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How is heavy water detrimental to the human body?
Heavy water (D2O) is known to be lethal to humans and other life in large quantities. All I've been able to find on the toxicity is that it's similar to chemotherapy chemistry. I'd like to know precisely how having a single neutron in two atoms of an otherwise non-toxic molecule can cause the body to degrade. What's the root cause here?

Well, its vapors can give you super-speed.

The question is already answered by Armand. I am just going to elaborate on that by referencing the paper.

Different isotopes of chemical elements have slightly different chemical behaviors, but for most elements the differences are far too small to have a biological effect. In the case of hydrogen, differences in chemical properties among protium (light hydrogen), deuterium, and tritium occur, in part because chemical bond energy (the strength of a bond) changes  with changed mass of the nucleus–electron system. The isotope effects are especially relevant in biological systems because of the prevalence of hydrogen atoms in biological molecules (even deuterated water can have significant effects in the human body).
Note that enzymes have a finely-tuned network of hydrogen bonds, both in the active center with their substrates, and outside the active center, to stabilize their tertiary structures. In a deuterated environment, some hydrogen bonds will be replaced with deuterium bonds which have different strength (Ref. 3), so normal reactions in cells can be disrupted.
Studies and experiments* show that heavy water affects cell division(mitosis), cell membrane changes and cellular heat stability, possibly as a result of inhibition of chaperonin formation. Also noted among the presumably wide-ranging cellular effects was the display of an altered glucose metabolism under deuterated condition in cells. $D_2O$ is more toxic towards at least some malignant cells, but the difference in sensitivity vs. normal cells does not seem high enough for therapeutic use.
In ref. 2, you will find a paper which shows the biochemical and pharmacological effects of heavy water on humans. Basically, to study the effects of heavy water on the metabolism humans, $D_2O$ and deuterated drugs were used and various changes were noted. Have a look for more details.
References

Effect on biological systems (Wikipedia)
Kushner DJ, Baker A, Dunstall TG. Pharmacological uses and perspectives of heavy water and deuterated compounds. Can J Physiol Pharmacol. 1999 Feb;77(2):79-88. PMID: 10535697.
Steve Scheiner and Martin Čuma. Relative Stability of Hydrogen and Deuterium Bonds. J. Am. Chem. Soc. 1996 118, 6, 1511–1521 DOI: 10.1021/ja9530376

*Experiments with mice, rats, and dogs have shown that a degree of 25% deuteration causes (sometimes irreversible) sterility, because neither gametes nor zygotes can develop. Mammals (e.g. rats) were given heavy water to drink die after a week, at a time when their body water approaches about 50% deuteration. The mode of death appears to be the same as that in cytotoxic poisoning or in acute radiation syndrome , and is due to deuterium's action in generally inhibiting cell division.

Since "normal" water has around 156ppm of deuterium, and "D2O is more toxic towards malignant cells" does this imply a slightly beneficial effect of the normal deuterium found in water?

Great answer. It might make sense to add that the physiological effects are similar to those of chemotherapy (anti-cancer) drugs because chemo agents also disrupt cell division.

At 50% deuteration, half of the molecules would be $HOD$, a quarter $H_2O$, and only a quarter $D_2O$. At 25% deuteration, only $\frac1{16}$ of molecules would be $D_2O$.

@Acccumulation In the body, hydrogen atoms are constantly exchanging with or being incorporated into other molecules as well as water, so the calculation is not so simple. I'm not sure if the rat water deuteration reported above is a measured value or (as I suspect) a predicted or modeled value.

Substitution of deuterium atoms for normal hydrogen atoms changes structure and function at the atomic scale, disrupting normal biological processes. It causes changes in protein conformation and changes chemical reactions, as more and more $D$ replaces $H$, in water, substrates, macromolecules etc. "Stuff" doesn't work quite right and works less well the more the $D$. Remember, $D$ is roughly twice the mass of $H$, so it moves/diffuses very differently.
This QA at physlink.com reports:

The reason for these adverse effects is that replacing hydrogen with
its heavier isotope deuterium slows down the rate of any chemical
reaction in which the chemical bond to the hydrogen atom is broken.

(additional explanation at the link)
An actual scientific review, "Pharmacological uses and perspectives of heavy water and deuterated compounds" Kushner et al 1999  PMID: 10535697 seems to be pay-only access.


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How much extracellular matrix is there in the human body?
I just found out that there is an extracellular matrix. I had imagined that the tissues, organs, and the whole body was a bone skeleton with cells attached to the bones and to each other. I imagined the cells to be joined directly to each other like atoms in a crystal.
In fact, most of the cells are not adjacent to each other. Rather the cells (except blood cells) sit in a solid matrix that is a mixture of proteins, especially collagen, which is like a plastic or hardened glue or rubber. The matrix is secreted by the cells, and holds them in place and connects them to each other, and separates them from each other. In bone, the extracellular matrix is strong, rigid and hard, while in cartilage it is strong but flexible like some types of rubber or plastic. In the brain it is very soft. The differences in rigidity, strength and hardness come from different mixes and densities of proteins, except in the case of bone which has a lot of calcium compounds (minerals) in the extracellular matrix (as an aside, for the sake of completeness, I'll just mention that some say the blood is a connective tissue, and that blood plasma is the extracellular matrix of the blood).
Finding out (so recently) about the existence of the extracellular matrix, for me has been absolutely amazing, and it has changed how I look at my own body.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995612/ (which has a lot of information about the extracellular matrix including a colorful and impressively detailed giant poster that you can magnify repeatedly) says, "Collagen is the most abundant fibrous protein within the interstitial ECM and constitutes up to 30% of the total protein mass of a multicellular animal. Collagens, which constitute the main structural element of the ECM, provide tensile strength, regulate cell adhesion, support chemotaxis and migration, and direct tissue development (Rozario and DeSimone, 2010)." but doesn't say how humans compare to the multicellular animal with 30% of the total protein mass being collagen, nor what the total mass of that collagen would be.
https://biology-pages.info/E/ECM.html contains the closest to an answer that I've found, though it speaks of 'bulk' and not mass and some multicellular organisms and not humans :"While it is true that all living things are made of cells, that is only part of the story. Most of the cells in multicellular organisms are surrounded by a complex mixture of nonliving material that makes up the extracellular matrix (ECM). In some cases, the ECM accounts for more of the organism's bulk than its cells."
So my question is: How much extracellular matrix is there in the human body? I leave it to you to decide whether blood plasma is extracellular matrix and similar issues. Also it's up to you how you want to quantify the amount, whether by mass (my preference), volume, or some other measure. Also, it's up to you how precise and quantitative (my preference) or approximate or qualitative (that could also be good) your answer is. My aim is to see, in my mind's eye, the human body as it really is.

Here's a rough estimate based on data found in this Nature scientific report :

Muscles (around 40% of our mass) contain around 11% of extracellular matrix proteins in mass.
Connective tissues (around 45% of our mass) contain a variety of values of ECM protein content :
31% (cartilage),
20% (tendon),
30% (bone)
(this is not exhaustive)

So combining these values we could estimate that around 17% of our mass is proteins in extracellular matrix.
If you're not just interested in proteins but anything that isn't cells, so including minerals in bones (85% of 14% of our mass), plasma in blood (45% of 7%), and fat in adipose tissue (90% of 20%) then around 38% of our mass is non-cell stuff.
Note that my values are not precise at all. The studies are based on values in dry tissue, but they took water into account to estimate the percentages for normal tissue. And then I took those numbers to estimate an average on the whole body, but obviously body composition, especially fat, can vary a lot. I also ignored nervous and epithelium tissues because I assumed they didn't influence the results much (and I couldn't decide whether dead cells in skin should be considered as cells or matrix)
Funnily enough, after calculating this I just found a wikipedia article that sums up what I said with a value of 34.3% "extracellular mass" shown in an image. Sadly the cited article does not contain that value, or at least I couldn't find it. It seems unnecessarily precise, but at least that indicates that we're in a reasonable range with 38%.
I hope that gives you the representation you were looking for about what our body "is", at least I came here hoping to find that kind of estimate and since there was no answer yet I tried my best.

source: Stack Exchange

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

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What is the difference between the cheeks and the near parts?
Linguistically, there should be the different property or feature between cheeks and the parts right near them for us to call cheeks “cheeks.” What is the main difference between cheeks and the other parts right near the cheeks? I mean, how do we distinguish cheeks and the other parts?

https://en.wikipedia.org/wiki/Cheek seems to cover it.

@user438383 It says the only difference is position.

"Cheek" isn't really a biology specific word with a specific definition within the field, it's more of an everyday expression. Vis-a-vis Grey's Anatomy 3rd Edition doesn't even use the word at all.
In fish, for example it's mainly defined as the space between important features which have a defined function (eye and front edge of operculum).
Even the Cambridge dictionary defines it by (mostly) what it's in-between:

the soft part of your face that is below your eye and between your
mouth and ear:

So definitions seem to be fairly consistently that the cheek is defined by its spatial relation to other features, rather than a "thing". Loosely speaking, this would be reification (treating something abstract as a physical thing), and it's quite commonplace.

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


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Would it be possible to create logical circuits out of insects?
Could one organise ants, bees or any insects to do addition using logical gates:

AND,
OR,
NOT,
XOR.

As inputs/signals one could imagine for example that 1 would be food and 0 would be no food.

http://dx.doi.org/10.1162/artl.2009.15.3.Michael.008

@Roland Can you please turn your link into an answer?

@jakebeal Link only answers are not allowed and I won't invest the time to summarize the study. Feel free to do so.

@Roland Done; it's not so hard to do a simple version.

Could you please explain why this is a problem in biology. Is it akin to one on whether you can train elephants to dance?

@David You just answered your own question. Logical gates can built from a lot of things, not just electric circuits, I was curious how they translate into insect behaviour.

In which case I would suggest it is really not on-topic here, as the Help makes clear.

@David How about this: "is there an insect with a special natural behaviour that resembles a logical circuit?"

How about it? Sounds on-topic. But a bit strange. I would have thought certain aspects of insect behaviour might qualify, but not the insect itself.

In short, yes, it appears to be possible, and a number of people have performed investigations in this area. For example, see the "Ant-Based Computing" article suggested by @Roland, whose abstract explains the concept at a high level:

A biologically and physically plausible model for ants and pheromones is proposed. It is argued that the mechanisms described in this model are sufficiently powerful to reproduce the necessary components of universal computation. The claim is supported by illustrating the feasibility of designing arbitrary logic circuits, showing that the interactions of ants and pheromones lead to the expected behavior, and presenting computer simulation results to verify the circuits' working. The conclusions of this study can be taken as evidence that coherent deterministic and centralized computation can emerge from the collective behavior of simple distributed Markovian processes such as those followed by biological ants, but also, more generally, by artificial agents with limited computational and communication abilities.

Whether such a computer is good for anything besides curiosity is another question, but curiosity and art are fine starting points for any investigation.

As an aside, this idea was explored by the sci-fi/fantasy author Terry Pratchet in his 1996 book Soul Music, prefiguring the actual research here.


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Identifying insect in Sri Lanka
I saw this one in our garden in Colombo, Sri Lanka. It seemed to be hiding from the harsh sunlight that was there. I have never seen this bug before. Anyone know what bug this could be?

Does it jump away if you disturb it?

This appears to be a springtail (Collembola). I'm not familiar with Sri Lankan fauna, but the overall body plan (kind of oval, pudgy, short-legged) reminds me of a subgroup of springtails, the Poduromorpha.
You can see similar-looking species in the Superfamily Neanuroidea, which are an example group in the Poduromorpha order:

 Brachystomella parvula from UK; Credit: Andy Murray (2012); Source: Wikimedia

 Red Poduromorph Springtails (family Neanuridae) ; Credit: Elahi Rayan (2018); Source: Wikimedia

FYI springtails are not insects but a closely related group of hexapods

Agreed all the way down to superfamily; going any further than that really needs a slide-mounted specimen, and (given the OP location) may actually end with a species that is as yet nameless.

@Arthur thanks for the comment. To clarify for others reading my post: I am only proposing this superfamily as a likely correct answer. I only include the specific species (found 1000s km away in the UK) for the sake of demonstrating visually the common body plan seen in the superfamily. I have no idea what the OP's species is, and Arthur is probably correct that neither does science :p.


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What determines if a compound is primarily taken up by the lymphatic extensions rather than the portal vein blood supply in the intestinal villi?
I am currently studying the intestinal absorption/transport systems, but am confused about one part specifically. There are hydrophilic and lipophilic compounds (to varying degrees), and they get absorbed by different methods.
As far as I can tell there are 3 main ways of absorption in the intestinal wall:

Passive diffusion of lipophilic compounds through the membrane.
Passive diffusion of hydrophilic compounds through pores and gap junctures.
Active transport of larger molecules by transport proteins.

But once a compound passes the enterocyte absorption cells in the lining of the villi of the intestine, there are primarily two paths into systemic circulation:

Capillaries of the blood supply from the hepatic portal vein, leading to the liver and first pass metabolism.
Lymphatic uptake through the extension of the intestinal lymph system in there.

From what I can tell anatomically, both of these are somewhat intertwined/overlapped to an extend — but which properties of a compound determine whether it is primarily taken up by the lymph system (getting it to the blood supply eventually circumventing first pass hepatic metabolism) or wether more of it is taken up by the local portal vein capillaries? Is it small differences outside of the general hydro/lipophilic nature like size etc.?
Please correct me if I'm misunderstanding some of these basic anatomic concepts. I would appreciate if someone can tell me whether there is a set of parameters involved in this biochemical branching.
I just read the lacteals, the lymphatic vessels in the villi, absorb digested fats. Does that mean the more lipophilic a compound is the more likely it is to be absorbed by the lymph over the portal vein capillaries? That sounds a bit too simple for me. There must be more factors involved.

The path used for a particular compound is determined by several factors:
Affinity for Plasma Proteins: Compounds with a high affinity for plasma proteins are more likely to remain in the bloodstream rather than diffusing into the lymphatic system.
Lipophilicity: Highly lipophilic compounds are more likely to be absorbed into the lymphatic system because they can be incorporated into chylomicrons, which are too large to pass through the capillaries of the blood supply and thus enter the lacteals.
Molecular Size: Larger molecules, especially those larger than the fenestrations in the capillary endothelium, are more likely to enter the lymphatic system for the same reason as above.
Solubility: Compounds that are not water-soluble may need to be transported in association with bile acids or incorporated into micelles to be absorbed. After absorption they are often repackaged into chylomicrons and enter the lymphatic system.
Transport Mechanisms: Some compounds require active transport mechanisms to cross the intestinal epithelium. These mechanisms can be selective and influence whether a substance enters the blood or the lymphatic system after absorption.
Chemical Stability and Metabolism: Some compounds may be metabolically unstable in the gastrointestinal tract or the liver. If they are metabolised in the enterocytes, the metabolites may have different properties that affect their route of absorption.
Charge/Ionisation State: The ionisation state can affect the compound's ability to cross the lipid-rich cell membranes. Non-ionized (lipophilic) forms are more likely to be absorbed through the lymphatic system, while ionized forms are generally more hydrophilic and absorbed into the portal circulation.
Formulation: The pharmaceutical formulation of a compound can influence its absorption. For example, lipid-based formulations may enhance lymphatic uptake of certain drugs.
Note that these paths are not mutually exclusive. The relative contribution of each factor varies with the specific properties of the compound in question. The extent to which each path is used can vary greatly and is influenced by these factors, and of course this implies that a molecule may use both paths, and this is determined by metabolites utilising different pathways, partial absorption by both routes, regional absorption variations and variable physiological conditions


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Do viruses do anything other than multiply?
Viruses are "on the edge of life ". They infect the cells and use it for multiplication of themselves  but other than that do they do anything else like "eat food" like an amoeba or move on their own like Euglena ? Do they share any other characteristics with living things other than being able to reproduce ?

To be clear, the OP's question is not about classification per se, but about function, motivation—perhaps even purpose—and properties.

@RyanG viruses do not have motivation or purpose. One can speak of their function as a part of an ecosystem, and sometimes viruses are co-opted by organisms, in which case they stop being viruses.

The way I understand the question, it is about comparing fubctioning of a virus with that of a living organism (in simplest case a cell). It doesn't really invoke the virus role in ecosystems.

They can also divide

@RogerVadim ".. is about comparing fubctioning of a virus with that of a living organism.." absolutely correct. I want to know whether a virus has ANY resemblance with ANY other organism other than being able to multiply. What is the purpose of its multiplication is whole another topic, I think.

look up giruses AKA giant viruses.

Skirting the Question's fringe, and too long for a comment:
On symbiosis with viruses, from some science magazine:

Most viruses are harmful, but some viruses have a mutually beneficial
relationship with their hosts. A lot of viruses help their hosts by
attacking their competition. For example, the hepatitis G virus slows
down the growth of HIV, the virus that causes AIDS, in humans.
Bacteria grow viruses inside their cells and infect competitors with
those viruses. Other viruses are needed for their host's physical
development. When wasps lay eggs inside other insects, their eggs are
equipped with viruses. These viruses fight off the infected insect's
defenses and guarantee the eggs' survival.

This doesn't appear to answer the question, which is about mechanism, what viruses do — not what role they play, but what routines their "firmware" implements.

@Ruslan that was my original thinking as well. But the question also asks whether viruses "share any other characteristics with living things other than being able to reproduce", which can be interpreted rather generally.

They infect the cells and use it for multiplication of themselves but other than that do they do anything else like "eat food" like an amoeba or move on their own like Euglena ? Do they share any other characteristics with living things other than being able to reproduce ?

Individual level
No, viruses are not considered living entities, because they do not extract energy from the environment (aka eating) and do not do any active work like moving or constructing themselves. They entirely rely for these functions on their hosts or random influences (like being carried by air in droplets).
Maximum of what some viruses are known to do are attaching to a cell and a simple one-time syringe-like movement to penetrate it.
Part of ecosystem
Being obligatory parazites, viruses certainly play a role as a part of their ecosystem: e.g., limiting the population of their hosts or even being in symbiosis with them (as pointed in the other answer). It is necessary to note in this respect that a "successful" virus is not the one that causes the maximum damage to its host, but rather the one that most efficiently uses the host to replicate and spread itself. This drives viruses towards co-existence with their hosts, since the extinction of the host would also mean the extinction of the virus.
Wandering genes
It has been argued that viruses play a role in horizontal gene transfer, gene duplication, etc. Some parts of mammalian genomes are identified as deactivated ancient viruses, which continue producing proteins essential for the functioning of the host organism. See, e.g., here.


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Poisonous Snakes consuming poison (chemical)
While travelling with my Son to a religious shrine, we saw a dead snake lying on the road.
My Son asked a curious question to me "Dad, if Poisonous snakes consume poison (Chemical), Will they die"?
I feel the answer is depends upon the type of poisonous snake viz Cobra, Python etc and how much the reptile has consumed the poison. i.e. quantity.
What is the correct answer?

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

Does this answer your question? If a venomous snake somehow gets it's own venom in its body, will it be affected by it?

If any living thing consumes enough of a poison it will die. But I feel that is not what you want to ask.
Perhaps you meant to ask if a snake will die if it drinks its own venom? That would make more sense as a question.
In English, venom  and poison mean different things when talking about a toxic chemical produced by an animal.
Poison is a toxic chemical produced by an animal that is meant to be ingested/eat/drink.
Venom is a toxic chemical produced by an animal that is meant to be injected into the bloodstream.
So a snake bite has venom, but a colourful tree frog has poison on its skin.
Venom is typically not nearly as harmful if ingested, even if by a different animal, because it is meant to act directly in the bloodstream


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What insect is featured in this picture?
At the end of the summer, we've been finding these insects in our apartment complex in Baltimore, MD. What are they and do they bite? The length is about the size of a US nickel (We've had mysterious bites along our legs the last few days and haven't found any fleas or bedbugs after turning over the bedroom!

Please update with approximate size, location, and species-identification tag. Thank you

This is a cockroach

Note the flattened body, long antennae, "hidden" short head, and spiny strong legs

Without more details, location or better photos, ID to species is not certain. The most likely species to be found as pests in buildings in the US include: Oriental, German, and brown banded roaches. Common outdoor species that also often come into the home or invade commercial buildings include two larger species: the American and less commonly smoky brown cockroaches. Both of these species are found in the highest abundance in the Southeastern US.
Your image does not immediately convince me you have one of these species. Oriental roaches are black and smoky browns are also darkly colored -- unlike your brown specimen. German (vertical) and brown-banded (horizontal) have stripes on their pronotum, which your specimen also does not clearly have. American cockroaches are unmistakably large with brighter pronotums having darker spots -- again, unlike your specimen.
there is a chance that this is a female brown banded cockroach with its colors washed out from the poor quality photo.  (I kind of see some banding along its abdomen).

 Female brown-banded roach. Credit: James L. Castner ; source UFL
Cockroaches really never bite. You'd have to have a really bad infestation for this to happen. Orkin supports this claim

Texas roaches are at least 3X larger as adults. Borax dust will control them if you can expose them to it . Borax is otherwise fairly innocuous. I blew borax into the cabinet containing the dishwasher and that has significantly reduced the number.

Borax can be dangerous for pets and kids. Use caution using this product. Follow safety guidelines recommended by product


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How is it determined which parts of an mRNA precursor are to be spliced?
According to my textbook, the same pre-mRNA sequence can get spliced in multiple different ways. But how is this regulated by the cell? How are the introns and exons to be spliced determined?

Welcome to SE Biology. Please finish the [Tour] and then How to ask good questions.  You will see there "Have you thoroughly searched for an answer before asking your question?… Tell us what you found and why it didn’t meet your needs. This demonstrates that you’ve taken the time to try to help yourself…" The term you should search for is "RNA Splicing". You will see related questions to the right here, a section in Wikipedia, and sections in Berg, Lodish and Alberts on NCBI Bookshelf.

Oh, and cells don't "know" anything. Acceptable scientific terminology would be "How is it determined which parts of a mRNA precursor are spliced?", "What is the mechanism by which a mRNA precursor is spliced at specific positions?" or "How are the splice sites recognized on mRNA precursors?". Precision in scientific communication is important. Sloppy speech leads to sloppy thinking.

As the textbooks available in NCBI Bookshelf are often older editions and the field of "alternative splicing" has advanced rapidly, try to find the 9th Edition of Lodish (2021) or the 6th Edition of Alberts (2017).

@Armand In an ideal world yes. But these are freely available and appropriate to a question at a completely naive level.

Your question is a good one, and has given rise to decades of intensive research, which continues today. The short answer is that many factors are involved, ranging from sequences within the gene up to chromatin-level changes.
De Conti et al. in their review "Exon and intron definition in pre-mRNA splicing" (2012 DOI: 10.1002/wrna.1140) note:

Most importantly, these influences act across several levels of
complexity starting from the relatively simple interaction between two
consensus 5' and 3' splice sites to much more complex factors: such as
the interplay between silencer or enhancer sequences, transcriptional
processivity, genomic milieu, nucleosome positioning, and histone
modifications at the chromatin level. Depending on local contexts, all
these factors will act either antagonistically or synergistically to
decide the exon/intron fate of any given RNA sequence.

In the big-picture view, there are two types of intron-processing complexes or "spliceosomes" found in most metazoan cells.  Akinyi and Frilander ("At the Intersection of Major and Minor Spliceosomes: Crosstalk Mechanisms and Their Impact on Gene Expression" 2021  DOI: 10.3389/fgene.2021.700744 ) summarize:

The majority of introns (more than 99.5% in humans) are recognized and
excised by the major spliceosome, which utilizes relatively poorly
conserved sequence elements at the 5' and 3' ends of the intron that
are used for intron recognition and in subsequent catalysis. In
contrast, the minor spliceosome targets a rare group of introns
(approximately 0.5% in humans) with highly conserved sequences at the
5' and 3' ends of the intron.

Finally, it now seems clear that intron/exon structure developed at roughly the same time as eukaryotic cells.
Rogozin et al. ("Origin and evolution of spliceosomal introns" 2012 DOI: 10.1186/1745-6150-7-11 ) write:

Reconstructions of intron gain and loss using the growing collection
of genomes of diverse eukaryotes and increasingly advanced
probabilistic models convincingly show that the LECA (Last Eukaryotic Common Ancestor) and the ancestors
of each eukaryotic supergroup had intron-rich genes ...

There is no indication that any prokaryote has ever possessed a
spliceosome or introns in protein-coding genes, other than relatively
rare mobile self-splicing introns.

Here's a review of the molecular machinery at work: "The nuts and bolts of the endogenous spliceosome" Sperling 2017 DOI: 10.1002/wrna.1377


text:
How fast does eyelid close when eyelash is triggered?
What is the reaction of blinking like when an unexpected piece of wood or something hits an eyelash and then an eyeball?
A piece of stone flew into my eyeball when we knocked a wall down, and it hit the white area. Another time, I walked into a piece of wood in the dark, and my eyelid closed faster than I was walking so it protected my eye.
So it got me thinking. Is there a fast neural network in between the lash and the the lid contractors, so that the eyelid can close very fast when the lash is contacted unexpectedly? How fast does the reaction happen?

The human eye is thought to react about 1/24 of a second, but I'm not sure how fast it is when it touches an eyelash

Thought by who? based on what? Please [edit] your posts to conform to the standards of this site.


text:
Do animals lie?
Have there been any studies that show or suggest that species known to be able to communicate information between individuals ever intentionally communicate false information i.e. lie?
(Apart from Homo of course).

Koko the gorilla once tore a sink from her living quarters, and when asked about it, blamed it on her pet kitten, signing, "Cat did it." If that's not a lie, then nothing is.

This question has been well studied by cognitive scientists who are interested in which aspects of complex human behavior are also exhibited by animals.
The only real problem here is that the word "lie" has a very complex bundle of meaning when we use it to speak about humans, and one can debate just how far various aspects of "lie" apply regarding other species. Cognitive scientists avoid this issue with more neutral terminology of "tactical deception."
At this point, it has been very clearly established that many species will engage in tactical deception. The most obvious and human-like manifestations (unsurprisingly) typically occur in more intelligent species with complex social interactions, such as primates and corvids.  Likewise, the subjects of deception also often occur in similar places as with humans, such as food, mating, and status/conflict.


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How is chicken egg a single cell
It is unexpected for ostrich or chicken egg to be single cell yet so large.
How could it happen, I thought egg is made up of several single cells.
If not, how is yolk a single cell http://www.alearned.com/egg/

Welcome to the site. Please take [tour] and visit the [help] to learn more about this Stack Exchange.  At this SE, we like questions that show that the person asking has done some research for possible answers for themselves.

Before the egg hatches, there is really only one intact cell inside the egg, that is the yolk. Before fertilization, the yolk is just an egg cell, but after fertilization, it is a fertilized egg. If the egg begins to hatch and the fertilized egg cells undergo cell division, there's not just one cell. A white spot on the surface of the yolk. The unfertilized egg is called an egg, and the fertilized egg is called a zygote, which further develops into an early blastocyst. The disc of the fertilized egg is about 3 mm in diameter, and the ovule of the unfertilized egg is smaller.

Welcome to the site, please visit the [help] to see what makes a good answer. In particular, this site (Biology SE) values answers that have some references to back them up.

But the yolk is too big for intracellular communication and exchange of mayerials @Jeffrey

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

"Hatching" refers to the process of the fully-developed chick (definitely a multicellular organism) exiting the egg casing. It only occurs at the very end of gestation.

Welcome to Biology.SE. Please take the [tour] and then consult the [help] pages for advice on [Answer] effectively on this site. In particular, answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Also note from [answer], Answer well-asked questions. Not all questions can or should be answered here. This is an inappropriate (under researched) question (see help) — please delete your post to avoid encouraging such questions.


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What are the oldest living plants in the world today? What can you know about them? Why can some plants live so long?
What are the oldest living plants in the world today? What can you know about them? Why can some plants live so long?

please ask only one question and try to be spesific,what type of research has you done so far.you have multiple questions here.

Arguably Pando, an aspen grove that is a single connected organism: https://en.wikipedia.org/wiki/Pando_(tree)  But for the many plants that spread by vegetative methods such as root suckers, the question of what exactly an individual plant is becomes rather difficult to answer.  For instance, I have many varieties of roses in my garden, all propagated (for instance, by rooting cuttings) from plants that were in some cases bred a century or two ago.  Are they still the same plant?

Just to be clear; you are asking for oldest individuals of plants, right? Not the oldest still living species (~living fossil)?

Great Basin bristlecone pines (Pinus longaeva) have been known to live to be thousands of years old.
The oldest known living individual is named Methuselah and is estimated to be more than 4,800 years old. It's been credited as the oldest living non-clonal organism on Earth.
There are multiple other trees over 1000s years old.


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Is there a way to use presence-absence data to inform a sampling design for a more specific survey?
I am currently in the process of designing a spatial survey to assess the abundance/density of woody debris across an ecosystem with multiple defined habitats (i.e. I am interested in not only the abundance across the entire system, but also any differences across habitat type). I have no prior data or similar studies to perform a power analysis to help determine how many sites I will need to address my questions, but I do have presence-absence data of woody debris within my study area. Is there a way to use this data to inform my design? I am likely going to be developing a small pilot study to collect enough data to run a power analysis, does presence-absence data help in any way?

What's your scientific question?

This might be better for CrossValidated. Power analyses always rest on some assumptions. You might be able to leverage presence/absence + some assumptions to get an estimate of variation in density, but you can also probably perform the power analysis with some sensible order-of-magnitude guesses about the degree of variation.


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Would green light look different if blue and red cones were deactivated
When looking at a graph plotting "blue", "green" and "red" cones reponses to different wavelengths, you can see that any wavelength trigerring a response from green cones is also able to trigger a significant response from blue and red cones.
Excluding colorblindness, that must mean the green we're used to is the result from not only green cones activation, but also red and blue cones activation.
My question is: given the current knowledge of cones, the optical nerve and image processing in the brain (or anything else relevent of course), if my blue and red cones suddendly stopped reacting to light, would a 520nm wavelength light look "purer and greener" than it would in a normal situation, or would the brain interpret this as a different "unknown" color? Or perhaps might it not be able to interpet it at all until it forms new connections in order to understand it?
(While this is most likely a hard question to answer, perhaps knowledge about how the brain processes images is advanced enough to form a "likely" hypothesis, which is why I asked.)

The genetic condition you are describing is called green cone monochromacy (GCM). This condition is exceedingly rare because it requires the dual inheritance of tritanopia (absence of blue retinal photoreceptors) and protanopia (absence of red retinal photoreceptors).1 Consequently, I can find very little information on the experience of people with GCM. In general, however, people with any type of monochromacy are considered completely colorblind. This is because color is perceived not by the excitation of specific cones but rather by the relative excitation of different cones and rods.  So, a person with only one functional cone type can perceive the intensity of light but not the color.
If you're interested in the science of how the eyes and brain work together to process color, I suggest reading up on opponent process theory.

References

Simunovic, M. Colour vision deficiency. Eye 24, 747–755 (2010).

I understand that, perhaps I phrased it wrong, what I meant is a more hypothetical (and possibly off-topic I am aware) where someone was trichromatic before switching to this situation, so that their brain would be wired for trichromatic vision and they would have memories of trichromatic vision to compare what they were now seeing to. While this is purely hypothetical (until very good prothetic retinas are invented I guess), I hoped current knowledge of the brain would have a crumb of hypothesis regarding the outcome. I will be checking that link, thanks.

(cont.) My line of reasoning was that "green" cones would send signals using the preexisting circuitry that was built up from living as a trichromat, but the total received signal would be unique in that the brain would be receiving nothing from "blue" and "red" cones, something that never happened in a normal situation since green cone activation implied red and blue also activated. Even if it's not the cones themselves that encode color, the circuitry behind, in the brain, would still be there (at least for some time).

@Uretki It was not that long ago when black-and-white monitors were in fact light-and-dark-green. ;)

Found a likely answer from the "See also" section of the link provided in acvill's answer.
Turns out it seems that you can somewhat approach this situation by exploiting cone cell fatigue to lessen blue and red cone cells's response to green light.
While this isn't exactly the situation described in the question (since I assume red and blue cone cells remain sensitive, just less), it seems to be pointing towards the "purer and greener" answer.
Link: https://en.wikipedia.org/wiki/Impossible_color#Chimerical_colors
Quote:

A chimerical color is an imaginary color that can be seen temporarily by looking steadily at a strong color until some of the cone cells become fatigued, temporarily changing their color sensitivities, and then looking at a markedly different color. The direct trichromatic description of vision cannot explain these colors, which can involve saturation signals outside the physical gamut imposed by the trichromatic model.
[...]
Likewise, staring at a bright magenta template may result in an impossibly highly saturated green afterimage.

So, I assume the result of deactivating red and blue cone cells and looking at a green light would be to see an exceptionally impossibly saturated green color.

one can trick the brain to see only green for a short time,spend some time in a room brightly lit by grow lights(red and blue light with all the green removed)when you leave the room everything will look green until the brain adjusts back to normal lighting.


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What is the highest concentration of sodium chloride for the oceans to be able to sustain life?
What is the maximum concentration of NaCl for life in the oceans to be possible?
Was it fortuitous that the concentration was originally no higher, in which case the evolution of life on Earth would not have occurred?

This is more of a biology question than a physics one. Try the Biology stack exchange.

Apart from answers given, here are some reference for you: https://royalsocietypublishing.org/doi/10.1098/rstb.2018.0011, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2329653/, https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-30123-0_57

There are organisms called halophiles which thrive in conditions of high salt concentration - and, indeed, require high salt concentrations in order to grow. According to Wikipedia:

Halophiles can be found in water bodies with salt concentration more than five times greater than that of the ocean ...

Since the earliest life on Earth originated in the oceans over 3.5 billion years ago, it is likely that it was adapted by evolution to suit the salinity of the oceans as they were then. If the salinity of the oceans had been significantly different then life would have evolved in a different direction.


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Can a species include only one subspecies?
Wikipedia says: A single subspecies cannot be recognized independently: a species is either recognized as having no subspecies at all or at least two, including any that are extinct. I do not understand this concept, please explain.

Heard today (TV) that red pandas are considered a single species .

it might be possible if a known specie goes extinct so only a subspecie remain,but then the subspecie will become the main specie and your whole question falls apart :)

Think about it like this:

How can a you subdivide 1 individual and still get a whole?

The answer is, you can't.
For there to be subspecies you need to have defining characteristics that can be used to separate individuals within the population into groups. This means that you need at least 2 to divide into.
Now there's a little tricky ground here - you could have an extinct subspecies as one of the subspecies (e.g. Homo sapiens neanderthalensis, if you follow the trend that Neanderthals are not a separate species) - meaning that the humans you see around you can't be subdivided into subspecies, but can still a subspecies that could be called Homo sapiens sapiens

In biological classification, the term subspecies refers to one of two or more populations of a species living in different subdivisions of the species' range and varying from one another by morphological characteristics. A single subspecies cannot be recognized independently: a species is either recognized as having no subspecies at all or at least two, including any that are extinct.

Thst is, subspicies are defined by opposition to each other: e.g., taller vs. shorter, bright vs. bleak, etc. Such a definition logically implies (at least) two types of specimen.


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What animal is this? Caution, GRAPHIC!
One of my friends stumbled upon this half part of an animal. It seems lizard-like...I don't think I've ever seen a lizard that large, though. We live in Greece. Can you figure it out? Close-up and a zoomed-out version with the pavement in it for scale included (length was ~10-15cm / 4-6 inches).

this is very likely some type of skink a type of lizard https://en.wikipedia.org/wiki/Skink

My guess is the ocellated skink (Chalcides ocellatus).

 Credit: Adel Ibrahim ; Source: The Reptile database
The species is names for its black/white ocellated, or eye-like, patched scales, similar to the ones seen in you specimen. C. ocellatus also would match your size (15-30 cm) and your location (generalist, including rocky).
It is found throughout the Mediterranean including in Greece.
See other similar specimens from Greece here and here


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Can someone identify this male Zygaenidae (subfamily Procridinae)?
Photo taken in 2018, Near Berlinchen, Germany.
The immediate vincinity is Calluna on sands. The area has a an interesting vegetation with heather and broom, species-rich grasslands on poor and sometimes raw soil, and extensive pine forest areas with a lot of lichen. Different Prunus species (including P. mahaleb and, sadly, P. serotina) occur. In a flight range agricultural areas (some with rather rare weeds, possibly organic agriculture), but also lakes, rainage ditches, and marshlands. A bit further paludal forests and remnants of (mostly drained) mooreland exist. Some areas within possible flight range have deciduous forests with Fagus, Quercus, Betula, Carpinus, Populus tremula, and some rarer species (planted, including intrduced species).


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How to reduce the quantity of (carcinogenic) mycotoxins in oatmeal?
Like all cereals, oat is commonly (nearly systematically) contaminated by several types of mycotoxin (produced by molds) known to cause cancer{1}. Oat is one of the most infected cereals{2}. Unless the package looks or smells bad (which is unlikely, and even dangerous to touch since some mycotoxin can penetrate through the skin), there is no way to know its level of toxicity.{3} Eating a large quantity of oatmeal (eg 250g/day) could thus be problematic, especially in a country that doesn't take this kind of food contamination seriously (even if the customer store the oats in a dry environment, it's too late: the molds have already grown (eg. while stored in a humid silo or warehouse, or during transportation).
There isn't much information about how to reduce mycotoxin in oat specifically but some studies done on other cereals suggest some procedures:

"Heating and cooking under pressure can destroy nearly 70% of aflatoxin in rice compared to under atmospheric pressure only 50% destroyed (37)".{4}

According to several studies, mycotoxins can be totally eliminated by cooking it at 160-180°C for 30 minutes {5}. But it doesn't make sens "Since [...] long-time cooking and overheating would destruct essential vitamins and amino acids in treated food".{4} (And it would not be easy to do: is it possible to reach such temperature in a pot ? Won't it burn? Plus this is quite an energy-intensive process and thus not ecologically responsible nor economically interesting).

Another study{6} mentions a more practical option: they reduced the quantity of mycotoxins (till 70-87%) by adding sodium bicarbonate. The study focuses on corn: they add 9 gr of sodium bicarbonate per liter. But the paper doesn't describe well the procedure: they wrote "the results obtained in this work correspond to an aqueous solution", which suggest they mixed some water, the corn (as flour?) and the sodium bicarbonate, but what quantity of water/corn, what temperature and for how long...?

And these pieces of information don't provide a practical way to reduce the mycotoxins in oats :
Oats aren't cooked like rice which needs to stay 10 (or more) minutes in boiling water. To cook oat, I simply pour boiling water on it and wait 15 min. It probably doesn't reduce much the aflatoxin (how many percent?). What about adding bicarbonate with the boiling water? (how many percent reduction?)
Is there a better way, or other steps that would decrease the amount of mycotoxins in oatmeal?
1:
https://www.tandfonline.com/doi/abs/10.3109/15569541003598553?journalCode=itxr20
2: https://www.sciencedirect.com/science/article/abs/pii/S2214799317300152
3: Aflatoxin is colorless and completely invisible. The loss of the nuts smell, which happens when the oats start to turn bad (just before they start to smell and then taste bad) is probably the only indication our senses can detect.
4: http://www.fao.org/3/x5036e/x5036e0q.htm
5 https://link.springer.com/article/10.1007%2FBF03032339
6: https://onlinelibrary.wiley.com/doi/abs/10.1002/jsfa.11001

Very difficult question. This review article discusses all of the above including oats (cereal). Can you buy whole hulled oats instead? Irish and UK oats seem to be lowest of European oats for mycotoxins. Just imho, trying to prevent cancer this way will be crazy-making. Carcinogens are absolutely everywhere.

Your refs 1 and 2 are behind paywalls and so generally unavailable. Can you remove them or at least extensively quote from them? Alternatively, @anongoodnurse provides a good review that's accessable.

@Armand do you know sci-hub?

@JinSnow Yes; Personally, I don't think that's an appropriate reference for questions here, but ymmv.

The methods adequately describe the NaHCO3 process - whole grains - how many or what weight is not described. "Solutions of sodium bicarbonate at 0.4, 1.2, and 3.0 g L−1 were added to the PDA culture medium. The inoculated corn grain was deposited in the center of the PDA, and it was incubated at 22 °C, measuring mycelial growth in millimeters, at 48, 72, 120, and 168 h." BTW this process sounds like nixtamalization - a process often used for corn products to increase availability of essential amino acids.

@bob1 What you quoted is the "Evaluation of mycelial growth inhibition of Aspergillus niger in corn with sodium bicarbonate" and not the "Evaluation of aflatoxin reduction". In other words, the goal (at our consumer level) is not to stop the growth of the mycotoxins (because it's too late, even if stored in a dry environment), but to destroy/reduce them.

Indeed it was - my apologies. The reduction section works with certified standard aflatoxin incubated (unknown time) with 9 g/l HCO3: "standard of aflatoxins (Trilogy TSL-108, USA) with a certified concentration of 2 μg mL−1 AFB1 and AFG1 and 0.5 μg mL−1 AFB2 and AFG2". So basically it is a vial with aflatoxins at the specified concs and the specified conc of HCO3 in water. There is no grain or flour/meal substrate in there.

This redearch is about rapid detection methods https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.olmix.com/sites/default/files/document-2-article-9-mycotoxin-analysis.pdf&ved=2ahUKEwj7vc_KkofzAhVJXRoKHSsWC04QFnoECCsQAQ&usg=AOvVaw0OQfUQr3jkhxTlCwL_w1WI

I’m voting to close this question for the reasons outlined in this meta post.

So far, the applications for the control of aflatoxins in food are experimental; and they require further evaluation by researchers. However, the use of basic products has been used and tested in Mexican tortillas through the nixtamalization process, which is part of the production of this food. I share a part of a review that I am writing that could help you:

"Since aflatoxins are susceptible to alkaline hydrolysis, the addition
of bicarbonate salts promotes their reduction. Nixtamalization can inhibit some
percentage of aflatoxins because it is a thermal alkaline process (Torres, et al. 2001)".

Torres, P.;  Guzmán-Ortiz, M.; Ramírez-Wong, B., Revising the Role of pH and Thermal Treatments in Aflatoxin Content Reduction During the Tortilla and Deep Frying Processes. J. Agric. Food Chem. 2001, 49 (6), 2825-2829. doi: 10.1021/jf0007030


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Are there any phenotypically visible examples of gene linkage in humans?
Are there any examples of two "visible" or "obvious" phenotypic traits in humans that are a priori unrelated, but which tend to be inherited together (i.e. their inheritance probabilities are correlated) due to genetic linkage from their proximity on a chromosome?
I know that peas' flower color and grain shape are genetically linked, but are there any similar examples in humans?

Sex-linkage would be the canonical example.
In other words, people with phenotypically male or female sex characteristics have non-random genetic predilections towards specific X-linked traits such as hemophilia, color-blindness, Duchenne dystrophy, etc.
However, other classic examples would include linkage between blood group antigens and peptic ulcers.
For a general review of how linkage has been used historically in human genetic research see here.

The blood groups/peptic ulcers paper linked is from 1954 and behind a paywall. Given that peptic ulcers' cause wasn't sorted out for another 40 years or so and isn't a gene, I don't think it really fits the question here.

Sex linkage certainly counts, but I think there's a big difference from genetic linkage of genes on non-sex chromosomes. If I understand correctly, chromosomal crossover is fairly common between homologous chromosomes, so genes are faraway loci on the same chromosome are inherited fairly independently because there is a high probability of a chromosomal crossover occurring between those loci, so gene linking is the exception rather than the rule on non-sex chromosomes. But chromosomal crossover is much less common between and X and Y chromosomes because they aren't homologous (except at the ..

pseudoautosomonal regions). So if I understand correctly, gene linkage is more the rule than the exception for genes on the sex chromosomes, so it isn't as surprising, but it's more the exception off of the sex chromosomes.

@tparker The ballpark genetic length of human chromosomes is around 100 centiMorgans so very roughly two genes on a given autosome will have a fifty-fifty chance of being linked -- not so exceptional.

@Armand I'll note that the asker's post mentioned as an example phenotypes from peas that were discovered to be linked in 1905 (taking the linked wiki example)- it's not as if the mechanistic basis of those linked phenotypes was sorted out! Asker doesn't seem to be interested in burden of causal evidence here. Their prompt is "inheritance probabilities are correlated". Also, I have located on openly available version of the peptic ulcers paper, editing answer to include.

@MaximilianPress The pea phenotypes were in fact due directly to different but linked genes. Blood groups and peptic ulcer assocations seem plausibly to be due to the same gene, in which case genetic linkage would not be involved, but rather pleiotropy.

@Armand- interesting, I was not aware of the direct functional relationship. I'll look for some other examples.


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Do bacteria select for "soap resistance"?
When people wash their hands with soap, this limits the spread of bacterial infections. That much, I am pretty convinced of. Duh.
What I don't get is how this doesn't lead to evolutionary pressure on the bacteria to become "soap resistant." I'm not talking about anti-bacterial soaps (I understand the FDA no longer recommends these), but just plain old soap and water.
The soap does something (I feel like I've heard a few mechanisms), but the net effect is that it makes the bacteria less likely to spread. How would this not lead to evolutionary pressure that drive bacteria to be less likely to be removed/killed/destroyed/whatever by soap?
Or is it not a problem because soap is just so "strong" that it's like evolutionary pressure for humans to survive underwater. Sure, if gradually introduced over 1MMM years, we might eventually get gills. But if you just keep drowning people, no one is gonna really evolve gills.

You make a reasonable analogy in the last couple of paragraphs - perhaps check out how soap works. There are 2 factors at play; chemical and physical.

Does this answer your question? Resistance to Antiseptics

I agree with @bob1. If you understand how soap works, you'll probably see why there's no selection pressure for soap-resistant bacteria. If after researching how soap works, you still have questions, please post what you found that confuses you.

Conceptually related: Do organisms use detergents to fight off viruses?

It would be an interesting experiment to supplement growth medium with small amounts of detergent and see how that affects evolution in a model bacteria over successive generations (something like Lenski's LTEE). Keep in mind, however, that bacterial killing is a secondary effect of soap in handwashing. The primary effect is to get the bacteria off your hands.

But wouldn't the bacteria then just evolve to not "get off your hands"? Like - whatever mechanism the soap works by, it's creates evolutionary pressure to resist that (be functionally stickier, in this case).

I must be misunderstanding something about the boundary conditions, because the argument I'm making seems to be mechanisms-of-soap agnostic...

@NateRush I think it would be enlightening for you to review the excellent answers to the question Why do some bad traits evolve, and good ones don't?

To avoid clogging up the comments, please continue discussion in this chat room.


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CCTV cameras in Microbiology (Pathology) Laboratories
Isn't it highly beneficial to have CCTV cameras installed in all Microbiology Labs in the COVID-19 times?
As the COVID vaccines are already developed, the research & development carried further in studying and analysing the COVID-19 variants by the Vaccinologists would be captured in real time on the Video monitors in as well as remotely from the Pathology labs.
This will assist the Vaccinology experts to analyse the COVID vaccine development (Including variants) in real time.
https://www.google.com/search?q=real+time+sequencing&source=lmns&bih=592&biw=360&prmd=invx&hl=en&sa=X&ved=2ahUKEwi46t2Us4LzAhWa0HMBHaKjD7cQ_AUoAHoECAAQAw
https://www.iaea.org/newscenter/news/how-is-the-covid-19-virus-detected-using-real-time-rt-pcr
https://www.illumina.com/systems/sequencing-platforms.html
https://i.stack.imgur.com/ToQo7.jpg
https://i.stack.imgur.com/cowUc.jpg
https://i.stack.imgur.com/65aPW.jpg
https://i.stack.imgur.com/380mk.jpg
https://i.stack.imgur.com/lvbeJ.jpg
https://youtu.be/NG44AEWHtRQ!
https://i.stack.imgur.com/SivW8.jpg
https://i.stack.imgur.com/8ehHn.jpg
https://youtu.be/8TaXtCOZV4o
https://sapac.illumina.com/products/by-type/informatics-products/basespace-sequence-hub.html
https://youtu.be/Ddavr_RASKA
https://www.fda.gov/news-events/press-announcements/fda-will-follow-science-covid-19-vaccines-young-children
https://i.stack.imgur.com/LewYd.jpg

No - cameras would not capture the detail of the experiments being performed, nor would many of the experiments make sense without some context for the individual labels, if the camera could see them.
All of the analysis of variants relies heavily on sequencing, which is run on a sequencer (such as these ones from Illumina). The data is then transferred directly to servers and processed there through bioinformatics pipelines. None of this could even conceivably be captured by camera.
Almost all viruses are far too small to be seen with a light microscope (for this one SARS-CoV-2 is about the same size as influenza). Bacteria are about on the limits of size that is useful for microscopy. The variants are all about the spike protein configuration and possibly some changes in morphology of the virion, all of which are way way too small to see with a microscope. Electron microscopy can be used to look at protein structure, but is too slow and imprecise to work out variant analysis - much better to do this by sequencing.

Thank you. Do you feel by modifying the sequencer machines (electronic circuit) by adding video camera can assist in this regard?

No, not at all. The data is already captured by a type of camera and is electronic, but it  wouldn't make any sense to the eye at all. These are massively parallel flowcells, capturing information in the order of millions of flashes of light per second, producing terabytes of information in a few hours. The data that comes out requires some fairly specialist software and knowledge to interpret - read the bioinformatics page on wikipedia for some small sense of the scale and challenges.

Thanks for the information provided. Customised Bioinformatics Software application/s can assist in this regard.

@PrashantAkerkar, most of the software used is already open source and such things are widely distributed, used, and discussed within the community. The datasets are generally open access too, so others can already access them and analyze to their satisfaction. I doubt that anything that you could add would improve the programs that are out there designed and programmed by CS and bioinformatics specialists.

Thanks. I feel the need of the hour is to manufacture Vaccines for the Delta variant of COVID19 as quickly as possible since three clinical pre trials will again consume time along with FDA approval. https://www.google.com/search?q=fda+approved+covid+vaccine&oq=FDA+appro&aqs=chrome.3.0i433i512j69i57j0i512j0i433i512j0i512.7604j0j7&client=ms-android-lava&sourceid=chrome-mobile&ie=UTF-8      https://www.google.com/search?q=fda+approved+covid+vaccine&oq=FDA+appro&aqs=chrome.3.0i433i512j69i57j0i512j0i433i512j0i512.7604j0j7&client=ms-android-lava&sourceid=chrome-mobile&ie=UTF-8

@PrashantAkerkar - not really, the time difference there is all taken up in recruiting people for the vaccine trials and then looking at the developing immunity. The sequencers run as fast as they can and the few hours they take are nothing compared to the weeks it takes to raise immunity. The Pfizer and Moderna vaccines are still highly effective against Delta with ~5% reduction cf wild-type.


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Are there any online resources for visualising on which band of a chromosome a particular gene is located?
I am studying some genes that are expressed in the brain. I use the online database UniProt to get information about the proteins encoded by the genes of interest. However, I would like to know on which chromosome and which band of the chromosome the genes are located.
I was wondering whether there are any online tools that I can use where I can type the name of a gene of interest and I can get a visualisation of which chromosome the gene is located as well as the band? Any insights are appreciated.

Well, given the protein, you can use http://www.ncbi.nlm.nih.gov/protein/ then just above the sequence it mentions the chromosome and band e.g 4q31. But no visualisation here. I did see a visualisation tool for human proteins 8 years ago but I forget where.

The UCSC genome browser is good for genome visualization. Searching for HBB, for example, gives the follow data by default:

You can also search by band and get a list of genes.


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Why does the time to reach equilibrium across a membrane decrease with concentration?
We're learning about flux and Fick's law and there's one point I'm having trouble understanding. Assuming we have a higher concentration of a species on one side of a membrane, I understand that increasing the concentration will increase the flux (net particle movement/(time*area)). We were told as well that increasing the concentration also decreases the time it takes to reach equilibrium. Why would that be?
Rephrased: If you have 10 particles on one side of the membrane and 0 on the other, it takes X amount of time to reach equilibrium (~ 5 particles on each side).
If you have 10 million particles, why would it take <X amount of time to reach equilibrium (~5M particles on each side).
Thanks

Considering Fick's first law, there must have been a misunderstanding between you and your teacher.

where

J is the diffusion flux, of which the dimension is amount of
substance per unit area per unit time. J measures the amount of
substance that will flow through a unit area during a unit time
interval.
D is the diffusion coefficient or diffusivity. Its dimension is area
per unit time.
φ (for ideal mixtures) is the concentration, of which the dimension
is amount of substance per unit volume.
x is position, the dimension of which is length.

As you can see, flux is proportional to concentration, meaning equilibrium time is not affected by concentration. Possibly, your teacher meant that either (1.) an absolute increase in concentration on both sides of the membrane (by the same offset) decreases the equilibrium time or (2.) that a proportional increase in concentration by down-scaling of the containers (x; length) would also shorten the equilibrium time.

+1, though this is relevant when you get closer to real world demonstrations: 1[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6648224/]. Where absolute concentrations can effect your lattice walking. I agree that this is more likely a misunderstanding.

I agree; it's definitely more complicated than that, including considerations like viscosity or temperature and Boltzmann distribution of corresponding velocities.


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How can you identify recessive mutations in a gene that has been disrupted by a chromosomal translocation?
I am reading a journal paper about a patient who has intellectual disability. The patient was found to have a balanced chromosomal translocation t(11;16)(q24.2;q24).
This chromosomal translocation disrupted two genes: CDH15 and KIRREL3. By using a genomic probe, the authors fine mapped the 16q24 translocation breakpoint to the second intron of CDH15. The chromosome 11 breakpoint junction sequence mapped to intron 1 of KIRREL3. Only one chromosomal copy of CDH15 and KIRREL3 were disrupted.
However, there is something about this paper that I don't fully understand. The authors state in the following:

We began by sequencing both copies of the CDH15 and KIRREL3 genes in
the patient with the translocation. No alterations were identified,
indicating that the t(11;16) translocation does not unmask a recessive
mutation in either gene.

In the above, it seems that the authors are trying to identify whether there are any recessive mutations in the CDH15 and KIRREL3 genes. I have read online that a recessive mutation is one in which both alleles must be mutant in order for the mutant phenotype of be observed.
However, since the chromosomal translocation disrupted one of the alleles for both CDH15 and KIRREL3, wouldn't you need both alleles of the CDH15/KIRREL3 genes to be intact in order to successfully identify a recessive mutation?
Any insights are appreciated.

You're reading too much into the authors statement.
The authors simply claim they have no evidence for any mutations in the working copies of the genes, and therefore not even preliminary evidence for a recessive mutation.
You're right that if they had found mutations in either gene, this wouldn't be sufficient evidence to conclude the translocation unmasks a hidden recessive mutation resulting in the given phenotype. But this is completely  moot in this case anyway.

They actually claim they have some evidence for a lack of mutations in the non-disrupted copies of the genes, which is stronger than no evidence for any mutations.

Yes agreed - I'd missed that subtlety (or really thought about it at all before)

Re:

I have read online that a recessive mutation is one in which both
alleles must be mutant in order for the mutant phenotype of be
observed.

Perhaps it's better to think of it as "all" rather than "both", as sometimes there are 3 or more alleles, and sometimes only one. When the authors write

does not unmask a recessive mutation in either gene

the unmasking refers to effective disruption of the translocation alleles, leaving only ("unmasking") one remaining non-disrupted allele in each of the two genes. If there were an obvious loss-of-function mutation in either of these alleles, that might be an explanation for the observed phenotype. They've checked to rule out this possibility.


text:
Does an N1-methyl-pseudouridine substitution in the first codon position (in mRNA) result in a different amino acid?
Because of the possibility of ‘wobble’ in the base-pair made between the third (5’) position of the anticodon and the third (3’) base of the the mRNA codon , single tRNAs with appropriate bases in this position are often employed by the cell to decode more than one codon specifying the same amino acid (synonymous codons). This is not possible and does not occur in the first or second positions of the codon.
N1-methyl-pseudouridine has been used to replace uracil in the preparation of mRNA for vaccines because it renders the mRNA less immunogenic. It has the same potential for base–pairing as uracil, so that even if its orientation in space is not absolutely identical, one would expect it to be able to form a base-pair with the wobble position of the appropriate anticodon.
But what is the situation with N1-methyl-pseudouridine at the first or second codon positions, where base-pairing is more stringent? Is there a potential for miscoding there, producing a proteins with incorrect amino acids?

Welcome to SE Biology. It is the practice here to allow editing of questions (and answers), although the poster can revert them, in order to improve them. I have done this to your question to make the chemistry and logic more precise. Please do not regard this in a negative fashion. On another quite different point I would ask you to think about how these modified mRNAs are made and whether they work or not. That may help you to answer your own question.

Have you looked at any space filled models for this? You can start to see how the wobble works, and then I think you can start to answer your question yourself as others have stated.

@AtlLED — How are you suggesting this be modelled exactly — onto what published structure using what software? And why spacefilling — one seldom sees spacefilling models of nucleic acid hybrids, except to give an overall impression of the shape of a molecule? Distances and angles are what is important, but to measure these one has to know whether and to what extent the bonding atoms in N1-methyl-pseudouridine are displaced from those in U. Not quite so simple.

Possible terminology confusion? "The first base of the anticodon binds the third base of the codon in the mRNA." "the same tRNA can base pair with different nucleotides in the third position (3′ base) of the codon, corresponding to the first position of the anticodon (5′ base)." https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/anticodon  (I'm no biologist)

Summary
The answer would seem to be NO, from the very fact that the vaccine works. My answer discusses why this should be so. It takes a somewhat different tack to well-documented, but different, answer from @endolith.
Answer
The term ‘wobble’ was originally introduced by Crick to describe and predict instances of non-Watson–Crick base-pairing between the  3′- base of a mRNA codon and the 5′-base of a tRNA anticodon. This was provoked by the finding of the base, inosine, at the 5′-anticodon position of some of the first sequenced tRNAs, and other examples (such as a 5′-anticodon G being used to decode both 3′- codon C or U) were found in situations where the pair of codons involved specified the same amino acid. (See also this SE answer)
The term ‘wobble’ was specifically applied the base pairing at this position as it did not occur at the other positions, where it would generally cause the incorporation of the wrong amino acid. Moreover, when the three-dimensional structure of tRNA was elucidated an explanation for this was found in the strong base-stacking at the 3′- and preceding anticodon position, but not at the 5′-anticodon position (see G34 below — explanation in answer cited above).

Nevertheless, the term ‘wobble’ is sometimes used to mean any sort of non-Watson-Crick base-pairing, which can be the cause of ambiguity in cases where the context does not clarify the situation. I shall try to be clear in this answer.

The question is concerned with the possibility of non-Watson–Crick base-pairing — and consequent mistranslation — between tRNA and m1Ψ (N1-Methylpseudouridine — above) at codon positions 1 or 2 in the artificial Covid spike protein mRNA used in the Pfizer and Moderna vaccines. I would suggest that this does not happen to an appreciable extent otherwise very little spike protein would be produced and the vaccine would be ineffective, which is certainly not the case. The developers of these vaccines were clearly aware of the possibility that m1Ψ in the mRNA might have a greater mispairing potential than the unmodified U it replaced, as they changed a number of codons in consequence. However these changes were specifically U→C at the 3′-codon position (red shading, below), as the tRNA that decodes cognate pairs of codons ending in U or C always has a 5′-anticodon G. Of course, it would have been very difficult to do anything if there were miscoding of m1Ψ at the first two codon positions, but one can assume that the developers either checked that this did not occur or guessed correctly that it would not occur there to an appreciable extent.

A possible objection to the above argument is that readthrough of termination codons (UAG, UAA, UGA) occurs to an increased extent in mRNA in which m1Ψ has replaced U at the 5′-codon position. (This may be one reason for the use of multiple termination codons in the artificial mRNA — see this answer to the SE question on that topic.) However the situation here is different from the miscoding of, say, tyrosine codon UAC. In that case miscoding would involve competition between the tRNA for tyr and those for his, asn and asp (see green shading, below). However termination involves competition for the codon between tyr-tRNA and the termination factors. The modification of the codon U may conceivable decrease its affinity for the termination factor, which depends on RNA–protein interactions, not base-pairing.

"although it was not mentioned in any answer to the SE question on that topic." It was mentioned in mine: https://biology.stackexchange.com/a/107186/3126

Apologies. Your quotation did include that, but the general tenure of the quote was so negative that I did not take it as a suggestion of an explanation of why the developers did it. I'll edit my answer. (also upvoted yours)

Detailed Dissection and Critical Evaluation of the Pfizer/BioNTech and Moderna mRNA Vaccines says that this can happen:

all U nucleotides were replaced by N1-methylpseudouridine (Ψ) [14,15]. However, Ψ wobbles more in base-pairing than U and can pair not only with A and G, but also, to a lesser extent, with C and U [16]. This is likely to increase misreading of a codon by a near-cognate tRNA. When nucleotide U in stop codons was replaced by Ψ, the rate of misreading of a stop codon by a near-cognate tRNAs increased [17]. Such readthrough events would not only decrease the number of immunogenic proteins, but also produce a longer protein of unknown fate with potentially deleterious effects.
…
There is another reason for recoding U-ending codons to C-ending codons. All U nucleotides in the two mRNA vaccines were replaced by N1-methylpseudouridines (Ψ) which can wobble with all [four] nucleotides and, therefore, should not be used in 2-fold codon families.

However, citation 16 is Kierzek 2014, which is about Ψ, not m1Ψ, and two others seem to contradict this:
The Critical Contribution of Pseudouridine to mRNA COVID-19 Vaccines says:

However, Ψ contains an extra hydrogen bond donor group (N1H) that contributes to a universal base character, i.e., it can not only pair A but also wobble base-pair with G, U, or C in the context of a duplex (Kierzek et al., 2014). On the other hand, N1-methyl-Ψ has a methyl group instead in the N1-position (Figure 1), thus eliminating the extra hydrogen bond donor. Consequently, N1-methyl-Ψ can only use its Watson-Crick face to base-pair with another nucleoside, thus preventing it from wobble-pairing with other nucleotides (G, U, and C).

It cites the same Kierzek source for wobble-pairing of Ψ, but doesn't cite anything for lack of wobble-pairing in m1Ψ.
N1-Methylpseudouridine substitution enhances the performance of synthetic mRNA switches in cells seems to say the same thing?

Interestingly, Ψ oligonucleotides showed two Tm  values, suggesting the existence of an additional unstable binding  pattern. This observation, together with the fact that Ψ has an extra N1 imino proton (26,27) for hydrogen bonding (Supplementary Figure S5), agrees with previous research, which concluded that Ψ can act as a  universal base to form wobble base-pairing with multiple bases (28) and may alter structural stability (29). Thus, together with the results above, we conclude that m1Ψ-containing  miRNA-sensing switches outperform other switches because m1Ψ allows  higher basal protein expression and enhanced miRNA sensitivity.

Since m1Ψ only has one Tm value, this implies that it doesn't act as a universal base?

This is a very interesting and well-researched answer, but unfortunately it only addresses the question of misreading in the 'wobble' (third-codon) position, whereas the question, despite its introductory reference to wobble, specifically asks about the first position. Much as your contribution deserves credit, at the moment it is not an answer to the question. Admittedly the logic of the question seems flawed — greater stringency should only affect alternative base pairing, not that to A — but perhaps you could finish your answer by pointing that out. Then it could be upvoted.

@David I'm no biologist, but if I understand correctly, my references are talking about about the possibility of wobble pairing of any base, irrelevant of position within the codon.

Having looked at the references, I felt it would be better to explain my reasons in a separate answer, even if the punch line is just "No, because it works."  I find the  arguments in the "critical evaluation" paper that they did almost everything wrong most unconvincing. Pfizer's product beats Xia's speculation in my book. And the question is base-pairing between mRNA and tRNA anticodon, so that the third paper on mRNA switches is irrelevant. It is change of mRNA conformation by intra-RNA bonds and not wobble by even the loosest definition. It just shows m1Ψ is different from U.


text:
Long strand of white eggs on balcony cat net - What insect do they belong to?
In the last few weeks we've noticed multiple strands of tiny white eggs appearing on our balcony cat net. It seems that they were always laid after rainfall (we had plenty in the last few days). Old eggs were washed away and new ones appeared soon after.
The way they're arranged, I have a feeling those could be moth eggs. Or is it something else? Should we get rid of it?
p.s.: We live in southern Germany.

Possibly snail eggs. Similar posts: what kind of hot pink eggs are these, what is this agglomeration of pink cells I found attached to a stone, can someone identify these eggs, and what made this is it an egg sac.


text:
Better understanding the life cycle of lasioderma serricorne (cigarette beetle, cigar beetle, tobacco beetle, drugstore beetle)
Lasioderma serricorne, commonly known as the cigarette beetle, cigar beetle, tobacco beetle, or drugstore beetle:

Live 2–4 weeks.
The female beetle lays as many as 100 eggs loosely on the substrate to be fed upon.
The larval period usually ranges from four to five months, but under very favorable conditions the development from egg to adult may occur in 6 to 8 weeks.
When the larvae are fully-grown, pupation occurs and they remain in this resting stage for 12 to 18 days.
The complete life cycle takes 26 days at 37 °C and 120 days at 20 °C.
In the Northeast (presumably USA, as the primary source is a USA university), there is usually only one generation per year.

Sources:
http://idl.entomology.cornell.edu/wp-content/uploads/Cigarette-and-Drugstore-Beetles.pdf
https://en.wikipedia.org/wiki/Lasioderma_serricorne
So it appears their life history cycle is:
EGG -> LARVA -> PUPATING -> ADULT
       2-5MO    12-18DAY    2-4WK

Given that the total cycle duration is much less a year, why do some regions only experience one generation per year?
Are the eggs just sitting for months on the substrate without hatching into larvae?

What happens when cold? Often eggs or pupae wait until warmer.

@PolypipeWrangler Thanks for your comment.  Would that mean in a climate-controlled environment they will prosper year-round?

With other indoor pests in climate controlled house; they do live and breed constantly year round.

@PolypipeWrangler Thank you for the update.


text:
Identify a copper fuzzy moth
Photographed in 2003 in Panama. Not sure of size.

Its a relative of dirphia horcana and dirphia brevifurca

Cerodirphia avenata, a moth of the Saturniidae family. An anonymous person identified it. The person did not give any evidence, and I know nothing about moths, but its seemingly-distinctive wing markings wing frontal edges, and antennae match this example image on wikipedia and those I can see on iNaturalist also made in Panama.

Thank you for posting the answer you found elsewhere. Please note that you are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that support this conclusion and supporting references or at least validated images. Without this post is indistinguishable from opinion and thus is not appropriate as an answer on this site. ——— You may also wish to take the [tour] and then consult the [help] pages for additional advice on [Ask] and [Answer] effectively on this site.

thanks, I've added a (quite likely naive) justification


text:
Can CNVs have a phenotypic effect unrelated to the direct modification of transcriptional units?
I'd like to know how (or if) copy number variations can have a phenotypic effect unrelated to the direct disruption/movement/duplication of sequences for coding regions, promoters, enhancers etc.
I ask this question with the premise that CNV duplications or deletions may change the organisation and shape of chromosomes in the nucleus, and that this may then affect the phenotype, perhaps indirectly affecting transcription or methylation.
However, I'm interested in any way that isn't just direct modification of sequences composing transcriptional units.

If I understand your question correctly, you want to know if gene copy number can have an indirect effect on transcription, i.e. an effect that does not arise from the dosage effects of the copied sequence or the direct disruption of proximal genes?
I think the answer is yes, insomuch that CNVs can change chromatin architecture.
In many eukaryotes, the genome is spatially organized into topologically associated domains (TADs). Though their necessity in all contexts is contested, there is research that suggests TADs delineate meaningful associations between distal regulatory elements like enhancers and promoters.1 Duplications can be pathogenic if they occur within a TAD or across a TAD boundary.2 Deletions at a single CNV locus have been implicated in causing genome-wide transcriptional changes at loci important for human brain development via ablation of TAD boundaries.3
Note that chromatin conformation capture experiments (i.e. Hi-C) are often confounded by CNVs due to the effect of copy number on library prevalence and, consequently, contact frequency calculations, making the inference of CNV effect on genome organization inherently problematic. However, new computational tools have been implemented to account for such biases.4,5

References

Beagan JA, Phillips-Cremins JE. On the existence and functionality of topologically associating domains. Nat Genet. 2020 Jan;52(1):8-16.
Franke M, Ibrahim DM, Andrey G, Schwarzer W, Heinrich V, Schöpflin R, Kraft K, Kempfer R, Jerković I, Chan WL, Spielmann M, Timmermann B, Wittler L, Kurth I, Cambiaso P, Zuffardi O, Houge G, Lambie L, Brancati F, Pombo A, Vingron M, Spitz F, Mundlos S. Formation of new chromatin domains determines pathogenicity of genomic duplications. Nature. 2016 Oct 13;538(7624):265-269.
Zhang X, Zhang Y, Zhu X, Purmann C, Haney MS, Ward T, Khechaduri A, Yao J, Weissman SM, Urban AE. Local and global chromatin interactions are altered by large genomic deletions associated with human brain development. Nat Commun. 2018 Dec 17;9(1):5356.
Servant N, Varoquaux N, Heard E, Barillot E, Vert JP. Effective normalization for copy number variation in Hi-C data. BMC Bioinformatics. 2018 Sep 6;19(1):313.
Wang X, Xu J, Zhang B, Hou Y, Song F, Lyu H, Yue F. Genome-wide detection of enhancer-hijacking events from chromatin interaction data in rearranged genomes. Nat Methods. 2021 Jun;18(6):661-668.


text:
Ancestral inference from demographic data
The question is inspired by this one, in the History community:
We consider a population, whereas the data we have the number of migrants arriving every year, as well as the initial and the current population size. We would like to determine what fraction of the population descends from the migrants that came in a particular year.
Naive approach
Let $n_t$ be the number of migrants arriving in year $t$ from the beginning of observation whereas $n_0$ is the number of individuals already present at year $t=0$, $T$ is the number of years. Let $s$ be the rate of increase of the population which we assume constant, so that the number of individuals descending from the immigrants from year $t$ is $$N_t=n_t s^{T-t}.$$ One can now estimate the parameter $s$ from the total size of the population at $t=T$:
$$
\sum_{t=0}^Tn_ts^{T-t}=N,
$$
and we obtain the proportions of interest as $$w_t=\frac{N_t}{N}$$.
Q1: is this a reasonable approach or is there a better way?
Haploid population
The approach above is correct for averages, if we assume haploid population. This is the case when we look only at Y-chromosome, i.e., only at the paternal descent, as suggested in the cited question. There is however demographic stochasticity (or genetic drift - depending on whether we prefer population ecology or population genetics language), which means that the fluctuations in $N_t$ may make our estimates obsolete. I could probably obtain estimates using birth-and-death process ($s=1+b-d$) or a colascent. I am wondering however, if there is a more canonical way of doing it. (this is Q2)
Diploid population
For diploid organism most currently living individuals will have many ancestors from different years. One can thus ask a somewhat different question: how many of the currently living individuals at least one ancestor that arrived in year $t$?
Q3: how could one perform such an estimate?

Since the above seems not to account for different individuals having different numbers of offspring, it doesn't seem well-posed to me. For example, it's certainly possible that limited numbers of individuals gave rise to very high proportions of following generations (I'm thinking of Genghis Khan for example).

@Armand This is what I ask in my Q2. This question can be reformulated as: for how many generations back the estimate is still reliable?

I would say it is never reliable :)

@Armand it is not 100% reliable for sure, but under some conditions the error could be small. E.g., if the population size is constant, we expect that few (and eventually) one genotype will dominate in the long run, but if the number of generations considered is small, the diversity is more or less preserved. If the population is growing we may have even more chances to discerne something.

Humans are well-known for not having uniform family sizes and not choosing mates randomly throughout the population -- that's why any approach that doesn't involve genealogy won't be reliable.

@Armand Genealogy would certainly give better results, but this is not what is given here. I imagine that carrying out a population-wide genetic study in the US is difficult for economic and social reasons.

As mentioned in the OP, one can perform an estimate using birth-and-death process. Let us consider an population from a particular year with the initial size $N_0$ - then the probability that the population has size $N$ obeys the following difference equation:
$$p^N_{t+1} = (1-b-d)p^N_t + b(N-1)p^{N-1}_t + d(N+1)p^{N+1}_t,$$
where $b$ and d are the birth and the death rates (per generation or per year - depending on how we choose the time scale).
Rather than solving for probability, we limit consideration to the mean and the variance:
$$ N_t=\sum_{N=0}^{+\infty}Np^N_t,\\
V_t=\sum_{N=0}^{+\infty}N^2p^N_t-N_t^2.$$
After some algebra we wrrive at:
$$N_t=N_0(1+b-d)^t,\\
V_t=N_0^2\left[(1+2b-2d)^t-(1+b-d)^{2t}\right]+
\frac{b+d}{b-d}N_0\left[(1+2b-2d)^t-(1+b-d)^t\right]
$$
The following analysis is simplified, if we assume slow population change, so that $|b-d|\ll 1$, so that we can switch to continuous time:
$$
N_t=N_0 e^{(b-d)t},\\
V_t= \frac{b+d}{b-d}N_0\left[e^{2(b-d)t}-e^{(b-d)t}\right]
$$
Constant population
Let us first consider the case of a constant total population size $b=d$. The equations above then reduce to
$$N_t=N_0,\\ V_t=N_0(b+d)t.$$
The relative error is then
$$
\frac{\sqrt{V_t}}{N_t}=\sqrt{\frac{(b+d)t}{N_0}}
$$
This error grows with time and eventually becomes large, which is the reflection of the fact that genetic/ecological drift will eventually lead to the extinction or fixation of the allele/population. However, as long as we look at times much shorter than $t\ll N_0/{b+d}$, the error is small and we can make a reliable estimate using the naive approach outlined in the beginning. Indeed, if we take birth/death rate as 1 per generation, and consider the time scales of up to 20 generations (Mayflower came to the US in 1620, 400 years ago) we have the relative error behaving as $\sqrt{40/N_0}$. Mayflower brought about a hundred of passangers, so that the error is relatively big, but for later and much larger imigration waves the error can bemuch smaller.
Growing population
If we assume growing population, $b>d$, and assuming in addition that we look at long time periods, $t\gg|b-d|^{-1}$, we can write the relative error as:
$$
\frac{\sqrt{V_t}}{N_t}=\sqrt{\frac{1}{N_0}\frac{b+d}{b-d}}
$$
This error is small, if $N_0\gg \frac{b+d}{b-d}$. With a birth rate of $3$ children per family, i.e., $b=1.5$ per person, this condition becomes $N_0\gg 5$, i.e., even small immigration waves shoudl be discernable, provided the community grows fast.


text:
Why do some viruses get deadlier over time?
I was wondering what reasons are that make some viruses become more lethal over time.
By "more lethal", I am not referring to acquiring more mutations which make the virus more infectious and result in more people dying.
I am referring to a drop in survival rate per infected person, because a virus changed in another way than becoming more infectious.

Welcome to the site. Please take a [tour] and visit the [help] to see what makes a good question. SE biology in particular values questions that make some attempt at indicating that the person asking has done some prior research attempting to answer the question themselves. So - what evidence do you have that some viruses become more lethal and that this occurs not because they are more infectious?

I think implicit to this question is that it is more beneficial for the virus if the host doesn't die. Could just boil down to statistics: More ways to go wrong than right so more likely to not coexist than coexist.

It depends on what is implied by over time in the question.
Virus may become more deadly (or otherwise harmful) simply due to a random mutation. However, virus does not specifically aims at harming the host - rather the negative consequences for the host's health are a byproduct of the virus hijacking and killing the host cells. This can be, e.g., due to the toxins generated during the viral replication, or due to the new virions bursting out of a cell and thus destroying it, or because of the overreaction of the host's immune system. E.g., HIV preys at the immune CD4+ cells, whose count eventually drops below the critical level, making the host susceptible to opportunistic diseases.
Thus, in a short run virus becomes more harmful/lethal, as the byproduct of being more successful in replicating and propagating itself. However, in the long run such success harms the virus, since, as an obligate parazite, it cannot exist without a host. Reduced number of hosts means reduced possibilities for virus to replicate. A virus that kills all of its hosts goes extinct. The viruses that continue exist do so either because they have reached an endemic equilibrium with their host or because they can survive in a host of different species, occasionally spilling into human population (like Ebola).

Sometimes, a virus may indeed benefit from specifically harming the host - a dead host may for example facilitate dispersal of virions.  A virus in the short run also may not become more harmful/lethal even if it becomes more successful in replicating. There are multiple levels of "trophism" involved depending on scale - subcellular, cellular, organ-level, whole organism, population, and kinetics may act against reaching an equilibrium state.  I think it's important to be specific about scale, time span, etc when asking such a question.

@Armand thanks, these are valuable points.


text:
Why is there no wavelength change in the hyperchromic shift in DNA?
From Wikipedia article on hyperchromicity (emphasis my own):

"When the bases become unstacked, the wavelength of maximum absorbance
does not change, but the amount absorbed increases by 37%."

However, theoretically speaking, any electron delocalization (in this case π-stacking) always lowers the overall energy of the system, hence the wavelength of maximum absorbance should be greater.
Why is this not the case in the hyperchromic effect?

Could you add the link to the wiki article in question?

Sure, here it is:
https://en.wikipedia.org/wiki/Hyperchromicity

We are dealing here with the quantities differing by (at least) two orders of magnitude:

energy corresponding to 260nm radiation is about 110 kcal/mol (here is a converter)
stacking energies of DNA double helix are of the order of 1 kcal/mol

The change in the absorption energy due to electron delocalization when unstacking is thus smaller than 1 kcal mol, and constitutes a negligible correction of less than 1% to the absorption energy.
Update
It is necessary to point out that:

The absorption at 260nm does not correspond to a specific electronic transition, but rather to the average of the transition frequencies of different bases (240-270nm) . Thus, the actual position of the peak of absorption is not necessarily at this wave length, but varies depending on the DNA base composition. Moreover, the peak is broader than the stacking energy.
The cited Wikipedia article (more precisely its English version) is the only source that I have seen so far, where it is claimed that the position of the absorption peak does not change. In fact, 260nm is not the position of the peak, but the standard wavelength where the absorption is measured and calibrated. In fact, the change in the absorption is so big, that a small shift of the absolute peak does not matter.

A quick Google search on stacking energy led me to this article (pubmed.ncbi.nlm.nih.gov/9199773), where it says, "the stacking energies in canonical B-DNA base-pair steps vary from -9.5 kcal/mol (GG) to -13.2 kcal/mol (GC)". And according to the converter, this would result in a quite noticeable shift to around 285-290 nm. Am I missing something?

@Rusty these values are very different from those that one finds in other sources.

@Rusty my initial answer was a bit simplistic. I have expanded it to include other aspects.

thank you so much, though I'm still uncertain as to the magnitude of the energies (still couldn’t find another reliable source), your updated answer is rather exhaustive!