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Interpreting replicator dynamic for simplest population model
Suppose the simplest population model where we track the size $y$ of a population:
$$\frac{dy}{dt} = ry$$
for a positive constant $r$ and some $y$ such that $y(0) > 0$.
For this population model there is a corresponding "replicator dynamic" model defined by
$$x_0 := \frac{1}{1+y}$$
$$x_1 := \frac{y}{1+y}$$
These are supposed to model "frequencies" of different variants in a population,
QUESTION
except its not clear to me what the different variants here. There is only a single species here so of course it is 100% of its own population or 100% of all populations being modeled here, so I feel that I must be misunderstanding what the "frequencies" of the replicator dynamic are. Can someone clarify what $x_0$ and $x_1$ correspond to here? Thank you!

The transformation carried here is a particular type of the more general one. As the linked text notes:

The continuous replicator equation on n types is equivalent to the Generalized Lotka–Volterra equation in n − 1 dimensions.

In the case described in the OP the number of types is $n=2$, although "Lotka-Volterra" is a bit too generous a term for the simple model in case.
So indeed an extra species is being added here with a zero growth rate. The advantage is that one can now talk about the relative fitness and otherwise use the rich theory developed for the fixed-size populations, since $x_0+x_1=1$ whereas $y$ may grow without limit. E.g., a lot of such intuition comes from the familiarity with Wright-Fisher and Moran models.

Thank you! Why is that needed for the replicator dynamic? I'm interested in using the replicator dynamic to prove ESS (obviously not in this model, instead suppose there are two populations $y_1$ and $y_1$ with growth rates $r_1$ and $r_2$ respectively, suppose $r_1 > r_2 > 0$ and I want to prove $y_1$ is an ESS), does the dummy population help for that somehow?

@John_Krampf one wants the total population to normalize to $1$. If one has two populations, $y_1$ and $y_2$, one could construct $x_1=y_1/(y_1+y_2)$ and $x_2=y_2/(y_1+y_2)$, but this would behave bad when both populations vanish. So $1$ is a kind of pseudocount here. But I must warn, that I am not a game theorist.


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Is there a functional reason why the right side of the heart has a tricuspid valve while the left has a bicuspid one?
Is there a functional reason why the right side of the heart has a tricuspid valve while the left has a bicuspid one? Why is it necessary that the right atrioventricular valve be 3-cusped?

This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic (citing reliable sources), and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

The reason why I asked this here is because I failed to get ANY information online (& therefore I have no nothing else to show).

That's fine, but if you don't include answers the questions I asked in your post, then we have to take that on faith — if you aren't willing to make that effort and have little reputation here why should we believe you? Many questions get asked here where little (or no) effort has been made, or the effort has been misdirected — if you tell us what you've tried then someone may be able to help ...

source: Stack Exchange

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

sort: votes


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What is this little (3mm) spotted insect in Northern Italy?
Every now and then I find one or two of these tiny bugs in my kitchen. They are about 3-4 mm long and seem to be very static on hard surfaces (furniture or walls). They rarely, if ever, more.
The one in the picture was found dead on the floor so I was able to take close-up pictures. The insect seems to have a very regular pattern of spots and presumably wings.
I tried to look online for Italian websites of "household bugs" but I could not find it.
Is it problematic, i.e. does it ruin food or something?
Location: Northern Italy, province of Vicenza

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


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Why do the COVID vaccines contain the cationic lipids they do?
Why did Moderna & Pfizer specifically pick their SM-102 and ALC-0315 cationic lipids with tertiary amines, branched tails, long linker chains, and small hydroxyl head groups? Are the large tails and packing parameter to keep the lipid from leaking out of the liposomal membrane? Why not use any other large hydrophobic groups? Thanks!

Are those vaccine's lipids very similar to our cell wall? I was told a while ago that due to the similarity, those lipid balls could just "merge" with cell walls and bring the content in the lipid balls inside the cell. I was pretty satisfied with that answer as I wasn't even aware of the amount of nuances that existed in the lipid itself.


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Do penguins "test the ice"?
Do penguins have a way to test the ice that they stand on to ensure that the ice will not break? In other words, do penguins make sure that they will not fall into the ice before stepping onto it?
I have conducted research but have come up short, which made me assume that penguins don't test the ice. However, I wanted to make sure before I just made an assumption.

What would happen to a penguin if the ice did break under their weight?

@BryanKrause They would fall into the water; they would be startled, but if the conditions are right, then they will be able to swim under the water, correct?

I could also envision a scenario that the ice reseals, thus trapping them under the ice -- perhaps a great distance from the next breathing hole. Seems like an interesting question to me. Please [edit] your post to explicitly indicate what type of research you've already done. (You say you've "come up short", but where did you specifically look and what have you learned along the way?)

This HIGHLY apocryphal blog post (https://thealchemistskitchen.blogspot.com/2013/02/how-penguins-do-it-testing-waters.html) suggests that some groups of penguins test water by pushing their leader off and seeing whether it's safe. However, I couldn't find any scholarly references that back that up (or otherwise suggest that penguins test water or ice). Regardless, I just wanted to caution against concluding that they don't just because it hasn't been specifically studied. A lack of research on the topic doesn't necessarily indicate that the phenomenon doesn't exist.


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How do physics notions of fluid dynamics relate to pressure gradients in circulation?
I'm having a hard time comprehending why sometimes physiology notions seem to contradict each other and contradict physics teachings.
More specifically I don't understand why aortic coarctation causes the pressure gradient to increase. In this condition the radius of the blood vessel decreases which should mean that pressure decreases too. According to Bernoulli theorem ΔP+Δvp/2=o
where v is velocity and p density. This theorem and the fact that velocity has to increase to maintain a stable flow through the coarctation should mean that the pressure gradient drops. Moreover in every textbook I've found it is said that tension on the aortic wall increases too but this seems even more counterintuitive, because if the radius decreases due to La Place T=Pr tension (T) should decrease too.
Then the most puzzling thing to me is the pressure drop when there vasoconstriction of  the arterioles, this is fine according to my reasoning so far (except it seems to contradict aortic coarctation) but resistance is supposed to increase too with vasoconstriction, and because of this equation: ΔP=Q*R (where Q is flow and R is resistance) the pressure gradient should go up. Now I think I understand that it increases because of the successive drop in pressure, correct? What am I missing with aortic coarctation? I'm sure it has to do with confusing the PTM in that specific place and the pressure gradient but I can't figure it out.

As far as we know so far, biology isn't able to break any laws of physics.
However, biology isn't passive: biological systems react to changing environments to maintain some level of homeostasis. Arguably this is one of the defining characteristics of life.
If you narrow the aorta, you will always get compensatory changes. Ultimately, the circulatory system is tasked with delivering sufficient blood to the body. It might be a bit of an oversimplification, but let's assume that blood flow stays constant, because flow is a good measure of the ability of circulatory system to deliver enough oxygen/nutrients to the periphery.
Blood flow is pulsatile, which also adds some challenges in understanding things simply, but let's simplify and think in terms of mean pressures. Again, this is wrong, but it's not terrible, kind of like when in a physics class you discuss a "uniform spherical cow" or something like that.
We can start with an equation you mentioned:
ΔP=Q*R
You write:

In this condition the radius of the blood vessel decreases which should mean that pressure decreases too

This is false. If we keep flow (Q) constant, but R increases due to a constriction, then ΔP, the change in pressure, must increase.
Consider:
ΔPaorta=Q*Raorta
If Q stays constant, but R (resistance) increases due to the decreased radius, then ΔPaorta must increase: there is a larger pressure drop. Perhaps you've confused the larger change in pressure with a "decrease in pressure" because there is this larger pressure drop?
Consider also that we can consider the rest of the parallel vasculature (all branches off the proximal aorta) in series with the aorta. If we think of the vasculature after the aorta as:
ΔPdistal=Q*Rdistal
then you can think of the whole system as:
(ΔPaorta + ΔPdistal) = Q*(Raorta + Rdistal)
If only the aorta is constricted and the distal vasculature keeps the same pressure and flow, then ΔPdistal must also not change. Therefore, the total pressure drop (equal to the difference in pressure between the aorta and great veins, the sum ΔPaorta + ΔPdistal) will be larger when ΔPaorta increases.

As far as Bernoulli:

This theorem and the fact that velocity has to increase to maintain a stable flow through the coarctation should mean that the pressure gradient drops. Moreover in every textbook I've found it is said that tension on the aortic wall increases too but this seems even more counterintuitive

Due to Bernoulli, if you go from large (A), to small (B), to large (C) diameter in some vessel, yes, you will have less outward pressure in the segment (B). You will also always have decreasing energy from A to B to C. However, think about what we were just talking about: if you want to keep the perfusion of the rest of the vasculature constant, that means you have to keep the energy at C (interchangeable with pressure in this context) constant, despite the constriction. You shouldn't be thinking about A B and C here when comparing a vessel with and without stenosis, you have to think about the non-stenosed case where you have large (X), large (Y), large (Z). In this case, you still have decreasing energy from X to Y to Z, but without the stenosis, you don't lose as much going through segment "Y". It is segment A that requires more energy/pressure/tension on the vascular wall compared to segment X.
There's some simplification here regarding vascular compliance, non-Newtonian fluids, and vascular permeability but these can be mostly ignored for these purposes. I think this website will help you a lot:
https://www.cvphysiology.com/Hemodynamics/H001
especially
https://www.cvphysiology.com/Hemodynamics/H012
for the part about Bernoulli's principle.

First, you are misapplying Bernoulli's law.  At each point, Bernoulli's law says that $$\text{constant}=P+\frac{\rho v^2}{2}$$  But remember, that constant is not constant in time for unsteady flows; it is constant in space.  To make use of Bernoulli's law, we should consider two different points in the fluid flow.
I will call the one closer to the aorta "upstream" and the one closer to the superior vena cava "downstream."  Since the constant in Bernoulli's law is the same for these two points, it cancels if we subtract.  Thus $$0=\Delta P+\frac{\rho}{2}\Delta(v^2)$$  (In fact, this is still not true, but it's a good place to start — see below.)  If the fluid returning to the heart is faster than the the fluid pumped out, then $\Delta(v^2)$ will be positive, but the vena cava will have lower pressure than the aorta, so that $\Delta P$ will be negative.
So yes, if the change in velocity increases, then $\Delta P$ will "decrease", but decreasing a negative number gives it a larger magnitude.
Now for the technicality: it might seem peculiar that I assumed $\Delta(v^2)$ is nonzero.  If fluid flows faster out of region than in, then either the density changes, or, before long, there will be no fluid left there!  So if $\Delta(v^2)$ is nonzero, either the heart will soon exsanguinate, or the blood is somehow rarefacting and compressing.  Is that the case?  Of course not!
Bernoulli's law does not apply to blood flow, because Bernoulli's law assumes viscous forces are negligible.  If viscous forces were negligible, you wouldn't need a heart; your blood would just flow on its own, a perpetual motion machine.  Instead, each millimeter of blood vessel has a boundary layer of slow-moving fluid at its edges — slowed down, because it touches the capillary walls.  Keeping this fluid moving absorbs some of the hydraulic head.
Since blood vessels are largely homogenous, the amount of head absorbed is proportional to distance traveled.  This means a good model for blood flow is actually pumping against gravity: we can consider "downstream" points as "pretend higher" than upstream points.
Bernoulli's law in the presence of substantial altitude (or "altitude") changes has another term: $$0=\Delta P+g\Delta h+\frac{\rho}{2}\Delta(v^2)$$  To translate between our model (in which fluid is pumped up) and blood flow, $h$ describes the length traveled by a blood cell and $g$ describes the viscous drag per millimeter.  Decreasing the arterial thickness increases the cross-sectional proportion of blood flow in which the viscous drag from the capillary walls is relevant.  In short, it increases $g$.  So capillary constriction has much the same effect as an increased $\Delta(v^2)$: it must decrease $\Delta P$ to compensate.  But now the same analysis as before shows that we are decreasing a negative number, giving it a larger magnitude.
(I've assumed in my formulations of Bernoulli's law that our density $\rho$ is constant.  This is not true, but a reasonable approximation, as Bryan Krause's answer says.)


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What is this very small black bug?
I saw a very tiny black bug crawling over my computer screen the other day. Having recently acquired a "fingertip microscope" for smartphone, I started investigating.
On a white paper it seemed like a small black dot. I think its in the 0.3 - 0.8 millimeter range.
It would have been fairly unnoticeable if it weren't for it to crawl over my screen.
What could it be? I was thinking about dust mites, but they say it should appear as white. So I'm not entirely sure.
I live in Western Europe.
Note: don't look at the scale. It is wrong.

Also related: Bug Identification: Tiny Bugs


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How likely is a lack of DNA match with a distant relative?
How likely is a lack of DNA match with a distant relative?
I have recently gotten interested in ancestry research and have had a DNA analysis performed by a prominent commercial provider.
I've been working on my family tree for a few months now and have gotten into contact with a lot of distant relatives of mine, which has generally been quite delightful. In one particular case, we discovered that we actually have a double-relationship about 5-7 generations back in time, depending on how you count (common links go back to about ~1790).
We found this quite interesting, and this distant relative had a DNA analysis performed on their own genome as well.
Much to our surprise, however, we didn't find any commonalities in our DNA, which seems odd given the double-relation, and the fact that we have what we believe to be original and authentic documents of all the relatives forming the link.
Of course, we began speculating about the possible reasons for this. Maybe a misattributed child somewhere in the family tree? However, this seems unlikely, given the double nature of the link - most likely, we would need two misattributed children to explain the lack of any commonalities.
The other explanation would of course be that the DNA analysis provided by these companies is less reliable than we think, and that just by random mutations and "unlucky" inheritance, any common DNA might have been lost or scrambled beyond recognition.
I would like to calculate the probabilities of this happening in order to judge whether it makes sense to dig further into the original documents to try and clear up this mystery, or whether a mismatch by chance alone is sufficiently likely to explain this oddity. Of course, I don't need super precise numbers, but a back-of-the-envelope estimation would be nice - are we talking a few percent, or one in a billion? Also, I would be curious anyway on how to calculate probabilities like this, given the publicly available data on these tests.
What are the relevant quantities for this calculation (number of SNPs, I suppose), and how would one define and calculate a probability like this?
About myself
I'm a physicist with a strong background in data analysis with some basic understanding of biology and genetics. Don't be afraid to hit me with those numbers and probabilities, but please explain any genetics jargon you're going to use!

Welcome! I think what renders this question difficult to answer is we don't know what test your commercial company employs. There are very, very many ways to compare DNA between individuals. It's complex: you can share a polymorphic gene variant with a great ape of another species that you wouldn't share with a grandparent, and parts of DNA are inherited paternally/maternally e.g. mitochondrial DNA is used to perform maternal ancestry tracing. To get an accurate picture, ideally one looks through the entire genome. If you provide the company/test name, it might help specify an approximation.

I didn't know if providing a concrete company name was against the site policies, but I'm happy to provide it. I was using the DNA Test Kit from myheritage.com.

myheritage.com uses autosomal DNA testing for ethnicity estimate and DNA matching. I assume you went for the latter. I know that different testing companies use different matching algorithms, so some estimates and likenesses for an individual will vary between tests, quite more than one might expect. I think this question is unanswerable in the way that you want; we can't perform an informed calculation for specific regions or genes, but we have no idea which regions myheritage.com uses nor prioritizes, nor with which weight. I hope you can see now that it is probably an intractable question!

I think the most help we could offer would be if you narrowed or refocused your question, perhaps after reading up a little about genealogical DNA testing. The wiki entry is more comprehensive than an answer you could expect here.

Thanks a lot for the Wiki pointer, I will take some time to study that article and see whether this helps me!

This may help you: https://dnapainter.com/tools/sharedcmv4

Also related: https://en.wikipedia.org/wiki/Pedigree_collapse

What is a 'double-relationship'?

Just so you know, "Genealogy & Family History Beta Stack Exchange" exists. -  https://genealogy.stackexchange.com/

With "double-relationship" I mean something like this: my father has a common ancestor with his mother, and my mother has a common ancestor with his father.

There's a very detailed analysis published by the International Society of Genetic Genealogy here with lots of charts and stats, including stats from various commercial providers.

Note that there are also "non-paternity events". That is, the actual father is not the stated father. These happen frequently enough that, excluding a solely maternal lineage, the family tree some generations back is typically not the real tree. You can see the effect here: https://isogg.org/wiki/Non-paternity_event#Table:_Cumulative_effects_of_NPE

First, if you haven't read it already, I highly recommend Carl Zimmer's "She has her mother's laugh." for anyone interested in ancestry/genealogy.
In it, he presents the following figure showing the probability of sharing any autosomal DNA with a given ancestor as a function of the number of generations separating you from that ancestor. (notably, this analysis excludes the very real possibility of intermarriage within a family tree).

So, for example, if you were to look at one single ancestor from 10 generations before you, there's a little less than a 50% chance that you share any of that ancestor's DNA (remember that at 10 generations you have roughly 1,024 ancestors).
So, at 5-7 generations there's still a high probability that you both have at least some genetic material from the same common ancestor(s). But, it's much less likely that you both share the same pieces of that genetic material (probably in the 10-14 range on this graph).
Plus, very few (probably none) of the commercial DNA ancestry sites do full genome sequencing for ancestry comparisons. They look at a limited number of specific regions that can help identify familial relations. So, even if you do share common ancestral DNA, it's less likely that it would be detected without whole genome comparison.
Image Credit: https://gcbias.org/2013/11/11/how-does-your-number-of-genetic-ancestors-grow-back-over-time/
Edit
I just wanted to edit and reference that the above analysis was calculated by Graham Coop and colleagues. I did a little more digging and he's got a blog post (How many genomic blocks do you share with a cousin?) with a more relevant analysis for you're specific question, showing the probability of two "cousins" having zero shared DNA blocks as a function of how many generations back the two shared common ancestors.

Reference: https://gcbias.org/2013/12/02/how-many-genomic-blocks-do-you-share-with-a-cousin/

Nice answer.  Another factor that might be significant is that there might be parallel relationships that I'm not sure have a specific term in English.  That is, siblings who each couple with other siblings.  For example, two brothers who marry two sisters.  The children of these couplings then are cousins on both sides.  This situation is probably was probably rather common in times when families were large, communities were mostly small and transportation was limited.

you have roughly 1,024 ancestors well, you definitely don't have more; you might have less.

@BenCrowell - According to the Coop Lab website, these calculations do seem to apply universally (at least with respect to autosomal inheritance), and are not limited to region-specific analyses. I've updated the references to link to the source page for both figures in the answer. Dr. Coop does a pretty good job of walking through these calculations and providing primary references to backup any claims. He has a number of other posts on the topic of genetic genealogy as well.

This doesn't seem to account for the most probable explanation: what we might politely call "misattributed paternity".  (IOW, "Your father's not your father".)  While estimates of the rate vary widely, 10% seems about average from a quick search.  If I'm doing the math correctly, that means that in 6 generations it's about 50-50 that there's at least one such event.

@jamesqf - In this particular context, that wouldn't really be a question of biology, per se, nor would it necessarily be the most probable explanation. Two people with a single shared ancestor 6 generations back would only have about 1 in 5 chances of sharing any common ancestral DNA (yes, that's assuming no misattributed paternity or maternity).

@MikeyC: Perhaps I'm misinterpreting the first graph?  It seems to show the probability of sharing some DNA with an ancestor 6 generations back as close to 1.0.

@jamesqf - That's correct, but I was speaking within the context of the original question, which is about sharing DNA with a contemporaneous relative (i.e. someone with whom at lease one common ancestor is shared). This point is better illustrated in the second figure. Even though there's a high probability of both individuals having at least some DNA from the same common ancestor after 6 generations, it much less likely that they will share any DNA with eachother (~20%).

5-7 generations is a long time
Mother and child or brother and sister each share 50% of their DNA.  If you find a link between two people that is five generations back, that means you take 50% of 50% of 50% ... for five generations.  For both you and the other.  Then there is a brother-sister link.  That means that 2^11 = 1 in 2048 pieces of DNA are held in common between the two of you.
If your ancestor had some unique form (allele) of a gene, the relationship could still be proved!  However, at least a quick glance at myheritage.com doesn't make me think they are doing a full genome sequence from scratch.  If they are focusing on known variations in the genome, (maybe SNPs, single nucleotide polymorphisms) then by definition those variations should not be unique.  There will be a certain percentage of identical forms between the results for any two people and the effect of changing that by 0.05% will be minimal.
Oh, hold on a minute...
After I received an unwarranted number of upvotes, the other response raised a great point: there will be potentially recognizable regions that have not been recombined in 11 generations.  A previous StackExchange question cited that about 53 meiotic crossovers per meiosis were observed in careful measurements of 8 human cells.  A genealogist addressing the question cites figures of 42 for females and 22 for males during gametogenesis. Taking a figure of 3.3E9 basepairs / (32 crossovers x 11 first-degree steps + 23 chromosomal ends), that means the segments of non-recombined DNA should still be about 9 million basepairs long!  With one SNP every 1000 basepairs or so, that gives 9000 SNPs in a row!  That's true, of course, only if you do inherit such a piece - the overall odds should be low, since that's 1/352 of the genome and only 1/2048 is inherited on average.  But ... that's still a 17% chance that a large block of syntenic SNPs might be found - one so large that it should jump out of the statistics if the myheritage data set contains a large number of SNPs.  That probability would be larger if your common ancestor was mostly via the maternal lineage.  It seems surprising to study linkage disequilibrium between two individuals, but with the preexisting SNP data set that isn't really the case.

+1.  Ancestry sites do use SNP arrays (source), so you're correct, and most determinations of relatedness are statistical

Your statement about a brother and sister is wrong. It's possible for a full brother and sister to share no non-mitochondrial DNA (e.g. each received the opposite contribution from each parent). However, sharing no such DNA is extremely unlikely, just as much so as non-twin brother and sister sharing 98% of their DNA. On average, it will be about a 48% share, but any amount between 0% and 98% is possible (can't be 100% and opposite sex). OTOH, two brothers or two sisters must share at least one chromosome from their father (i.e. either the X or Y chromosome from their father).

@Makyen: I don't think I said anything to disagree with what you said (aside from my ignoring mitochondrial DNA, that is - you remind me that if the genetic relationship happens to be entirely maternal, they should see a very clear confirmation by that means!).

@MikeSerfas Your first sentence in this answer says "... brother and sister each share 50% of their DNA." That's what I was saying is inaccurate.

When used to predict a simple numerical expected value for the overall amount of shared DNA, we can use the average figure.  Besides, the binomial distribution gives a >98% probability of inheriting more than 6 and fewer than 17 chromosomes in common even without crossing over - adding say 64 more fragments (they overlap, so I can't really use binomial distribution accurately in that case) would give 38% to 62% shared genes.

It's not all that surprising for no actual segments of the genome to be shared between distant relatives.
The back of the envelope figure I've heard is that there's about one crossover per chromosome arm per generation. So, when you're composing the chromosomes for your child, you pick a point along each arm of each chromosome, and splice your two chromosomes together at that point to make the chromosome to pass along.
This means that there's a fairly limited number of chances to share DNA: if you overlay all the crossover points that happened between you and your relative, they don't define that many distinct segments. Each segment has a chance to be shared or not shared via descent from the common ancestor in question, but can't really be fractionally shared.
23 chromosomes * 5 generations * 2 lines of descent * ~2 crossovers per chromosome * 1 segment created per crossover = ~460 segments

If each segment has a 1 in 2048 chance of being shared, as @Mike Serfas suggests, then it has a 2047/2048 chance of not being shared, and if you AND together not being shared across all the segments you get:
(2047/2048) ^ 460 ~= 0.799

So there's about an 80% chance of seeing what you observed, by my back of the envelope math. If you fudge the numbers up and down a bit, the probability still stays in the realm of "could go either way".

+1.  I handwaved this issue out of mind, but as you showed here, it is quite relevant.


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How might IV-saline cause kidney damage that seems to be less likely with "balanced fluids" IVs instead?
The ABC News article What's in the IV bag? Studies show safer option than saline includes:

Saline — salt dissolved in water — has been the most widely used fluid in the U.S. for more than a century even as evidence has emerged that it can harm kidneys, especially when used a lot.
Other IV solutions called balanced fluids include saline but also contain potassium and other things that make them more like plasma, the clear part of blood. They're widely used in Europe and Australia.
The studies involved 28,000 patients at Vanderbilt University who were given IVs of saline or a balanced fluid. For every 100 people on balanced fluids, there was one fewer death or severe kidney problem.

and refers to research "...which were discussed Tuesday at a critical care conference in San Antonio and published by the New England Journal of Medicine."
Presumably the traditional saline solution does not contain a "wrong" or dangerous concentration of salt, but it seems that it's now conclusive that a balanced combination of ingredients beyond NaCl is safer.
Is there any understanding of the particular mechanism by which saline alone lead to issues with kidneys that seems to be alleviated by the addition of other natural constituents of blood plasma?
At first I thought the issue may be connected to "...especially when used a lot." by itself, but (also presumably) the study would have accounted for this.

I've won a Tumbleweed badge with this question, a dubious honor. Any ideas how the question might be improved? https://i.sstatic.net/NwioR.png

Short answer
There is not likely to be a single mechanism involved, but the study authors suggest that high chloride is the main issue; they refer to previous work showing a whole variety of issues that can be caused by higher-than-normal chloride levels.
Although saline contains roughly the same sodium content as blood plasma, it contains a lot more chloride than usual, because blood plasma contains several other anions such as bicarbonate.
However, please see the rest of my answer: this study shows a fairly modest effect and is certainly worth some more investigation but might not be as definitive as the news makes it seem.
The study in question
I assume the news article you reference refers to this recent paper:

Semler, M. W., Self, W. H., Wanderer, J. P., Ehrenfeld, J. M., Wang, L., Byrne, D. W., ... & Guillamondegui, O. D. (2018). Balanced crystalloids versus saline in critically ill adults. New England Journal of Medicine, 378(9), 829-839.

I am constantly befuddled by why journalism considers it appropriate to refer to a study with no citation at all of the original article, only barely noting one of the original authors and only after mentioning an interview with someone completely different. Even their link to "New England Journal of Medicine" is not a link to the journal but to other articles written by that news organization that also refer to NEJM.
Careful interpretation of the study results
First, note that this study is talking about a fairly small difference. It isn't like saline is causing people to just drop dead, and you recognize this in your question, writing:

Presumably the traditional saline solution does not contain a "wrong" or dangerous concentration of salt

Rather, the study showed that 1139/7924 (14.3%) with "balanced fluids" had an adverse kidney event versus 1211/7860 (15.4%) with saline.
They also reference two previous papers, one from the same authors:

Young P, Bailey M, Beasley R, et al. Effect of a buffered crystalloid solution vs saline on acute kidney injury among patients in the intensive care unit: the SPLIT randomized clinical trial. JAMA 2015;314:1701-1710.
Semler MW, Wanderer JP, Ehrenfeld JM, et al. Balanced crystalloids versus saline in the intensive care unit: the SALT randomized trial. Am J Respir Crit Care Med 2017;195:1362-1372.

each of which showed no difference between "balanced fluids" and saline.
Therefore, I think concluding

"...that it's now conclusive that a balanced combination of ingredients beyond NaCl is safer."

is not necessarily true. In Young, et al., 102/1067 (9.6%) versus 94/1025 (9.2%) of patients showed signs of acute kidney injury for the "balanced" versus saline groups - a difference that was not significant (i.e., there are not enough subjects in the study to know that an effect this size is unlikely due to chance), but numerically the "balanced" group was worse. In Semler, et a. 2017, major adverse kidney events were 128/520 (24.6%) "balanced" versus 112/454 (24.7%) saline - literally as close to "no difference" as possible with this number of subjects (i.e., 111/454=24.4%).
Therefore, although this latest work shows a significant result with a larger population size, if you consider the previous work in this area the results are definitely mixed. The more recent Semler et al. 2018 paper's result is based on a p-value of 0.04, which is just below a commonly used threshold of 0.05 for deciding whether a result is significant. That doesn't mean the result is wrong, but it means that it should be considered in the context of other work being done in the area.
This study is also focused specifically on kidney issues, and although they have some other general secondary measures like deaths, the study is not designed or able to tell whether certain patients may actually be harmed by use of 'balanced' IV rather than saline IV.
To your actual question,
How might IV-saline cause kidney damage that seems to be less likely with “balanced fluids” IVs instead?:
The authors refer to other work showing that high chloride levels lead to a variety of issues; saline has a higher chloride level than normal blood plasma levels, so they suggest that if there is an issue with saline, the chloride levels are a likely cause, but this study has no ability to test those mechanisms.
Relevant quotes from the article, with emphasis mine:

In preclinical models, the high chloride content of saline has been reported to cause hyperchloremia, acidosis, inflammation, renal vasoconstriction, acute kidney injury, hypotension, and death. Studies involving healthy volunteers suggest saline may decrease renal perfusion through chloride-mediated renal vasoconstriction.

Thank you for taking the time to write such an in-depth analysis of the paper's statements, analysis, and it's citations, and locating the relevant xkcd to go with it as well.

You might want to re-unite "...that it seems..." with the block-quote snippet from my question, and include the "..." to indicate that words are still missing.

@uhoh I added the ellipsis - I prefer leaving out the "that it seems" - in the context, you wrote both "it seems" and "conclusive" which are sort of contradictory. I've been trying to remove "it seems" from my own writing in that context, because it sort of hedges something that isn't meant to be hedged. If it didn't seem, you wouldn't be saying it in the first place, so it's sort of redundant.

I chose "...seems...conclusive..." to allow an opportunity for the answer to be instructive and cautionary about concluding too much from one paper or one study, which you did quite nicely! I may combine those words again in the future if something seems conclusive to me, but I am not certain that it is, and I'm asking a question about it. Thanks!

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


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Is it unusual for populations of archaea to be found living inside trees?
The NPR News article and podcast Getting Fire From A Tree Without Burning The Wood begins with

A scientist walks up to a cottonwood tree, sticks a hollow tube in the middle and then takes a lighter and flicks it. A jet of flame shoots out from the tube.
It seems like a magician's trick. Turns out, there's methane trapped in certain cottonwood trees. Methane is the gas in natural gas. It's also a powerful greenhouse gas.

and describes the discovery that quantities of methane have been observed to be produced within cottonwood trees.
There is a video of the methane tapped from a tree being set on fire.
The article continues:
"The wood in this particular species naturally has this condition called wetwood, where it's saturated within the trunk of the tree," says the lighter-flicking scientist, Oak Ridge environmental microbiologist Christopher Schadt.

This wetwood makes for a welcoming home for all sorts of microorganisms.
"You can't actually see a lot of the organisms because we can't grow a lot of these organisms," says Melissa Cregger, a staff scientist at Oak Ridge. "So we're able to identify them using their gene sequences."
Some of those organisms turned out to be species of archaea that are known methane producers. So it's not the trees themselves that are making the methane, it's the microbes living in the trees.

It's not clear to me if the use of "wetwood" refers to the natural condition of cottonwood trees, or if this is meant to refer to some kind of bacterial infection. For example, Mirriam-Webster defines wetwood as:

wood having a water-soaked or translucent appearance because of abnormally high water content sometimes due to bacteria and sometimes to physiological factors

Question: Is it unusual for populations of archaea to be found living inside trees? Is this something new and surprising or is this well documented?

The exact term — wetwood, is used only once in the original article (Yip et al., 2018).

Others have found that water content of heartwood tissue was the best
predictor of methane flux across multiple plant species (Machacova et
al., 2016; Wang et al., 2017), however this was not a strong predictor
of methanogen relative abundance in our analyses. It is possible that
within trees characterized by wetwood such as Populus deltoides,
other factors may become more important than water content above a
certain moisture threshold.

However, if you look at these lines from the introduction of the paper, it seems that wetwood just means wood that has a high water content. It definitely does not refer to a disease or infection.

Indeed, both mechanisms may be important depending on tree species
(e.g. those containing dry and dense vs wet and porous wood) and
ecosystem under study (e.g. wetland vs upland forest soils).

Based upon past work and our own informal observations of odors
associated with tree coring at these sites indicative of fermentative
environments, we hypothesized that an anaerobic community including
methanogenic archaea would dominate woody tissue, particularly in
heartwood tissue which is often water‐soaked.

Now coming to your question on whether it is unusual for populations of archaea to be found living inside trees.
Roots have been known to harbour microbes; plants establish this symbiotic relationship with the microbes for nitrogen fixation (See mycorrhiza and root nodules). So, it may not be very unusual that archaea interact with plants but it may possibly be unusual that they are living inside this part of the tree. Yip et al. (2018) highlight that although microbial composition of the wood has been studied in the past, these studies have been done ex situ. This means they are the first to study these microbes in situ.

Microbiological investigations of living wood have been conducted in
the past (Zeikus & Ward, 1974; Zeikus & Henning, 1975; Ward & Zeikus,
1980; Schink et al., 1981a,b, 1982), but these studies primarily
focused on ex situ wood incubations and the isolation of microbial
representatives, rather than overall community characterization across
tree conditions. For example, Zeikus & Ward (1974) demonstrated that
methane production occurred from extracted wood tissue from Populus
deltoides and were able to isolate pure cultures of a new species,
Methanobacterium arborphilicum (Zeikus & Henning, 1975), later
reclassified as Methanobrevibacter arboriphilus (Balch et al., 1979).

So, it seems that people have been working on this area since 1970s.
However, it also appears that there is not much research on archaea as a part of the plant microbiome (Taffner et al., 2018).

IMPORTANCE: Archaea are still an underdetected and little-studied part
of the plant microbiome. We provide first and novel insights into
Archaea as a functional component of the plant microbiome obtained by
metagenomic analyses. Archaea were found to have the potential to
interact with plants by (i) plant growth promotion through auxin
biosynthesis, (ii) nutrient supply, and (iii) protection against
abiotic stress.

So whether this is unusual or not depends on whom you are asking (hence a bit opinion based).

This turns out to be more complicated than I expected, thank you for the interesting and well-sourced answer!


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Is there a link between SASP and fibrosis?
1/ Fibrosis: Fibrosis is the formation of excessive fibrous connective tissue in an organ or tissue during a reparative process.
2/ SASP: SASP is the accumulation of molecules and senescent cells in tissue, that triggers "dead" parts in the body
Is there a link between these two phenomenon? I'm specially thinking about the fact that SASP in an organ would not be able to replicate and recreate parenchymal tissue, leaving the place to connective tissue to replicate: This would end in fibrosis?
Question: Is SASP one of the factors leading to fibrosis?


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In atherosclerosis, why do apoptosed macrophages stay on the endothelium?
In atherosclerosis, the following process happens:

Lipid deposits of LDL-cholesterol happen on the endothelium
They triggers an inflammatory reaction of the endothelium: macrophages circulating in the bloodstream comes in and assimilates the LDL-cholesterol
The macrophage enters apoptosis when they are full of LDL-cholesterol, and this triggers collagen production which ends in creating a plaque

My question is: in a common inflammatory reaction, the secretion of caspase triggers the apoptosis of the macrophages that have assimilated foreign material. Then the macrophages migrate to lysosomes where they are degraded. Why does this migration not happen in atherosclerosis?
Might be linked with this question: Why oxLDL accumulate to form foam cells?

Why do you write "the macrophages migrate to lysosomes"?

I think you have some problems with your terms - perhaps look up what lysosomes are, and whether this might be something that a macrophage could migrate to? You might also want to look up whether caspases are secreted for initiation of apoptosis.

@bob1 Thanks but could you please be more specific about the interrogation? For caspase for example, I have read an article about a study asking whether caspase triggering apoptosis is a unique or multiple effect of caspase. What is the problem with that?

The term "secrete" means a specific something in biology and I don't think you are using it correctly. Caspases do trigger apoptosis, but is this done by secretion of the caspases or not?

My understanding is that caspase is secreted by cells and that caspase triggers apoptosis by linking to chemical receptors on other cells


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Is proliferating stem cells dangerous on some aspects?
By searching on internet about replication of stem cells, I came across numerous articles speaking about how to activate stem cell proliferation, most articles searching "natural" means for that. This looks to me as some "magical words" for speaking of a good health.
My question is: what are the benefits of activating stem cells in our body, since:

Cicatrization mechanisms activate "when needed", when the body is underinjury
Activating stem cells could be a cause of tumors appearance (AFAIU)?

There are lots of different types of "stem cells" in the body, with many different roles, and varying degrees of "stem-ness". That article seems to be conflating iPSCs, which are highly pluripotent, with lineage stem cells like MSCs, with progenitor cells like the ones found in the crypts of the intestines that only differentiate into one or a few different cell types. It then combines this with a lot of hand-waving about good health practices in general. Basically the take-home should be that if you live a healthy lifestyle and eat well, your body will be taken care of. Duh.

Keep in mind the source of the article, too - they sell supplements just like the kinds recommended in the text. How surprising.

Thank you for your comments. I understand the "buy what I sell" side of the article, but my question is about proliferating stem cells in général. About the different type of stem cells, do some of them create cancers?

They can. And, in a way, all cancers have some stem-like qualities to them, as they proliferate continuously, given enough nutrients, blood supply, and protection from the immune system. Some "cancer drivers" are actually mutated or dysregulated genes that are active during stem cell proliferation and division. Stem cells can grow in a cancer-like manner, but they are typically regulated by surrounding tissue and the body as a whole, so they don't form tumors. It's only when that regulation goes awry that true cancers form.

So I understand that stem cells duplication can be activated by different elements entering the organism
But besides the nutrients, is there a need for "signalling" and "planning" of how and where stem cells will duplicate? Like an organ should not grow up in all directions

Yes, there's a tremendous amount of signaling and regulation going on. Stem cells don't just decide on their own to proliferate or differentiate, there's all sorts of inter-cellular signaling going on so each individual cell is acting in concert with its surrounding cells, as well as the needs of the tissue, organ, and body as a whole.

Would you have some information on this signalling and regulation. I think this is the path that answers the best my question

There's so much available online using Google or Google Scholar, and searching with terms like stem cell signaling or regulation of stem cell differentiation. It's a huge area of research, so you'll need to be more specific about what exactly you're looking for. This review might be a decent place to start.


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Why can DNA tests with mixed DNA of several people not be used to detect a criminal in a database?
Scenario: Two males attack another pair of two males with a weapon. The attackers are fought off and the weapon remains. Why does the police require DNA samples of the two who have been attacked to be able to find out if the two attackers are in the national criminal database?
Or without the specific scenario: Can a DNA profile be created from a sample where several individuals have been involved and it is not possible to separate the cells and assign them clearly so that this profile can then be searched for in a database?
Disclaimer: This happened to me and several years later, I'm simply curious why I had to give a sample to help police find the perpetrators.


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Clarifying Resting membrane potential
I need some help understanding how the resting membrane potential is maintained in neurons. I understand that there are more K+ leak channels than Na+ leak channels, meaning that more K+ ions leave the cell membrane than Na+ ions enter.
However, where I am confused is with Na+/K+ ATPase. 3 Na+ are pumped out and 2 K+ are pumped in. From what I understand, this pumps out Na+ as fast as it leaks in. But if K+ leak out faster and less are brought in, then won't there be eventually no K+ left in the cell?

Better to not worry about the pump ratios at all. They don't matter appreciably. Learn and use the Goldman/GHK equation.

Think of it this way, the rate at which K+ and Na+ try to leak to the side with the least concentration  of that ion  is counteracted by NA+/K+  pump. So while K+ is leaking out and Na+ is leaking in, this process is balanced by the pump (pumping K+ in and Na+ out). This is process will come to a balanced equilibrium, where ions will still be leaking, and still being pumped, but the net sum of these two opposing processes is zero change in concentration.


text:
Would there be more amino acid residues in the extracellular or intercellular space?
I am working on a bioinformatics project with HMMs and want to write some initiation probabilities for the location of amino acid residues. I know for different transmembrane proteins there will be different cases, but, in general, which regions of the protein would correspond to more AA residues: intracellular or extracellular? Or is there no general pattern?

This would probably vary a lot with cell type, is there a certain type you're interested in?

Not really, I was wondering more in general terms. It makes sense that there is a lot of variety.

Yes ,there are some patterns.
First you have to determine which group of membrane proteins you're talking about.
According to Molecular Cell Biology Lodish et al 8th ed chapter 13, there are 6 types of ER membrane proteins ( and therefore in the cell membrane)
The 6 types are type 1,type 2 ,type 3 , type 4,Tail anchored proteins ,GPI anchored proteins.
Nearly all AA residues in type 3 or  the tail-anchored type are located in the cytosolic side of the membrane ( their difference is in their N/C terminus orientation) whereas GPI anchored type has almost its entire AA residues in the exoplasmic side.
For other types there may not be a general pattern.
See E. Hartmann et al., 1989, P. Natl. Acad. Sci. USA
86:5786, and C. A. Brown and S. D. Black, 1989, J. Biol. Chem. 264:4442.
By the way , you can also think of it in another way. Antigens , Hormone Receptors , Structral proteins in exoplasmic leaflet of membrane usually have more AA in the exoplasmic side.


text:
Why is loud music much louder after pausing and resuming it?
If I pause a sufficiently loud song (in headphones) for several seconds, then resume it, I perceive it as deafeningly loud, even painfully. Yet, if I first lower the volume, resume, and then gradually increase it over a span of as little as two seconds, there's no problem.
Like turning on lights when someone's sleeping, but for ears that were awake six second ago.
Why does this happen?

This is probably a good hint that listening to loud music in headphones is bad for the ears!

Hearing is capable of sensory adaptation such that prolonged constant stimulus is perceived as less intense. In hearing, the adaptation to loud sounds is called acoustic reflex and is mediated by two muscles: the tensor tympani muscle and the stapedius muscle. Both of them involuntarily and quickly contract when a loud sound comes to the ear in order to minimize any possible hearing damage.
However, they do not respond immediately, which you observed yourself. Depending on the loudness and the frequency of the sound, the response time generally ranges from several tens of milliseconds up to several hundreds of millisecond1,2. Therefore, gradually increasing the loudness gives the reflex enough time to respond and decrease the sensitivity of your ear.

1 Bell, A.
A fast, "zero synapse" acoustic reflex: middle ear muscles physically sense eardrum vibration (2017)
2 Narayanan, R. Characterization of Acoustic Reflex Latency in Females (2017)

@chivracq There are many more than just five senses. The classical five are only a few; there's also your sense of balance, your kinesthetic sense (i.e. your sense of where your body parts are relative to each other--how you know that your arm is at your side and not raised up, for instance), your sense of hunger, the sense that tells you when you need to use the restroom, and most people consider "touch" to be a combination of several senses, including your sense of pain and your sense of temperature. And there's your sense of humor! (that last one was a joke, just in case yours is impaired.)

@Hearth, alright, I actually wanted to add "physical + psychological" to the word "Perception" that I used in my previous Comment... OK, I understand (a bit)... Thanks for your explanations/clarifications, and I'll stop "polluting" this Answer, the "System" is complaining about "extended discussion + moving to chat"...

Oh...!?, "good"... Some High-Rep User removed the "Like many other senses" I was "complaining" about, => +1 from me for both the Qt + Answer. // There is a Typo btw in the Answer: "several hundreds of millisecond[+s]" (missing 's'). Hum, and in the Qt also: "six second[+s] ago" (also a missing 's').

Based on this answer, I got that it needs some time to adapt to loud sound, but how about the reverse? Does it need much time to adapt to no/quiet sound at all? Or otherwise, will pausing only for a very short time (either voluntarily or musically) not amplify the subsequent loudness?


text:
Can we produce sugar using chlorophyll dissolved in ethanol?
I can't find anything about this on the net.
I read in my (high-school) textbook that if plants get sunlight, water and carbon dioxide, and the catalyst called chlorophyll, they can make sugar.
I'm just thinking... We CAN extract chlorophyll by dissolving the boiled leaf in ethanol! So can't we just bubble CO2 in and let the sun shine on it and add some water? Shouldn't that make sugar in the solution?

An interesting thought, but your textbook has presented photosynthesis in a highly simplified way. I suggest you go through https://www.khanacademy.org/science/biology/photosynthesis-in-plants (it's fairly detailed!). Then think again about why the method you described may or may not work.

The mechanism of photosynthesis proceeds via light-dependent reactions and light-independent reactions within the chloroplasts (organelles in cells which house the photosynthetic machinery, and indeed chlorophyll itself).
To produce glucose via photosynthesis, you certainly need the pigment chlorophyll - it is necessary but not sufficient by itself. For that, you need the Calvin cycle, which is part of the light-independent reaction within photosynthesis.
The light-dependent reaction requires chlorophyll and uses H2O and sunlight to produce ATP and NADPH, with oxygen as a byproduct. ATP and NADPH are necessary for the Calvin cycle to proceed, which takes atmospheric CO2 and produces glucose and other sugars. This is simplified into basic photosynthetic equation which you are familiar with.
     6 CO2     + 6 H2O  -->  C6H12O6 +  6 O2
carbon dioxide + water  -->  glucose + oxygen

Here is an illustration:

The red arrows point to the light-dependent ("light"), and light-independent ("dark") reactions.
Take a look at this slideshow, which answers all your questions with illustrations.

We CAN extract chlorophyll by dissolving the boiled leaf in ethanol! So can't we just bubble CO2 in and let the sun shine on it and add some water? Shouldn't that make sugar in the solution?

Unfortunately you destroy the chloroplast structures during the extraction you describe. These structures, and especially the membranes, are necessary for photosynthesis in its entirety to proceed.


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Why does water flow from low to high concentration? Shouldn't it be the reverse?
So my understanding of water flow is as follows:
Basically, water moves about randomly because it has thermal energy. It will occasionally hit other water molecules and "bounce" back. As such, in areas of high pressure, water bumps into other water molecules a lot. However, if a high pressure water tank were connected to a low pressure empty tank, some water would be hit in the direction of the empty tank, but it wouldn't get hit back. Over time, more and more water is hit over until the water pressure equalizes. A vacuum doesn't suck so much as not push back, if that makes sense. So my trouble with hypotonic/hypertonic solutions is as follows. In a hypotonic situation, the solute concentration outside the cell is lower than inside the cell. A hypertonic solution is the reverse. So a hypotonic solution has fewer water molecules, so you would expect water to flow out of the cell because it's not getting hit back as much. But it flows in. The reverse is true for hypertonic solutions. Why is this? Thanks!

Why do you think a hypotonic solution has fewer water molecules?

A hypotonic solution has lower solute concentration outside the cell than inside the cell. In other words, the ratio of solute to water is higher inside the cell than outside. In order to equalize the concentrations, the solution inside the cell must be diluted, by drawing in water from outside the cell. A hypotonic solution has more water molecules per solute molecule than inside the cell, so water moves into the cell.
Your mistake is in thinking that a hypotonic solution has fewer water molecules than the cell. In a relative sense, it's the opposite - the hypotonic solution has a lower concentration than inside the cell, and therefore more water per solute than inside.


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Why doesn't the polar side of the plasma membrane block nonpolar diffusion?
It is often stated that small molecules or nonpolar molecules can diffuse through the plasma membrane because they can pass through the middle nonpolar bit, but why don't the polar sides block these nonpolar molecules. Estrogen is nonpolar and can diffuse across the membrane right? Why don't the polar heads of the phospholipids block it? Or look at H+. H+ can't diffuse across the membrane because it's charged (it's not like nonpolar molecule have a repulsive force against it, neutral objects don't repel charged ones as far as I am aware, I don't get why we say polar and nonpolar repel each other, as I understand they just stick to themselves better than each other). Regardless, H+ a small charged molecule would be able to get past the hydrophilic heads right? Estrogen wouldn't be. Where am I going wrong here?
Thanks!

You might get the answers you're looking for on the chemistry stackexchange

Polar and nonpolar molecules don't actually "repel", it's that polar molecules attract each other much more than nonpolar molecules attract anything. Therefore, to take a polar molecule from the (polar) water on one side of the membrane and bury it in the nonpolar region in the middle of the membrane is difficult because it means breaking its relatively strong interactions with the polar water molecules without forming new strong interactions to compensate.
In the case of a nonpolar molecule passing through the membrane, it is already in water when it approaches the membrane, and transferring it past the polar head groups isn't much "worse" (there's likely a slight effect of the often charged head groups attracting ions that bridge them to one another, but this would be small). The large effect of it being nonpolar, however, is to make it less unfavorable to move it into the middle layer of the membrane where there aren't polar groups for it to interact with.


text:
Can alleles have cyclic dominance?
Do the relationships between alleles always form a hierarchy? Ignoring partial and codominance, can alleles have a cyclic relationship? For example, is there anything that exists analogous to the following 3 fictional alleles:
Rock -> Scissors -> Paper -> Rock
If so, it's easy to see what would happen in a diploid relationship and which phenotype would be expressed. But what would happen in a triploid organism? Would nothing be expressed because each allele was dominated by another?

Have you thought about what dominance is caused by?

I understand situations like a pigment being produced or not being produced. But what I'm asking abouot if any boundary conditions exist that are outside the norm. Specifically, modes of inheritance that have non-binary causes.


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What are these structures inside a cut open Allamanda blanchetti?
As suggested by @tyersome in my previous question on the same topic which I posted yesterday, I have cut open few flowers of Allamanda blanchetti
in order to observe if any reproductive structures could be found.
I took 2 buds in different stages of opening as well,if they had some kind of bud pollination. But it seems there is no difference in the bud and bloomed flower.

then I found these  yellow long stiff hairs all stuck together, with some transparent secretion on them,no pollen. I think that these hairs cluster together to form this small star shape projection inside the flower we usually see when it is in bloom.

and this small green bulb like thing with a thread like extension to attach it to the base of the pedicel.
and then on further extending the incision this small swollen part almost like a ovary. But on its transverse section I didn't observe any ovules or placenta inside.

I don't have microscope or other high resolution equipment, I tried looking at it with a magnifying glass but no new details appeared.
So what are these structures? Do they enable sexual reproduction for the plant? Links to related reliable websites are also welcome.

+1 for the dissection and photos. Good work!

This is great — I'm glad you got a good answer. If you have lots of flowers, you might want to try dissecting them at different times (e.g. over a number of days after the flower first opens to see how the fruit develops). You can also try some experiments to see whether these flowers are self-pollinating (e.g. enclose a flower in a bag before it opens) and see whether it makes a fruit.

The third photo gets to the heart of the matter. Here's an enlargement:

The gold-colored areas are the anthers of some of the stamens, the filaments of which are fused with the tissue of the petal.  (This is typical of the Apocynaceae, the family to which A. blanchetti belongs; they have epipetalous stamens, that is the stamens are "adnate" i.e. fused with the petal.) This is the male part of the flower; the anthers have the pollen grains which the plant is trying to get transferred to another flower.
Above the knife is the style.  This part of the female structure is a hollow tube which runs from the openings in the stigma (the out of focus green blob) down to the ovary (not in photo). The central part of the fourth photo is presumably the ovary (missing its style). The ovary contain the ovules which will become seeds after fertilization from pollen which sticks to the stigma and grows a tube down the style.

So the fertilization occurs just like any other flowers[like a hibiscus]? because the anthers and stigma seem hidden .

@AmarylisVaselaar, yes, much like other flowers. Some of structure tries to route the pollinator to the stigma first, then the anthers, for out-crossing. See  1, 2,

Great research articles I couldn't have found them out myself.


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Red flowering climber ID
Here's another climber from the same garden in Araku Valley

So what is this climber?
Does it have any economical uses?

It's an Ipomea also known as a Morning Glory. There are 600 species of Ipomea including the sweet potato. There are many colors of mixed Ipomea, your one is probably a fairly random hybrid. It is perhaps most similar to Ipomoea Rubriflora and Ipomea Coccinea:


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Why do Oak Processionary caterpillars form processions?
Firstly ,I don't live in Europe. I live in South India, and my garden has a Night Flowering Jasmine tree.
And these trees are quite popular, but notorious for their caterpillars. In our region ,there are no specific names or identification these caterpillars and the thick mat they form on the tree trunks.

And one day, I was looking through images of caterpillars online ,when one seemed similar. It was called Oak Processionary.I am not sure if the caterpillars found in my area are the same species or something else entirely, but their behavior is similar .  As per as Wikipedia and some other websites, they are usually found head to tail moving together.
My question is

Do they have some chemical signaling agent like pheromones ,or like ants when they follow each other?
Why do they form such processions in the first place? Wouldn't having such a large ,conspicuous gathering make it easier for predators to spot them from afar?

https://en.wikipedia.org/wiki/Selfish_herd_theory

Would it be to their advantage to look like a snake?

@PolypipeWrangler they don't look much like a snake, rather a kind spiky doormat.:)

Here's a paper that gives the distances traveled, the directions, phototactic strategy of the leading caterpillar (away from shade). He doesn't state a reason, it's presumably a variety of protective reasons, because they burrow and cocoon in trees socially, and because of birds/crows/lizards https://movementecologyjournal.biomedcentral.com/articles/10.1186/s40462-020-0189-x


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What changes do ants make to the soil they use for building ant hills
I live in South India ,and among the many species of ants in and around our house, some of them except the weaver ants build the typical small ant hills in the garden.

I have examined the coarse sand like grains on the top of the ant hill. They are somehow modified and don't mix with normal soil or disintegrate in water.The region I live in has red soil.
A quick search on ant hills brings up information from here

The ant hill is a byproduct of ants building their colony. As ants dig their long and winding tunnels beneath the ground, the excess dirt and debris is carried out and placed near the colony entrance, creating the ant hill. At the top of the hill, there will be a small hole that serves as the entrance and exit to the colony.
Typically, an ant hill will be made from a combination of dirt, small rocks, pine needles, and whatever other materials were left over after the ants have dug their colony.

Other sites also state same facts on the composition of ant hills, but nowhere I can find any secretion or something which changes the properties of the ant hill soil.

So do they secrete enzymes or something or mix the soil with plant
debris to change the size of grains?
Does doing this confer some added protection to the ant colony living underground ?


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Natural Toxins and Medicine
How are natural venoms and toxins (e.g. spider and snake venoms) used to make antidotes? In other words, what is in that venom that is part of a harmful substance but, when used correctly, can actually help us, and why can these molecules help or harm in different situations?
Also, why are we looking to natural toxins to produce new medicines instead of synthetic chemicals we could make or already have?

You are probably thinking about antivenom using immune serum.
You give the venom to a host animal to induce an immune response, and then purify (to the extent possible) antibodies collected in serum from that animal, and then inject these to the patient to neutralize the venom. You don't use the venom directly.
Isolating components of venom could also allow for screening for molecules that will bind to them strongly and possibly block their action, though I'm not aware of specific antidotes that have been produced this way.


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Tiny deep red flower shrub species ID
I found this plant with maple like leaves blooming after rains this july.I am in Bhubaneswar,India.

It's Jatropha gossypiifolia, a medium-sized (maximum 15m) shrub.The leaves are similar to the leaves of a cotton plant (Gossypium). Often categorized as an agricultural weed. Poisonous for mammals also. Commonly used for the production of Biodiesel.
As per wikipedia-

There are many common names for Jatropha gossypiifolia including bellyache-bush, black physicnut, and cotton-leaf physicnut in English; pinon negro, pinon colorado, and tua-tua in Spanish; medicinier noir and medicinier rouge in French; mamoninha and peao-roxo in Brazil; jarak merah and sibidigua in India.[4]

NCBI Taxonomy ID: 454931


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Is Panmixia very rare?
I'm reading the wikipidia page on Panmixia.

Panmixia (or panmixis) means random mating. A panmictic population is one where all individuals are potential partners. This assumes that there are no mating restrictions, neither genetic nor behavioural, upon the population and that therefore all recombination is possible. The Wahlund effect assumes that the overall population is panmictic.

In genetics, random mating[4] involves the mating of individuals regardless of any physical, genetic or social preference. In other words, the mating between two organisms is not influenced by any environmental, hereditary or social interaction. Hence, potential mates have an equal chance of being selected. Random mating is a factor assumed in the Hardy–Weinberg principle and is distinct from lack of natural selection: in viability selection for instance, selection occurs before mating.

Now, I would guess from this definition that Panmixia is a condition that almost never occurs, that in the vast majority of cases, there is some sexual selection going on which makes some pairings more likely than others.
But the way the page is written seems to suggest that this is a pretty normal condition of populations, or at lead doesn't mention that it is a "spherical cow" abstraction.
Am I missing something here?

Broadcast spawning aquatic animals such as clams, and wind-pollinated plants like grasses are all panmictic - both randomly discharge gametes into their environment, where they are randomly mixed and eventually matched, meaning that in theory any individual in such a species can produce offspring with any other individual in that species. And the textbook is correct - aquatic broadcast spawners and wind-pollinated plants are ubiquitous in their respective environments, so panmixia isn't unusual or rare at all.

I agree, it is very common. Maybe not in vertebrates, but plants, fungi and bacteria (if you consider horizontal gene transfer a type of sex) tend to be panmictic.

Not fungi. Fungi can have potentially hundreds of  "mating types", and two fungi can only procreate if their mating types match.


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Genome-wide association study (GWAS) search engine?
I am not a biologist and came across the term genome-wide association study or 'GWAS' for the first time today.
Now I would like to see if there is a GWAS on the particular condition I am interested in finding out about. Is there a search engine that collates all known GWAS and makes them searchable?
Note: the backup plan is to use Google, but I wonder if there's anything dedicated to this particular task.

Try this https://www.ebi.ac.uk/gwas/

When researchers write meta-analyses etc. of such studies, they still use the traditional literature search tools, pubmed etc. So I don't think there is a database that has taken off just for gwas.

Thanks @Fizz (you're a human encyclopedia). Also, you may be interested in this question, which is somewhat related to another question you answered


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Are there any biometrics that can measure tiredness (sleepiness)?
Are there any biometrics that can estimate how tired someone is? I specifically refer to tiredness in the sense of sleepiness (as opposed to physical tiredness that might happen after a workout, for example).
For context, I'm trying to quantify "tiredness" through methods other than counting hours slept, and I'd like to explore some other way(s) of measuring (approximately or otherwise) how someone is. Also, regarding granularity/accuracy it's okay if a metric can't accurately detect a sudden slump (as may happen after a heavy meal), that would still be of interest (more accurate/granular is better, obviously, but not vital).

I would pretty much guarantee that artificial intelligence and a learning algorithm of eye movement And  Iris dilation would be able to tell when the eyes are alert and when they are lethargic.

Most of the sleep-deprivation studies I've seen measure cognitive impairment as a way of quantifying sleepiness, similar to some of the metrics taken in drug and alcohol intoxication studies.
Here's a recent proof-of-concept study using a phone app designed to measure things like simple attention, arithmetic ability, episodic memory, working memory, and executive functions like cognitive conflict and behavioral adjustment (using something called a Stroop test). They also included a subjective "sleepiness" survey self-reported by participants on a 1-10 scale.
It's a Frontiers journal, so I would take the results with a grain of salt, but the methods seem well defined to me (a non-expert), which is more than I can say for many of the Frontiers articles in my field of Microbiology. Seems to me like it would be prudent to include some control metric that isn't expected to fluctuate with sleep-deprivation, but, not being an expert in the cognitive science, I'm not sure what that would be.
Reference:
Holding BC, Ingre M, Petrovic P, Sundelin T, Axelsson J. Quantifying Cognitive Impairment After Sleep Deprivation at Different Times of Day: A Proof of Concept Using Ultra-Short Smartphone-Based Tests. Front Behav Neurosci. 2021 Apr 13;15:666146. doi: 10.3389/fnbeh.2021.666146. PMID: 33927603; PMCID: PMC8076531.

Lactate production is a direct measurement of fatigue, also described as tiredness. You may want to consider ATP Synthase production and the results as they relate to temperature and oxygen.

lactate can measure muscle fatigue it is basically useless for mental fatigue.

Mental fatigue happens because muscle fatigue happens. That’s how we measure an athletes performance, you need a brain in order to contemplate.

mental fatigue has little to do with muscle fatigue.


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How many senses do humans have?
I recall learning that humans have 5 senses, but that may have been an over-simplification to focus on the most notable ones, or simply that no others were known about at the time. Wikipedia says:

Although traditionally around five human senses were known (namely sight, smell, touch, taste, and hearing), it is now recognized that there are many more.

Is there a known, discrete number of senses (and, if so, how many are there)?
Note: If there's disagreement in the scientific community about the answer it would be interesting to learn what most biologists consider most plausible.

Downvotes? Really? Why!?

This post has 3 close votes as "opinion based" — probably be because this requires sharp distinctions among  fuzzy groups. ——— In addition, the Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may also be subject to down-voting and closure. For example, you could start with the wikipedia on senses.

@tyersome is it opinion based or just not well enough understood to have consensus yet? I presumed the latter. I did 3 things before asking: 1. Googled (lots of unreferenced articles I didn't trust), 2. Wikipedia'd it (see link above), and 3. Searched Biology SE (not previously asked here). I guess a 4th was look for an example of a nebulous biological concept (I searched for an article I read some time ago stating there were 13 different definitions of 'species', but I couldn't find the article so left that analogy out). BTW, if there's not consensus on this, that itself is an answer

This kind of question generally isn't interesting to professional biologists (in fact they are actively disliked). In part this is because even if you could answer it you wouldn't have learned anything particularly interesting (Let's say that it's 13 — so what?). This is also inherently dependent on how you define a sense and where you put the (somewhat) arbitrary boundaries among them — even within the traditional 5, smell and taste overlap. That makes it difficult (maybe impossible) to enumerate the "senses". More research could change this, but efforts aimed at counting won't get us there.

Would a brief explanation of why it doesn't work like that be a valid answer by the Biology.SE rules?  I think I could manage that myself, if nobody else wants to.  As you guessed it might be, stevec, the answer is that, like species - in fact, more so - once you know more about the details it becomes clear that different senses can't be classified neatly enough to be counted.  As tyersome said, what's usually referred to as "taste" is partly the same as "smell" and partly not, whereas "touch" is a lot of things (heat, vibration, pressure) which are actually separate systems.

@A.B. I think that would be helpful! Please include leads for what to look up for the genuinely curious if you can

@A.B. — Welcome to Biology.SE! It is unlikely that (m)any of the established users will see your question. The correct way to get that type of feedback is to post it as a question on the [meta] site with a link to this question (click where it says "Share" to get such a link). To me what you propose seems reasonable (depending on how brief and how well referenced your answer is), but I'm a relative newcomer and wouldn't want to lead you astray!

I'd like to challenge your question.
What is a sense?
Are you looking for a complex organ that integrates with the central nervous system? Or just any part of your body that can be used to determine the property of something in the outside world? For example, you can use your toenails to test whether a hot plate is of sufficient temperature to melt dead keratinous biomaterial, like your nails. This would count as an integrated sense for a specific physical chemistry.
Or do you think a sense is a thing that detects a singular property of the world? For example, do you discriminate proprioception from gravity sensing, even though it may be performed by the same organ? Historically, each classic sense is limited to one property, but this I think is outdated. For example, skin is not only capable of performing touch and texture detecting ("tactile" sense), but also heat, pain, and other things like sensing noxious poisons such as bee stings.
Also, do senses have to detect stimuli in the external world? Plenty of sensing goes on internally, both in interstitial spaces and fluids in your body, on the surface of cells, as well as within cells, and the variety of cellular and sub-cellular equipment is hugely various. Should light receptive cells only count as 'vision' or 'light receptive' when they are found in the eye, or can light-sensitive cells found deep within the body can also be classified as part of the visual sense? There are many animals and tissues in biology where light-sensitive receptors are not exclusively found in eyes.
These are only 3 things you did not consider. There are many other questions you must answer along these lines to have a clear, at least temporarily operational definition that can be used to make distinctions to answer what things can count as a separate, countable sense.
Just as a proof of concept, I can list more than five senses off the top of my head to show you that the "five senses" concept is woefully outdated in my view, and I'm sure some others would agree. I will pick some weird examples just to demonstrate the complications that the above questions illustrate.
Chemosensory systems
(considered a sense for chemistry? or a collection of senses?)

Olfaction (smell, as carried out by neurons in the nasal epithelium; e.g. smell of vanilla, and smell of bad food)
Gustation (taste, as carried out by neurons on the tongue; e.g. salt, sugar)
Antigen chemosensing (chemical sensing, as carried out by, for instance, immune antigen receptors on B cells)
Hormonal signaling chemosensing (chemical sensing of hormones such as insulin, as carried out for instance by myocytes)
Starch sensing? (amylase in saliva can be used as a test for digestable starch)

Visual system, at the retina?

Visible light (sensing electromagnetic radiation on the order of a few hundred nanometers in wavelength)
Internal methanol sensing (the visual system as a sensor for methanol, which disproportionately affects myelin surrounding the optic nerve)
Pressure sensing (see phosphenes)

The vestibular system

Gravity sensing
Balance
Coordination
Motion sensor
Head position sensor
Spatial orientation

Skin

thermosensation (touching a hot kettle!)
Nociception (pain sensing)
allergen sensing
sensor for gamma rays, X-rays and UV light (indicated by radiation burns, development of skin cancer, sunburns, etc.)

Bones and muscles?

Kinesthetic and bodily proprioception

Brain/mind/mental/social senses?

mental pain
boredom
mental or spiritual distress
sense of self and other, including friendship, power, place in social hierarchy, reputation, companionship
motivation and love (oxytocin, dopamine, etc. in limbic systems and other neural correlates)

I'm sure some would agree, and some would disagree about the specific cases I provide. Thus the definition of senses, or sensing, seems to be opinion-based or at the very least very sensitive to an agreed-upon operational definition, for which there is none.

This is better and covers more things than what I was going to say (which was much the same thing, otherwise), so I won't.


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why are dizygotic twins genetically dissimilar
I am a high school student and I am a little confused in a topic related to dizygotic twins, I get to know that dizygotic twins are genetically dissimilar because they are formed as a result of two different fertilizations but my question is that we know sperms are formed by meiosis in germ cells and each germ cell produces 4 sperms which are genetically different from each other but there is not only a single germ cell ,they are in millions so every time meiosis occurs 4 sperms are produced from each in millions so 1/4th of them should share common genetic material? so dizygotic twins can be genetically similar ,isn't it?

When sperm cells are formed via meiosis, all resulting mature sperm cells are unique from each other due to meiotic recombination; their genomes are shuffled in such a way that they will never be identical, even between daughter cells of the same germ cell. The deck of cards is always shuffled uniquely, so even if the same daughter pair of sperm meet with a pair of same-daughter eggs, it will still produce a unique individual (zygote). See here.

Dizygotic twins are formed as a result of fertilization of 2 different eggs by 2 different sperms.
For the 2 zygotes to be genetically identical it is necessary that both eggs and sperm have exactly same genetic material.
You cannot say that 1/4 th of sperms will share same exact same genetic material..during meiosis there is recombination..now there is no defined way that only a certain gene will recombine  with the homologous pair..these recombinations are quite random..so each time a new recombinant is formed. Further variation comes during Anaphase as the sister chromatids seperate hence generating even more variant sperm.
Even if 2 in million sperms are same..it is not certain that these 2 will fertilize eggs..it can be any other sperm
Moreover for dizygotic twins to be genetically identical the 2 eggs should also be genetically identical..but again the above reasons show that this is quite difficult..(here the eggs won't be in millions.. instead 2 eggs will be released during ovulation but recombinations happen still)
Now probability of  fertilization of these 2 similar eggs by 2 identical sperms out of millions is almost nil

It would be best to include citations.  Also, while you talk about meiotic recombination you completely neglected to mention the more fundamental concept of independent assortment, which in and of itself yields an identicalness probability of roughly 1 out 70 trillion on humans.


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Plasmolysis and turgor pressures
I am a high school student and I am a little confused in plasmolysis,
when we study plasmolysis, we say that at limiting plasmolysis, the turgor pressure OR pressure potential reduces to 0 what do we mean this by saying that turgor pressure becomes 0, like in gases if pressure becomes 0atm it simply means that there is no gas molecule left which can collide with the walls of container, but here water is still left in cell, but still we say that turgor pressure has become 0? why?
And if plasmolysis still continues we say that it has not become negative and starts contracting the plasma membrane and separates it from corners of cell wall {incipient plasmolysis} ? How can the water starts attracting the membrane and not colliding with it? what do we mean by saying negative turgor pressure or negative pressure potential? please explain in simple language and by giving as many examples as possible because its my first time I am studying this and it will become easier for me to then understand.

A pressure potential of 0 doesn't mean there isn't any water left in the cell, it just means that the existing water available in a cell is not able to exert any force on the cell wall. This is because in extremely hypertonic solutions (solutions with a higher solute concentration than the cytoplasm), enough water leaves the plant cell that there is not enough water to "fill" the entire volume created by the rigid cell wall. This leads to a pressure potential of 0, i.e. no force (since pressure is force/area) applied on the cell wall.
Now if there isn't enough water to fill the entire volume of the cell wall, which is rigid, the plasma membrane detaches and pulls away from the cell wall (plasmolysis) in order to be able to surround the remaining cytoplasm. It would be physically impossible for this not to happen (I would guess that a vacuum would end up forming because of the empty space that was once occupied by the water, creating enough negative pressure to physically pull apart the plasma membrane).
This brings us to the idea of a negative pressure potential. This can often be observed in vascular tissue, such as the cells of the xylem, where water is physically being pulled from the cell, creating a situation where, in simple terms, a "vacuum" of sorts is created due to the lack of water, which ends up "pulling" the water from xylem cells (called vessel elements) via the cohesion of water molecules. This "negative pressure" can also be called tension, where the inside of the cell actually exerts a "pulling" rather than a "pushing" force (here the "pulling" is what causes water to travel up the xylem against gravity).
Source: Campbell Biology 11th ed., Chapter 36: Resource Aquisition and Transport in Vascular Plants

Might be worth saying explicitly at the beginning that people often use "pressure" as a shorthand for "pressure difference" or "relative pressure" since we don't have a separate specific word for it (like we have "voltage" for "electrical potential difference"), and/or that "pressure potential" is different from "absolute pressure". OP doesn't seem to know the differences.

I have 1 more confusion,,,,  we know that, xylem vessels have a diameter in the range of 15um -200um{ you can search for this} and in one of the videos of "Veritasium" he makes a statemen hat if have a capillary of diameter of about 10um then it could hardly raise water upto a height of 1m ,,if that's true then the "cohesion tension theory" should be wrong because it is entirely bases on cohesion of water molecules with themselves and with xylem walls, but water actually rises due o the pressure difference , i,e by transpiration plans actually generates a negative absolute pressure.

Negative pressure means that the liquid is under tension i,e if it has no air bubble in it so that cavitation can't occur, it actually can act like a solid o some extent, like when we stretch spring it generates tension in it which wants to regain its shape back jus like this I think that if we have a huge water loss then liquid molecules are no longer pushing the wall and themselves , they are now attracting themselves and their surrounding? I know it sound weird but his is the only way people can explain it


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What spider is this? Is this invasive or dangerous?
Hi the picture below has been taken here,
I've never seen such a spider, is it an invasive specie or a dangerous one?

thank you

That appears to be a zebra jumping spider (Salticus scenicus). It is fairly widespread throughout North America. It does not post any kind of threat to people or to the environment:
Here is a map of iNaturalist observations for zebra jumping spiders.

And here is a gallery of photos you can view: https://inaturalist.ca/taxa/68901-Salticus-scenicus/browse_photos


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Are animal cells animals themselves?
If all life can be divided into several kingdoms, and if the cells that make up organisms are the smallest units of life, does that mean that cells are part of those kingdoms as well? E.g. are animal cells classified as animals themselves too?

This is like asking if your arm is considered an animal. No, (like the cell), it's a sub-organismal part of the animal. Recognize that our classification systems (which are arbitrary ways of trying to conceptually organize a continuum of genetic diversity) organize genetic diversity at the organismal level. I feel like this is sort of related to the fallacy of division. I think you'd also benefit by reviewing the criteria to be an animal.

Also, If an animal cell was capable of living as a unicellular organism, I would posit that either the cell or the organism as a whole may get reclassified.

Eukariotes are more logically defined as unified multicellular groups in science.
You are right that Eukariote cells share many traits with unicellular organisms, like meiosis division, cell walls, inner metabolism, and it is an intelligent view to consider them as related to unicellular organisms in most ways, although your proposition is mostly of comparative and philosophical us, rather than a scientific biological reasoning and description.
Animal cells share the same chromosomes, which is different from species of micro-organisms, so that eukariote stem cells can differentiate into the specialized cells. Most species definitions contain a strong reproduction framework which applies to all species whereas Eukariote cells start from zygotes and then communicate with each other with signalling hormones to form a specific superstructure which are used to produce more zygotes, which contrasts with procariote definitions of a species.

So far as I know (per https://www.genetics.org/content/181/1/3 ) meiosis evolved early in the history of the eukaryotic lineage.  Also, there is no direct connection between multicellularity, hence zygote formation, and the domains of life - so far as I know, eukaryotes simply happened to be the ones that developed it.

I didn't upvote your answer because i agree with it, just because it showed some effort and contained some accuracies. I said that animals are defined by reproduction type, i.e. multicellular animals reproduce as indivisible groups, typically through zygotes. animals can be a colony which has arms and legs and nerves stemming from the brain to the toes, so they are considered as a unified multicellular groups, because it simplifies useful communication.

My opinion is yes, but note this could be subject to debate.  This is a semantic question and someone could decide arbitrarily the other way, but I'm not aware of a formal counterargument, and logic seems to demand it...
Consider Devil facial tumor disease.  I've linked a Wikipedia article there, and Wikipedia usually is very good about providing taxonomy for organisms and it's a shame they didn't do it here, as they are experts in semantics.  NCBI also does not provide a taxonomy.  But logically, if we were going to provide one, how could we possibly categorize those cells?  They are living, they reproduce, they evolve, they are eukaryotes, and based on their DNA ... they are animals!
A less clear-cut instance leading in this direction can be seen with Sacculina carcini, a parasitic barnacle of crabs.  That does have a multicellular larva, but it is not a very typical mollusc, and it illustrates that it is the cells and descent of an animal, not its form, which determine its status.
Based on these things, I would say an animal cell can potentially survive, thrive, and in reproducing itself, become recognized as an organism despite its form.  However, there is a contrary semantics to be considered, notably in the case of the HeLa cell line.  In that instance, in part due to the genetic instability of the tumor cells and their dependence on human intervention, a proposal to name them as a species did not gain traction, while I believe some argued with an eye to legal issues that the cells were still essentially part of the individual Henrietta Lacks.  However, in nature the definition of an individual can be fluid - in polyembryony one individual can divide into many, and even in humans one individual can become identical twins, so I wouldn't say that an isolated cell must remain part of the parent individual.  Meanwhile, cells of different genetic origins can join into "a" slime mold, though they usually sort themselves out by species.  In that instance we have a clear precedent of deciding the taxonomy of individual cells of an organism ... but it's not an animal.
Love it or hate it, biology will do whatever it can, without regard for how we choose to think about it.


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Have cruciferous vegetables been genetically altered to reduce cooking odors?
As a young girl my mother always kept a bottle of "Air Wick" under the kitchen sink. When she cooked cabbage, cauliflower, broccoli, etc., she would open the bottle, pull out a green sponge that was on a wire, and place the opened bottle on the counter. It absorbed the strong odors of those foods that would normally penetrate other rooms. Today when I cook those same vegetables I don't notice those strong odors of my youth. Have those vegetables been genetically altered to reduce their strong, lingering odors?

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, it is important to define what you mean by "genetically altered" — almost every food we eat has been under selection by humans for many generations. Is that what you are trying to ask about? ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

perhaps she cooked it for longer and used difference of oil/salt/vinegar.

Perhaps your sense of smell is not as good as it was when you were young?  I'd also be more than a little skeptical about the "absorbing odors" claim.