text:
What are the characteristics of a living organism?
It seemed fairly basic at first, and yet I have to ask because even a quick Google search reveals that it doesn't seem to be quite so straight-forward anymore. After more research, I found multiple lists, some with six points, others seven or eight. Some lists shared six points and only differed on one, but others had five different points and divided and named the points differently such as Respiration vs Metabolism, Adapt vs Evolve, Homeostasis vs simply consisting of cells, etc.
Maybe it never really was simple, but when I learned basic middle school life science in the 1990s I seem to remember a clear and concise list of 7-8 distinct terms. I know they were just the summary given by the author of whatever textbook we used, but I remember several sources having similar lists (cannot say for sure if they were exactly the same), including a textbook, an educational video game, and a poster.
I'm also told that this has become a bit of a debate in the biology community, whether such a black and white distinction of "living" or "not living" is prudent. Questions such as this one on viruses are an example of how it is difficult to categorize life. However, I noted in my research that there was still clearly overlap in meaning of definitions, it was just in description and division of points that they differed. This suggests to me there is still a generally agreed upon core definition that is simply described by different people, specifically authors, with a few areas of possible debate.

What are the current generally agreed upon characteristics, the common denominators? (They all reproduce?)
What characteristics are commonly debated and therefore would unwarranted to claim? (Specifying cell structure?)

With the understanding that an answer will require an objective synthesis of a range of content and opinions, debate on what should or should not be characteristics is discouraged. Rather, an impassioned summary of the current  scientific consensus on this question is what I am looking for.
It seems to me that even if this is a topic of opinionated debate, it is certainly at the core of Biology and would be worthwhile to be addressed in an academic manner, be accessible, and available to reference on this site.
(PS - Not in any way a homework question, never was, just a curious 30-year father. Unless you are counting questions I have to answer from a curious little boy.)

I asked a related question. "Does it have it's own ribosomes?" is a good objective classification, but why should anyone care? Ultimately any answer is subjective.

The definition of any subject is open to subjectivity. Asking "What is maths?", "What is programming?", "What is beginners English?" or "What is religion?" in the respective SEs would all be equally be off topic. Additionally, I think the attitude of approaching a new community expecting their answers and then insulting the community is particularly unpleasant.

@James I agree...if that is what I had asked. But I am asking "What are agreed upon characteristics?" This can be done objectively by simply reviewing  all the subjective definitions and summarizing what they agree upon. As you say, everything is subjective at some point, so that is why scientists have peer reviews and such, so by the use of consensus of experts we can arrive at a conclusion that can be labeled objectively correct. And I still believe that voting to close a question with no comment as to why, when it is not obvious, is far more insulting than anything you think I've said.

@James if I am simply not communicating it well I will try to make an edit this evening. But it is a bit difficult to know what to correct with no constructive feedback (besides your own recent comment which did help) so if you or anyone else thinks they can see where I'm going wrong here I'm still just not sure, even after an edit, that it won't be closed again for some unknown reason. Maybe I've expressed my frustration poorly, but can you see that the attitude of approaching a new member of a community and expecting them to know what's wrong without telling them is equally unpleasant?

I didn't mean to say everything is subjective. There are empirical evidences. The issue comes when trying to devise a test to answer "what is living?" Many philosophers have moved away from the living/non-living divide & prefer something a little more nuanced. You've unwittingly stumbled into an age-old, unoriginal, unanswerable question. Here, we like questions that are answerable & want to avoid questions that induce debates. Because of this I'm not sure if any amount of edits will help. Recently in the chat we even considered closing that virus question for the same reasons.

@James I hope with my edit you can see that an answer to this can be even more objective and less contentious than your own on viruses. I'm simply looking for summary and synthesis of material. Not conjecture. Trust me, from my time at Christianity.SE I've learned the fine line between a "truth" question and a verifiable summary.

In meta we're struggling with hwk questions and how to deal with poorly researched/trivial questions & there is some over-zealous closing in the meanwhile. Personally I closed the question because it is too subjective to be answered with empirical biology. A similar question was closed on Philosophy.SE. They said there was no line & the division came down to semantics. It's very unsatisfying.

If you want a practical answer, you can just ask: Is this thing in the tree of life?

@joshua if you read the help pages and meta regarding homework closure you will understand that it was closed not because we literally thought it was your homework

@rg255 Yes, I realize this. I did read it. (Which is why I make light of it mentioning my boy...) And its why I detailed my prior research better in this edit. I considered giving a few sample lists, but...well research it with "characteristics of living organism" Google search and you'll see what I'm talking about. Me quoting multiple lists in the question isn't going to benefit anyone who is actually attempting to answer the question.

I don't think bio.se is the place for this question. However, I'd thoroughly recommend Koshland's 2002 Science article "The Seven Pillars of Life". It has excellent detail & justification for what "life" is. P(rogram), I(mprovisation), C(ompartmentalization), E(nergy), R(egeneration), A(daptability), S(eclusion), PICERAS, for short—are the fundamental principles on which a living system is based.

First of all, you have to note that there is no such thing as a scientific, objective definition of life, and that many scientists disagree on a given definition, and that every definition has it's limits.
However, the one from wikipedia

Since there is no unequivocal definition of life, most current definitions in biology are descriptive. Life is considered a characteristic of something that exhibits all or most of the following traits:[10][12][13][14][15][16][17]
Homeostasis: regulation of the internal environment to maintain a constant state; for example, sweating to reduce temperature
Organization: being structurally composed of one or more cells — the basic units of life
Metabolism: transformation of energy by converting chemicals and energy into cellular components (anabolism) and decomposing organic matter (catabolism). Living things require energy to maintain internal organization (homeostasis) and to produce the other phenomena associated with life.
Growth: maintenance of a higher rate of anabolism than catabolism. A growing organism increases in size in all of its parts, rather than simply accumulating matter.
Adaptation: the ability to change over time in response to the environment. This ability is fundamental to the process of evolution and is determined by the organism's heredity, diet, and external factors.
Response to stimuli: a response can take many forms, from the contraction of a unicellular organism to external chemicals, to complex reactions involving all the senses of multicellular organisms. A response is often expressed by motion; for example, the leaves of a plant turning toward the sun (phototropism), and chemotaxis.
Reproduction: the ability to produce new individual organisms, either asexually from a single parent organism, or sexually from two parent organisms.

Encyclopedia Britannica

Metabolism
Respiration
Sensitivity (responding to stimuli like gravity and sunlight)
Nutrition
Excretion (getting rid of CO2)
Growth
Reproduction
Homeostasis

"you have to note that there is no such thing"... Part of this question is about dealing with just that. Generally agreed upon. Consensus. But you dismissed it and just gave me the results of a Google search (which I've already done). Was hoping for more. The latter encyclopedia version is what seems to me to have been a pretty standardized answer in the 90s. It was in textbooks, educational video games, etc. So if there was consensus then, why not anymore?

@Joshua "textbooks" are not consensus. They are the opinions of the publisher. Anybody can write one, and if it's cheap enough schools will buy them. Textbook authors generally take the viewpoint that younger readers can't handle ambiguity, and so create facts where none actually exist. I'm willing to bet if you traveled back to your childhood, all the media you mentioned didn't completely agree.

@MattDMo if you combined that with a summary of what various definitions do agree on and what they don't, you'd have a winning answer.

Just wanted to alert you that the question has been edited considerably. I believe its still the core question I intended, but hopefully I'm more clear this time. Thanks.


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Estimating RNA concentration from Specific Activity of Labeled RNA
The question reads, Using T7 RNA polymerase to transcribe in vitro a 100-nt RNA off a DNA template. This RNA contains 19 Adenosines. In your 100 uL transcription reaction you added 1.00 µL of α32P•[ATP] that had a specific activity on its reference date (May 6th) of 10.0 µCi/µL. The concentration of "cold" (non-radioactive) ATP in  your transcription reaction was .500 mM. At the end of a 2.00-hour transcription reaction, you run a calibration curve using autoradiography on standards of radioactive ATP plus 2 µL of your reaction to obtain the following data:
Sample-------------------------------------------------------------Pixels
1:1000 dilution of α32P•[ATP] Stock (10.0µL)-------------3.211x10^7
1:10,000 dilution of α32P•[ATP] Stock (10.0µL)-----------2,483,565
1:100,000 dilution of α32P•[ATP] Stock (10.0µL)---------299,215
1:1,000,000 dilution of α32P•[ATP] Stock (10.0µL)-------31,444
Your transcription reaction (2.00 µL)-------------------------102,784
-
Estimate the concentration of RNA (in pmol/uL) that exists in your remaining 98 uL of the reaction.
I am using the equation: S.A = (Chn*(.5)^d/14.3 *Vhn * N * cf)/
                                        Vt*Ccn
where Chn = concentration of the S.A. of the α32P•[ATP] in µCi/µL =10 µCi/µL
Vhn = volume of α32P•[ATP] used in the labeling reaction =1.00 µL
N = the number of A nucleotides in the NA= 19
cf = calibration factor from the standard curve (“pixels”/µCi)= 10278.4 pixels/uCi
Vt = volume of the reaction=  100µL
d = number of days past your isotope’s “reference date” = 7 (May 6th to May 13th given in problem)
Ccn = concentration of cold ATP in the labeling reaction (pmol/µL) =.500 mM =500pmol
After I calculate the S.A. how do use that to estimate the concentration of RNA that exists in my remaining 98 uL of the reaction. I am beyond confused, any help would be greatly appreciated.

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What is the difference between sequence alignment and sequence assembly?
I read the wikipedia page about sequence alignment and sequence assembly but I have not been able to find any difference between the two. What is the difference between sequence alignment and sequence assembly? If there is no different why are the terminologies different?

Sequence alignment
It is done for checking sequence similarity between two or more different sequences. This will give information about how two sequences are different, what is their evolutionary relationship, which residues are conserved etc. Take a look at following sequence alignment between different sequences. (Image courtesy: Wikimedia Commons)

You can see conversation of different amino acid residues in variety of organisms like human, mouse, rat etc.
Sequence Assembly
It is done for creating long consensus sequence from short fragments of same sequence. Generally you would do sequence assembly after sequencing some genome or large DNA fragment. Take a look at following representative image of sequence assembly (Image courtesy: Wikimedia Commons)

Here black sequence is your original sequence which you wanted to sequence. However because of technical difficulties you can't sequence all at once. Hence you fragment and sequence different fragments which are shown in red, blue and green). Looking at overlapping region between different sequenced fragments you calculate consensus. Potentially problematic repeats are shown above the sequence (in pink) Here you are ideally sequencing only one large sequence and assembling it.

but its the same thing right? I mean both could have been given the same name...

Well, yes. Sequence assembly is kind of multiple sequence alignment ! Naming is for avoiding confusion I guess.

@Rishika As Dexter's answer shows quite clearly, it's not the same. It would be inaccurate to say that you are doing Sequence Assembly, when you are in fact comparing genomes (doing sequence alignment) from different species (e.g. as part of a phylogenetic analysis). To say that you are doing Sequence alignment when you are doing Sequence assembly could be correct (for some steps), but slighlty misleading and not very specific.

@fileunderwater is correct. I would say sequence assembly is special case of sequence alignment.

okay, understood

@Dexter Again, it is not. Sequence alignment is a part of sequence assembly algorithms, but that does not make assembly a special case of alignment.

okay, debatable nomenclature

The two tasks are quite different.
Aligning means comparing sequences to find differences between them.
Assembling means that you take a bunch of short sequences and try to stitch them back together to reconstitute the original DNA sequence.

Fig1: Screen capture from DNA Baser Assembler of an 'assembly to reference'. The reference is in purple color. The forward and reverse sequences are red and green. The contig is blue.
Note about the input of the two processes:
The sequences that enter into an alignment have (supposedly) already been cleaned up. Every base is correct/accurate.
The sequences that enter into an assembly are 'dirty' and inaccurate, because it is highly likely that the sequencing machine will generate 'bad' bases at the ends of the sequence. The user will have to manually inspect and clean up the sequences (even though today there are smart assembly programs that can fully automate the process reducing the time from 10 minutes per contig to basically nothing (under 1 second)). It is preferably that multiple overlapping sequences are used for redundancy. This way 'bad' bases are discovered and eliminated.
Once the assembly job is done, the clean contig can be used for further operations (such as alignment).
raw sequences

after reverse complement

final contig

Not necessarily. A good analogy for differentiating the two sequencing strategies (not to be confused with sequencing technologies i.e. illumina, smrt, oxford nanopore etc...) would be a puzzle. In the case of sequence alignment, you would have a bunch of puzzle pieces i.e. your reads and a picture of the finished/completed puzzle i.e. your reference genome to guide you in putting together the puzzle. In sequence assembly, you only have the puzzle pieces and no picture, no reference genome. This makes assembly a much harder task.
In the first case, you would compare the N reads against only 1 reference genome. In the second case you would compare N reads against N "quasi" reference genomes.

Both comparisons are nice, but only half of the truth. I can do alignment of two puzzle pieces (pairwise alignment) without a reference. And I can do reference guided assembly (what you describe is de novo assembly), by using alignment to a closely related reference as a guide for assembly. ( so assembly with a picture that does not show the current puzzle, but a similar one).

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Indoor plants acidic soil
I have a ponytail tree plant. The new growth look anemic, pale and thin. And several leave have browned from the midway to the ends of the leaves. The stem is woody and firm. Though it is in a solid pot, the soil tests dry, and there seems to be reasonable space for root growth. I have just moved it so it can get eastern morning sun for several hours. I have tested the pH of the soil and it tested to be a pH of 4.0. Can someone help me diagnose and treat my plant.
Thank you.

could you add a picture?

That's a super low pH, and I kinda doubt it's real. If you used a cheap home test, it's more likely analytic error (not necessarily your fault, it's just a hard thing to measure) than a real result. 4.0 pH is lower than most plants can tolerate--it's in the range of vinegar. Most plants (I have no experience with this species) prefer a slightly acidic soil, ~6.8pH. So, if your pH is really 4.0, then that's almost certainly a problem. It messes up the cation-exchange capacity of the soil, so even if you fertilize, the plant can't access the nutrients.
You can easily amend with some lime--if you don't want to dig it up, you can just scratch it into the top of the soil, and water through it. It will leech down through the pot. Hope that helps.

I used a Dr Meter soil survey instrument

Although pH 4 is low, it's not impossible. Natural sandy soils in my country can have a pH even below 4 (with aluminium toxicity as result). I agree that liming could work here though.


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Are STOP codons impacted by base insertion or deletion mutation?
I am learning about base insertion and deletion mutations. An example in my textbook is given below.
GUU CCA CAU AUC.
So if there is an insertion (of guanine):
GUU GCC ACA UAU C_ _ (there will be a detrimental effect on the protein created).
I'm a bit confused about how the stop codon will be read. If we have a new example with a stop codon:
GUU CCA CAU AUC UAG
When the mutation occurs (insertion of guanine) will it become:
1) GUU GCC ACA UAU CUA G
OR
2) GUU GCC ACA UAU C_ _ UAG
If mutation 1) occurs, there would be no stop codon, but mutation 2) looks strange to me. So which is the right one?
Thanks

Yes. Mutations can affect STOP codons and they do relatively commonly. These are important because they can lead to significant changes in the resulting peptide and are likely to affect protein functions or phenotype.
For a point mutation (a single base substitution), there are several possible effects:

silent mutation is a synonymous base substitution which does not change the encoded amino acids (this is neutral variation).
missense mutation is a non-synonymous bass substitution which changes only one amino acid in the protein (these can affect protein functions but do not always).
nonsense mutation is a change in a coding codon to a STOP codon (this truncates the encoded amino acid sequence prematurely resulting in a shorter peptide).
nonstop mutation is a change from a STOP codon to a coding codon (this means the amino acid sequence will continue to the next STOP codon resulting in a longer peptide).

Insertions and Deletions in DNA sequence (InDels) are important because they change all codons that follow it (not just the base substituted):

frameshift mutation adds or removes a base which resulting in a change in the reading frame: all bases following will result in new codons, including STOP codons (this commonly results in entirely new protein domains and proteins of different lengths as STOP codons will also be changed. They are encoded in the reading frame like all other codons.

As you can see, mutations which affect STOP codons are very important as they drastically change the protein sequence. This usually disrupts the protein function and causes diseases or inviable embryos. Most of these are removed from populations long-term by natural selection. However, it can rarely lead to entirely new proteins beneficial to the organism and evolutionary changes. This is more likely with duplicated genes where one can change while the other retains the original function.
As such, mutations involving STOP codons are among the most biologically important.  Another important case is splice functions. Point mutations and frameshifts can also affect intron-exon boundaries, resulting in new splice variants, skipped exons, and reading further into introns (which may contain splice junctions or STOP codons).

Let's start with your example:
Wild-type gene looks like:

GUU CCA CAU AUC UAG*

After G insertion, you end up with

GUU GCC ACA UAU CUA G

There are 3 stop codons: UAG*, UAA*, UGA*
You don't see those in your mutated gene, because you truncated sequence. Let's imagine that gene actually goes like this:

WT: GUU CCA CAU AUC UAG* GCG UCU AAA ACG CUA
Mut: GUU GCC ACA UAU CUA GGC GUC UAA* AAC GCU A...

In mutant you got now new stop codon created
Gene, transcribed into mRNA doesn't stop at stop codon, there is whole bunch of sequence after it too (3'-UTR and poly-A tail for Eukaryotas)

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What is the difference between multiple allelism and polymorphism?
From the Scott Freeman textbook Biological Science 4th Edition:
https://www.amazon.com/Biological-Science-4th-Scott-Freeman/dp/0321598202,
Multiple allelism is defined as "the existence of more than two alleles of the same gene within a population."
Polymorphism is defined as "the occurrence of more than two distinct phenotypes of a trait in a population."
I don't really understand the difference - unless it means that two alleles may not result in two different phenotypes?
Additionally, another definition of polymorphism also in the textbook was "the existence of more than one allele at a certain genetic locus."
What does this mean? I was under the impression that all genes had at least two alleles.

can you cite where you are getting your definitions?

There are many different meanings of polymorphism and not all involve different phenotypes. Please [edit] your question and give us more context. Neither of the definitions you use are really correct.

Well, my original definitions came from my teacher, but the definitions provided in my textbook have both cleared up some confusion AND yet further confused me. Which definition of polymorphism is most common?

Can you please indicate what is your textbook and indicate on what page you found these definitions?

The name of the textbook was already given above, but for further detail it is the 4th edition (2011). The definitions were part of the glossary, on pages G:19 and G:23.

The term polymorphism is broad and can have different meanings. Here are your definitions

Multiple Allelism: The existence of more than two alleles of the same gene within a population.
Polymorphism: the occurrence of more than two distinct phenotypes of a trait in a population.

Considering your definitions only, then multiple allelism has to do with genetics while polymorphism has to do with the phenotype.
Most loci (=position in the genome) that contain more than one allele (=genetic variant) have no effect on the phenotype. So multiple allelism does not necessarily yield to phenotypic polymorphism.
On the other hand, plenty of phenotypic variation in a population is due to environmental variation (including what an individual eats) and not to genetic variation. So phenotypic polymorphism is not necessarily caused by a case of multiple allelism.

This answer refers to polymorphism within genetics (for clarification), which as far as I know is the more common use of the term (but that could just be because I'm a geneticist).
Polymorphism in general refers to genetic variation of traits within a population (or species), due to mutations.
A 'single nucleotide polymorphism' is a single change in the DNA sequence of an organism at some point. So:
A -> C
or
T -> G
Or some other combination of these. It is simply a change of a single nucleotide. More specifically, a SNP is present in at least 1% of a given population.
As these mutations (and other types of mutations) accumulate it results in multiple allele variants of a gene.
Here is a good reference: http://www.nature.com/scitable/search-scitable?criteria=Polymorphism
You are right to say that not all alleles will yield a different phenotype.
Finally, in principle, genes do not necessarily have to have more than one allele, it is the result of mutations that cause this.

Please add references to your answer.

My apologies. Reference has just been added.

unless it means that two alleles may not result in two different phenotypes?

That is correct. Due to codon degeneracy.. ie one amino acid can be encoded by more than one set of 3 DNA base pairs... you can a difference in DNA but no difference in the protein. This synonymous base changes leads to no phenotype.
Also it is possible for an amino acid change to occur in a protein and cause no phenotype either, as the change may occur in a region that has no over effect on the protein function, folding and interaction with other proteins.
So as you have eluded too, not all allelic variation leads to a phenotypic  variation.

Is a slightly difference:

polymorphism is a variation in an allele at the sequence level. A common one is Single Mutation Polymorphisms SNPs.
Multiple allelism means that in a population there are more than one alleles for a certain gene.

Please add references to your answer.

My genetic Professor

Welcome to Biology.SE. Please provide non-anecdotal references for your claims, i.e. information that can be checked by others as well. Also take a look at the guidelines on how to provide good answer and consider taking the tour. Have fun on Biology.SE!


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Human Demography - Where can I find this statistic?
In "An Introduction to Genetics" by David J. Merrell, copyright 1975 by W.W. Norton + Co., p. 742, in the Chapter "Genetic Counseling and Eugenics," the author states: "... 50% of the women produce 85% of all children born in the United States."
The author provides an Additional Reading list, but I'm not a geneticist, nor do I have access to much of the listed material.  With that in mind, 1) where can one find the statistic mentioned above? and  2) has this number changed over time?
OP EDIT: In response to comment (a few examples from Reading List of 30 items):
Davis, 1970, Prospects for Genetic Intervention in Man, Science, 170 279-1283
Dubos,1965,  Man Adapting, Yale Univ. Press
Dunn, 1962, Cross Currents in the History of Human Genetics, Amer. J. Human Genet, 14: 1-13
Ehrlich, 1968, The Population Bomb, Ballantine NY
...
Lynch, 1969, Dynamic Genetic Counseling for Clinicians, C. C. Thomas, Springfield, Mass.
...
Petersen, 1969, Population, 2nd Ed. Macmillan
...
1969, WHO Expert Comm. on Human Genetics, "Genetic Counselling(sic), Tech Rept 416, pp. 1-23
I know I can find stats like average ages, etc from the Statistical Abstract of the United States, but where do geneticists find items like the one cited in the Merrell book?

Welcome to Biology.SE! Could please copy paste the reading list or any source that Merrell has indicated?

Note that it is more a question of human demography than genetics. It is still on-topic though.

Isn't this just an interpretation of the rate of childlessness? Say 41.2% of women don't have children. This means that the remaining 58.8% of women produce 100% of children and therefore that 50% of the women produce 85% of children.

If a reading list is given, but it isn't clear from which book the statement is derived, it often works to google the unique aspects of the statement. If general search, which includes books, doesn't work: google scholar, with temporal filter for years prior citing work, often manage to retrieve original source

The CDC has some good stuff. http://www.cdc.gov/nchs/data/nhsr/nhsr051.pdf
But keep in mind that number from your book is likely based on yearly findings in which more than half the women would not be able to have children due to age, voluntary contraception, or other conditions. So it is not reflecting how many children they have over their lifetime. Even in the CDC study more than half the women had no children but few had no plans to have children, couples are moving their first pregnancy to later and later in life, which is going to make it look like few are having children at all on first glance.
 And it's probably not accounting for death rates, the poorest people tend to have the most children but they also have the fewest number live to maturity, which is why they tend to have more (not necessarily consciously mind you) .

That information seems to be censored very often. In certain countries there are even laws preventing asking certain quesitons about demography, i.e. France, and In America you should have transparency for the government censors on household numbers, but apparently the official numbers discreetly use 4+, to not publish families of 8,9 and 10.
Your question doesn't say if that figure holds for 1-2-3 generations.
Big family traditions extend for more than one generation. so 5*5 becomes 25, and 2*2=4
If you square the figures, the add up very fast... Unfortunately the statistics don't measure higher than 2 children... What you need is a graph like this:
It illustrates that "4+" children actually averages about 5.5-6.5 children (vaguely)...
If your square that sum, his statistic may be true.
If you multiply the household percentage and the number of children you get a bell curve that is different:

The 50 percent of the women represented by the black and white graph, it seems to 3.5 children at that village, and the number of children is in the top graph, so it indeed appears that in only one generation, women with more than 3 children, for that graph, indeed produce 75 percent of the population.
Sorry that's my lame attempt to answer the question. Having checked it may help a teeny bit. it's not a sci reference though. sorry.
family size is a factor of education, professional ambition, culture, religion and ethnicity.
https://www.mtholyoke.edu/courses/rschwart/encounters/family_size.htm
http://www.pewsocialtrends.org/2015/05/07/family-size-among-mothers/

You can try to use some standart data sources, for example:

NASA's Gridded Population of the World - LINK
Geonames - LINK


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What kind of bee can dig through stone?
My house (in Israel) has a concrete structure, with a decorative veneer of Jerusalem Stone at least an inch thick. Yesterday I came out to discover a little hole in the wall - and a pair of bees coming in and out of it! (See video)

This wall is no more than 5-6 years old, and I have never drilled anything there; they're not reusing a human-made hole. I must conclude that the bees somehow dug that hole.
Is that possible? What kind of bee could do this?
Update: As interesting as these bees are I didn't want them living in my wall, so I filled up the hole with a silicone-type glue. A few hours later, they had dug through that, too.

I don't know the answer to your question, but from the video it looks possible that the bees adapted an existing hole/crevice and added mud around it, giving the appearance that they drilled a perfect hole.

Here's a paper in Current Biology1 on the discovery of a species of bee (Anthophora pueblo) in Utah (US) that burrows through sandstone. Pretty cool!
Sandstone is harder than limestone, so I suppose it could be possible for this type of bee to get through your wall material, though Utah is a long flight from Israel.
Perhaps you have discovered a related species of Anthophora local to where you live (perhaps this one?), except that it is unclear if the bee in your picture has the same large mandibles that would help it dig through stone:

As sandstone is harder than other substrates bees excavate (e.g., sand or soil), higher energy and time costs are expected. Mandible wear is consistently seen in older females, a consequence of excavation that likely limits their further use.

Unless you have a lot of similarly-sized and -shaped holes in your wall material, with large-mandible-d bees coming and going, it seems reasonable to infer that this hole came from something else and that these particular bees are just reusing it.

1. Orr, M.C., Griswold, T., Pitts, J.P. and Parker, F.D., 2016. A new bee species that excavates sandstone nests. Current Biology, 26(17), pp.R792-R793.

It's best practice to spell out references to papers in full, as links may go dead after a while.

I would not expect a DOI link to go dead.

Thanks for changing all that.

Can you explain why you would expect lots of similar holes if these were excavating bees? It's my understanding that these are solitary bees, so they wouldn't necessarily have other relatives trying to live nearby? Also see my update - these bees definitely can dig through glue, at least.

@Shaul Behr: And, moreover, given how compatible the size of the hole and size of the bee are...

My expectation was based on similarity with the linked species of bee, which appears to excavate many similarly sized and shaped holes in a concentrated area. But you have added more information to your question, and hopefully that will help others answer your question correctly. More pictures of your bees may help others, as well.


text:
Why does vision gradually becomes dimmer in bright setting?
I don't know if this is only happens to me, but if I am in a well lit room and I stare at one point or just look at one area without moving my eyes around my vision in that specific light setting becomes dimmer. I can look around and everything feels like it is dim and lacks the bright light that originally radiated through the room. So I was wondering how and why this happens? I suspect(I am quite dusty in my ophthalmology) my eyes maybe relaxing and taking less notice of the intensity of the light, if so what makes it do so? As a side note this occurrence hasn't affected my life, I am just curious as to why it happens. Another note response to some of the comments, this isn't like walking into a well lit room and get bombarded by the light and eventually adjusting to it. This is like sitting in a well lit room for 15 minutes and then things just become dimmer and less intense. I've also observed this only happens with artificial light and may have some link to the type of light bulb.
I would like to add that this happens if I concentrate on one area or object. So if I were to read a book or be on my laptop, the light around me would feel dimmer. I suspect it has something to do with my eyes focusing on one source, if I were reading a book and this happens, the words become more prominent.

You mean when you just enter a bright room then things appear bright and they seem to dim down after a while?

Answer is linked to expression of proteins and sequestration of those proteins as amechanism to adjust light intensity percived by eye

WYSIWYG not really, I understand what you are saying, this is more like sitting in a well lit classroom for 15 minutes and suddenly everything becomes much less intense and much more dim and gloomy.

Always Confused I feel like your description of pupil becoming narrow might have something to do with this I'll look it up and see, but if any of you could beat me too it I would be grateful.

Always Confused, this is not the case, as the issue only occurs after some time. Light-adaptation is not nearly that slow, so that explanation is invalid.

I get this too, but I understand exactly what you mean unlike previous comments. Only happens when staring, can be almost blurry sometimes.


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Why does a high osmotic pressure pull water in, yet a high hydrostatic pressure pushes water out?
When I normally think of high pressure, I think of it as pushing something away from the zone of high pressure.
Yet for a high osmotic pressure, water is pulled IN to this high osmotic pressure region.

Why is this the case?

Thanks for the response @AlwaysConfused.  Sorry if it was unclear. I am just confused as to why a "high osmotic pressure" like in the picture above, doesn't push water away from the high pressure region.  Because if we are talking about e.g. air pressure, the air would be pushed away from the high pressure region.

Great question, the answer has to do with the definition of osmotic pressure and the difference between this pressure and "hydrostatic pressure" which is the water pressure you are thinking of.
Here is the definition of "osmotic pressure" given by Google:

the pressure that would have to be applied to a pure solvent to prevent it from passing into a given solution by osmosis, often used to express the concentration of the solution.

Osmotic pressure in this definition is best illustrated by the commonly used tool to show osmotic pressure, often seen in a textbook as something like this:

In this picture, osmotic pressure is roughly how hard do you have to push down on the water on the right to make the levels the same on the left and right, despite the difference in concentrations. Osmotic pressure is not a pressure of water, as your question seems to imply, it is a pressure of the solutes in the water.
If it helps, I think it would be appropriate to think of this as sort of a "suction" on the water. Net flow of water stops when:
osmotic pressure - hydrostatic pressure = 0
...on the right side of the diagram.

Hi, @Bryan. Another user was asking about this and was confused about the pressure being applied to the pure solution. I think the quote about pressure being applied to the pure solution is a widely spread error (or maybe the pressure is doing something weird). As you say, you're pushing down on the right (non-pure) side of the tube and textbooks agree with this. So it might be a good idea to fix the quote in your answer. Thanks

Osmotic pressure is simply... Negative pressure exerted by solutes in the solvent.. That will draw the solvent into the solution.
External pressure,(+VE)exerted on the solution side to prevent the flow of solvent into solution across semipermeable membrane measures... Total magnitude of OSMOTIC PRESSURE (-VE) created by solutes.

Hi and welcome to Biology_SE. Answers are much more appealing if they cite references to books/papers and if they are formatted in a more organized layout.


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Plaque rupture flow chart reading
I am having a bit of trouble interpreting flow charts given in my biology question sets.
Given the following stimulus

The Question is :
In which of the following options does each substance play two different roles in the series of events from plaque ruprture to MI?

ADP and collagen
Collagen and Fibrinogen
Antithrombin III and collagen
Fibrinogen and antithrombin III

The answer is:
"Fibrinogen binds to the glycoprotein (GO) IIb/IIIa leading to the cross-linking of platelets. It is also converted into fibrin which stabilises these cross-links and leads to aggregation. Antithrombin III inhibits the activation of the coagulation cascade and also inhibits the production of thrombin. The answer is D.
My issue is:
This answer doesn't make sense to me.
The fibrinogen square connects to the "Cross links-platelets via GPIIb/III receptor" square, which THEN connects to the "Platelet cross-links stablised" square (i.e. "Fibrinogen" doesn't directly connected to "Platelet cross-links stablised").
Why does this count as "two different roles" yet e.g. "Exposure of collagen" connecting to "platelets adhere to collagen" which connects to "Platelet activation release of TXA2 and ADP" not count as "two different roles".

The given correct says fibrinogen has two roles. It links to itself, and it links to other proteins. These are two separate functions. The drawing makes it harder, but it still shows fibrinogen in two distinct places. You seem to have missed it under "thrombin".

I see. The arrow coming out of "converts fibrinogen to fibrin" is a bit faint and I missed it. Thanks for pointing that out, spent hours trying to figure it out.


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Why is the resonance frequency of a neuron defined by peak impedance?
I'm relatively new to the field of electrophysiology, so if anything is unclear or incorrect, please let me know.
One thing that continues to confuse me throughout my reading is the property of resonance frequency of a neuron.  Generally, I've seen resonance frequency defined as the frequency at which neurons respond best to inputs of injected current, which makes sense.  What does not make sense to me is why it has also been defined as the frequency at which peak impedance is observed because in circuit analysis, resonance frequency is the exact opposite (the value of frequency at which you have minimum impedance).  The definition for electronics is logical in my mind because that's also the value at which current is at a maximum (since the impedance is lowest).  I'm assuming that the relationship between impedance and resonance frequency is flipped in neurons because of another property I'm not considering (like driving force of ions, voltage-gated channels, etc.), but I'm genuinely curious what the reason is.  If anyone could be of assistance on this, I would greatly appreciate it.
EDIT WITH POTENTIAL RESOLUTION BY QUESTIONER:  I believe one of the pioneering texts discussing neuronal resonance was a Trends in Neurosciences paper by Hutcheon and Yarom (Volume 23, Issue 5, published in 2000).  However, after reviewing this text, I think I may finally understand the idea.  As described in the referenced article (which I would highly recommend), membrane properties of a neuron allow it to act like a band pass filter. A little more poking around the internet led me to the conclusion that it is specifically a parallel resonant band-pass filter (for a brief explanation, visit  http://www.allaboutcircuits.com/textbook/alternating-current/chpt-8/resonant-filters/).  I believe this might be the correct interpretation, but have left it as an open question because if there is something wrong in my interpretation, all you bright individuals out there can point out my mistakes or elaborate further on the concept!  Thank you!

Can you state your source, please.

My apologies, thank you for the response!  I have made that edit and hopefully resolved my question in the process.  Though I would still appreciate hearing your thoughts on this topic!


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What happens to eyeball when you push your eye muscles harder?
I have myopia and I read that the rays of light intersect before the retina.
When I can not see clearly I can push somehow my eye muscles and can see a bit clearly. The object gets clear but moves some distance ahead (getting smaller).
My question is: What is in fact happening to the eyeball? Do the eye muscles contract it and make it more round than ellipsoid thus bringing the retina forward  so the light intersects on it?
In fact I have the feeling that the eye ball gets longer (ellipsoid).

Do you mean squinting? Any sort of tension on the eyes would result in changing of the shape of the eye. A change in shape will bend light differently. The perceived effects you're describing are most likely from you changing the shape of your eyeball to take in more light.
In terms of squinting, eye strain like that won't lead to blindness or worse vision. There's more danger with UV from the sunlight (cataracts) or getting wrinkles from squinting too much in the long-run.


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Self-thinning: slope of log (biomass) vs log (density) is -1/2 whereas slope of log (weight) vs log (density) is -3/2, why?
In self-thinning or intraspecific competition (more relevant for trees I guess) why does logarithm of Biomass vs logarithm Density give you a slope of -1/2 whereas logarithm of Weight vs logarithm of Density gives you a slope of -3/2? Biomass is mass (or quantity) of an organism per volume(or area), weight is mass scaled by gravitational acceleration which is a constant, unless the organism you are dealing with is very very tall. So the plots can be shifted accordingly but shouldn't slopes be more or less the same ?
source: Ecology: Concepts and Applications
by Manuel Molles
www.mheducation.com/highered/product/ecology-concepts-applications-molles/M0077837282.html
.

Welcome to Biology.SE. This is a question of statistics, not biology. You should give it a try on Stats.SE.

I would not expect the slope of y~x to be equal to the slope of log(y)~log(x) (to the exception maybe of when the slope is 1?). Consider this R code for example. x=rnorm(100,40,7);y=x/6+rnorm(100,0,1);plot(x=x,y=y);lm(y~x);lm(log(y)~log(x))

@Remi.b I understand log plots. For example, if you know Stephan's law of radiation; radiated energy E is proportional to fourth power of temp T, in this case, if we plot log(E) and log(T) we will get slope to be 4. But that (value) is not my concern, why are they different is my concern.

@Remi.b I don't understand how is this a Stats question, I think definition of biomass and physics are more relevant here !

I though your question was "why does y~x has a different slope from log(y)~log(x)?" but it rather seems to be "why does log(y)~log(x) has a different slope from log(k*y)~log(x)?" (which is still a stat question). Actually, they should not differ. So either your definitions of Biomass and or weight are wrong (in other words weight != k*Biomass) or you misinterpret / misplot your graphs. You should include your data (or link to the source) and explain how you treated them.

Oh ok, you are comparing graphs from the book you added I suppose. Most of us won't have access to the book so you should show the graphs and also the text that define the variables used in the graph.

@Remi.b I know that this is not exactly a Biology question, it is more about the understanding of those quantities, physics behind them and the mathematical analysis of it. I am not exactly sure where to post it. I googled definitions of Biomass and weight and crosschecked if there was any misinterpretation, but there wasn't any. And as far as I understand it should only offset ( y = mx + c, I mean c by offset ) the plot and not change the slope. BTW I still don't get it how is it a Stats question XD.

Let us continue this discussion in chat.

Biomass here refers to the total mass of all the organisms in the population (in a unit of area), added together.
Weight here refers to the average weight or mass of an individual.
If biomass decreases, that could be because the individuals got lighter, or it could be because there are fewer of them, or both.

Added
I think I see what's happening.
Let $W$ be the average mass of an individual, $N$ be the number of individuals, and $B$ be their total biomass. Then of course,
$B=WN$
Let's start with:

$W$ is proportional to $N^{-\frac{3}{2}}$
$N$ is proportional to $N$ (duh). Let's rewrite that though, as:
$N$ is proportional to $N^1$

But that means:
$B=WN$ is proportional to $N^{-\frac{3}{2}} \cdot N^{1} =N^{-\frac{3}{2}+1} = N^{-\frac{1}{2}}$
Density increases with density (N). Weight per individual  decreases with the -3/2rd power (W). So their product, biomass decreases with the -3/2 + 1 = -1/2nd power  (B=WN).

Plants do not get lighter, the loss of leaves is not considered in this theory and it would apply to all individual in the stand, only the stem density is discussed.


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Confusion about Lotka_Volterra model for two competing species
Lotka-Volterra model for two competing species in Boyce's Elementary Differential Equations and Boundary Value problems' is given by:
\begin{align*}
   \frac{dx_{1}(t)}{dt}&=r_{1}x_{1}-a_{11}x_{1}x_{1}-a_{12}x_{1}x_{2} \\
&=r_{1}x_{1}(1-\frac{a_{11}}{r_{1}}x_{1})-a_{12}x_{1}x_{2} \\
&=r_{1}x_{1}(1-\frac{x_{1}}{K_{1}})-a_{12}x_{1}x_{2},\quad x_{1}(0)>0 \\
   \frac{dx_{2}(t)}{dt}&=r_{2}x_{2}-a_{22}x_{2}x_{2}-a_{21}x_{1}x_{2} \\
&=r_{2}x_{2}(1-\frac{a_{22}}{r_{2}}x_{2})-a_{21}x_{1}x_{2} \\
&=r_{2}x_{2}(1-\frac{x_{2}}{K_{2}})-a_{21}x_{1}x_{2},\quad x_{2}(0)>0 \\
K_{1}= \frac{r_{1}}{a_{11}}\\
K_{2}= \frac{r_{2}}{a_{22}}
\end{align*}
$ r_{i}, i=1, 2 $:is the intrinsic growth rate for prey species.
$ a_{ii} $ :are intra-species interference coefficient of the two prey species.
$ K_{i}, i=1, 2 $ : the environmental carrying capacity for ith prey species.
$ a_{ij} $:  are inter-species interference coefficient of the two prey species.
While in the book by Murray 'Mathematical Biology: I. An Introduction' is given by:
\begin{align*}
   \frac{dx_{1}(t)}{dt}&=r_{1}x_{1}\left(1-\frac{x_{1}}{K_{1}}-\frac{a_{12}}{K_{1}}x_{2}\right),\quad x_{1}(0)>0\\
   \frac{dx_{2}(t)}{dt}&=r_{2}x_{2}\left(1-\frac{x_{2}}{K_{2}}-\frac{a_{21}}{K_{2}}x_{1}\right),\quad x_{2}(0)>0\\
\end{align*}
Trying to match them I get
\begin{align*}
   \frac{dx_{1}(t)}{dt}&=r_{1}x_{1}\left(1-\frac{x_{1}}{K_{1}}-\frac{a_{12}}{K_{1}}x_{2}\right) \\
&=r_{1}x_{1}- \frac{r_{1}}{K_{1}}x_{1}x_{1}- \frac{r_{1}}{K_{1}}a_{12}x_{1}x_{2} \\
&=r_{1}x_{1}- a_{11}x_{1}x_{1}- a_{11}a_{12}x_{1}x_{2},\quad x_{1}(0)>0\\
   \frac{dx_{2}(t)}{dt}&=r_{2}x_{2}\left(1-\frac{x_{2}}{K_{2}}-\frac{a_{21}}{K_{2}}x_{1}\right) \\
&=r_{2}x_{2}- \frac{r_{2}}{K_{2}}x_{2}x_{2}- \frac{r_{2}}{K_{2}}a_{21}x_{2}x_{1} \\
&=r_{2}x_{2}- a_{22}x_{2}x_{2}- a_{22}a_{21}x_{2}x_{1},\quad x_{2}(0)>0\\
K_{1}= \frac{r_{1}}{a_{11}}\\
K_{2}= \frac{r_{2}}{a_{22}}
\end{align*}
so here we have an extra factor in the inter-species terms.
How they are equivalent?

Do you use upper and lower case ‘k’ by purpose for Murray’s version?

Sorry for the mistanke it is upper case K in all , the environmental  capacity.

This is probably not a very satisfactory answer. The very next step in Murray's book (3rd Ed) there is a non-dimensionalised version of the model (eq 3.32) which looks like the one given in Boyce's book (10th Ed) except $\epsilon_i$ and $\sigma_i$ (eq 2, Ch 9). If you plug in $\epsilon_i = \sigma_i = 1$ in Boyce's book you get the same fixed point expression (eq 36) as Murray's book.
The idea is: in the RHS of a $\frac{dx_i}{dt}$ term the $x_i x_i$ represents intra-specific interaction and the $x_i x_j$ represents inter-specific interaction between species $i$ and $j$. You can put constants wherever you like to scale these terms with an interpretation. But the qualitative behavior of the system doesn't change and the coefficients persist in algebra, based on how you plugged them.
But to literally interpret the extra factor in the second set of equations: you can think of them like if $a_{ii}$ is the scaling of intra-specific interference, then $a_{ij}$ is a scaling of $a_{ii}$ for inter-species interaction, i.e. the species $j$ interfere with species $i$ with $a_{ij} a_{ii}$.

Thanks for the contribution. The problem is that both books define the parameters biologically in similar way which doesn’t make sense for me. I think $a_{ij} $ is scaled with $a_{ii} $ and not the opposite without any explanation given.

I agree with @Cheesebread I think that one of the books misdefines the parameters because rescaling is super common and often times mathematically-oriented authors more easily forget about the underlying biological interpretation. This is especially true, as pointed out in this answer, when the qualitative behavior is the same.


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Can mitochondria with "depleted" mtDNA reproduce?
Background
There's a popular group of antibiotics known as fluoroquinolones, abbreviated FQs. They're quinolone abx with a fluorine atom added at position 6 to increase cell permeability. Popular varieties of these drugs include ciprofloxacin, levofloxacin, norfloxacin, and many others. They also go by brand names Cipro, Levaquin, etc. They have a well known side effect of wreaking havoc on the body's mitochondria through numerous pathways.

This stunning image shows the in-vitro result of administering a clinically relevant dose of ciprofloxacin to human tissue for 24 hours (1). The study notes "short, swollen, fragmented mitochondria (smaller aspect ratio) with highly reduced branching (smaller form factor)"
Because the fluorine atom allows for deep tissue penetration, FQs can cross the double membrane of mitochondria, and because FQs are designed to target "double helix" DNA of some bacteria, they also appear capable of targeting the same double helix DNA structure in mitochondria. In bacteria, the FQs bind to the DNA-gyrase, causing breaks in the DNA that are fatal (2) to the bacteria.
Question
A study published in Molecular Pharmacology (3) shows that mtDNA is "depleted" by Cipro:

Analysis of mtDNA from ciprofloxacin-treated cells revealed the presence of site-specific, double-stranded DNA breaks. These results suggest that ciprofloxacin may be causing cytotoxicity by interfering with a mitochondrial topoisomerase II-like activity, resulting in a loss of mtDNA.

The full text of this study is not available as far as I can tell. I can find scientific literature on depletion of mtDNA (4) but what does this mean for the long term health of the mitochondria / cell?

Can mitochondria with "depleted" mtDNA reproduce, passing on the damage from breaks in the DNA? Or is the mitochondria and cell doomed?
More open ended: Is there any literature suggesting mitochondria damaged by oxidative stress can recover (first image), or are they also doomed?

References

Bactericidal Antibiotics Induce Mitochondrial Dysfunction and
Oxidative Damage in Mammalian
Cells
Fluoroquinolones: Mechanisms of Action and
Resistance
Delayed cytotoxicity and cleavage of mitochondrial DNA in ciprofloxacin-treated mammalian cells
Mitochondrial DNA metabolism targeting drugs

Can mitochondria with "depleted" mtDNA reproduce ?

If by depleted, you means reduced number of mtDNA copies, then yes, as long some copies still remain, these can be replicated.
Mitochondrial genome is replicated asynchroneously from nuclear genome [Bogenhagen, 1977], through a particular process (review [Holt, 2012]), and is present in multiple copies. These copies can be different, due to mutation.
Mitochondria do not "reproduce" in the common sense, as they do not undergo mitosis, but have a fission and fusion mechanism (review [van der Bliek, 2013]). The fission products get their half of the mtDNA copies at random when the two mitochondria separate.
Mitochondria with depleted mtDNA can (and do, according to your image) undergo fission.

passing on the damage from breaks in the DNA?

There are DNA repair mechanisms for the mitochondrial genome. In this case, the mechanism of choice to repair double strand break is  microhomology-mediated end joining (MMEJ) [Tadi, 2016], that try to align the ends of the DSB through use of 5-25 bp homologuous sequence. This ususally results in the deletion of some material near the break.
The resulting mutation is conserved, and passed on through replication of this particular mtDNA instance. The mitochondria will contain a mix of mutated and non-mutated mtDNA from now on.

Or is the mitochondria and cell doomed?

One could say a particular mitochondria is "doomed" if there is no [viable] copy of mtDNA; if it is not able to maintain adequate internal membrane potential, it will try to fuse with other working mitochondria, or be eliminated through autophagy/mitophagy.
The cell itself could be "doomed" if there are not enough mitochondria left to meet energetic demands. (or, through mitochondria-induced aptotosis). Some particular human cell type have hypersensibility to fluroquinolones (tenocyte, chondrocyte, osteocyte), with increased cell death, but other types have not manifested this behaviour. [Barnhill, 2012] The reason for this sensibility/resistance is not elucidated.

Thanks! Lots to digest. Do you mind if I edit in some relevant studies? Also, the image doesn't show fission I believe, the first scan just happened to include one mitochondria and the second happened to include two.

Hmm, there is one cell on the first picture, and two on the second. The mitochondria are the green fluorescent-marked structure inside these cells. (using Mitotracker green marker, this is explained in the Mitochondrial morphometry paragraph of your first paper). OK for the edits.

Ah ok I think I initially misinterpreted the image then. So the mitochondria are only the blurry green areas inside the black circles? Does the non-triangular look of the surrounding tissue imply anything? I believe these are two separate samples as I understand it, not a before and after picture.


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What species of insect is this, spotted south-east of Berlin? Habitat: forest near lake shore, Size: body 40mm, w/o antennas and ovipositor
This insect has been spotted south-east of Berlin (2021-10-31).

Please [edit] your post to include as much of the following essential information to improve your chances of getting a good answer: 1) habitat information; and 2) an estimate of the size of the organism. ——— Please see the [tour] and the [help] pages starting with [Ask] questions effectively on this site for details.

does this answer your question?

For starters, looks like in the family ichneumonidae

I found a picture on the internet with a resembling insect that was specified as Rhyssa persuasoria. But when I looked this species up it shows a much darker color (black). This is puzzling me. Also bob1's response points to a species of the same shape but different color.

@VolkerOtto there will be some natural variation in colour within the species. At best you could probably say Rhyssa genus or perhaps the closely related Megarhyssa, but I think those have some brown/red in them rather than just black and yellow/white.

There's a nice PDF guide to the british species of wasps etc. here I'd expect similar species in most of Western Europe, though maybe not the exact species.

@bob1 thank you very much for sharing this guide and your profound answers - very helpful.


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What is a good method to test the effect of gibberellin concentration?
I was just wondering what a good method would be to test the effect of gibberellin concentration on growth. I know it is prevelant in many flowering plants but am unsure as to what would be suitable. I have been looking into tepary beans as one but am unsure as to how exactly I would measure 'growth'/the effect of gibberellin.
Thanks!

Exactly, the 'good' plant would depend on how you measure the effect of gibberellin. I think you should change the wording of the question from good plant to good method.

Could you possibly direct on me on how to apply the gibberellin as I have not found a simple methodology for this. I have also read in a number of papers that it also effects root length, germination period etc. Would it also be possible to explore these? How would I also go about applying it as a root drench?


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How does alum help in blood coagulation?
I recently came across a test in my chemistry book which says that potash alum, $\ce{K_2SO_4.Al_2(SO_4)_3.24H_2O}$ is used on cuts and bruises, because it coagulates the blood quickly. The explanation it gave, was that blood is a colloid of proteins in water and the $\ce{K^+}$, $\ce{Al^{3+}}$ and the $\ce{SO_4^{2-}}$ ions coagulate(=precipitate) them, causing a blood clot (quickly). However, from biology, I know that blood coagulation(=clotting) is brought about by formation of fibrin network which traps the WBC and RBC in blood. The formation of fibrin from fibrinogen involves a series of reactions with many factors like $\ce{Ca^{2+}}$ , but not $\ce{K^+}$ or $\ce{Al^{3+}}$.
So, I was wondering what the actual explanation might be.

Do people actually use alum to stop bleeding, or only as a disinfectant? Does alum have any disinfectant effects?
Does precipitation of proteins in blood help clotting?
Does alum contribute in any way to the process of blood clotting?

Note: This is a question involving both chemistry and biology, but I posted the question here as I thought that this is more of biology than chemistry.

If English is not your native language, please use a spelling checker, especially for the titles of questions which are indexed. Every web browser has one built in — just set the language temporarily to English.

I will answer the three questions one at a time. Lets begin with the first one:

Do people actually use alum to stop bleeding, or only as a disinfectant? Does alum have any disinfectant effects?

Yes, alum is also used as a disinfectant, and it works in the same way as it does in blood coagulation. In aqueous solution, potash alum dissociates as:
$\ce{K_2SO_4.Al_2(SO_4)_3.24H_2O -> 2~K^+ + 2~Al^{3+} + 4~SO_4^{2-} + 24~H_2O}$
Now, as is known, blood is a colloidal solution, in which the plasma proteins are charged (see Rügheimer et al, 2008). These ions from alum neutralize the charges on plasma proteins, causing the blood to coagulate. Similar effect is observed in disinfectant where these ions react with the free organic acid and thiol groups of proteins on microbes and free proteins, resulting in their precipitation (Williams, 2001). Thus alum can act as disinfectant.

Does precipitation of proteins in blood help clotting?

Coagulation of both plasma proteins and RBCs takes place on application of alum, since both of them are charged (Fernandes et al, 2011) as is discussed in next point. However, it is difficult to say whether coagulation of plasma proteins plays a significant role in clot formation or not.

Does alum contribute in any way to the process of blood clotting?

Yes, alum does contribute in the process of clotting: it makes clotting faster. Although the term 'clotting' is generally used for formation of what is called as platelet plug, the actual process of clotting also depends on coagulation of colloidal particles in blood. When the blood is exposed to the extracellular matrix (due to damage to blood vessel), platelets activate and, via a cascade of reactions, lead to formation of a platelet plug. Red Blood Cells get tapped in this plug (which is actually a fibrin meshwork) and lead to formation of clot. A nice and simple representation of this process is below (from here):

Without alum, RBCs would take longer to coagulate due to mutual repulsion. By neutralizing them, alum makes this process easier and faster. Hence, alum helps in the formation of blood clot via coagulation of red blood cells.
I hope this helps.


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What is the "stimulus" that initially triggers an action potential?
There are many steps detailing the depolarization and repolarization of axon nodes to describe how an action potential is transmitted from a neuron. But, after looking at many different sources, I still see one clear thing missing: what causes the action potential in the first place? Every source simply says something vague like "stimulus" or the ever redundant "depolarizing current." But, how is this stimulus generated, and what exactly does it do to which chemical to start the chain reaction of moving sodium ions to create the depolarization in the first place?

In addition to my answer, I would add that there is absolutely nothing redundant about the phrase "depolarizing current."

"how is this stimulus being generated" -- have you heard of neurotransmitters?

@BryanKrause Yes there is, simply explaining what triggers depolarization as a "depolarizing current" does not explain much.

I disagree somewhat, but please see my answer.

That answer requires wayyyyy more detailed than "depolarizing current."

I didn't say "depolarizing current" was sufficient as an answer, just that I disagree that it is a redundant term. Hyperpolarizing current can also trigger action potentials in some cases, for example, due to activation of intrinsic conductances and deinactivation of sodium channels.

But if a stimulus is sufficient, then by the definition of an action potential, the axon must undergo depolarization anyway.

There are several possible answers, which is partly why the sources you are reading are being vague: they are discussing the chain of events that happen after the initial depolarization, the source of which doesn't matter much for that chain of events.
Receptor potentials
Sensory receptors consist of some machinery that eventually lead to ion channels opening, often cation channels. This machinery can be direct, where a stimulus directly opens an ion channel, or it can me mediated through g-protein coupled receptors. There are many many examples, but one favorite toy example is the TRPV1 receptor, part of the "transient receptor potential" family.
TRPV1 channels open when exposed to high temperatures or chemical agonists like capsaicin (which gives chili peppers their 'heat').
There are mechanically gated channels in the inner ear that are stretched open as sound waves pass; there are G-protein coupled receptors in the retina that are activated in response to light - when they are activated, they close channels which reduces neurotransmitter release and therefore changes the amplitude of the post-synaptic polarization.
Ligand-gated ion channels
Synaptic transmission between neurons is often mediated by ion channels that are gated by neurotransmitters. A presynaptic cell releases a neurotransmitter, for example glutamate, and that neurotransmitter binds glutamate receptors on the post-synaptic cell, for example AMPA receptors. These receptors are non-specific cation channels, and when they open sodium comes in and depolarizes the cell. Other neurotransmitters, including inhibitory ones, work a similar way.
Gap junctions/eletrical synapses
Although they only occur between particular populations of neurons in mammalian nervous systems (for example, some inhibitory networks in the brain and between cardiac myocytes), some cells are coupled through channels that allow ions to pass between cells. Therefore, depolarization in one cell can be transmitted by ions flowing through that gap junction and begin to depolarize the adjacent cell.
Intrinsic conductances
It doesn't really apply in the context of a "stimulus" but in some types of cell there are intrinsic conductances that can bring a cell to threshold and trigger an action potential. One example would be in the pacemaker cells of the sinoatrial node that initiate cardiac contractions.


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What is the biological potential for vision of wavelengths outside the human visual range?
Humans eyes have evolved to perceive light only between approximately 350-700nm, because that form of light is most common to our lifes. Other animals can perceive lights with slightly different fequencies. Can eyes theoretically evolve in a way that they can observe all light as we know it today? If not what would approximately be the maximum amount of frequencies that can be perceived?

Hmm, interesting question. I think there are 2 aspects. 1: As the range of frequencies increases then input of signals increases which needs a better brain. 2: Since visible spectrum has wavelength in range of nm but otherwise like radio are in metres to KMS in wavelength, I think neurons( or other special cells) could not act like antenna , so there will be limit .

"...approximately 350-700nm, because that form of light is most common to our lifes." This is not correct. It just so happens that we evolved to see in this spectrum.

@anongoodnurse it is certainly no coincidence that it just happened this way. I am on my phone so I cannot link it, but there are charts that show the amount of light that reaches earth.  Most of it is light between 350-700nm. It is crucial for survival to see colour and therefore we evolved into seeing it.

There are some limits on what light can be detected biologically based on physics and chemistry. Although there are animals that can sense more UV or more infrared than humans, they are still subject to these limitations.
How Vision Works
The way most types of vision operate is by using photons to cause a conformational change in an opsin protein by influencing a chemical bond in a sensitive molecule (a chromophore, for example retinal, which changes from 11-cis to all-trans) bound to the opsin. To sense a particular wavelength of light using this mechanism, it is necessary that the energy of the light is sufficient to cause this chemical change in the opsin-chromophore, without being enough energy to destroy the molecule entirely by breaking a bond.
Sensing low-energy (long wavelength) light
Longer wavelength light ('infrared') is also known as heat. Detecting "heat" photons is difficult because they don't have much energy. Therefore, you need a molecule that is very sensitive. It turns out that the opsin-based vision strategies use chromophores that are too stable to sense long wavelength light.
Some snakes have particular sensitivity to infrared, for example the pit viper. However, these animals do not "see" infrared using their eyes: they have another specialized organ called the pit organ. The pit organ uses receptors that are much more like the heat receptors in your skin than the photoreceptors in your eye, but the pit organ uses a pinhole camera effect to organize the incoming light onto a very sensitive heat-sensitive membrane.
Humans of course are able to sense infrared, too, but the same way: through the skin rather than the eyes, and at low resolution. However, if you stand outside in the sun and close your eyes, you can probably still "see" the direction of the sun: one side of your body will feel warmer than the other! In a way, this is like a form of low-resolution "vision" if you want to define that term very broadly. The snake's infrared sensitivity is more like this sensation than eyesight.
When you get to very long wavelengths, for example radio waves, the wavelength is too long and too low-energy to even be relevant at a molecular level: these forms of light will travel right through cells, and individual photons don't carry enough energy to influence molecules in ways that can be sensed by biology.
Sensing high-energy (short wavelength) light
Very short wavelengths of light have the opposite problem: too much energy. Ionizing radiation (from the upper ultraviolet range and shorter) has enough energy to actually free electrons and create ions. This type of radiation damages biological molecules, including DNA, so organisms have a lot of good reasons to avoid these types of radiation. Exposure to short-wavelength radiation can also cause bleaching (permanent destruction) of photosensitive molecules and potentially damaging heating of tissue surrounding pigments, in addition to direct effects on other molecules in the cells.
Insects and other organisms that can see into the UV range see mostly in the near-UV range, >300nm, not too far from our own vision range (roughly corresponding to "UVA"). However, it isn't true that humans can't see these wavelengths due to some lack of sensitivity of our photoreceptors: instead, UV light is (at least partly) blocked by the cornea and lens, presumably to protect the retina from damage!
Humans and other organisms do have some sensitivity to damaging UV wavelengths, just not through vision. Instead, humans and other organisms sense UV based on the damage done within cells, which recruits repair mechanisms and apoptosis to prevent damage from leading to cancer.
Summary:
The chemical processes behind vision determine the range of potential wavelengths that can be sensed. Animals on earth are able to sample from this entire range. Mechanisms to sense wavelengths outside that range would require wholly different approaches, and maybe even a unique biochemistry. The mechanisms would have to be so different that we probably wouldn't refer to those mechanisms as "vision" (for example, even the infrared sensitivity of the pit viper isn't really though of as vision) but we would come up with a new term, such as "radio sensitivity" or "radiation sensitivity" just like we have different names for "hearing" relatively high-frequency pressure waves with the ears but we have "vibration sensitivity" for low-frequency pressure waves felt through the skin.

A very informative answer. However is it possible that some species could evolve a "sight" process not based on opsin? For example could a species evolve a structure capable of receiving AM radio? This article (https://www.seas.harvard.edu/news/2016/12/world-s-smallest-radio-receiver-has-building-blocks-size-of-two-atoms) describes a very small radio that is "biocompatible". Although using "sight" to describe this wouldn't match the current meaning of the word very well.

@Χpẘ Yeah this is exactly what I was referring to in my Summary: I think the pit viper is a great example of a place where we might colloquially say vision, but if I search Google Scholar for "pit viper infrared" the scientific literature mostly if not exclusively refers to vision only in quotes; the other terms used are "infrared detection" or "infrared imaging"; it's a stretch to call it vision because it isn't from the eyes.

@Χpẘ Also as far as biocompatibility in the article you linked, what they are referring to is that diamonds don't cause an allergic/foreign body response. No known biological mechanism can create diamonds nor substitute single carbon atoms in a diamond with nitrogen.

Yes, but that doesn't mean an evolution isn't possible. Another example, IBM has built a radio out of a carbon nanotube. Looking at the future from the point of view of earliest life, I'd venture that it wasn't predictable that human sight was in the future (setting aside for a moment the question of who would've been making predictions!). The OP says "eyes theoretically evolve" which is fairly ill-defined. "Evolution" is not even limited to earth based evolution. Second "theory" could refer to a host of disciplines, such as physics, genetics, etc. Third, meaning of "eyes" would likely change.

@Χpẘ There is "possible" in a science fiction sense and "possible" in the sense that it could happen from known biological principles. I agree that if one leaves behind known biology in favor of non-earth based life origins and completely different biological paths that a lot is "possible" but it mostly belongs on WorldBuilding.SE, not Biology.SE.

"known biological principles" doesn't include unknown biological principles. Unknown biological principles aren't SF, they are merely not known. It wasn't too long ago (75 years?) that life surviving in temperatures above 100 C would've been SF. Radioresistant organisms are a lot more common than was thought prior to Chernobyl. It's a mistake, IMO, to equate what is known to what is possible (in real sense, not SF)

@MrX In this answer I write: "Exposure to short-wavelength radiation can also cause bleaching (permanent destruction) of photosensitive molecules"; what is the intent of your comment?


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What causes paresthesia from compression?
Compression of a nerve causes loss of afferent and efferent information in it. What is the physiological basis of this?

Seems like it results from a loss of blood flow as the Vasa Nervorum is compressed. Vessels, like arteries or tubules within the kidney, are compressible since they have a vacuous lumen, while an axon is cellular and resists compression. I was thrown off a bit by an answer by a Bryan Krause to this question here, Neurons during Numb feeling, "the feeling of paresthesia is not from loss of blood flow", but, seems like that person was wrong.

Another commenter noted my comment was mentioned here; it was made in haste and probably misleading, probably I should have added a word and said "complete loss of blood flow". I was referring to the article linked in the question there that implied that blood flow to entire limbs is cut off; if this would happen there would certainly be tissue damage in short order. The distinction I meant to make was between compressing major blood vessels versus compressing nerves themselves.

It can likely happen if vessels proximal to vasa nervorum are compressed too. Loss of blood flow to vasa nervorum does cause tissue damage, but increases in severity with time. And for the axon conductance to shut down (however it is axons actually do conduct signals), likely very deplete of oxygen, glucose, or whatever it is lacking that makes it not signal anymore.

@BryanKrause if its caused by oxygen/glucose deprivation, that proves the saltatory conduction theory that the action potential has to "boost" itself at the nodes of Ranvier. do you happen to know if electrolyte exchange is in any way stifled in the peripheral nervous system where the nodes of ranvier are a bit "covered" with projections from the myelin cell?


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Coronavirus and temperatures
An article on bioRxiv, Evaluation of heating and chemical protocols for inactivating SARS-CoV-2, recommends certain treatments to inactivate SARS-Cov-2 for lab work.
The abstract notes: "Although heating protocol consisting of 92°C-15min was more effective rather than 56°C-30min and 60°C-60min to achieve 6-log reduction, it is not amenable for molecular detection on respiratory specimens because of important decrease of detectable RNA copies in the treated sample vs untreated sample."
Do I understand correctly that 56C/30min is broadly as effective as 60C/60min? Given that 56C from previous research seems to be more effective than 22C, I would have expected 60C to require less time to achieve a similar effect to 56C. Especially with 92C/15min being more effective still, though more disruptive.
I'm curious what the explanation may be why effectivity might drop between 56 and 92C. Or why I may be misunderstanding the temperature/time scales. Please keep it simple. Thank you.

They only tested 3 heat treatment regimens: 56C/30min, 60C/60min, 92C/15min (6 if you consider the "with BSA" and "without BSA", but only 3 combinations of temperature and time). They didn't measure the time required at certain temperatures to get to a certain level of inactivation. It seems they chose some of these particular protocols because they have been recommended in the past for other viruses.
They don't really have sensitive enough data to compare the 56C/30min to the 60C/60min or really enough to do any sort of statistical comparison whatsoever (as far as I can tell they only tested a single sample of each); yes, you can say they were roughly as effective, but it would be a leap to say 56C is the same as 60C.

Thank you.
Does anyone know or a have an idea why 60C/60m levels off at an effectiveness comparable to 56C/30m?

@user345360 In 2 of the tests they ran (one at each temp) they got no detectable virus. In the other one they got a small amount. That's not enough information to make any conclusions about things "leveling off". The temperatures aren't that different, the time isn't that different. At best they might be able to detect a 10-fold change, and even then not be too certain about it.


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Can anyone identify this object?

It was found on the shore of the Ohio River in Kentucky. It is very hard, like bone, and feels hollow but does not rattle.  It is translucent.  I do not think it is skull of a water fowl even though the blunt end appears beak-like. I cannot figure out if it is plant or animal.  It was found in an area where arrowheads were found.
It appears to be hollow. I do not believe it is a shell since there is no margin or growth lines. It appears to be shriveled or desiccated.

This may be, though not sure, one of the supporting bones of the dorsal spine of the black drum,

Pogonias cromis also known as drum or drummer.
It is the only species in the genus Pogonias.
Reference

Freshwater drums are native to Ohio, preferring habitats of deeper pools of rivers and in Lake Erie with clear water and clean bottoms. They spawn from April to late summer.
Reference

Pogonias courbina is distinguished by the following characters: the occurrence of character-
istic thickening of the dorsal spines VII to XI in all specimens larger than 250 mm SL; all pter-
ygiophores in the dorsal-fin laminar, thin; anal-fin pterygiophores slender excluded those of
spines; lateral projections of gas bladder with few finger-like projections; genetic distance
between both species 1%

An important site that helped me to identify this-
https://txmarspecies.tamug.edu/otherdetails.cfm?scinameID=black%20drum%20pterygiophore

Thank you.  Additional sources say it is a Tilly bone, perhaps from a large catfish.  A Tilly bone is caused by hyperostosis, or excessive bone growth and is found in many fish.

@Kevin Oravec you may accept the answer if you are satisfied, for the future references.


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Do human women smell different before they enter labour?
Surfing youtube I found a video where a cat shows a protective behaviour towards a pregnant woman soon to enter labour.
In the miriad of average (dumb) comments I found another person stating that her cat felt precisely (via olfactory means I guess) that her (the woman's - not the cat's) day had come to give birth and started acting weirdly.
Do mammals leave a clear olfactory footprint before labour? And is this footprint noticeable by cats and dogs?
Is this definetely myth? Is this something yet to study? or is this something well known?
If the latter is the case: is it based on the sense of smell? is there anything to read to study the topic?

There is plenty of anecdotal evidence of this happening. However, studies cost money, and knowing when a woman is about to go into labor is not a particularly compelling reason to spend a significant mount of money doing a controlled study. On the other hand, predicting a seizure or detecting a cancer has some significance, and those have been studied.

Ty for the feedback. Well... I guess a lot of women would disagree on that: knowing that "today it'll happen" might be more than useful - especially in emerging countries where people can't manage a thorough monitoring of the pregnancy. And given this, the compelling reason might have also an economic basis. But I get your point.


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What are the various types of plugs found in a bee house and how do they help us with identification?
I have a Mason bee house with small tubes that is currently buzzing with life but I am completely clueless about what's in there. Some plugs seem made of clay, some of crushed leaves, some of resin, some look like just a little film...
I figure it's possible to learn about what is living in there (approximately) going by the type of plug, and maybe the size of the tube, but I don't know where to start. I'm in Eastern Canada if this makes a difference.

Not an expert on bees, but there 39 known genera of solitary bees in eastern Canada1.  That reference contains a key, so at very least you can start to identify your tenants when they emerge next year.
The clay plugs are due to one of the genera of "mason bees", but that doesn't really appear to narrow things down much.
Your area does have "leafcutter bees" in the genus Megachile that use cut leaves to line and separate the chambers of their nests1,2, so that probably explains the holes containing crushed leaves.
There are also "resin bees", but the only species in your area (Paranthidium jugatorium) I've read about that fits that description is supposed to nest in the ground.1
Finally, bees in the genus Hylaeus and Colletes are known to use a membrane rather than a plug.2
1: Packer, L., Genaro, J. A., & Sheffield, C. S. (2007). The bee genera of eastern Canada. Canadian Journal of Arthropod Identification, 3(3), 1-32.

2: Michener, C. D. (2000). The bees of the world (Vol. 1). JHU press.

ETA: A guides to wasps in your region from the Canadian Journal of Arthropod Identification may also be of help.

That's a good start, thank you! I believe I may have wasps in there as well so it's a bit broader than just bees.

You're welcome! I'll add links for a couple of identification guides for wasps in your region.


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Do hormones make it more likely to perceive sexual forms in otherwise non-sexual objects?
People can see sexual forms in many things. It seems that this varies with age, but this is not enough to claim it is because of sexual hormones. The question is: is it?

Pareidolia is a common phenomenon, and certainly is not limited to "seeing" phallic or other objects as sexualized; the canonical example is seeing objects as face-like, such as the headlights and grill of a car appearing as eyes and mouth.
There seem to be some sex-based differences in pareidolia (see Proverbio 2017) but if there is hormonal cause it is probably developmental rather than acute, and this is related to face-specific perception, not anything sexualized.
I don't see any literature on, say, puberty and sexual pareidolia, though absense of evidence is not necessarily evidence of absense. It isn't surprising that there are changes with age, but this need not be due to hormones per se but rather due to exposure to different stimuli (or their salience). I think this is probably not an area of much biological study because there isn't an associated medical concern and it's a fairly subjective phenomenon.
Proverbio, A. M. (2017). Sex differences in social cognition: The case of face processing. Journal of neuroscience research, 95(1-2), 222-234.


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Why is "mutual search" of some disadvantage/loss of power? (in Darwin's The Descent of Man)
I read a book "The Descent of Man" from Charles Darwin. What is the reason for the following statement?
"It would be no advantage and some loss of power if both sexes were mutually to search for each other."
I know that in most species it is the male having an active role in the search of a partner to mate, but Darwin provided no fact in supporting the quoted statement about the disadvantage of mutual search.
Mr. Darwin died 139 years ago, so his books became a public domain (70 years after his death). Here is a link to a pdf file:
The Descent of Man - Charles Darwin
There it is page number 273, in the pdf file page number 322, in the lower half.
EDIT: The explanation provided on Wikipedia, that I just found, is the Batemans principle. It says that the females are "more valuable", because of greater time and energy they put into producing offspring, compared to that of the males. Hence, the males compete for the females.

I’m not sure what exactly Darwin was getting at, but the answer to why males perform the search (generally speaking) seems to me to be the same as to why there isn’t mutual searching.


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Can mrna spike protein block other proteins entering cells?
When vaccinated with pfizer a mrna is injected which eventually creates spike proteins. These will bind to cells. Now there is a rumour that when these spike protein binds to cells it can block other important proteins from binding to that cell. Is this true? Can someone debunk this.

I’m voting to close this question because this site doesn’t exist to debunk rumours about things that do not happen, but to answer questions on biological problems about things that do happen.

Skeptics.SE exists for just this sort of question. As with any SE site, search for a similar question before asking.

Short answer: No.
What I am going to do here is some back-of-the-envelope style calculations and a bit of explaining, so bear with me...
The way that these vaccines work is by causing the mRNA to enter the cell, where it is translated into the encoded protein sequence. This is then translocated to the surface of the cell and in some cases into the extracellular space (ref 1; see figure 2).
This means that some of the protein produced is floating around and could bind to a cognate receptor on another cell (or even on the surface of the cell it came from, in which case it won't go any further). However, in the case of the spike protein, this receptor is the Angiotensin converting enzyme-2 (ACE2) protein, which is a receptor for Angiotensin II. In a natural infection it is thought that the levels of spike protein (ref 2) produced by the replicating virus are high enough that it prevents the normal function of ACE2 and enhances damage and further infection.
We (by that I mean I, myself) don't know what proportion of the expressed protein is released from the cell into the extracellular space, but based on my experience in the lab using similar methods for DNA transfection, it will only be a small proportion of the protein produced. It may be that this information is known or it may be proprietary, but I would be willing to bet it is less than 50%, and maybe much lower.
We do know the sequence of the mRNA in the vaccine and can make at least some order-of-magnitude estimates of the number of RNA molecules in a dose (30 micrograms for Pfizer, or about 0.5 ug/kg body weight, assuming 60 kg average body weight per person). Not all of these molecules will be fully functional - some will have manufacturing errors that terminate the protein early, some won't be packaged properly, some will be degraded during preparation, some won't make it into a cell, etc.. However, we can assume about 1-10 trillion (1-10 x 1012) molecules, which as it turns out, is about the 10-100 times the number of viral genome copies that your lungs produce at peak infection (ref 3; see fig 1). Now, if we assume that each produces a single protein before being degraded, we have a corresponding 1-10 trillion protein molecules.
This sounds like a lot, but rest assured that this number is tiny in terms of what we are looking at - there's about 1021 sugar molecules in a teaspoon of sugar (4.2 g/teaspoon, molar mass sucrose = 342.3 g/mol).
Now, back to the virions. If we assume that each one of these genomes produces a virion (whether functional and infectious or not), and that each virion contains 24 spike trimers (ref 4), or 72 individual spike proteins (24 trimers x 3 spikes per trimer), then we have roughly the same number of spike proteins produced by the virions as by the vaccine, and we know that the virus can do some damage via this route (see ref 2). So, in theory, we could produce enough protein to effect some damage to your cells.
The other major variable here is the amount of ACE2 in a cell - I don't think this can be quantified easily. It is known that some cell types have more than others, but in terms of molecules per cell, it is unlikely to be static and would be very very hard to determine. This means that maybe there are only 10 (very unlikely, it is an important molecule) or maybe there are millions of molecules per cell (also unlikely). If we take a number somewhere between the two - lets say 100,000/cell (105/cell) - that means we would need 107 (10 million) cells to mop it all up. There are about 4-6 million cells in a ml of blood, so we would need about 2 ml of blood to cope with that. I can also say, just to give you some sense of scale, if you clumped the cells together, 10 million cells is about the size of a large drop of water while it is hanging.
However, it's not that simple in any biological system, these sorts of things have kinetics of production, so we wouldn't produce all that protein in one big hit. Here's some known kinetics (ref 5; see fig 3) for a test of these sorts of vaccines, which shows that about (I estimate) 50% of that protein is produced within a few hours and then tails off over the next day or so.  Indeed these people (ref 6) showed for their experimental spike vaccine version, that the vaccine peaked at 12 hours and was gone 48 h post injection. Spreading the production out means that the body has time to produce more ACE2, minimizing the affect of the spike production. Some (as I mentioned before) won't make it out of the cell or won't be released into the extracellular fluid. The vaccine particles are also spread via the blood, so the effect is not localized and any effects somewhat diluted because of that.
Whatever actually happens, we know that this type of vaccine has almost no short-term serious side effects, and is very unlikely to have longer term effects too. The vast majority of people experience a sore arm for a day or so and maybe some other symptoms (aches, tiredness, fever), almost all of which can be attributed directly to activation of the immune system.
So, the (very) long and short of it is - while it is plausible that this vaccine could IN THEORY produce enough protein to block the normal function of ACE2 in some cells, we don't see this happening in real life for a huge number of reasons.
References:

Park et al. Int J Biol Sci. 2021 17(6):1446.
Sriram and Insel. Br J Pharmacol. 2020 Nov;177(21):4825-4844
Sender et al. PNAS.  2021 Jun 22; 118(25): e2024815118
Ke et al., Nature. 2020 588:498–502
Pardi et al., J Control Release. 2015 Nov 10; 217: 345–351.
Zhang et al., Cell. 2020 Sep 3; 182(5): 1271–1283.e16


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Why do ion leak channels exist?
I've recently learned about ion leak channels in the context of membrane potential and action potentials. Neurons have ion pumps that require energy in order to maintain the resting membrane potential and concentrations of K+ and Na+, yet the K+ and Na+ leak channels seem to directly oppose this purpose. It seems like, if left unopposed, the ions would eventually diffuse across the membrane such that there would be equal concentrations on both sides and a membrane potential of 0.
If the ion pumps spend energy and store it in an electrochemical gradient, don't leak channels let that potential energy dissipate back across the membrane? Wouldn't it be more efficient to tightly seal ions into their respective sides until the energy is released during action potential?
Am I missing:

An important function of leak channels directly involved in maintaining membrane potential or causing action potentials?
Some broader evolutionary purpose of leak channels that help ensure a cell's health in other ways?

Additional clarification requested: Would it be correct to say that leak channels function in facilitating changes in membrane potential (and return to "baseline") until the threshold, at which point the voltage-gated ion channels allow for a much larger influx/efflux?

Check the parameters that go into the Goldman equation... it shows that permeability of ions is as important as their concentrations. If the permeability is zero, there is no potential. Because other conductances are mostly closed at rest, the leak channels are almost entirely responsible for the resting membrane potential (there is a minor component, a couple mV, supplied by the sodium-potassium pump itself, that is missed by the Goldman equation). If there were no leak channels, there would be effectively no resting potential, and certainly no useful one.
Additionally, there would be no return to "baseline" after a signalling event.
Leak channels are entirely integral to nervous system functioning (and the function of other excitable cells, including muscles and immune cells) - a system without them would be nothing at all like what we actually observe in any biological nervous system. The membrane potential massively amplifies the concentration differences into an electrical signal, such that large changes in voltage occur merely by opening and closing channels: very few ions need to move for this to happen, making a very efficient signalling system, requiring only the maintenance of ion concentration gradients (which change very slowly).
I would say it's correct to say that the role of leak channels is quite diminished during an action potential, since voltage-gated conductances ultimately overwhelm the leak conductance. You can see this from the Goldman equation, too. But they are quite important in setting threshold itself, and in returning to rest after an action potential. However, even during an action potential there is very little actual ion flux. Electrical forces are very strong, so not many ions need to move (see again the answer I linked above).