous fitness published fitness studies, he has published some work trying to study evolution in "digital organisms."

One can readily design such an evolutionary simulation. There are many such programs, many of them designed for educational purposes. Others are used to explore the theoretical effect of varying certain parameters including formalized environmental factors. Is that what you mean?

Yes. Fisher wrote on this (hypersphere). Then it was improved by Kimura. Now, as the other commenters mention, there are modern much better ways of simulating this.


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How do we know genes that are considered endogenous retroviruses are actually endogenous retroviruses and not just ordinary genes?
What makes these genes different as to be classed as an endogenous retrovirus? I've read the entirity of Wikipedia on retroviruses and didn't find the answer. I think it could be that these genes are identical to some viruses making the conclusion appear sound. But I'm not sure. If this is the case is there any other ways to conclude a gene is an endogenous retrovirus?

That’s a good question. However on this list you need to tell us what research you have done already to try to find the answer. You should also tell us what possibilities you have come up with yourself after thinking about the problem. You can check out the form here in the Help on asking good questions.

The APMIS article link I provided in my answer to your earlier question (https://biology.stackexchange.com/questions/101276/what-book-teaches-you-about-endogenous-retroviruses) answers your question, either directly or in its references (e.g. refs 2 and 3). In particular "HERVs have been historically classified within several different groups, formerly designated as families, based mainly on sequence similarity and other structural features"

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Could you identify the species of this animal attaching to a fish in the Aegean Sea?
While wading within a few meters from the shoreline today, I observed and was observed by a number of curious fish. One of them had a blackish attachment, which was reminiscent of a small aquarium catfish, probably because of its size and because its colour was not homogeneously black and appeared to have dense brownish spots. But it had no apparent thin parts like fins or tail and was quite plump overall. For this reason, I do not believe that it could be remora or lamprey, but could it be a marine leech? It was probably less than an inch long and one third of that wide. Could you identify what species could it be considering that it was in Toronean Gulf to the south of Kallithea village? I attach a collage of somewhat blurred photos captured through the surface of the water.

Update: I've seen three more examples today in the same spot. No pictures this time. The host fish species was the same. The parasite looked the same. The rear part of it is narrower and thinner than the rest of its body and the rear edge is uneven in comparison to the rest of its contour. In three cases out of four, it was attached to the same place at the right side of the fish. In one case, it was attached to the same place but on the left side of the fish.

Given the rough shape I lean towards an ectoparasitic isopod. I have no idea which one of the roughly 2700 species it might be, but I would guess from a quick search that it probably belongs to the families Cymothoidae or Gnathiidae as these seem to be the more common and well described (at least they have more complete Wikipedia entries, wheras the other families don't).

Looking at the parasitic isopods which were reported in Aegean Sea (per Kirkim F, Kocataş A, Katağan T, Sezgin M (2008)), I lean to Anilocra physodes because of its overall shape, dark colour without longwise stripes, attachment to the rear side of the fish ("Caudal peduncul" per Öktener A, Alaş A, Türker D (2018)). The fish looks like Lithognathus mormyrus, which is a common host for it.

Gnathiidae ("fish gnats") would be 1–3 mm (see Williams E, Bunkley-Williams L (2019)).

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Pedigree probability question - complete penetrance
The inheritance pattern of a common trait that shows complete penetrance is shown below:

What is the kind of inheritance? If III-1 is a carrier, what is the probability of IV-1 (from III-1 and III-2 marriage) showing the trait?
a) Y-linked; 0
b) Y-linked; 1/2
c) Autosomal; 1/8
d) Autosomal; 1/6
It cannot be Y-linked because then II-2 could not have transmitted it to her son. It can only be autosomal (recessive).
Since III-1 is a carrier (heterozygous, Aa):
i)If III-2 is also Aa, the kid will have a 1/4 probability of getting aa
ii)If III-2 is AA, the kid will have zero probability of getting aa
iii)If III-2 is aa(unlikely because it is not colored in the pedigree), the kid will have a 1/2 probability of getting aa.
I am unsure how 1/8 or 1/6 probability is calculated.

You have correctly identified that the trait is autosomal recessive.
Now for the probabilities. We know that:

II-1 is $Aa$ and
II-2 is $Aa$ (because they don't show the trait, but their son does),
III-1 is $Aa$ (because he is a carrier),
III-2 is either $Aa$ or $AA$ (because she doesn't show the trait).

IV-I will show the trait if it is recessive homozygote, $aa$. Because we are not sure about the genotype of III-2, we have two distinct scenarios:

III-1 is $Aa$ and III-2 is $AA$
III-2 is $Aa$ and III-2 is $Aa$

Let's first calculate the probability for each of the scenario. Here, we have to be careful not to fall into the trap by ignoring the conditional probability. The probability of III-2 being $Aa$ is not $1/2$ as we might wrongfully assume from simply drawing a Punnet square of their parents ($Aa \times Aa$). Because we know that III-2 doesn't show the trait, he cannot be $aa$. Therefore, we have to eliminate this possibility from the Punnet square, and we are left with the probabilities $1/3$ for her being $AA$ (scenario 1) and $2/3$ for being $Aa$ (scenario 2).
Scenario 1 (probability 1/3)
III-1 is $Aa$ and III-2 is $AA$.
Their child cannot show the trait.
Scenario 2 (probability 2/3)
III-1 is $Aa$ and III-2 is $Aa$.
Their child will show the trait with the probability $1/4$.
Conclusion
The probability of IV-1 showing the trait is now the product of probabilities for the scenario 2 to be true and the probability for their child to show the trait. Therefore,
$$\text{probability for IV-1 to be } aa = 2/3 \times 1/4 = 1/6.$$
As you see, not being careful about the conditional probability will lead you to the wrong result: $1/2\times1/4 = 1/8$.


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Is it possible for a plant extract to have different effects, depending on the type of cell line it was tested on?
My plant extract (ethyl acetate fraction) seems to have two different effects depending on the cell/cell line it's being tested on. On liver cancer cells (HepG2), it is moderately cytotoxic. But on lymphocytes and macrophages, it helps increase their proliferation. Is this really possible? What do you think is the possible explanation for this?
I've been trying to find studies that might have similar results as mine, but none so far. I found one study wherein their extract both exhibited anti-proliferative effects on both cancer cells and fibroblasts. However, the effect is much stronger on cancer cells.

"I found one study wherein their extract both exhibited anti-proliferative effects on both cancer cells and fibroblasts" - Could you please cite that article?

I couldn't find the study anymore (forgot to save it, I guess). But I found another one - similar results, wherein the extract had a lower level of toxicity against fibroblasts, compared to cancer cell lines: https://www.frontiersin.org/articles/10.3389/fphar.2017.00371/full

Cell lines can do wacky things
Have a look at Zhou, 2019, which discusses the genome of HepG2 cells.  These typically have 49 to 52 chromosomes... and many other interesting aberrations.  Awortwe, 2014 commented on the irreproducibility of drug-herb interaction studies in cell lines; they note Caco-2 cells could vary 100-fold in their ability to transport mannitol.  Cell lines are frequently subject to genetic instability associated with their immortalization from a tumor, followed by in vitro evolution that changes their behavior.  (Fusenig, 2017)  The old traditional cell lines are useful in some contexts - if you would like to find a protein that binds something you are interested in, for example - but they can't be counted on to react in a human way.

Thanks for the references. I would think the cell lines are useful for preliminary studies, like screening of plant extracts. I do primary cultures, I get murine macrophages and lymphocytes, since I want to screen for potential immunostimulants. My colleagues test their extracts on cancer cell lines.

Finding a consistent interaction is useful.  I imagine you could fractionate the extract and identify the compound that affects the HepG2 cells.  Injected into a mouse, maybe it causes elevated liver enzymes ... maybe it cures liver cancer. :)  Either way, it might be something that a person taking an herbal supplement would like to know about.

True! I'm still screening but this plant extract can be one of the candidates for further elucidation. Thanks!

Of course different types of cells, or even the same type of cell in different conditions, may react differently to the same stimulus.  Regarding your "plant extract", it likely has many different molecular components. A typical biochemistry way to investigate further would be to separate the extract into fractions containing different components, and see whether an effect can be prodced by one or more of the components and not others.

Oh, actually, I used the ethyl acetate fraction. The hexane fraction is highly toxic based on my preliminary assays. I will edit my question to add this info, sorry for the missing info.


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What are the chances that the primary oocyte that created me contained atoms of the primary oocyte that created my maternal grandmother?
This isn't so much homework help but more related to personal curiosity. I know that it's generally accepted that all oocytes are created prenatally and once a baby is born, no new oocytes are created. However, even if no new oocytes are created after birth, I would assume that much of the oocytes molecular and even atomic makeup are not the same overtime because of molecular turnover to maintain homeostatic. I assume that there is a very slim chance that the oocyte that created me contains any atoms of the oocyte that created that created my grandmother. Is my assumption correct?
If this isn't the right tag for this type of question please let me know which tag is the right one and I can redirect the question.
Edit: Forgot the word "not" in the third sentence of the paragraph.

Well, sure, there's a statistical chance, but incalculable and probably infinitesimal. I think some of your underlying assumptions are probably incorrect around the molecular turnover; I would have thought degradation of the molecules and loss of these via waste mechanisms rather than recycling, but I know very little about oocytes at that level.

@bob1
I noticed that I forgot a word in the 3rd sentence of my original comment. I meant to say that an oocyte's molecular/atomic makeup is not the same overtime due to molecular turnover to maintain homeostasis. I understand that there is probably no numerical statistical figure to such a question but your answer that the numerical chances are very small supports my assumptions but I wasn't sure if I was missing something. Thanks for the answer!


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Mutations in a Petri dish overnight
How long does it take for a bacterial culture in a Petri dish to experience all possible single base pair mutations? Can 12 hours be enough?
I want to get an intuition for whether a given mutation is a rare event we can only hope for or something that is all but guaranteed to happen.

Remember that not every mutation is beneficial or conveys some sort of survival advantage, especially in a rich environment like a Petri dish where you are theoretically growing the bacteria on some sort of nutrient agar or in a nutrient-containing solution. Also remember that populations evolve, not individuals.

Sure! Maybe I should delete the last paragraph. The surprising part for me just that mutation is not a matter of "if" but "when". Like in https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6242871/ I can see antibiotics resistance evolve in a matter of days. Super cool.

A number that gets passed on will be in the non-coding set, I wonder where they get the value for P - presumably from viable specimens, or is it total likely mutations... Question followed.

I don't understand your question, as you give no value for P. Are you saying that the twit quoted some value and you wish to know what it is? In which case your question would appear to be "What is the frequency of mutations per base-pair of E.coli during cell division?" and by extension "How many mutations occur in a petri dish in a period of (say) 24h, and how does this compare with the number of base pairs of DNA in the E.coli genome?". If this is the case please say so explicitly.

@David: Thanks! Yes, that's exactly the case. I've updated the question to be clearer. I'll also try to add an answer based on what I can Google.

It occurs to me that you might be interested also in our sister site, [skeptics.se]. They specialise in challenging notable unreferenced claims in the various media.

@ARogueAnt. Good point! But I can't even find the claim. I decided to cut down the question radically and just ask about how long it takes to get all point mutations. I also cobbled together an answer.

Note that your question, while it takes the usual framing of single base pair mutations, ignores a very large number of possible mutations in the form of structural rearrangements, transpositions, etc., which do most of the real work of changing genomes. Contrary to single-base mutations, there is no way to saturate the space of all such mutations in culture.

We can calculate the number of base pair copy errors in a Petri dish per hour by multiplying the number of base pairs (B), the copy error rate (P), the number of divisions in an hour (D), and the number of cells in a Petri dish (N). (We assume a stable population in a saturated medium.)
$$
B \times P \times D \times N
$$
I've looked up some articles and tried to pull out numbers from them:

B: E. coli has 4.6 million base pairs. [1]
P: Mutation rate per base pair per generation is around $10^{-10}$. [1][2]
D: The doubling time can be as little as 20 minutes. So 3 divisions per hour. [3]
N: Around a billion E. coli per ml. [4] A few billion in a "colony". [5] Let's call it 3 billion for the Petri dish.

$$
B \times P \times D \times N
= 4.6 \times 10^6 \times10^{-10} \times 3 \times 3 \times 10^{9}
$$
This comes out to 0.9 mutations on average per base pair per hour.
Each base pair can change into 3 different base pairs. After 3 hours we will have had almost as many mutations as possible! We can get the same mutation multiple times. But even accounting for that, it's almost certain that a given mutation will happen within a day:

(Click the chart for an interactive view where you can try different numbers.)
Indeed we can see research [6] where selection can give rise to new mutant strains every day:

In general if the inverse of the base pair copy error rate is close to the population size, we will see a large subset of all possible single base pair mutations in each generation.
How likely it is that truly 100% of mutations have happened is known as the "coupon collector's problem". Its solution tells us that the expected number of mutations needed to cover all 3 × 4.6 million point mutations is $3 B \times log(3 B)$. With our numbers above we are doing around 4.1 million mutations per hour, so we would on average need around 55 hours.

Spontaneous mutation rates come into focus in Escherichia coli, 2014 by A B Williams

DNA replication fidelity in Escherichia coli: a multi-DNA polymerase affair, 2012 by I J Fijalkowska, R M Schaaper, and P Jonczyk

Organization of sister origins and replisomes during multifork DNA replication in Escherichia coli, 2007 by S Fossum, E Crooke, and K Skarstad

General calibration of microbial growth in microplate readers, 2016 by K Stevenson, A F McVey, I B N Clark, P S Swain, and T Pilizota

Role of the RuvAB protein in avoiding spontaneous formation
of deletion mutations in the Escherichia coli K-12 endogenous tonB gene, 2004 by K Mashimo, Y Nagata, M Kawata, H Iwasaki, and K Yamamoto

Access to high-impact mutations constrains the evolution of antibiotic resistance in soft agar, 2018 by N Ghaddar, M Hashemidahaj, and B L Findlay

The tweet was from an expert and I don't know the first thing about any of this. So I'm pretty sure this answer is wrong. But which part?

I got the whole formula wrong! That's error rate PER BASE PAIR. Then the claim is 100% good. I'll fix this!

All fixed. I'm quite unsure about the number of cells. But https://doi.org/10.1016/j.bbrc.2004.08.078 also gives cell counts in the billions so I hope it's roughly correct.

One needs to compare the total number of mutations, $P\times D\times N \times T$ with the total number of base pairs $B$. If $P\times D\times N \times T > B$, i.e., $P\times D\times N \times T/B >1$, then the mutations explore all of the genome. In fact the condition is even more stringent, if we take into account that it is a stochastic process, i.e., some bases will mutate multiple number of times.

10 mL is a very large volume of cells to be growing on a plate (solid media). Cells do not grow in the medium but on top of it. I would suggest instead using a number of cells in a colony 3.3e9 (https://bionumbers.hms.harvard.edu/bionumber.aspx?s=n&v=6&id=104458). Alternatively, one could instead assume that the culture is in liquid medium of 10 mL, in which case your 1 billion cell number is close (though other estimates are higher, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3146540/).

Additionally, on the right side of your equation you still have $T$, but you also have a "3" (?). I think that you meant to remove the last $\times T$.

Thanks for the comments! @RogerVadim: But P is the error rate per base pair. So you will have $B\times P$ mutations for each division.

@MaximillianPress: Thanks, I'll use the colony size. It's the same ballpark. The 3 is there because we have 3 divisions per hour. $T$ is the number of hours.

I'll just drop $T$ and talk about mutations per hour! There are so many variables already anyway!

@RogerVadim: "In fact the condition is even more stringent, if we take into account that it is a stochastic process, i.e., some bases will mutate multiple number of times." I've added a paragraph to address this too. Looks like this pushes out the timeline a bit! Thanks!

@DanielDarabos Another thing that is missing is that the number of cells is treated as a constant, although they divide, i.e., it grows geometriclally (unless we also allow them to die).

Oh man. I was hoping the population stabilizes at some point. ($N$) But maybe they just stop dividing when they go hungry?!

@DanielDarabos it stabilizes, because many mutations are deleterious and/or because there are limited food supplies... in which case they either do not divide or there is strong selection. I think you need to ask a more pointed question: do you want to know how many mutations are there or whether all the mutations have been explored? Under what conditions they grow (in terms of food, selection, growth rate, etc.) - if they do not replicate, why use doubling time?

Yeah. Whether we want to go into that I think depends on why we are asking the question. I edited it now to say that my goal was just to get an intuition for how likely it is to get a specific mutation in a day. On that I'm satisfied even if the answer is lax on population size. I'll also add to the answer a practical example where selection is used to force mutations in a matter of days.

Be careful about what you call a specific mutation. You proved that each site might have experienced a mutation over the night, but it doesn't mean that all the possible genomes were explored: for $B$ base pairs one may have $4^B$ different genomes - it would take much longer to explore all of them.

@RogerVadim: You're right! I forgot this is not binary! I think I've fixed it now. I've also added an interactive thing where you can change the parameters and see how the probability over time changes. Even if we consider 3 mutations per bp, the probability goes up very high in 16 hours or so. Thanks for all the help!


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What is the difference in the function of tractus rubrospinalis and tractus corticospinalis?
What is the difference in the function of tractus corticospinalis and tractus rubrospinalis? I know, that they begin in different parts of the brain, but from what have I read on the internet*, I can't see any difference in their function. The only difference I can see is, that tractus rubrospinalis is having impact only on the upper half of the body, but still this isn't difference in their function (at least on the upper part of the body).
Edit:
* for the rubrospinal tract I have read

The tract is responsible for large muscle movement regulation flexor and inhibiting extensor tone as well as fine motor control.

and for the corticospinal

The primary purpose of the corticospinal tract is for voluntary motor control of the body and limbs.

Both are from wikipedia, but this is just because it is was the fastest source of something in english. I learned it from sources in my language so I can't post them here, but I understood it very similarly as it is on the wikipedia.

Can you perhaps add a short quote (with references) on what you've read about each and why that makes you think it's the same?

@BryanKrause, sorry, rn I don't have time, but I'll do it about an hour later. BTW, I also don't think, that they do the same thing, I just also don't know what is the exact difference. This is the reason, why I am asking. Anyways, thanks for tip how to improve the question.

@ARogueAnt., humans, there is the human-biology tag.

Fair enough, I'd missed that.

Assuming those quotes are from Wikipedia (and wherever you quote from it's always important to cite your source), did you happen to read the sentence before the first one, and the paragraph after the second?

@BryanKrause, Yep I did. For the sentence, yes, it is smaller, but I am asking if (and if yes, what) there is something different in what kind of things they do, not just, that one is smaller and the other is bigger, so it can transfer more informations. And for the paragraph, yep, that is my mistake, I forgot to say it, but I am asking only on the motor part of it's function.

Before the first: "It is one of the pathways for the mediation of involuntary movement, along with other extra-pyramidal tracts including the vestibulospinal, tectospinal, and reticulospinal tracts." After the second: "After patients are lesioned in some part of the pyramidal tracts, they are paralyzed on the corresponding side of the body. However, they can re-learn some crude, basic motions, just no fine movements.[2] This implies that the connections to these tracts are crucial for fine movement, and only partial recovery is possible if they are damaged."

Oh sorry, so we were probably referencing to different senences. This is probably the answer, so thanks.


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How to reduce PPi concentration in blood samples by PPase
I have some samples of whole blood that are a little bit expensive and I want to significantly reduce the concentration of PPi in the samples by causing a reaction. I don't have any experience in practical chemistry, but I understand that in theory, there are enzymes that can hydrolyze pyrophosphate into orthophosphate (e.g. inorganic pyrophosphatase).
I see that I can purchase inorganic pyrophosphatase suspended in 3.2 M ammonium sulfate solution, (pH approximately 6), from yeast, on Sigma-Aldrich and in theory converts 1 micromol pyrophosphate to orthophosphate per minute at room temperature (in the presence of Mg-ions). For my purpose, the reduction in pH is not a problem. I am more concerned about whether PPi concentration would actually go down, or if I could expect cell lysis or other effects to occur, causing PPi to rise.
Can I use this reagent to reduce the measurable PPi concentrations in the blood samples? And if so, how would I do it?
EDIT: I am doing an experiment with bacterial growth in plasma, and comparing with serum deficient in pyrophosphate. I want to have a rough idea of the appropriate way to hydrolyse the PPi.

I guess it might be helpful to know the reason you are removing pyrophosphate? Like this paper suggests, pyrophosphate activity might be inhibited by compounds present in blood, and it would help if you tested on a different sample while monitoring the pyrophosphate level as they do in this paper

@PrashantBharadwaj I added the information that you requested.

@MikkelRev, you mention whole blood, plasma, and serum. Which of these are you ultimately using as your bacterial growth medium? This will affect the steps of your protocol.

Bernhard et al. 1 describe a method for the treatment of human plasma with yeast inorganic pyrophosphatase. The PPase-treated plasma is used as both a diluent and a negative control in their PPi conversion assay. The use of a salt solution as a secondary negative control confirms the depletion of PPi from PPase-treated plasma samples. I've quoted their protocol and validation steps below, but here is my summary:

Centrifuge whole blood and transfer supernatant. This serves to remove most of the cells from the plasma fraction.
Filter plasma with 300 kDa filter. This will remove any remaining cells so the amount of PPi contributed by any cell lysis is negligible.
Add PPase and mix by inversion. The authors do not supplement the plasma with Mg2+ nor any buffers.
Incubate for 30 minutes at room temperature.
Filter plasma with 30 kDa filter. The recombinant PPase from NEB has a mass of 71 kDa 2, so this step likely serves to remove PPase from the plasma, which would confound the use of PPase-treated plasma as a diluent for PPi measurement.
Aliquot and freeze PPase-treated plasma.

Generation of Pyrophosphatase-treated Plasma
For human plasma, blood drawn from donors (everything at room temperature) was spun down at 3500 rpm for 15 min, and plasma was then transferred to a 15-mL tube. Then, 2 mL of plasma was filtered through a Centrisart® I 300 kDa mass cutoff filter at 2500 × g for 30 min. The filtered plasma was transferred to a fresh 1.5 mL Eppendorf AG tube. Yeast inorganic pyrophosphatase (PPase; New England Biolabs Inc) was added at 1:1000 plasma, mixed well by inverting 4 times, and incubated for 30 min at room temperature. Five hundred microliters of PPase-treated plasma was filtered through a Nanosep Centrifugal Device With Omega Membrane 30K (Pall Corp) at 13,200 × g for 5 to 10 min. The PPase-treated, filtered plasma was frozen at −80°C in 500 µL aliquots. A new stock was made every 2 months.

Assay Description and Validation
The assay utilized ATP sulfurylase to convert PPi to ATP, which was then detected by a luciferase/luciferin luminescence detection kit. The luminescent signal is directly proportional to the amount of ATP present; the assay is a semiquantitative assay (regulation 493.1256(d)(iii) of Clinical Laboratory Improvement Amendments of 1988). Target analyte of assay validation was PPi. The specimens were human platelet-free plasma samples. The low limit of detection was 0.15 µM; the quantitative range was 0.15 to 10 µM. Normal ranges, determined by testing PPi levels of 50 healthy adult volunteers (50% male), were 1.43 to 7.40 µM (unpublished data). For validation and clinical testing, a standard curve was generated for each run by titrating measured amounts of PPi in PPase-treated pooled human plasma. The PPi standard curve was prepared by diluting powder PPi in water; thus, concentration was equal to 1 mM PPi final. One millimolar of PPi was diluted 1:100 in PPase-treated donor plasma and mixed well. Defined concentrations were achieved by serial 1:2 dilutions in PPase-treated donor plasma. A negative control of Hank’s balanced salt solution alone and PPase-treated pooled human plasma were included on each assay plate. Each concentration was run in triplicate.

References

Bernhard E, Nitschke Y, Khursigara G, Sabbagh Y, Wang Y, Rutsch F. A Reference Range for Plasma Levels of Inorganic Pyrophosphate in Children Using the ATP Sulfurylase Method. J Clin Endocrinol Metab. 2022 Jan 1;107(1):109-118.
https://www.neb.com/products/m2403-pyrophosphatase-inorganic-yeast


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Can the effect of an allele on height be context-dependent?
Some data is available on the effect alleles have on height. For example Common DNA Variants Accurately Rank an Individual of Extreme Height
However after browsing the literature I was not able to easily answer the following.
If we take a genome and allow only one gene to change there is going to be an allele maximizing the genetic potential for height. If we take two different genomes and allow one gene to vary are the optimal alleles going to be the same?
If this can happen then linear polygenic scores cannot fully capture the genotype–phenotype map.

Linearity is an assumption of convenience established by Fisher 1918 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456325/) to make the math easier. There really isn't any biological reason to believe it's true; even the existence of dominance is sufficient to make it obvious that linearity isn't complete. I recommend reading about epistasis (https://www.nature.com/articles/nrg2452). That said, linear predictions yield pretty good predictions under the assumption that most pairs of loci don't interact (also shown by Fisher I believe).

See also e.g. https://pubmed.ncbi.nlm.nih.gov/31761530/. Even if polygenic scores can be used for prediction, they're honestly not doing a very good job! They suck even for highly "heritable" traits, showing the weaknesses of the concept of heritability (but that's a different conversation).

Linearity is an assumption of convenience. In fact, since Fisher himself allowed for the effect of dominance in his 1918 paper, it made the math more complicated, not easier (though it may be easier today in, say, GWASs). The additive model was created based on empirical data to address flaws in the prevailing dominance/epistasis model at the time. There are a number of biological reasons why most alleles are additive; deviations from additivity are very rare.

Polygenic scores are empirically doing an excellent job for prediction; in fact, Alzheimer's disease and height are completely "solved" so to speak (i.e., captured ~all SNP heritability). Heart disease polygenic scores predict better than pre-existing conditions or family history.

Polygenic scores are very good at predicting height.
This figure, from https://arxiv.org/pdf/2101.05870.pdf, predicts height using common SNPs at r = ~0.65.
In a different study, "combined with sex, a polygenic risk score captured 71.1% of the total variance in adult height in the UK Biobank."
As you can see below, polygenic scores are about as good as the height of your parents at predicting your height.

Yet another study found an r^2 of ∼0.82. In fact, this is greater than some heritability estimates of height.

A good starting point is to understand why Fisher used a linear/additive model. It wasn't just due to convenience or to make the math easier, though that may have been a factor. Fisher's model was empirically driven. He observed that some physical human traits, like height, were normally distributed, and then found that his additive model correctly predicted how similar in height relatives would be. In fact, he incorporated dominance into his models in the 1918 paper, allowing for effects of both dominance and additivity at the same time. The additive model was created to address the shortcomings of dominance models, which already existed at the time.
Fisher said in 1930: "The biometrical facts as to the inheritance of stature and other human measurements, though first regarded as incompatible with the Mendelian system, have since been shown to be in complete accordance with it, and to reveal features not easily explicable on any other view. The approximately normal distribution of the measurements themselves may be deduced from the simple supposition that the factors affecting human stature are approximately additive in their effects."
Forgetting Fisher's result that many complex traits are highly polygenic is what ultimately led to the candidate gene era and its frequent failures.
So why is the additive model so predictive? Is it just a quirk of chance?
Not quite. It is inherent to natural selection. Additive effects are more stable across generations, as they do not depend on the particular combinations of alleles an individual has (unlike dominance or epistasis). This stability makes additive effects more consistently "visible" to selection.
Imagine if a gene for having a long neck was dominant in giraffes--it would be impossible to eliminate the recessive allele from the population (aside from genetic drift), as there is no phenotypic difference between heterozygous and homozygous long-neck individuals. Now imagine if there was simultaneously a different, additive pathway to having a long neck. Selection would favor increasing neck length via the additive pathway, as there would be decreased risk of one's offspring having a short neck. In this case, selection inherently favors additivity.
The second reason why additive effects are biologically preferred is due to the fact that mutations happen randomly. By definition, in order for a new dominant interaction to occur, two mutations must happen. If the mutations require each other to be useful, they'd have to occur simultaneously to be selected for. On the other hand, a new additive mutation being selected for only requires that a single new mutation is beneficial.
The third reason why additive effects are predominant is because most allele frequencies are biased towards one extreme or another. Therefore, the remaining genetic variation between individuals is likely to be of small effect and polygenic.
The final counterintuitive reason is because multilocus epistasis itself mostly contributes to additive variance.
As you saw from the paper you cited, very tall people are not tall because of rare dominant mutations, but because they happen to have a very large number of "tall height" alleles.
Yes, if you take a genome and allow only one SNP to change, there is going to be some change which maximizes the genetic potential for height; if you repeat this with two genomes, the allele will probably be the same unless the individual already has that allele or has a different ancestry than the first individual.
I'm not sure how this means that a linear polygenic score would not fully capture the genotype–phenotype relationship. You are completely correct that SNP-based polygenic scores cannot capture the full heritability: they can only capture the SNP-heritability at best. You are correct that it is possible for alleles to be context dependent. If there is a strong GxE component, and you are measuring between environments, a SNP-based polygenic score's accuracy would be attenuated for the trait.
There are other factors besides this that limit SNP heritability and the maximum accuracy of SNP-based polygenic scores, such as:

Rare variants (not yet included in many GWAS or polygenic scores)
Large insertions, deletions, duplications, or rearrangements
Gene-gene interactions (e.g., dominance): though additivity is more common, dominance is still extremely important, especially for certain Mendelian diseases or non-polygenic phenotypes.
Copy number variations

TL;DR:
Your intuition is correct, but for many traits like height, linearity happens to be a good assumption due to biological constraints.
P.S.
Since we all learned about dominance in school, it can be surprising to hear that it is really not that common. For example, Okbay et al. 2022 with N = 2,574,253 found that their "dominance GWAS identifies no genome-wide-significant SNPs. Moreover, with high confidence, we can rule out the existence of any common SNPs whose dominance effects explain more than a negligible fraction of the variance in EA." The "combined variance explained by dominance deviations in common SNPs is negligible."
A different study analyzed 70 complex traits on 254,679 individuals in the UK Biobank. The authors "found strong evidence for additive variance," but negligible dominance variance" and "epistatic variance... not significantly different from zero." "Genetic variance for complex traits is predominantly additive." "Epistatic variance is likely to be extremely small in human complex traits." This replicated a similar earlier result that looked at 79 phenotypes. This was replicated again here with 50 phenotypes. Each time, dominance is negligible.
Hill et al. "evaluate the evidence from empirical studies of genetic variance components and find that additive variance typically accounts for over half, and often close to 100%, of the total genetic variance." This is why Crow states "the breeder's custom of ignoring epistasis usually gives a more accurate prediction than if epistatic variance were included in the formulae."
Keightley shows from a biochemical standpoint that polygenicity alone is sufficient for a lack of dominance effects.
Even after accounting for correlations between alleles (LD), "independent of the type and strength of gene interaction, the epistatic variance contributes little to the total."
Twin studies also support the additive model being predominant, with no effect of dominance for most phenotypes.


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Does the gas in blood remain constant when breathing? Is O2 and CO2 replaced by N?
Am a software dev and working on a non-scientific game that shall include "somewhat realistic" elements of the pulmonary system.
Effectively I want to roughly model the exchange of O2 and CO2 between blood and air when breathing.
From what I was able to gather here, roughly 20% of O2 are bound to blood when we are at full saturation: https://www.cvphysiology.com/Microcirculation/M002
Furthermore that O2 is replaced by CO2 due to our metabolic processes. As a result, the gas remains roughly constant (ignoring what's solved in the water and plasma).
However what happens if a human exhales all their air and then breathes an atmosphere of pure Nitrogen (besides suffocating, obviously)?
Will the exhaled gas contain any O2 or CO2? If yes, does that mean N is solved into blood in significant amounts? I haven't been able to confirm the later at all. Or does the overall gas concentration in blood decrease after all?
Hope someone has a rough answer.
Huge thanks in advance :)

If you want the model to be "somewhat realistic," no one should be able to exhale all their air.

I'm no expert, but my take is that there will initially be some CO2 diffusing from the dissolved CO2 in the blood into the pure N2 in the lungs and thus exhaled if there is breathing.  This will continue while the body's remaining metabolism continues to produce more CO2 and the heart moves blood, which primarily transports it as bicarbonate and carbonic acid.(1)  There would probably be trace amounts of O2 diffusing into the lungs.  There would probably be only slightly more N2 in the blood, as the partial pressure of N2 would not change much between air and pure N2.
I'm not sure what you meant by "the gas remains roughly constant" as the O2 and CO2 (and N2) in the blood are not in gaseous form.  They exist as dissolved molecules in the aqueous plasma, not as bubble of gas.
(1) "Transport of Carbon Dioxide in the Blood"


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Do we know all the possible human hair colors?
I occasionally see people with blue hair and I always assume it is dyed. I wonder how justified is that assumption. Have biologists determined all the possible human hair colors? Or is it possible that if an embryo was exposed to the right amount of radiation in the right place it could get green hair or some other hitherto unseen color?
NCBI lists some alleles of MC1R together with their effects on the phenotype but I don't know how exhaustive their data is (and also other genes might be at play).

Have you checked Wikipedia? https://en.wikipedia.org/wiki/Human_hair_color

Do you mean natural? I spent a lot o time in a cancer hospital with my wife and I have seen, for example, pinkish hair that I could bet was not dyed. I've also seen bluish and greenish, but can't begin to guess if it grew like that or was coloured artificially.

Melanin is the only biologically coded for pigment amongst mammals and most animals broadly speaking. Some birds are exceptional in this case where reds and greens can be seen (in which case often some dietary component is required for the synthesis of these abnormal pigments).
In humans, the entire variation in skin, hair, and eye color is a consequence of varying treatments of melanin. Melanin traditionally comes in two forms, namely eumelanin and phaeomelanin. The former can come in a brown or black variety while the latter is responsible for the reds and oranges seen in human pigmentation (e.g., localized to the lips, nipples, and nether regions).
Red pheomelanin serves as an accent and does very little as far as protection from UV radiation is concerned; the brown-black melanin serves that purpose. The cells in your body that produce melanin are known as melanocytes, and the MC1R gene you mentioned codes for a receptor that localizes to the membrane of these cells. This receptor acts as a light switch that indicates whether the melanocyte ought to be producing red pheomelanin or brown-black eumelanin. An agonist that binds to this receptor is coded for by the ASIP gene and is also partially responsible for pigmentation differences throughout the animal kingdom.
In most people this receptor functions as intended, and melanocytes in the skin produce varying degrees of brown-black eumelanin (the extent of which depending on one's ethnic background) while pheomelanin is switched on in the few key areas listed above. When both copies of the MC1R gene inherited from each of your parents are disfunctional, this switching mechanism no longer works and your melanocytes will produce primarily pheomelanin ubiquitously across your body. This is what we know as 'redheads'.
What isn't immediately obvious is that red-haired individuals are not unique in just the aspect of their hair. Their whole body presents with a deficiency in eumelanin and as such they also carry a pale/rosy complexion as well as an inability to tan and a propensity to sunburn easily. This is a consequences of the fact that eumelanin is our primary defense against UV radiation.
While melanocytes in the skin and eyes are responsible for the production of melanin, the melanin in one's hair gets there as a result of a handoff between melanocytes and the keratin producing keratinocytes. Melanin within melanocytes is produced and stored within organelles known as melanosomes and, through a complex formed by the 3 genes MYO5A, RAB27A, and MLPH, the transfer of these melanosomes through the tendrils of the melanocytes to the keratinocytes is facilitated. Defects in any of these 3 genes can result in a condition known as Griscelli syndrome (types 1, 2, and 3, respectively) where the transfer of melanin from melanocytes to keratinocytes is impaired.

As a consequence the hair of one of these individuals appears silver, and when looked at under a microscope you can see the inconsistent nature of the melanin being transferred to the hair during its development:

To summarize, the only pigment that appears in hair is melanin, and thus the only possible hair colors are: the entire spectrum between blond and black; red in the case of MC1R defects; silver in the case of the Griscelli syndromes; and of course white in the case of albinism (which I needn't cover).

You mentioned blue hair color but I think this might be due to a misconception about how blue eyes came to be. Blue eyes are not due to a blue pigment (rarely is blue ever found in nature), but rather due to a physical manipulation of the light being reflected due to the microscopic structure of the eye. So in the same way that the sky and  water can appear blue due to manipulation of light, so can the human eye. The blue of human eyes is typically covered up by melanin, except in the case of those carrying a specific one-letter mutation within the HERC2 gene that results in the absence of melanin in the eye.
Not just black and white: pigment pattern development and evolution in vertebrates
Signaling Pathways in Melanogenesis
Rab27a and MyoVa are the primary Mlph interactors regulating melanosome transport in melanocytes

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

Bright bird coloring, like butterflies, is usually not the result of pigmentation but microfibers forming a texture that refracts and reflects light almost the same way as a holograph - which explains why the same bird can appear different colors based on the angle they're viewed from.  Viewed up close, those feathers are not actually blue or whatever color they appear to be from a distance.

Is it conceivable that human hair could develop (via some mutation) with the microscopic structure needed exhibit other colors via reflection & refraction?

@R..GitHubSTOPHELPINGICE funny you should ask, theres a mutation that causes a condition know as "pili annulati" where the hair follicle has air bubbles in it and they create reflective bands in the hair. I always have my eyes peeled for any new papers about this because the genetic origin of this is not known

In that case, it seems plausible that there may be more colors (depending on your definition of color).

Time to break out the CRISPR set and get my follicles to produce some turacoverdin.

Technically, isn't the silver of Griscelli Syndrome the same thing that causes blue-haired cats (most famously the Russian Blue and British Shorthair), when it occurs in someone with what would have been black hair? Looking at wikipedia, I think it's the same gene, too, at least for the non-lethal variant of the syndrome.

@nick012000 But blue cats aren't really BLUE, at best they're just a sorta-kinda cool toned grey. Another option would be mixed hair like a bluetick hound or a blue roan horse, but this also isn't BLUE, just kinda-sorta-maybe-blueish. You get this with some people who have black hair and are greying from age, but the light conditions have to be very favorable to describe it as blue.


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What is harvest mortality and how is it calculated?
My background is not in biology, however for the work I'm currently doing, I am reading some papers in ecology and the term "harvest mortality" appears. I could not find the meaning of this term or an equation explaining the way it is calculated.
Can someone please define the term "harvest mortality rate" in the context of wildlife ecology and sustainability, and also provide a formula explaining the way it is calculated please?

“I am reading some papers in ecology and the term "harvest mortality" appears.” — could you please link one or more of the papers that use that term?

"Harvest mortality" usually refers to the proportion of a population that is killed by humans for economic purposes (e.g. birds or terrestrial mammals that are shot by hunters, fish caught in nets or on lines, trees cut down by loggers, etc.). For a specified population and time period, it will be something like (number harvested/total number alive at time 0).
The first hit of this Google Scholar search for "harvest mortality" is by Solberg et al. They describe a complicated procedure for estimating the number of moose of a given age and sex alive in a given year. Basically, they add up the reported number of moose shot by age and sex in each year, combine it with estimates of the non-hunting mortality by age and sex, and do the accounting to back-calculate how many animals of a given age/sex must have been alive in a given year (they do the book-keeping up to a maximum age beyond which few animals survive).
Once they've done the hard part, estimating the total number of moose of a given age that were alive at the beginning of a given year,

The  age-specific  harvest  mortality  was  calculated
as the annual number of moose harvested divided by
the annual number of moose present in the respective
age groups.

Solberg, Erling Johan, Anne Loison, Bernt-Erik Sther, and Olav Strand. “Age-Specific Harvest Mortality in a Norwegian Moose Alces Alces Population.” Wildlife Biology 6, no. 1 (2000): 41–52. https://doi.org/10.2981/wlb.2000.036.


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The village of Twins — Mystery behind and Scope
With the presence of more than 200 twins,  Kodinhi , a village situated in Malappuram District in Kerala , India , is popularly known as the "Village of Twins".This phenomenon of large number of twin births is not only unique to Kodinhi.It has also observed in : (a)  Cândido Godói , a municipality of 6,151 inhabitants in the state of Rio Grande do Sul in Brazil , (b) in Igbo Ora in Nigeria and also (c) in Hiệp Hưng in Vietnam .
a) Kodinhi/Kodinji : The village of twins in Kerala

The village entered the international spotlight when a survey done by locals found an unusually large number of twin births in the region. A report by The New Indian Express Staff Correspondent Mithosh Joseph from Malappuram had brought the attention of several people outside India to the attraction of the spot. His report had featured well the ongoing researches in the area, the total number of twins, the peculiarities of parents and a few other comments by doctors who studied the strange phenomenon. Though initial estimates put the instance of multiple births at 100 pairs, follow-up surveys found the figure to be closer to 204 pairs (408 individuals) of twins, and two sets of triplets.Despite several studies being conducted, the exact cause of this phenomenon is yet to be ascertained. Women from Kodinhi married off to far away places are also known to give birth to twins.According to doctors, this phenomenon is due to chemicals present in water in the Kodinhi area .According to locals, the oldest known twin pair in the village was born in 1949. The number of twin births in Kodinhi has been increasing over the years, with surveys showing over 79 pairs of twins within the age group of 0–10 years.
In 2008, around 30 pairs of twins from Kodinhi, along with their parents, got together to form The Twins and Kins Association, the first such association of twins in India.The forum, according to its founders, aims to bring to wider attention problems peculiar to people of multiple births, such as those concerning their education and health.

b) Cândido Godói in Brazil

The rate of twin births in Cândido Godói is 10%, significantly higher than the overall 1.8% rate for the state of Rio Grande do Sul. This rate is unusual, exceeding the highest observed national twinning rate (4.5 to 5% for southwestern Nigeria).Nearly half (8 of 17) of twins examined in one study were monozygotic (identical) twins, a few more than the average of 30%.Twin births were noted from the early twentieth century, when the first immigrants included seventeen sets of twins, and have been observed through several generations in the latter part of the twentieth century.
The population is largely of Polish or German ancestry, with many tracing ancestry to the Hunsrück region of Germany, which has a higher than average twinning rate. The rate in Cândido Godói could reflect genetic founder effect: rare genetic traits occurring by chance among a small group founding a community will be more common among their descendants than in the population at large.

Note : Founder Effect
c) Igbo Ora in Nigeria : The Twin Capital of the World

In Igbo-Ora, research has suggested that the multiple births could be related to the eating habits of the women in the region.Though no direct relation between dietary intake and twin births has been proven, a research study carried out at the University of Lagos Teaching Hospital has suggested that a chemical found in Igbo-Ora women and the peelings of a widely consumed tuber (yams) could be responsible.
A possible explanation that the large number of twins being born here could simply be a matter of genetics

d) Hung Loc Commune in Vietnam
From the article: The hamlet of Twins ,

The high rate of twins in this area is not due to marriages between families who produce twins.In many families with twins the parents come from different regions of country with no background of twins in the family. It is a rumour that the water in this region consists of a special mineral that helps women get pregnant and produce twins.

What can be the reasons for such a phenomena? Is it just genetics or may because of some chemicals present over that particular area (what chemical)? What all ways this phenomenon can be beneficial (scope) ?

More Reference :
A Case Report : A Non-Identical Twin from the village of Twins with identical occlusal characteristics — A Non-Identical Twin from the village of Twins with identical occlusal characteristics
Website : International Journal of Health Sciences and Research (IJHSR)
Volume : 6 ; Issue : 10 ; October 2016
Pages : 260 - 264
Date of Publication : 05.10.2016
Corresponding Author : Praveen Jodalli
Abstract : Abstract of the case report
Accessed on : 20.11.2021
(Note : Based on Kodinhi/Kodinji village of Kerala only)

it's related to dulebobvulation.

This is interesting, and it's nice - lovely actually - to see sources. But what about research into a possible answer? What did you find when you googled why some areas are blessed with so many twin births?

some info here: https://www.google.com/search?q=factors+that+increase+chances+of+indentical+twin+birth&biw=1213&bih=645&sxsrf=AOaemvLCw958js4B4SfLX2XiVMhuRh-1aQ%3A1637570137571&ei=WVabYdOvIoO7lwTewoPYCQ&ved=0ahUKEwiTwOCSyKv0AhWD3YUKHV7hAJsQ4dUDCA4&uact=5&oq=factors+that+increase+chances+of+indentical+twin+birth&gs_lcp=Cgdnd3Mtd2l6EAM6BAghEApKBAhBGABQAFi6QmCqRmgAcAF4AIABkgGIAdokkgEEMS4zN5gBAKABAcABAQ&sclient=gws-wiz and general science https://www.google.com/search?q=hormes+that+affect+twin+birth&oq=hormes+that+affect+twin+birth&aqs=chrome..69i57j33i22i29i30.4538j1j4&sourceid=chrome&ie=UTF-8

@LifeInTheTrees Your links relate only to general factors increasing the likelihood of women conceiving twins, not the reason why there should be an abnormal geographical concentration of twins. If you know a source relating this please provide it.

You really need to examine the null hypothesis: that a few villages (out of perhaps millions on Earth) having a higher than average number of twins is simply due to chance.

Comments have a habit of doing that. Did you manage to find a more apt reference?


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Can genetic material actually provide a physical description of appearance?
A bodies genetic material provides the blueprint for your appearance. Your predisposition to be tall, freckled, blue eyed and blonde are encoded from birth.
However, external and environmental factors can influence the manner these instructions are carried out. For example malnutrition during childhood will affect bone and tooth growth. A lack of oxygen can lead to cerebral palsy with dramatic affects on the bodies muscle development (amongst other things).
Does your current genetic material indicate how you physically appear in real life and not just the genetic markers or 'potential'?
eg : If a scientist had a bloodsample taken today, I know they could say that the subject has obesity markers but could they actually say how fat the person was. Could they determine the difference between what the markers say and what the subject actually appears like?
Is current research limited but indicating that this might be possible in the future?

Is the wealth of information about how many cells, and what each of those cells are doing encoded within every other cell, or more generously--a blood sample? Probably not. On average you'd probably be able to determine a lot of characteristics somewhat accurately. In 2016, I'm neutral on the likelihood. In 2 or 3 decades, maybe we'll figure out some more bio that unlocks what you're asking.

A blood sample can tell you a lot about a person's level of obesity, but not necessarily from reading the DNA sequence, although that may help in some limited circumstances. Blood levels of HDL and LDL cholesterol can be measured, as can concentrations of glucose, insulin, and other indicators of diabetes, which is often related to weight and body mass index (BMI). However, I could not take a sample (or several samples over a timecourse) of blood from you and determine that you're 175 cm tall and weigh 95 kg.

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


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Could Omicron be the variant of a variant?
I read that the newly discovered variant of Covid-19 has a higher number of mutations than the other variants. Isn't it more likely that it is the variant of a variant? It would be absolutely normal, after all, viruses of this family mutate so frequently that they are continuously evolving.
There would be a missing point though, is the intermediate variant a known one or is it a variant that passed under the radar?

It's pretty straightforward (in theory) to determine whether a new variant is a sub-category of an existing variant, or a new variant on the same level as e.g. Delta, by building a phylogenetic tree and looking at where the new samples fall.

Useful resource: https://cov-lineages.org/lineage.html?lineage=B.1.1.529

From what I've read (which isn't much beyond a few synopsis articles), despite containing some genetic features of some previously identified variants of concern, Omicron genomes are not directly descended from any of these other variants. Apparently the closest ancestor is from a mid-2020 lineage that hasn't been of much concern. There's a twitter thread from Trevor Bedford (Fred Hutch faculty member)  here breaking it down into a pretty digestible chunks and citing some cool interactive resources.

At the point of its discovery, Omikron wasn't a "variant of a variant", but goes down directly to the Pango lineage B.1.1.
Now we know something more, with the discovery of the outgroup now named BA.2 and the original Omikron being BA.1: There was a common ancestor to the two sister lineages, now named B.1.1.529.
Note that this still does not make it a "variant of a variant" because for being named a variant, a lineage must fulfill some additional criteria, such as becoming dominant or at least a notable fraction of all cases in some region, or being in other terms different and interesting enough to be worth additional attention.


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What is the thickness of the mucous, submucosal, muscular and serous membranes of the stomach wall of a piglet aged 60-75 days? (Large White pig)
There is publicly available data on the thickness of the layers of the stomach wall of piglets aged no more than 20 days. But at an early age, the thickness of the layers of the stomach wall increases extremely non-linearly and there is no way to predict how the layers will change by 60 days. Maybe there are specialists among the community who participated in the experimental determination of the thickness of the layers or those who have met studies on similar topics?
I will be glad of any constructive answers on the merits of the question. Thank you in advance for your response.
For those who are interested, I attach drawings with the dynamics of the thickness of the layers in the cardiac (a) and pyloric (b) parts of the stomach of piglets.


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What is this large long-legged orange and black insect?
Around and inch long. 6 legs, bigger than a wasp, and orange and black. Found near the coast in the woods in South Carolina.

Welcome to Biology.SE. Please [edit] to include an estimate (in cm or inches) of the size (length) of your bug. Larger than a wasp isn't very precise, especially since there are many different types of wasp! Clearer photos (ideally from multiple angles) would also be helpful. Also note that "is this dangerous" is open to interpretation — I'm going to edit your post to better fit this site's standards, make additional changes as you see fit. Please take the [tour] and consult the [help] starting with [ask] for details.

Thank you! I’m just learning about this website! I will try to upload more pictures although I didn’t want to get too close.

You're welcome. This is almost certainly not especially dangerous to you. One way to avoid a painful bite while getting a sharp close-up would be trapping it in a sealable container and putting in the fridge for ... try 10 min and work up until it is very sluggish ... happy 'hunting'. Alternatively if you have a clear non-distorting container that could also work.

From these photos, the main features to go on are the dorsal black and red markings, the coloured bands on the legs, the white dots on the abdomen, and the shape of the body. These features does match well with this species, which is common in southern North America:
Milkweed Assassin Bug
(Zelus longipes)
The bite from this species is supposed to be very painful.

While not a threat to humans, if not handled properly, a Zelus longipes bite can cause a burning sensation with swelling that may last for several days.
https://entnemdept.ufl.edu/creatures/beneficial/bugs/zelus_longipes.htm

Additional resources:
https://www.insectidentification.org/insect-description.php?identification=Milkweed-Assassin-Bug
https://www.thoughtco.com/red-and-black-bugs-4138391

I agree, but this is close to a link-only answer. Answers (and questions) are supposed to be self-sufficient (not require following external links, especially since those can (and do) break making the post much less useful. Please [edit] to explain why your identification is correct, including a discussion of key features that led you to this conclusion and supporting references or at least validated (as well as public domain & properly attributed) images.

(+1) Thanks for the edits!

I agree. I have edited the post, which hopefully made it more useful.

Hi @Michael. welcome to BIO.SE! We appreciate the answers and quick involvement over the last 2 weeks. Willingness to edit and improve posts is a huge bonus -- thanks!! My only suggestion to you is that when answering questions (especially [tag:species-identification] Q's) that you avoid citing non-reputable sources. There are so many misidentified organisms (especially insects, plants, and fungi) all over the internet, that we want to avoid sending people to these sources. I think your ThoughtCo piece is decent and relevant in this case, but certainly be mindful moving forward. Thanks!

Thanks for the welcome and friendly advice. It is much appreciated.


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Do the cells of any multicellular lifeforms discard their genetic material after differentiating?
There are many types of cells which will never again divide. Some of them may not need DNA to perform their function. Are there any cases where the DNA is discarded after a final differentiation?

I recommend looking into terminal differentiation.
As one extreme example of terminal differentiation, xylem cells that form plant vascular tissues are simply dead. This is a case where not only the genome but also physiologic activity in these cells is irrelevant to their function.
A more famous case is red blood cell enucleation, wherein the genome of mature cells is lost in cell division.
In other words, yes, this happens.

But how does this answer the question? The instance  you explain is for cells that just die — not an example of what the poster is asking about, and we have no idea from your answer what is in the review you link to. Please either explain in your answer or restrict yourself to commenting.

Your answer didn't answer the question I meant to ask, but it did answer the question I wrote in the title. Rather than say your interesting reply was unfit, I have decided to change my question to match it. I'll ask a new question about what I really meant later. :-)


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Are there any species whose cells do not copy the DNA that has been inactivated during cell differentiation?
According to this paper, the ATP cost of a having (not counting transcribing) a gene in a diploid eukaryote is about $5\times 10^3$ ATP per base pair, while the lifetime ATP usage of a mono-cellular eukaryote might be around $10^{9+3}=10^{12}$ ATP. The human genome contains about $3\times 10^9$ base pairs, and all taken together this implies that the cost to the cell in a multicellular organism of copying its genome may be a respectable fraction of its total lifetime energy costs. (I am not willing to say anything more specific than that, because these are ballpark numbers and vary widely from organism or organism and even cell to cell.)
The process of cell differentiation inactivates large blocks of genes. This paper suggests that only ~6% of mammalian genes are ubiquitously expressed, while each tissue tends to express only 30-40% of the whole genome it carries.
Taken together, these two facts imply that an organism whose cells did not copy permanently inactivated genes could save as much as half the energy it would have to spend otherwise on genetic replication, which in the first paragraph I argued was not insignificant. Nonetheless, all of the organisms I can think of put full copies of their entire genomes in every cell that will ever need to multiply (mature red blood cells do not contain copies of the full genome, but that is only because they do not have a nucleus). Are there any species that exhibit this parsimony?
I recognize that a mechanism for doing this would be nontrivial, because some genes are inactive during differentiation but must be present to become active later, but life, uhh, finds a way.

To put these numbers in context, the human body has a daily ATP budget on the order of 100 moles. Translating that to numbers of ATP molecules ($\approx10^{26}$), the quantities you cite are minuscule. Looking at figure 3 of the paper you link, those estimates are more burdensome (accounting for the whole genome) but are still tiny as a fraction of the energy budget (bottom axis).

Also: you might be interested in the ciliate micronucleus/macronucleus organization as a related strategy.

@MaximilianPress The ATP budget of the whole body is not a good number to compare the costs of a single cell with. There is a lot of ATP available every day, but there are also a lot of cell divisions.

Fair enough, to me it was not clear which those numbers referred to, though going back and rereading I see it now. Also, only just noticed: you write $10^{9+3} = 10^{11}$ where I'm pretty sure it should be $10^{12}$. I still think that Figure 3 pretty much has the answer, which is the same: this is not a very large cost for selection except at astronomical population sizes (bacteria), which have quite compact genomes already (possibly related).


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Is Zayed et al.’s revision of Orthornavirae robust?
Zayed et al. (April 7, 2022) in Science “Cryptic and abundant marine viruses at the evolutionary origins of Earth’s RNA virome” report several major hitherto-unknown Ribovirial phyla:

The two most sampled, Taraviricota and Arctiviricota, had the lowest normalized abundances.
To mitigate issues of subjectivity, their RdRp-based phylogenetic analysis was developed to recapitulate the established ICTV-accepted taxonomy (97% agreement).  Their new tree shows a very different early evolutionary history, for example splitting Duplornaviricota into 3 distant phyla:

Are these findings robust?  The unknown megataxa and the revision of Orthornavirae?

Do you really think that there is someone on this list who has read and is better able to assess this paper than the referees assigned to it by Science? I presume you feel it important — I have no idea — but if it is I’m afraid you will have to wait either for direct responses to the journal, or future publications citing it. This is a question and answer site  about biology, not a journal club.

Can you identify the evidence supporting alternate tree topologies? If you show that evidence here we might be able to judge it.

Paper certainly looks robust - you would need to dig out the original data and analyse for yourself if you wished to compare. You can find the annotated data here: https://datacommons.cyverse.org/browse/iplant/home/shared/iVirus/ZayedWainainaDominguez-Huerta_RNAevolution_Dec2021

@David Sometimes in phylogenetics the reviewers of science are just a joke (see the Omicron evolved in west africa retracted paper where the non-omicron raw reads were just contaminated with later omicron strains)

The main difficulty here is that it is risky to feed mafft directly with so distant RdRp, the resulting alignment will be a mess for sure. You can try running a MCMC optimizing both the tree and the alignment (after subsampling the dataset) and see if the deep branches topology stays comparable.


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How does the SNS increase the heart rate when it causes an increase in cellular uptake of potassium?
Since β-Adrenergic stimulation increases cellular uptake of potassium, this will reduce the plasma concentration of potassium. Thus, a more negative membrane voltage will arise as the potassium ions flow out of the cardiac muscle cells more easily due to the more steep ionic gradient set.
This, consequently, makes it more difficult for an action potential to fire, and as a result, a decrease in the heart rate. So now since the sympathetic nervous system increases the heart rate, then why does this beta adrenergic stimulation occur? It would decrease the heart rate, so what is happening?
This information is from the medical physiology Guyton and Hall textbook, page 384, put into my own words if I have understood it correctly. This is the entire quote from it:
"β-Adrenergic Stimulation Increases Cellular Uptake of Potassium:
Increased secretion of catecholamines, especially epinephrine, can cause movement of potassium from the extracellular to the intracellular fluid, mainly by activation of β2-adrenergic receptors." Or does this mean that the stimulation causes a direct intake of potassium ions FROM THE PLASMA INTO THE CARDIAC CELLS, hence causing a less negative membrane potential and an easier firing of an action potential?
Many thanks in advance!

It's important to keep in mind that extracellular potassium concentration is normally very tightly regulated at 4.2 mEq/L (±0.3 mEq/L in nonpathological circumstances.) It's precisely because so many cells are so sensitive to extracellular potassium levels.

Since β-Adrenergic stimulation increases cellular uptake of potassium, this will reduce the plasma concentration of potassium. [Emphasis mine.]

If this were the case, the entire body would need respond to increased K+ levels, which would present some difficulties. So your second interpretation is the correct one.

Or does this mean that the stimulation causes a direct intake of potassium ions FROM THE PLASMA INTO THE CARDIAC CELLS, hence causing a less negative membrane potential and an easier firing of an action potential?

The effect of receptor stimulation is localized to the cells which have that receptor. So β-adrenergic receptor stimulation causes in increase in heart rate and contractility, whereas β blockers decreases same.
More than I knew and more than you probably want to know at this point abot about β-adrenergic receptors in the heart
One of my mnemonics for β-adrenergic receptors was "1 heart, 2 lungs" to remind me that the heart was predominantly β1 and the lungs β2. β2 stimulation in the lungs decreases smooth muscle contractility, which is why we used to give epinephrine to those with asthma attacks. That's been replaced with albuterol and atropine, but epi is still useful if the attack is severe enough.

Hey thanks very much for your help! So do you mean that the heart does not have as much of β2-adrenergic receptors? But so they still do have some, right? So during for example exercise, the SNS is activated stimulating the β2-adrenergic receptors to cause an influx of potassium, hence causing a more positive membrane voltage, and as a result, the heart muscles are able to contract more easily, increasing the heart rate? Many thanks again!

Yes, they have both, but β1:β2 is about 70:30. If this answers your question, you might consider accepting the answer. Thanks.

okay cool! And so just to summarize it, is the answer to this: "So during for example exercise, the SNS is activated stimulating the β2-adrenergic receptors to cause an influx of potassium, hence causing a more positive membrane voltage, and as a result, the heart muscles are able to contract more easily, increasing the heart rate?" a yes?

Well, it's also linked to CAMP and Ca++, but for the purposes of your question, yes. See the source I linked to for how complex it is, and this was the easier of a number of papers. Most of the papers dealing only with K+ involved the treatment of heart failure... so weren't too helpful.

great! thanks so much!


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COX enzyme inhibitors
The use of aspirin inhibits COX-1 and hence the production of TXA2. This would prevent the aggregation of platelets. However, inhibition of COX-1 should also inhibit the production of PGI2 which is an antithrombotic prostanoid. How is the overall effect of aspirin leaned towards antithrombotic if it also has prothrombotic effects (inhibits PGI2)? Many thanks in advance!


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Is 50Hz noticably worse for eyes than 60Hz on a 4K monitor?
I was told in ux.stackexchange that this question is better suited for biology.stackexchange, so, here we go ;).
I have a 50Hz 4k monitor (28 inch and using 1920x1080 scaling - so, the text is super smooth and pixels are non visible from my 90 cm distance as I sit) but I can't set it higher to something like 60Hz.
Does this equals to some problems long term or the 10Hz difference is not something I should be worried at all?

Welcome. Why would any refresh rate be harmful to your eyes?

@AliceD people have different views on this topic. A lot of people say higher refresh rate is easy on eyes. That indirectly says 60Hz is less good for your eyes. See this https://superuser.com/questions/302415/is-60hz-refresh-rate-as-bad-as-i-believe-it-is The discussion in comments is not clear.

Also, the more I read that higher refresh rate like 120Hz is easy on eyes, why we still have 60Hz monitors? They would potentially be straining eyes more for maybe half of the customers?

Yes, flickering can cause eye fatigue and headaches, but 50Hz vs 60Hz would only be relevant if your 4K screen was built in the old CRT technology, which certainly not the case.
Todays screens do not flicker at the refresh rate frequency, instead you should check the backlight flicker, which is, sadly, not always disclosed  by the manufacturer.
Read more at: https://www.rtings.com/monitor/tests/motion/image-flicker


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Does ellagic acid dissolved in DMSO react with Brain Heart Infusion media?
I dissolved 2mg of Ellagic acid in 500 microliter of DMSO. I used 100 microliters of this solution to test for antimicrobial susceptibility against E.faecalis by adding it to 100 microliters of BHI media. After incubation for 24 hours in 96 well plate, I noticed precipitate at the bottom of the first row in the wells, which was confirmed not to be microbial growth . Another observation I made is that there was a distinct change in color(brownish) in the well. I tested other antimicrobial compounds as well but I had no issues. I repeated the experiment but got the same results, which lead to high optical density values.  I maintained the ideal pH range mentioned for the media.
My question is what caused the formation of precipitate? Is there a reaction that takes between ellagic acid and the media?
EDIT: Ellagic acid is poorly soluble in water(0.82 g/L) hence DMSO(dimethyl sulfoxide) solvent is used. The media requires pH  7.4 ± 0.2 for its properties to be stable. The reason I posted this question here is I am not sure if there is any reaction taking place, or if any other factor is responsible for the formation of precipitate and also because it is about antimicrobial susceptibility testing.

Please [edit] the following information into your question: 1) What is BHI media? 2) What is the solubility of Ellagic acid in water? 3) Is Ellagic acid's solubility dependent on pH and if so how does this relate to the pH of your media? Have you tried mixing equal volumes of Ellagic acid and your media? How about with just water? ——— Finally, if this is a reaction with the media, then this would be better moved to [Chemistry.SE] — either delete from here before reposting or request migration because cross-posting is impolite.

Hint : look at the structure of Ellagic acid. Is it like tannins? How do tannins react with proteins? All in Wikipedia.


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What is mechanism of action of ellagic acid as an antimicrobial compound?
Ellagic acid (a polyphenol) works as an antimicrobial compound. But what is its mechanism of action?
I found these 2 research papers related to this, however the mechanism of action is not clearly explained in either of them. Is there a paper that effectively explains the mechanism of action?

doi:10.3389/fmicb.2019.00829(in page 2, it is mentioned that the compounds are known to involve many sites of action at the cellular level, but why does it affect the site of action?)
doi:10.1002/chem.202000354 (In page 3, It has been postulated that ellagitannins inhibit the growth of microorganisms by sequestering metal ions critical for microbial growth, but direct bacterial targets remain unidentified.
Is there a paper which explains why it inhibits growth more clearly?

What do you mean by mechanism of action? I would argue that those papers both present possible mechanisms of action related to cellular adhesion. Why does that not answer your question?

@MaximilianPress Indeed, in the first one, the entire second paragraph is entirely about this question; in the second one, it's a picture within the abstract - pretty rare to find a picture in an abstract, for sure, but certainly not hidden information. OP - can you clarify what is missing/where the gap is between these papers and what you want to know?

Thank you for editing, but I don't think you've adequately addressed the above comments and thus have voted to leave closed. For example, as noted by Bryan the abstract of the second paper you link shows a clear mechanism that you seem to be ignoring. ——— Also note that questions on this site work best if they are narrowly focused — an example would be asking why biofilm disruption is important for antimicrobial activity, or better yet how biofilms contribute to infections in Streptococcus (including a summary with references of what you've learned about the question from your research).


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Are, or how are, polyuria and diuresis different?
Polyuria - Wikipedia states:

Polyuria (/ˌpɒliˈjʊəriə/) is excessive or an abnormally large production or passage of urine (greater than 2.5 L[1] or 3 L[6] over 24 hours in adults). Increased production and passage of urine may also be termed as diuresis.

whereas Diuresis - Wikipedia states:

Diuresis (/ˌdaɪjʊˈriːsɪs/) is the excretion of urine, especially when excessive (polyuria). The term collectively denotes the physiologic processes underpinning increased urine production by the kidneys during maintenance of fluid balance.

These are incredibly similar definitions, which even appear to reference each other. Can anyone here provide any clarification?

We expect questions to show some evidence of the effort you've taken to understand the problem. If you've found definitions of these terms that seem the same, could you cite those? Perhaps quote them briefly with a link, and point out why they seem the same, and why you think they should be different?

@BryanKrause, I believe that I have added what you request.

Probably better on SE Medical Sciences.

@David, are you able to transfer it? Nobody appears to be able to answer this.

No, only the mods like @BryanKrause (the diamond indicates he is a moderator). So what you can do is raise a flag and under "other" ask for the transfer. But it would be a good idea to first modify your question as he suggested. Alternatively, delete and post there.

@David, see https://medicalsciences.stackexchange.com/q/33937/28762.

Ok, I will close it as double-post. No need to migrate it.

I’m voting to close this question because it has already been double posted to medical.sx: https://medicalsciences.stackexchange.com/questions/33937/are-or-how-are-polyuria-and-diuresis-different

Thanks, @Chris.


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Why isn't the resting membrane potential at equilibrium?
There has been a question asked regarding the purpose of ion pumps, and the main answer was that the resting membrane potential isn't in an equilibrium state, so the potassium keeps flowing out. Other sources claim this, too.
But why is this the case? For example(in this case considering only sodium and potassium), wouldn't potassium be forced out the cell when sodium starts to enter, and in the same way that potassium builds up an electric force to match its diffusional force to reach equilibrium, the electric force of potassium get stronger to the point that it can counter sodium's inflow? This would create a new equilibrium, albeit different from potassium's Nernst potential, but still an equilibrium.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Short Answer

This would create a new equilibrium, albeit different from potassium's Nernst potential, but still an equilibrium.

The Nernst equation is how you determine the voltage at which an equal number of potassium ions move in each direction across the membrane; that seems to be what you are calling "equilibrium" for potassium. If you have two ions and you'd like them both to have zero net flow, their Nernst potentials must be identical. The Nernst potential depends on relative concentration; the only way to change Nernst potential is to change relative concentration.
The Goldman equation will help you find a different "equilibrium": the voltage at which net total flow of all ions equals zero. This gives you the membrane potential with multiple ions present; however, at this equilibrium, as you've read, individual ions are not at equilibrium; for a typical neuron, you can expect that at the resting potential given by the Goldman equation you will have about equal potassium leaving the cell as sodium entering.
Longer Answer
In a typical neuron, there is more potassium and less sodium inside the cell relative to outside.
This makes a negative Nernst potential (=reversal potential) for potassium: to stop net flow of potassium down its concentration gradient and out of the cell, you need negative charge inside.
Similarly, there is a positive Nernst potential for sodium: to stop net flow of sodium down its concentration gradient and into the cell, you need positive charge inside.
The resting membrane potential is a weighted sum of these potentials that are driven by concentration gradients. The relative contribution of different ions to the membrane potential depends on their permeability; the more permeable the membrane is to an ion (through specialized channels), the more important that ion is for setting the overall membrane potential.
For a typical neuron, the resting membrane potential is near the potassium reversal potential, but not quite as negative, due to sodium (and other ions, but for now we can just think in terms of these two).
Let's say, for example, potassium reversal is -90 mV, sodium reversal is +50 mV, and the membrane potential is around -70 mV. The reason it's around -70 mV would be because that's precisely the voltage where as many potassium ions are flowing out of the cell as sodium ions are flowing in.
If pumps keep the concentrations of sodium and potassium constant inside and out, this will stay the same indefinitely: concentrations stay the same means reversal potentials stay the same which means the membrane potential stays the same, as long as ion permeabilities stay the same.
However, with no pump, the sodium concentration inside is rising, and the potassium concentration is falling. That means the reversal potentials won't stay the same. As the potassium concentration in and out becomes more similar, the Nernst potential for potassium drifts towards zero: you don't need any voltage to stop net potassium from flowing if the concentration is equal inside and out. As the sodium concentration in and out becomes more similar, the Nernst potential for sodium drifts towards zero. These potentials are not intrinsic to the ions, they are entirely a function of relative concentrations inside and out. If you lose the relative concentration gradients, you lose the voltage, and, importantly, you lose the ability to influence membrane voltage by changing the permeability of particular ions.

What I'm curious about is why potassium just leaves the cell without forming an electric gradient (by leaving behind anions) when sodium starts flowing in. Wouldn't potassium eventually be attracted back, match the sodium inflow, disable more sodium from coming in, and reach an actual equilibrium as the resting membrane potential?
This is the same way the electric force matches the diffusional force to reach the potassium Nernst equilibrium (which is when we're only considering potassium), but this time also matching the added diffusional force by the sodium inflow.

@SentientRays At the resting potential, the sodium entering equals potassium leaving; that's what the Goldman equation tells you: what voltage will the cell be at when the charge moving is equal. If 100 potassium ions leave and 100 sodium ions come in, there's no electrical change: +100 - +100 = 0. If enough ions move so that concentrations change (like if a pump isn't keeping them constant), you need to redo your calculations.

Oh. So then would the reason sodium increases the membrane potential a bit be that there's initially some space for the sodium to go to, therefore making multiple sodium entering equal one potassium ion leaving for a while until it fills up and one sodium equals one potassium? But then, after that other ions will not affect the membrane potential. If calcium enters after potassium and sodium establish themselves, since the cell is in a state where one charge entering one charge leaving, one calcium would kick two ions out and not affect the membrane potential at all.

@SentientRays Not really following and I don't think anything you are writing is grounded in reality. Use the Nernst and Goldman equations, they tell you everything about what will happen in the cell: Goldman equation tells you what the membrane potential will be, Nernst equation tells you the equilibrium for each ion. Ions will always move according to their Nernst potential relative to the membrane potential.

Alright. I was just wondering if you could explain the mechanics behind exactly why ions change the membrane potential before reaching the inflow-outflow balance.

@SentientRays If the membrane potential is more positive than the Goldman equation gives, you can know the change in membrane potential will be towards the Goldman equation potential. That means slightly more positive charge leaving than entering, making the cell more negative and closer to the equilibrium potential.


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What happens to the empty space ion pumps create?
Sodium-potassium pumps pump two potassium ions in and three sodium ions out. That means that it creates space for one more ion. Eventually, it's going to be filled. The concentration will be fine, as it would be 3 sodium out and 3 potassium in (because one potassium ion flowed in), or 2 potassium in and 2 sodium out (as three goes out and one comes in).
However, sodium-potassium pumps supposedly change the membrane potential by pumping more positive ions out than in. Wouldn't this be nullified if another ion comes in to take its place?

I’m voting to close this question because it: 1) contains multiple questions; 2) shows no evidence of prior research; 3) is unclear; and 4) appears to based on an assumption that seems to reveal a lack of basic understanding of chemistry — if so, this is best rectified by taking an chemistry course or an online equivalent (e.g. from Khan Academy).

There is no special "empty space" due to the action of these pumps. Ions are very, very small and even in liquid there are always gaps between molecules/ions/atoms. If you dissolve a bunch of salt in a glass of water, the volume doesn't change noticeably, but even if you measure carefully you find it actually decreases. That's because water molecules surround the ions and take up a bit less space than they would in a pure solution.
Additionally, sodium, potassium, other ions, water, etc. can all cross membranes by a variety of mechanisms. For charged ions, they cross the membrane primarily through ion channels though also through transports, some of which use ion concentration gradients to move other things (see https://en.wikipedia.org/wiki/Cotransporter).
Though flow through these channels is indeed somewhat random, in aggregate you can predict how much ions will move. It isn't as though a random ion will "replace" a sodium ion that has moved, rather, all ions will have net flow according to their concentration gradient and any electrical gradient across the membrane. You can determine the direction of net flow for given ion using the Nernst equation.

Well ... this does not apply to ammonium sulphate, and is one reason for the popularity of nomograms.  Try dissolving 50g ammonium sulphate in 100ml water, for example, or try dissolving 30 g SDS (sodium dodecyl sulphate) in 100 ml water: in both cases there is a very considerable increase in volume.  (In my experience, a very common mistake in biochem labs is to dissolve 30g SDS in 100 ml water, ignore volume changes, and assume this is 30% (w/v) solution: it isn't (the final volume is considerable greater than 100ml).

What I actually meant by "empty space" is how much ions can enter before before potassium flow and sodium flow equalize, and did not mean actual space (don't really know why I termed it that way). I can imagine a pump leaving one charge worth of "empty space (that is, one ion is needed until potassium and sodium flow equalize. This obviously isn't exact, but is true on average)", therefore slowing down potassium flow a tiny bit (less diffusional force), and allowing sodium to build up in the cell (one sodium ion on average), nullifying the pump's contribution to the membrane potential.

@SentientRays The pump's contribution to membrane potential is fairly minimal, a couple mV perhaps. If you want to use a water analogy, think about it as pushing some water to one end of the pool; there's nothing preventing it from flowing back, yet you can have slightly more water on that side indefinitely if you keep pushing. I've repeated this a few times to you now, but use the Nernst equation and Goldman equation; have a look at them and play around with possible values to input. These are the important things.

Related questions I've answered: https://biology.stackexchange.com/questions/88730/when-is-voltage-generated-across-a-membrane/88777#88777 https://biology.stackexchange.com/questions/81570/neuronal-membrane-resting-potential-for-large-cells/81571#81571 https://biology.stackexchange.com/questions/95192/why-do-ion-leak-channels-exist/95193#95193

Your question implies that proteins are like metal tubes (i.e., constant shape and form). This, however, is a bad assumption since there really is no "empty" space. Proteins have active sites and their movement is a highly chemical process; they often change shapes (e.g. hemoglobin) as well. Additionally, proteins are really "smart" (i.e., highly specific) and won't accept different ions. This "space" you refer to is very small, diagrams are misleading in that sense. You can look up 3D renders of proteins and quickly realize that they are difficult to understand. There is always the possibility of taking in different ions. This can definitely affect cell metabolism and function not because the cell cannot get rid of the unwanted material (homeostasis), but because when they do, they expel the material onto neighboring cells.
I am sure my answer is probably unsatisfying because you've asked too many questions under one post making it difficult to focus in on one topic. Try researching each question on your own first and if you do not find a satisfying answer, you can always ask a question in this forum :)


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Is this a Sunflower? Well over 10 ft tall
Huge stem but not the broad heart-shaped leaves like I have seen in pictures of sunflowers. Leaves look more like those of Helianthus. Stem is a good 6 inches around and smooth not hairy. The red branches are also throwing me off. No flower yet. . This is an Elementary School garden in Clermont, (central) Florida. We planted sunflower seeds, which is why, when they began growing that is what I thought they were. After much research I couldn't find any pictures that look like these plants. I have tomatoes and pepper plants in the same raised bed and it gets misters every 12 hrs for 3 hrs. Full, hot, Florida sun. If they are not sunflowers nor vegetable, we didn't plant it on purpose.

The trunk's glabrous whereas in sunflowers it would be hairy. As to Identification - is it developing a flower head of any sort anywhere? That might help pin it down if you can post a photo of that.

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 plant. The location can be an essential clue for identifications. Clear, closeup photos of a leaf from above could also be helpful. Such questions should also use the species-identification tag. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

I've made a few (what I hope are) improvements to your post — please check and make sure I've not misstated anything. In particular, I'm not sure what the red lateral structures are — I think they are branches rather than petioles (leaf stalks), but please change that if I am incorrect. ——— Also, this looks like it might be a school garden — do you have any way of finding out if these were planted intentionally or whether they are "volunteers"?

Could be pokeweed, though I associate that with reddish stems. Can you please edit with photos of the leaf blade

Pokeweed is a good guess. Whatever it is, it's definitely not a sunflower. Did you plant a maximillian sunflower by accident? Doesn't strongly resemble that, either, though.