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PCR for gene expression
Could somebody please explain the basic principle behind how qPCR can detect if a gene is expressed or not? I tried looking at literature on ScienceDirect and other websites but I could not find any information. I understand what qPCR is supposed to do - amplify a target DNA and provide numbers for the resulting DNA after cycles. I am familiar with the concept of gene expression.

For detecting expression (mRNA), you need RT-qPCR (quantitative reverse transcription PCR). You can read more about it here or here or here.

it is precisely the jargon you linked which I am unable to comprehend

Welcome to Biology.SE. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and [ask] a good question. In particular, please provide more detail about what isn't clear to you — are you unfamiliar with reverse transcription? Did you try reading the relevant wikipedia page? I also encourage you to put useful information in your bio rather than impersonating a dead man.

What is qPCR? What's the central concept?
qPCR (or more stringently, qRT-PCR, a term that is less ambiguous) usually refers experiments which use quantitative polymerase chain reactions to quantitate (measure) gene expression in real time ("RT"), and when the source material is RNA, it is reverse-transcribed first ("RT") because PCR does not work well with single-stranded nucleic acids such as RNA.
The idea behind it is simply two-fold:

we amplify DNA (using PCR), and
we measure the DNA in real time during each step/cycle of the PCR, until the reaction is exhausted or plateaus or is sufficient for making a determination about DNA amount.

Over many PCR cycles, say 40 or 50, the amount of DNA product reaches a plateau that is not directly correlated with the amount of target DNA initially. So we must survey the amount of DNA before we hit the plateau! That's why we do it in real time. Simple.
How is DNA actually measured?
We measure DNA at the end of each PCR cycle using reporters. Typically, a fluorescent dye that intercalates (binds) with DNA is used. To simplify somewhat, more fluorescence means more DNA strand. We can measure absolutely (comparing to known amounts, or DNA standards, which we calibrate to) or relatively (relative to another gene or segment of DNA which we are amplifying using known primers). When you do quantitation, you must make sure as best as possible that your sample and the standard have the same amplification efficiency, so that the assumption that each cycle will amplify equally across samples will be assured.
How does qPCR measure gene expression specifically? DNA is not gene expression.
We use the amount of DNA transcript (mRNA) as a proxy for the expression of the gene. We can treat expression as numerical quantities. For example, 5 mRNA strands that act as transcripts of the insulin INS gene are assumed to be a tenth of what 50 insulin mRNA transcripts are. In the second case, you have a 10-fold higher expression than in the case with only 5 transcripts.
However, qPCR does not work with RNA (single-stranded nucleic acids) since PCR depends on two-strandedness of DNA. So to quantitate a gene's expression (mRNA) we must first reverse transcribe all the mRNA into complementary DNA (cDNA) which we can then put into the qPCR machine!
So, the proxy for gene expression is mRNA amount, but now we are using a proxy for mRNA amount in the form of cDNA.
With this cDNA, we can now precisely quantify how much of it there is. Then we can make an indirect statement about how much mRNA for specific genes we found in our sample (e.g. biopsy, lysed cells, bodily fluids, harvested tissues, etc.). So we've achieved quantifying expression of our sample.
The devil in the details
Importantly, the whole process takes place within PCR conditions, so you are very dependent on your primers and thermal cycling conditions. If your extension temperature step is too short, long strands may not have enough time to complete duplication by the polymerase. If your primers are designed incorrectly, or are in conditions in which they cannot anneal efficiently, you will have incorrect amplification and the quantitation will not be possible. If you do not prepare the initial reaction with sufficient dNTPs (DNA building blocks), your reaction will be exhausted prematurely. If you forget to add a polymerase enzyme, there will be no amplification. For some reactions, you need to use specific polymerase enzymes which are more thermostable, more efficient, or are more stringent in that they make fewer errors in duplicating DNA strands. A lot of little things must be satisfied in order to run a good qRT-PCR with dependable read-out, so please refer to standardized practices and considerations. Here is an old but good one to familiarize yourself with.


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Possible fishbone identification
It's my first post to this forum so I really hope, my question is not misplaced here!
I found this item on the beach La Línea de la Concepción, Spain and it resembles pictures I found of certain spine bones of larger fish. Acutally, I have no idea about any of that and as far as I know, it could be some piece of pottery washed by the sea into this shape.
Interesting is the small "V"-shaped mark. The object is 5.5cm in diameter.
Thx for your helping me identifing this object!

Welcome to Biology.SE. Not an expert, but that is almost certainly not a fish vertebra (try an image search) —  looks like part of a ceramic to me.

agree with Tyresome, the texture is all wrong for a vertebra especially the broken portions, a piece of shell is more likely. bone has a very recognizable porous texture, massive or solid texture like that is either shell or man made.

In addition, the reddish coloration is the result of iron oxide - used in the glaze probably, or possibly iron from the clay. There is also a very clear "V" mark in images 1 and 4 - this has been stamped in. Definitely man-made.

It might be the base of a broken ceramic mug or vase; @bob1 has provided excellent evidence of it's origin. That is a maker's mark (I used to throw pottery before the pandemic and makers marks were required to identify which piece of pottery belonged to whom coming out of the community kiln.)

This is definitely man-made. It has none of the features of a natural (biological) product and several features of man-made.
First - it has impressions on a smooth surface. In nature, smooth surfaces such as the interface between bones tend to be completely smooth, with no impressions or shapes that might cause friction. This has two features that appear man-made - the "V" which appears stamped in and might help an expert identify where, and who (company) made this. On the obverse (image 2) of the V surface are two shapes that appear like blobs or holes (at the "10" and "1" positions; if the object were a clock). I suspect that these are from the manufacture and that this object is made using a ceramic method known as slip-casting, which is where liquid clay (slip) is injected into a mold and allowed to set before firing. This technique produces a form of stoneware which is cheap and highly reproducible, so it is used for most ceramics these days. If you have a mug or plate handy - have a look on the bottom, you'll likely find similar shapes to those on this object (on my mugs it tends to be the bottom of the handle often smoothed a bit). This is where the slip has been injected into the mold.
Second - The reddish coloration on the surface is highly likely to be iron oxide. This could come from two sources in man-made objects. One of these sources is a glaze. In ceramics glazes are often used to create smooth, impermeable surfaces and are frequently made with metal oxides, but this would create a more even surface coloration, so I suspect that it is iron oxide present in the clay from which this was cast. On this object, most of the glaze has worn off, but you can still see the residue inside the "V" mark, which is shiny. This is a clear glaze making it likely to be a lead-glaze. Lead glazes are very commonly used on ceramics for their clear and shiny effect.
Third - this has fracture patterns consistent with ceramics rather than bone. I'm struggling to find things to illustrate this, but ceramics and stones chip in remarkably similar ways, with chips coming off the edges, leaving sharply delineated edges and rounded spall. Bones tend to chip in a more jagged manner.
Fourth - the texture is wrong for bone. Bone texture tends to be porous when broken, but yours looks crystalline (not easy to see in the images though), which is not a characteristic of bone, but might be for something like a sea-shell from a gastropod or mollusc.
Conclusion: Man-made stoneware ceramic, not biological.

source: Stack Exchange

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

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What are layers in the Blue Brain Project?
I was watching Bedlewo: Topology meets neuroscience when the lecturer mentions that data is available here. I might find it an interesting challenge to do some exploratory data analysis, but I want to ensure I understand the jargon.
The download page has some of the data broken down by layers, but I am not sure what a "layer" is in this context. They have a glossary of terms, but layer is not explicitly defined here.
I found the SE post L1 - L5 layers of the brain that looks like it might answer my question, but I have also been burned by jargon for different things coinciding (kind of like a hash collision but for words). Since neuroscience is outside my background, I would rather not assume.
What are layers in the Blue Brain Project (specifically the Digital Reconstruction of Neocortical Microcircuitry)?

One interesting part of the brain is called the neocortex. In the human brain, the neocortex is the largest part of the cerebral cortex, which is the outer layer of the cerebrum, with the allocortex making up the rest.
The neocortex is formed of six layers, numbered I to VI, from the outermost layer I – near to the pia mater, to the innermost layer VI – near to the underlying white matter. Each cortical layer has a characteristic distribution of different neurons and their connections with other cortical and subcortical regions. There are direct connections between different cortical areas and indirect connections via the thalamus.
This wikipedia is a reasonable start point for a neuroscience beginner.

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


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What's the term for "Amino acid regulating the expression of components used to synthesize it"?
In the tryptophan operon wikipedia page, it says under the Attenuation title:

A similar attenuation mechanism regulates the synthesis of histidine, phenylalanine and threonine.

If my reading is correct, this means that these amino acids also regulate expression of componenets that synthesize them.

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.

What's the term for "Amino acid regulating the expression of components used to synthesize it"? , maybe the lack of a question mark '?' in the question body stimulated this bot to write this.

The method of inhibition of the operation an anabolic metabolic pathway by the final product synthesized is called:

End-product Inhibition or Feedback Inhibition

Of more biochemical interest is the mechanism, which is:

Allosteric regulation

In general terms, the end product of the pathway is a negative allosteric effector of an early (often the first unique) enzyme of the pathway.
However this is quite distinct from Attenuation. Attenuation regulates the transcription of the trp operon, i.e. the synthesis of the mRNA that encodes the enzymes of the pathway. That summarized above relates to catalytic activity of the already-synthesized enzymes. Attenuation is restricted to prokaryotes†, whereas allosteric regulation is a more general phenomenon.
Although semantically the term “end-product inhibition” could also be applied to attenuation or even repression of transcription, in practice it is not. I do not believe that there is a specific term for attenuation of the transcription of a polycistronic mRNA for synthesis of an amino acid by its tRNA.
End-product inhibition is covered in all biochemistry text books. The best web example I can give that covers all the above terms is from Alberts et al., Molecular Biology of the Cell, freely available on NCBI Bookshelf. This example involves the pathway for the synthesis of CTP, rather than that of an amino acid, the enzyme inhibited being aspartate transcarbamoylase. However the principle is the same.
You can pick up a secondhand copy of an old edition of Berg et al. Biochemistry cheaply on eBay, for example. Well worth it to ready an authoritative account of basic topics in biochemistry, such as this one.
† The reason that attenuation is restricted to prokaryotes is that it depends on the coupling of transcription and translation. In eukaryotes, however, transcription occurs in the nucleus whereas translation occurs in the cytoplasm.


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Comparison of different glassy matrices for protein immobilization at room temperature
I am completely new to protein biology experiments. I care about experiments where proteins are immobilized near a surface with the help of a glassy matrix or similar materials.
I am looking for a reference that will allow me to compare the performance of various matrices in immobilizing proteins at room temperature. In particular, I want to know which matrices are the best at limiting protein tumbling at room temperature.
In particular, I am interested in matrices that outperform Polylysine matrices at room temperature by a good margin, if that's possible.
I am aware that the melting point of the glassy matrices is probably a good proxy for their ability to immobilize proteins. So perhaps a reference describing the melting points of these matrices would be enough.
If this is more appropriate in the Chemistry forum, let me know.

Hmmm. I am sure that someone will have looked at it, probably in a commercial field, so there could well be difficulties finding this information with IP concerns etc for companies.


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Are there animal species who would sacrifice their lives to save their offspring?
In the comment section of YouTube animal videos, there are people who say that animal mothers love their offspring very much as if human mothers do. But are there actual animal species whose parents are willing to lose their lives to save their offspring's lives?
Thinking purely in the perspective of spreading its genes more, it seems to me that it will be better to save the parent's own life and produce more offspring in the future than losing his or her life to save current batch of offspring, so I cannot think animals have that much "love" for their offspring, but it could be wrong.
Also, exclude the species that reproduce and automatically die afterwards, like salmon.

Why exclude the species which are the clearest examples of the circumstances you describe? Especially because I'd wager that a majority of animal species follow that pattern.

Is it actually true that human parents are willing to sacrifice their lives to save their children? It's a saying that gets a lot of advertisement, but does data actually back it up?

animals are willing to kill to save their offspring and are at the risk of getting killed by doing so.i think that it is fairly close to sacrfice their life?

The pelican is often used in Christian symbolism because of the belief that a mother pelican will kill herself to feed her brood. However, I'm having trouble finding any zoological / scholarly sources that confirm or refute this phenomenon.

In support of the other side of the argument, pelicans have been observed cannibalising their own chicks.

"Thinking purely in the perspective of spreading its genes more, it seems to me that it will be better to save the parent's own life" My understanding is that this tends to be the case not that long ago when people had many more children than they do now and infant mortality was much higher. At that time, it was arguable that losing your spouse was more traumatic than losing your child. Also social insects routinely sacrifice themselves to save their progeny.

@trondhansen Yeah, tell me an example of a species that actually takes very real danger to its own life to save its children.

@DKNguyen The social insects example, I think, is not applicable here, because they are not parents but copies. That is, the individual who sacrifices itself have the same genes as the ones that it saves. I was talking more about parents whose children have only 50% of one parent.

Large herding animals do this all the time. Surround the weak and young

Plovers fake injury to draw predators away from their nest, drawing the attention/interest of the predator to themselves. Parents die trying to save their kids somewhere in the world all the time: parents drown holding the child above them, push their kids out of the way of oncoming traffic, mothers forgoing chemotherapy while pregnant and allowing the cancer to advance and become fatal, etc. Animals may not love their offspring in the same way, but they do love them (read Jane Goodall's work.) But I suspect you'll reject any answer just for the sake of argument.

@anongoodnurse Brings up a thought...you probably need to look at animals that live in communities and can rear the orphaned offspring. The parent sacrificing itself to save an offspring is pointless if all the offspring die. I am unsure if a single parent could do the job unless that was the normal arrangement for that animal, but in that case it is also less likely, though not impossible, that the non-caregiving parent would be around to sacrifice itself in the first place. If just you and your 5 year old live in an isolated cabin in the woods, it is quite pointless to sacrifice yourself.

Which also brings up the fact that dying in an attempt to save your offspring is not the same as willingly sacrificing yourself so your offspring lives on. In that respect, it may be impossible to know what an animal's intentions were because you do not know how they think since you are not that animal.

For the human side, if wikipedia is to be held reputable in that matter (1 and 2), filial infanticide has been observed in humans as a form of population control in situation of scarcity. It was quite common, it was transversal to all cultures and it had been there since before the invention of agriculture. Concerning sex-selective infanticide, I take the liberty to remark that a reasoning like "I can raise another two sons, but not a second daughter" is a rather sophisticated take on scarcity.


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Help identifying small snake in southern India
I found a baby snake near a hill in Karnataka, Southern part of India.
It's monsoon season here.
Approximate length - 15 cm


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Can anatomically modern human siblings have three decades of age gap?
In my story titled La Maison Sapiens, there is a HUGE nuclear family composed of the father, the mother, and their seventeen biological children.
To be exact, the male human being and the female human being, who are the starting members of this nuclear family, were respectively 18 years and 10 months, and 19 years old and 6 months when their first biological child was born. When their second child was born, the father was 22 years and 3 months, and the mother was 22 years old and 11 months. When their third child was born, the father was 26 years old and 5 months, and the mother was 27 years old and 1 month. When their first pair of twins were born, the father was 29 years and 4 months old, and the mother was 30 years and 0 month old. When their second pair of twins were born, the father was 34 years and 1 month old, and the mother was 34 years and 10 months old. When their first set of triplets were born, the father was 39 years and 6 months old, and the mother was 40 years and 2 months old. When their second set of triplets were born, the father was 44 years and 9 months old, and the mother was 45 years and 5 months old. Finally, their last biological children, who are quadruplets, were born when the father was 48 years and 11 months old, and the mother was 49 years and 7 months old.
So, the question is: is it realistic for anatomically modern human siblings to have three decades of age gap?
Note: here is a link about multiple pregnancy : https://www.healthline.com/health/pregnancy/chances-of-having-twins#assisted-reproduction.

Depends what you mean by 'realistic'. Possible - sure, the constraining factor would be the age of the parents, the Mother in particular. Mother's can have children well into their 70s, so the scenario from this story seems totally plausible. Whether it's common, that's another question...

Cross-posted from worldbuilding.

Worth noting, this is a biology site. You should use biological terminology here rather than psychosocial neologisms.

I’m voting to close this question because it: 1) lacks evidence of the expected prior research, 2) is unclear (examples: unneeded detail about the exact timing of fictional births, "anatomically modern siblings" doesn't seem to be meaningful), and 3) is crossposted on a more appropriate site. Please take the [tour] and consult the [help] starting with [ask] for details of what is expected on this site.

49 - 19 = 30
So the 1st Child would be 30 when the last children would be born, as long as the parents stay healthy and the mother delivers the child in a natural way (No Surgical Procedure to deliver the child) and the Mother has not had Menopause (Menopause usually happens around 50 Years of age) the sibling age gap would be very possible, but lets take a look at how many children the mother had, if I am correct they had about 16 Children, many people in countries that have a considerably low life expectancy have many children, lets take a look at the world record for most children born from one mother...a person named Valentina Vassilyev, gave birth to 69 Children! Thats a lot of children, so giving birth to 16 children with a 30 age gap should be very possible and realistic as well.

If you downvote my answer please feel free to say why in the comments. (Somebody Downvoted)

I'm not the downvote, but you could improve this answer by providing some references to some of the topics (menarche and menopause would be good) and you could also provide data on the oldest natural and potentially the youngest mothers (IIRC, 5 years old, not sure how verifiable this is).


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Fly identification (Michigan)
Recently we've seen lots of this small fly in our house in Michigan. They are smaller than regular houseflies and don't have the distinctive green/blue sheen that houseflies have. I assume they bite, because at least once I've killed one and it spewed red (which I assume was blood), although I haven't actually been bitten by one to my knowledge.
The fly is about 8mm in length. They tend to sit on walls or ceilings without flying a lot, and they're not difficult to kill, i.e., they don't immediately fly off when approached unlike a regular house fly.
Is it possibly a cluster fly?
Here are two images. The first image is a live fly, the second is dead which is why the wings aren't flat to the body.

Some insects have internal body fluid and organs that can appear reddish upon disruption of the exoskeleton (aka - squishing). I wouldn't be so quick to assume it's blood.

@MattDMo Fair enough but then wouldn’t all of them behave the same way when crushed? I’ve killed quite a few and only one had that result.


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Bioavailability -- what is the effect of absorption rate?
I learnt about Bioavailability and this is the definition given by many sources:

...the fraction (%) of an administered drug that reaches the systemic circulation.
(https://en.m.wikipedia.org/wiki/Bioavailability)

In some other places, it was defined as:

Bioavailability (F) is defined as the rate and extent to which the active constituent or active moiety of a drug is absorbed from a drug product and reaches the circulation."

This 2nd definition is supported by sources including:

Essentials of Medical Pharmacology by KD Tripathi; 8th Edition; Page 22 (photo attached)

https://www.sciencedirect.com/topics/medicine-and-dentistry/bioavailability

https://www.msdmanuals.com/professional/clinical-pharmacology/pharmacokinetics/drug-bioavailability

However, I find it very disturbing to accept that the rate of absorption affects Bioavailability. And this is my reasoning:
Let's say you have 2 drugs, A & B
20g of A is administered and a total of 10g is seen in systemic circulation where A is absorbed at a rate of 1g/hr (taking 10hrs to be fully absorbed at 10g)
20g of B is administered and a total of 10g is seen in systemic circulation and B is absorbed at a rate of 2g/hr (taking 5hrs to be fully absorbed at 10g)
I am assuming both drugs experience same degree of 1st pass Metab and that every other factor that affects Bioavailability is constant.
Isn't the bioavailability of both drugs same at 50% irrespective of the difference in rate of absorption?
Please help.
PS: This source, https://www.sciencedirect.com/topics/medicine-and-dentistry/drug-bioavailability#:~:text=Drug%20bioavailability%20is%20the%20fraction,which%20the%20drug%20is%20absorbed , says:

Bioavailability does not take into account the rate at which the drug is absorbed

I am even more confused!

I think you will frequently find that measures in biology are not defined in a consistent manner, largely because experimental constraints often require a different operational definition. People prefer to keep the same term for the underlying concept, but recognize that different operational definitions may give slightly different answers. I'd consider this in the realm of "all models are wrong, but some are useful".
In the case you describe here, I would argue this is a conflict between a theoretical and practical version of the same concept.
For drugs, the concept of bioavailability generally applies to different dosing strategies and contrasts intravenous injection (bioavailability = 100% because the entire injection is immediately introduced to systemic circulation) with other routes (e.g., oral, transdermal).
Operationally, though, people don't typically measure bioavailability by counting individual molecules in the systemic circulation versus not. Instead, they measure serum concentrations at multiple time points, calculate the area under the curve, and use a ratio of area under the curve to determine bioavailability.
Here's an example of how that might look from Wikipedia:

For the IV curve, you just have decay kinetics; for PO you have absorption and decay. To compare them, you integrate to get area under the curve which has units of concentration*time, and look at the ratio of PO to IV to report PO bioavailability.
Sort of the "null hypothesis" or basic assumption for kinetics in pharmacology is that everything is single exponential unless you find otherwise. That is, rates of absorption and clearance are directly proportional to concentration in different compartments, or in other words every molecule behaves independently like you expect for any process driven by diffusion or unsaturated enzyme kinetics. Under that assumption, this AUC ratio is equivalent to "fraction of an administered drug that reaches the systemic circulation" and it's also true that "Bioavailability does not take into account the rate at which the drug is absorbed": it doesn't matter "when" a molecule enters the systemic circulation, if you calculate AUC you will at some point have that molecule enter and then leave and it will spend exactly the same amount of average time in circulation as a molecule entering at any other time.
However, drugs aren't always going to perfectly obey exponential kinetics, and another meaning of bioavailability is just "area under the curve", whatever the contributions to the area under the curve might be. That might include a drug that enters circulation very fast saturating an enzyme that metabolizes it, leading to a slower clearance for a drug absorbed quickly versus slowly. If that's the case, your AUC ratio no longer precisely represents bioavailability in terms of "fraction of an administered drug that reaches the systemic circulation" but it retains a meaning of bioavailability in terms of "dose*time".
Your definition:

Bioavailability (F) is defined as the rate and extent to which the active constituent or active moiety of a drug is absorbed from a drug product and reaches the circulation."

is consistent with this practical measurement issue from AUCs.
In contrast, if you are using some sort of pharmacological model with explicit terms for absorption, decay (including higher-order decay terms), etc, you would want to use the theoretical definition for bioavailability.
I'll add that when you read:

Bioavailability does not take into account the rate at which the drug is absorbed

I would interpret this as trying to emphasize that bioavailability is not about peak concentration. In medical practice, this is very important to understand, whereas in a pharmacokinetic sense the other nuances may also become important.


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What's the terminology for the deformity between the halluces and index toes caused by sandals?
In Japan, especially in the past, people tended to wear wooden sandals or the like, which separated their halluces from their index toes.

As a result, there is often a gap between their halluces and index toes.

What's the terminology for this kind of deformity? I searched a potential terminology, Bunion or hallux valgus, but all pictures I got were the ones where there was no gap between the hallux and the index toe. Besides, it's said that 'proposed factors include wearing overly tight shoes, high-heeled shoes, family history, and rheumatoid arthritis', where geta is not mentioned at all.
I searched hallux varus, the pictures and the description I got is nearer to what I expected, yet when I search 'hallux varus' + 'japan' or 'japanese', the results I got were all about hallux valgus. To add yet another twist, in the abstract of  The etiology of hallux valgus in Japan, the author even says:

Until recent years, hallux valgus did not exist in Japan.

I'm confused. What's the correct terminology?

@JiminyCricket. This article says the gap is a healthy deformity, not a pathological one.

Yeah. I deleted my comment because I'm unsure of my ground in arguing that or any position. I have feet a bit like that anyhow, so you can put it down to personal bias. You might still have more luck on medical I suspect.

Fwiw, my toes are separated like that and I have never worn that style of shoe in my life. The article you link is not loading for me...

@BryanKrause It can load easily for me. Its name is 'A comparative study of foot morphology between Filipino and Japanese women, with reference to the significance of a deformity like hallux valgus as a normal variation'.

there is some evidence this is actually the normal condition or at least far more common, and people without it have a deformity caused by wearing closed shoes. It is very common in hominid and fossil human footprints.

This is sometimes called a "sandal gap." See here.

Gap between the 1st and 2nd toes (sandal gap).

The above NIH link lists 58 known conditions with this feature+.
...
Other sources emphasize "halux varus" as a common cause for a larger interphalangeal gap between the first two toes. (Though, note, such a gap is unlikely to appear as in the OP's photo, which is lacking characteristic "bent" toes commonly seen in such deformations of the big toe and surrounding anatomy).

Hallux varus is a deformity of the great toe that is characterized by adduction of the hallux and medial subluxation of the first MTP joint.  [Source]1

See linked source for photos. See here2 for more technical information.

Interesting, radiopaedia suggests that these two terms (sandal gap and hallux varus) are linked.

A sandal gap deformity, also known as hallux varus, is an imaging observation in antenatal ultrasound (typically second trimester) where there is an expanded first interspace, i.e. the gap between the great toe of the foot from the rest of the toes (likened to the gap caused by a sandal).

I think the intent to synonymize these terms is inappropriate based on the other more detailed and peer-reviewed sources I linked/cited. However, I also include this quote due to their usage of the phrase "expanded first interspace" to describe this gap -- However, I cannot find much reputable relevant usage of this phrase in a quick Google or Google Scholar search, so I don't think it's the broad-usage term the OP is looking for.
Other conditions to rule out
FYI: Plantar plate disruption (or injury) is related but not what you're looking for. It's a v-like gap due to injury vs a genetic anatomical characteristic that you're describing.

Also, according to an article in the The Journal of Rheumatology3, "A gap between toes can be an indication of rheumatoid nodulosis, a relatively benign variant of rheumatic disease."

However, this condition appears between any toe due to rheumatic disease during life, and images from the linked paper rule it out as the more general genetic morphological condition the OP is asking about.

Citations:
 1. Vanore, J.V., Christensen, J.C., Kravitz, S.R., Schuberth, J.M., Thomas, J.L., Weil, L.S., Zlotoff, H.J. and Couture, S.D., 2003. Diagnosis and treatment of first metatarsophalangeal joint disorders. Section 3: Hallux varus. The journal of foot and ankle surgery, 42(3), pp.137-142.
2. Boike, A.M. and Christein, G., 1994. Hallux varus. Hallux Valgus and Forefoot Surgery, pp.307-312.
3. Prati, C., Brion, B.B., Leclerc, G. and Wendling, D., 2014. Spacing of Toes Reveals Rheumatoid Nodulosis. The Journal of Rheumatology, 41(5), pp.973-974.

 + below is an unformatted quick list of the 58 conditions (listed alphabetically) copied in case the cited link dies. One could certainly explore the literature for each of these conditions to determine if some other common phrase/term is additionally used to describe this gap across these conditions.

Acromesomelic dysplasia 4; Acrootoocular syndrome; Al-Raqad syndrome; ALG12-congenital disorder of glycosylation; Arthrogryposis, distal, type 2B2; Arthrogryposis, distal, with impaired proprioception and touch; Atelosteogenesis type II; Atelosteogenesis type III; Autosomal dominant intellectual disability-craniofacial anomalies-cardiac defects syndrome; Cardiac malformation, cleft lip/palate, microcephaly, and digital anomalies; Chromosome 6q24-q25 deletion syndrome; Clark-Baraitser syndrome; Cleft palate-stapes fixation-oligodontia syndrome; CLOVES syndrome; Coffin-Siris syndrome 1; Coffin-Siris syndrome 5; Congenital disorder of glycosylation, type iit; Coxopodopatellar syndrome; Cranioectodermal dysplasia 3; Cutis laxa with severe pulmonary, gastrointestinal and urinary anomalies; Desbuquois dysplasia 1; Developmental delay with autism spectrum disorder and gait instability; Duane-radial ray syndrome; Ectodermal dysplasia with facial dysmorphism and acral, ocular, and brain anomalies; Endocrine-cerebro-osteodysplasia syndrome; Growth delay due to insulin-like growth factor I resistance; Hydrocephalus-costovertebral dysplasia-Sprengel anomaly syndrome; Intellectual developmental disorder with dysmorphic facies and behavioral abnormalities; Intellectual disability, autosomal dominant 1; Intellectual disability-facial dysmorphism syndrome due to SETD5 haploinsufficiency; Kohlschutter-Tonz syndrome-like; Larsen-like syndrome, B3GAT3 type; Lethal acantholytic epidermolysis bullosa; Lethal hemolytic anemia-genital anomalies syndrome; Linear skin defects with multiple congenital anomalies 2; Mandibuloacral dysplasia progeroid syndrome; Meier-Gorlin syndrome 6; Menke-Hennekam syndrome 1; Menke-Hennekam syndrome 2; Microcephalus cardiomyopathy syndrome; Micrognathia-recurrent infections-behavioral abnormalities-mild intellectual disability syndrome; Microphthalmia with limb anomalies; Myofibrillar myopathy 10; Neurodevelopmental disorder with dysmorphic facies and distal limb anomalies; Neurodevelopmental, jaw, eye, and digital syndrome; Nicolaides-Baraitser syndrome; Oculofaciocardiodental syndrome; Orofaciodigital syndrome 18; Orofaciodigital syndrome V; Oto-palato-digital syndrome, type I; Seckel syndrome 1; Short stature, facial dysmorphism, and skeletal anomalies with or without cardiac anomalies 1; Short stature-optic atrophy-Pelger-HuC+t anomaly syndrome; Short-rib thoracic dysplasia 16 with or without polydactyly; Specific granule deficiency 2; Toes, space between first and second; X-linked intellectual disability Cabezas type; Zechi-Ceide syndrome;

Note: I'm not an expert in this. I'm a biology professor who teaches human A&P and has the internet (e.g., Google Scholar) available to me. So take my answer as a summary of 10 minutes of compiling relevant knowledge/info. There may be a better/broader answer. (In fact, I feel like I've come across something in the past -- I'll take a look at some of my A&P textbooks when I return to my office).

So, how about your 'look' when you return to your office?

@Michael turned out none of them mentioned this explicitly. So, I'll leave my answer as is.


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Is retinoblastoma truly an autosomal dominant condition?
I am getting, in my opinion, very conflicting information from sources about the inheritance of retinoblastoma, a type of cancer. Hereditary retinoblastoma is associated with defects in the gene encoding the cell cycle-regulating, tumor suppressor protein RB1. Most sites claim that retinoblastoma is inherited in an autosomal dominant manner, which would suggest that the offspring only need one defective  allele to inherit the condition. At the same time, however, all online sources claim that only one working copy of a tumor suppressor gene is required to maintain its functionality and that both copies of a tumor suppressor gene must be defective for the onset of cancer. This understanding is known as the two-hit hypothesis. But to me, this idea clearly conflicts the claim that retinoblastoma is an autosomal dominant condition and suggests the opposite: that, in order to develop retinoblastoma, there can be no working copies of the RB1 (tumor-suppressing) gene (hence making retinoblastoma an autosomal recessive disorder).
I don't know if there are any flaws in my interpretation and if somehow both explanations are correct with the issue being me not understanding it clearly. How can a condition be autosomal dominant (i.e. requiring only one affected allele) while also only requiring one working allele to prevent it? It seems illogical.

Welcome to Biology.SE. Please add references and/or links for your sources. In addition, it would be helpful if you included a quote from at least one of the sources claiming autosomal dominance for retinoblastoma — there may be some context you are missing. Also note that it is possible for a gene to have both dominant and recessive alleles or even for an allele to be both depending on the phenotype under consideration ...

"Dominant" and "recessive" have a philosophical quality, and this makes them more confusing than an introductory course will suggest.
You could argue that Rb "really" has incomplete dominance in that Rb(+/+) embryos survive, Rb(-/-) embryos mouse embryos die at E13.5-E15.5, whereas Rb(+/-) embryos often die from tumors after birth.  But from a practical point of view, if you have a patient with retinoblastoma or achondroplasia, you'll be drawing a pedigree in which anyone inheriting one copy of the gene has the same issue.
Additionally, we have the issue of cell-autonomous phenotypes.  In the case of retinoblastoma, any given cell has a very low risk of losing the other copy, and you can think that at the level of the cell it is almost like it is "recessive".  The risk of forming a tumor is higher, but you won't see that in any random cell under your microscope.  So the phenotype in this case isn't cell-autonomous.  (I haven't researched whether there is any other cue you can observe that would allow you to score single cells as Rb(+/-) on sight, but I know they don't get tumors!)
Bottom line: when describing an allele as "dominant" or "recessive" at the level of the organism, think about it from a genetic counseling point of view.  Do both parents transmit the allele (or an allele that subsequently underwent mutation) to affected offspring, or just one?

Hi, I think you were hinting at this in your answer though I've found a rather lucid explanation: "If a person has inherited a[n autosomal dominant] cancer susceptibility gene, it does not mean they will automatically develop cancer. It simply means that the person has inherited a mutation in a gene that gives them a higher chance to develop cancer than someone without the mutation" from https://www.urmc.rochester.edu/encyclopedia/content.aspx?contenttypeid=85&contentid=p07104. Thanks a lot for the reply!

@ZuhairQureshi Retinoblastoma is, unfortunately, a poor example for this.  The penetrance of the tumor phenotype is over 90%, and 40% of affected children develop tumors in both eyes independently.  There are lower-penetrance variants of the condition, but whenever it takes only one allele to increase the chance of a tumor, it is still dominant.

Two-hit theory/Knudson Hypothesis is for sporadic development of retinoblastoma, once it develops it is transmitted to the offspring in an "autosomal dominant" fashion.

https://eyewiki.aao.org/Retinoblastoma#cite_ref-Shields_text_3-1 read this for more info

So the sporadic form of retinoblastoma requires both copies of the alleles to be defective, but then when transmitted to the offspring in a hereditary manner, requires only one defective allele? If not, then how are you defining " 'autosomal dominant' fashion"? I read the link you posted and it feels quite similar to what I was reading yesterday: saying the disease requires both alleles being defective to develop while still calling the disease autosomal dominant. Thanks for the help.


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How do mosquitoes know if they are going 'up'?
I have read articles that say mosquitoes detect humans through carbon dioxide exhalation and body odour. When we wave our hand around a mosquito, it usually flies away from ground (even if it initially moves towards it after immediate stimulus). How do indoor mosquitoes 'know' that they are moving 'up', that is, against gravity?
My hypotheses is that instead of detecting whether their direction of motion is against gravity, they somehow measure their distance from the ground but I doubt this because I chased a mosquito up the stairs and its distance from the steps remained almost constant. When I ran down the stairs, the mosquito still tried to swerve around me and move upwards.
If the above hypotheses is wrong, can you link to some experimental evidence as well? (Not necessarily experiments on mosquitoes)
What I could find

Honey bees
(Apis mellifica) were unable to fly normally and tumbled in weightlessness.
House flies (Muscus domestica ) mostly limited themselves to walking on the
walls.  When they did fly, they apparently could control motion in all three
axes, although flight only lasted for a few seconds.  Moths (Anticarsis
gammatalis) that developed in space, learned not to fly and preferred to float
without wing beat.  Whereas adults that were developed on Earth, then sent
into space, had problems controlling pitch.

This answer links to sources which directly consider the idea of the influence of Earth's magnetic field (not gravity) but looking at the comments, I am having second thoughts.

Invertebrate solutions for sensing gravity

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.

Insects also use the skylight and horizon to maintain attitude. Did those experiments provide for that? Of course, it doesn't explain how insects fly indoors. They obviously integrate many methods.

Coordination between Cerci (on last segmet of body) to detect gravity; compound eye (can se 10-15 feet) ;vector memory of their home & surrounding and body organs (as mentioned in above comment of user:domen) to detect inertia (inertia inturn detects direction and acceleration)

We're looking for long answers that provide explanation, context, and include references to reliable sources. Don't just give a short answer; explain why your answer is right with appropriate citations. This is a good example of how to format references.


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Role of the CD3 proteins and ζ chain
Could someone please explain which of the following is correct and why?

The role of the CD3 proteins and ζ chain on the surface of the cell is to:
a) transduce signals to the interior of the T cell
b) bind to antigen associated with MHC molecules
c) bind to MHC molecules
d) bind to CD4 or CD8 molecules
e) facilitate antigen processing of antigens that bind to the surface of T cells

From what I have read I believe a) to be the correct answer but I am unsure if I have understood it correctly. This is based on this paragraph in the book "The Immune System 4th Edt":

"By inducing this organization of molecules in the T-cell membrane, the interactions
of MHC ligands with T-cell receptors activate cytoplasmic protein
tyrosine kinases, which phosphorylate particular tyrosine residues in the cytoplasmic
tails of the CD3 cell-surface proteins and the associated ζ chain
(CD247), a purely cytoplasmic protein (see Figure 5.6, p. 118). The tyrosine residues
that become phosphorylated are part of short amino-acid sequence
motifs called immunoreceptor tyrosine-based activation motifs (ITAMs).
Enzymes and other signaling molecules bind to the phosphorylated tyrosine
residues and thus also become activated. In this way, the extracellular binding
of antigen to the T-cell receptor initiates pathways of intracellular signaling
that lead to alterations in gene expression and end with T-cell differentiation."

The quote from the textbook is incorrect in that $\zeta$ has both transmembrane and extracellular domains, so it is not "purely cytoplasmic". The ECD is small, but not non-existent.

A is most likely the answer they're looking for. However, CD3$\epsilon$ and either CD3$\delta$ or CD3$\gamma$ associate with CD4 or CD8 (depending on cell type) in the TCR complex, bringing in kinases like Lck to phosphorylate the ITAMs on the CD3 chains' intracellular domains, leading to further downstream signaling. So, CD3 does associate/"bind" CD4/CD8, making D correct as well, at least in my opinion.


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Correlation between polygenic scores and reproductive success
I was looking through this article in the journal Behavior Genetics. The researchers has investigated 400 000 people in the UK Biobank and calculated polygenic scores for 33 traits. Then they investigated how much offspring the 400 000 people had generated and coupled the traits to fecundity (number of children).
They found that people with a genetic composition that suggested that they had a high risk of (for instance) ADHD, obesity, and becoming smokers in general had better reproductive success.
I am having some problem understanding how big the effect is. If you look at the main results in figure 2, you get a list of polygenic traits with some measure of association, but how large a difference in reproductive success does the measure indicate?
If the number they get for "ADHD" is slightly above 0.03 does this mean that people with a very high genetic probability of having ADHD statistically have 3% more children than those with virtually zero risk of getting ADHD?
Question:
What is the interpretation of figure 2 in this paper? How many more children are people prone to various polygenic traits such as ADHD, high BMI etc. statistically supposed have according to the research?
Is says under the figure: "Each point represents a single bivariate regression of RLRS on a polygenic score. P value threshold is 0.05, Bonferroni-corrected for multiple comparisons."

RLRS is defined as respondent i’s number of children, divided by the mean number of children of people born in the same year

They fit a regression:

RLRSi=α+β * PGSi+εi

In this equation, RLRSi is the normalized number of children by subject i. α, the intercept, is probably something around 1 but not necessarily exactly 1, but would account for bias in the sample in the study vs. the reference population they used to normalize number of children.
"β" is the key variable they are estimating with the equation. Note that β is multiplied by PGSi, so β is not in units of RLRS but in units of "RLRS per PGS". If PGS was, say, height in cm, you would interpret β as "change in RLRS per cm of height".
However, in Figure 2 they only state they are plotting "effect size". They do not, however, report what effect size they actually use in the paper. This is bad. Effect size is not one thing, but rather a family of approaches meant to quantify the relative size of an effect, usually relative to variability. However, unstandardized regression coefficients (i.e., "β") are also used as effect sizes.
Peaking at the code for the paper, I think this is probably what they are reporting: raw β coefficients that they then label "effect size", but I didn't go through the trouble to actually download and run the code and verify I'm reading their output correctly. It's quite a jumble.
However, they do mention:

The “selection effect”, β, reflects the strength of natural selection within the sample. In fact, since polygenic scores are normalized, β is the expected polygenic score among children of the sample (Beauchamp 2016).Footnote1

and Footnote1 is:

The selection effect  β  equals Cov(RLRS, PGS)/Var(PGS). Since PGS are normalized to variance 1 and mean 0, this reduces to  Cov(RLRS,PGS)=E(RLRS×PGS)−E(RLRS)E(PGS)=E(RLRS×PGS) . This is the polygenic score weighted by relative lifetime reproductive success, which is the average polygenic score in the next generation (Robertson 1966).

Those conclusions seem consistent with the idea that these are indeed the unstandardized regression coefficients. It also seems like these are better numbers to use to interpret the results of the paper, rather than converting to number of children.
So, in summary, it is not trivial to convert these to "number of expected children", but if you knew the PGS for a given individual, you would multiply that by these numbers and add to α to get the RLRS. If α is exactly 1 and the PGS for an individual is 1, then yes, β=0.03 would mean their RLRS is 1.03 which would be 3% more children than the reference, not considering any of the other possible weighting or confounding factors.


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Can you identify this seedpod (Malvaceae)?
I collected this seedpod from a plant I was pretty sure belongs to the mallow family (Malvaceae). Location = Central Europe. Unfortunately I lost my picture of the whole plant. Can you help me to identify the genus/species?

Welcome to Biology.SE. Please [edit] additional detail into your question based on the detailed tag info page. In particular, it could be helpful to have: 1) a size estimate of this fruit; 2) a description of the whole plant — ideally including the arrangement and positioning of the fruits/flowers, but even herb vs. bush would help; 3) more geographical specificity; and 4) some idea of the environment the flower was in (e.g.s: marsh, grassland, forest) — including other plants you could recognize, dryness, and elevation.

Lavatera trimestris (flower became-fruit & dried & exposed and seeds are dispersed)

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 led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion.


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What animal is this from the kitchen
The following picture has been taken in August  inside a box
I’m the kitchen in a city at the center of France. What animal is this? The real size is about the size of a grain of rice

Welcome to Biology.SE. This is a common question, but hard to find the answer if you don't about image searches e.g. Google Lens — please have a look at the links posted in the comment by @theforestecologist here.

Thank you! I just tried with Google lens that suggests this is a larva of Varied carpet beetle.

it is the larva of many possible skin beetles (carpet beetles) including, possibly, the varied carpet beetle.


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How do I help an injured plant avoid infection?
A hail storm came through my town while I was at work and my innocent cactus was outside! I'm pretty sure this exists, but is there something I can put on these open wounds to stop them from rotting/getting infected?

I would like to point out that I did try to google this, and I was unable to find an answer, which is why I'm here.

I think this would be a better fit for [Gardening.SE]. If you agree that is a better site for your question, please delete your post from here before reposting there because cross-posting is impolite. Alternatively, you can request migration of this question by flagging your post for moderator intervention and explaining what you want and why.

Petroleum jelly thin coat with clean fingers would work in my opinion.


text:
What does ‘per DNA fragment’ mean?
In "[Genomics: A Very Short Introduction]" by John Archibald, the author discusses the DNA sequencing:

In living cells, DNA rarely exists in isolation; it is typically bound tightly to proteins (see Figure 2), proteins that serve to compact it and to regulate the process of gene expression. Consequently, the act of purifying (or ‘extracting’) DNA from the multitude of proteins, lipids, and other macromolecules inside the cell requires the use of harsh chemicals and subjects it to physical damage. While it is possible to estimate the size of intact chromosomes in the lab, modern DNA sequencing instruments typically collect at most 1,000 base pairs of nucleotide sequence per DNA fragment.

What does this sentence mean?

They are referring to sequencing strategies where you chop a longer stretch of DNA into fragments, sequence each of these, and stitch the sequences back together.
The sentence is explaining that the lengths of DNA actually sequenced from these fragments are relatively short, up to 1000 base pairs per fragment.

Are you sure? If this the case why don’t they just say so without reference to the sequencing machines. Without knowing any more about it, I would interpret the sentence to mean that regardless of the fragment length, the machines become inaccurate after 1000 nt.

I agree with David. Depending on the method of fragmentation (restriction enzyme, sonication/shearing, etc.) you can sometimes end up with fragments that are a lot longer (or a lot shorter) than 1000bp. I think the sentence is talking about the maximum usable length of a read, not the fragment size itself.

@MattDMo Updated to clarify that this is the sequenced length from a fragment, not the size of the fragment itself.


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CDRs and antigen-binding sites
Are complementarity determining regions (CDRs) not the same thing as antigen-binding sites?
If not, what is the difference?
An old exam question states:

"Clarify how CDRs are related to the antigen binding sites"

To answer this I would simply say that CDRs provide a binding surface that is complementary to that of the antigen. Is that what is meant by the question or am I missing something?
All help is appreciated!

Each antigen binding site (also known as paratope) is made up of six complementarity-determining regions (CDRs) - three from each of the light and heavy chains.


text:
Common House Spider got shrunked and appeared lifeless when touched by water
I was trying to save a house spider which was on my water tub, it was desperately trying to move out of the tub but due to the smooth surface couldnt manage, the tub was wet but not filled with water so I tried to assist it with a net, but it end up slipping into tiny puddle of water (like a drop or two) and it got shrunked (the water probably made its legs closed due to surface tension of the droplet)
I then managed to gently soak the water with paper towels but the spider appears lifeless.
Is it dead? The whole process of getting soaked in water and being dryed up with paper towels was less then a minute.
Now I saw some reference where it says that it takes hours for spider to drown. So is it likely that the lifeless spider on my paper towel is most probably still alive?

Update (1 hours passed) I notice some twitching of one of its legs, very subtle though. Not sure if it is still alive or just muscular spasm.
Update (2 hours passed) 3 of its legs seems to be oriented in a way that they are touching the base of paper towel. Maybe the twitching action was to fix its legs? The spider still appear lifeless though :(
Update (2 days later) no movement as the spider appears lifeless. Most likely died but I want to know why? how can a drop of water kill a spider, when ants and other insects survive. Is it the crushing force of water droplet tension that cramped its legs? I could see very subtle adjustments of its legs after I dried it. The final form it took is in the picture is below. Looks like it managed to re-orient its legs but in the process didnt survive.

Was the "wetness" in the tub hot, or in any way soapy?

your link shows a giant house spider - was it one of those, or a common house spider (a cobweb weaver)? If it was juvenile, like a recently hatchling or maybe past one molt phase, it can drown in a drop of water. Alternately, if the spider was old and near the end of its life, the trauma of getting pushed around and into water. It's hard to fully grasp in what way "it got shrunked". If it remains still, you can probably get a very clear picture to share

@JiminyCricket. the tub was cold, I am not sure about the soapy

@JimN the spider was common house spider about the size of a pea. But I dried it up quickly with paper towel. It seems lifeless in day 2 so I am certain its dead. Its quite delicate creature and I felt quite sad when it shrunked because of mere drop of water. Its still on my paper towel and I shall share picture once i am back.

@JimN eventhought it somehow managed to get all its legs on the paper towel to orient itself upright, it looks lifeless to me now :(

@JimN I have shared the picture.

@user0193 thanks for the update and photo. A spider that size should not drown that quickly upon contact with water. Where are you geographically located? This is not any 'house spider' I'm familiar with (not parasteatoda sp, not Eratigena sp like you linked). It is coloured like dysdera crocata, but I would need a look at its face/jaws to be sure. Not that its identification will lead to any answer on how it died, but for completeness' sake, a correct ID would improve the question quality.

@JimN, Ok I tried to open up its legs using cotton buds and since I am no expert it may appear botch job. I am currently in Dubai, does that narrow it down? I tried searching if the spider is in dormant state / hibernation because it did managed to fix the orientation of its legs rather slowly (over few hours) but under observation for 2days didnt come back to life.

Perhaps the reason it could not climb out of the tub was because it got soap residue on itself, and then when it fell into the drop of water that residue was able to cover the spider's body.

It seems like [Brown Recluse Spider[https://en.m.wikipedia.org/wiki/Brown_recluse_spider]], also that twitching was from changing cephalothorax pressure which they do to to extend their legs (she was alive at that moment) unlike other insects spiders have muscle only to flex their legs not to extend so in order to extend their legs they use their body pressure/ hydrostatic pressure for hydraulic legs they do this by changing heart rate. Also when they die they curl up for the same reason(heart stops hence no hydrostatic pressure to extend the legs)

@daemon looking at your link, it does appear that it was indeed Brown Recluse, so looks like it could be combination of factors that could have killed her, soapy water, drying action, lack of energy, potential damage during picking up with paper towels (even-though I was very careful and held paper towels from the further ends so as not to have any hand pressure applied). Also with your Iink realized that they are one of the species whose venom do require medical attention.

@DKNguyen so a soapy water can kill a spider if it is covered with it?

@user0193 Soapy water is used by exterminators on wasps. It coats them in a suffocating film.

This is not a brown recluse. The carapace is too shiny (like a Cicurina) and unmarked (unlike the brown recluse, which would have the notorious fiddle mark). Also, there are no brown recluses in that area. This looks like a Sahastata  https://inaturalist.org/observations/124127 (which does exist in that area).


text:
Given a vaccine, can you deduce that a disease exists?
For example, if a scientist from 2018 found one of today's Covid vaccines, can they tell that it is a vaccine to a hitherto unknown disease, and therefore infer that Covid exists?
I'm guessing that the answer depends on the type of vaccine, in which case I'm interested in all of them.

@JiminyCricket. that sounds like the answer I'm looking for. (Although how can you tell it appears to be an inoculation of some kind?)

I'll write an answer.

The main giveaway that it's designed to produce an immune response would be the presence of an immunological-adjuvant:

a substance that increases or modulates the immune response to a vaccine.

Now, of course, adjuvants are used in cancer treatment, but the difference with inoculations for pathogens is that there'd be an additional molecule or set of them which triggers a specific immune response.
There are nearly a dozen types of "vaccine" for COVID and variants, the majority are focusing on making use of the spike protein of the virus to create a response, but there are some which are designed to create a response to the capsid proteins, i.e. the viral-shell. Neither the spike protein nor the capsid would be expected to be found natively existing in the human body.
This doesn't mean they all contain the spike protein (or any other target protein), the mRNA version for example is designed to induce the body's own systems to produce the spike.
Some contain an adenovirus - a familiar companion found usually in the mucus membranes of human populations causing a number of familiar respiratory diseases. This being also designed to induce the body to produce the spike protein and only that. They would be otherwise reproductively inert.
Some contain artificially produced virus-like particles which have some characteristic in common with the target virus.
The one producing arguably the broadest response would be the virus particles themselves, artificially cultured then inactivated before administration. This would be straight-up identify the virus that the vaccine is designed to combat. At the time of writing, these seem to have been primarily developed and deployed in China.

Thanks for answer. I take it the short version is yes - it's possible to tell that the unknown substance is an artificially produced vaccine. Do you know if it's obvious or if it's only obvious in hindsight?

I guess I didn't explicitly say, but yes. If the mRNA vaccine, we should have been able to identify that from about 1990 onwards as its development began in the 1980s. The rest is older and would be recognised. An exception might be the virus-like particles which resemble other things found in nature - like the substances found in the sting of some parasitic wasps - it might be suspected that we're trying to mind-control caterpillars if not for other clues like the adjuvant ;) @Allure


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Is uncoating required for completion of reverse transcription of HIV?
The p24 capsid plays an important role in the replication of HIV, particularly in the reverse transcription and nuclear entry processes. The capsid protects the viral reverse transcription complex (RTC) from antiviral sensors of the host cells, and breaks apart to release the pre-integration complex (PIC) for integration. However, the precise timing of the uncoating is unclear. It’s generally accepted that HIV can initiate reverse transcription in intact viral capsids because the p24 hexamers can alternate between closed and open conformation, which opens up a tiny pore that allows nucleotides to get in and out. So the uncoating is likely to occur during or after reverse transcription. Some researchers speculate that the capsid is uncoated before the reverse transcription is finished. The reason is that the capsid is too small to accommodate the DNA product (however, the RNA template is hydrolyzed at the same time of reverse transcription, which means the volume of nucleic acids should remain the same), and double stranded DNA is more rigid than single stranded RNA. As the reverse transcription proceeds, the pressure builds up inside, which eventually ruptures the capsid. The rupture of the capsid also makes room for the reverse transcription to finish.
So I come up with an interesting idea. If the uncoating of the capsid is mandatory for the  completion of the reverse transcription, can we test it by using mutations or small molecules like lenacapavir to stabilize the capsid and prevent its rupture? If the reverse transcription is unable to finish inside intact capsids, the uncoating must occur before its completion.

Reference:
Jacques, D., McEwan, W., Hilditch, L. et al. HIV-1 uses dynamic capsid pores to import nucleotides and fuel encapsidated DNA synthesis. Nature 536, 349–353 (2016). doi.org/10.1038/nature19098
Zila, V., Müller, T. G., Müller, B., and Kräusslich, H.-G. (2021b). HIV-1 capsid is the key orchestrator of early viral replication. PLoS Pathog. 17:e1010109. doi: 10.1371/journal.ppat.1010109

Note - you should provide attribution for your images - it is good practice for writing, and also because links are susceptible to rot, so ideally your article links should also be listed as references.

Could you provide an example about how references are added?

It seems the image is adapted from the first linked publication. Here is a link to a blog that contains the composite image.

That’s why I didn’t include the link to the blog. The rearrangement is too trivial to be included.

@哲煜黄 it's still good practice to link all sources of images that are not your own.

@哲煜黄 simply by quoting the reference details, your first one is: Jacques, D., McEwan, W., Hilditch, L. et al. HIV-1 uses dynamic capsid pores to import nucleotides and fuel encapsidated DNA synthesis. Nature 536, 349–353 (2016). https://doi.org/10.1038/nature19098. Most articles have a "cite this article" link or simply a cite button that will produce a pop-up with 1 or more citation styles.

Thanks for giving insight about the interesting characteristics of HIV Capsids and Reverse transcription! In order to fully judge the viability of your proposed experiment, we need more information about your model. How does culturing HIV work? Does it work like any other viral culture using a host cell culture? Or are there simpler/safer in vitro models? I suspect that one needs the full length HIV-genome? If so, you could run a PCR of the medium using primers that span the complete/incomplete genome to test for complete reverse transcription?

At the time I couldn't find any info on this, but I recently came across a review covering the recent literature investigating this subject. To summarize, evidence currently supports entry of the intact capsid into the nucleus through the nuclear pore complex (NPC), (this is a surprising result!) reverse transcription occurring mostly in 'nuclear speckles', and capsid uncoating most likely occurs near the end of or shortly after cDNA transcript is complete.
The authors suggest the conical shape of the HIV capsid facilitates NPC entry, but there's no direct evidence for that yet.
Electron tomography and AFM studies directly observed partially broken capsids with nucleic acid exiting, both in cell nucleus and isolated capsids. This means there's likely no signal-mediated disassembly of the capsid and makes it more likely rupture is caused by internal stress.

Two observations that undercut the "cDNA > internal pressure > ruptured capsid" hypothesis are as follows:

However, the in silico model (130) also predicts that compaction of HIV-1 nucleic acids by the viral nucleocapsid (NC) protein, present within the core at high concentration, strongly alleviates outward forces acting on the capsid shell, and NC-mediated condensation of DNA into a tightly packed globule has been demonstrated in vitro (135). The limit of dsDNA length that can be accommodated within the HIV-1 capsid under authentic conditions is currently not known.

lentiviral vectors packaging RNA much smaller than 10,000 nucleotides have been shown to efficiently transduce cells and are thus capable of genome uncoating and integration.

OP seems to be familiar with the details of the subject, so I recommend reading the review in full if you have access.


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What do Wild Silverfish Eat?
Silverfish are famous for eating wallpaper paste.

The paste is made of starch mixed with water.  Wikipedia says silverfish love starch

They consume matter that contains polysaccharides, such as starches and dextrin in adhesives.[4] These include book bindings, carpet, clothing, coffee, dandruff, glue, hair, some paints, paper, photos, plaster, and sugar.

But all of these are artificial substances. I wonder what do they eat in the wild?
I suspected they eat wood but a cursory search suggests they do not. Or maybe the articles I found are talking about them not eating wooden furniture. Perhaps they prefer to eat damp wood such as rotting logs in the wild.
Most of the obvious info on Silverfish is about what they do inside your house, rather than in the wild. Does anyone know what they eat in the wild?

Related Bio.SE posts: Do Termites and Silverfish metabolize cellulose the same way?, What is this tiny bug,

Silverfish are shredders. Shredders are...

...responsible for processing coarse particulate organic
matter (CPOM). CPOM is greater than 1 mm in size and typically derived
from allochthonous sources, such as woody debris, leaves, and other
vegetation [..].

Their diet includes sources of starch and protein, including grains, vegetables, fibers, sugars and fabrics. Silverfish can actually digest cellulose, a feat not shared by many animals. They are able to do so thanks to cellulase activity in microorganisms that live in their gut (Lasker & Giese, 1957).
Reference
- Lasker & Giese, J Exp Biol (1957) 33(3): 54–553

Good info's, nearly all animals that bore into wood or use wood to build a nest can digest cellulose, some beetles, termites, moths, barnacles, grasshoppers, leaf cutter ants, worms, wood mollusks, sea cucumbers, wood crabs, leafhoppers, gnats, weevils, aquatic insects, something like 15% of invertebrates can.

The answer to this is in their habitat some points to note are:

They inhabit moist areas, requiring a relative humidity between 75% and 95%

It avoids light

Silverfish are a cosmopolitan species

Silverfish can live for a year or more without eating if water is available

They are agile runners

Citation:
(1) https://en.m.wikipedia.org/wiki/Silverfish
(2) https://animaldiversity.org/accounts/Lepisma_saccharina/
This concludes that they dwell (in wild) on the lowest strata of forest (i.e forest floor - especially if its wet and humid) and it is rich in detritus (eg:fallen leaves specially) also since they are cosmopolitan they can infest a rotting tree trunk (for loose parts since they can not bore into it like termites) which will provide a suitable shelter and food for them, also they are pretty tough since they can live for almost a year without food barely surviving on water. They are also agile/quick thus got large area at their dispense to explore for food. They aren't so voracious feeders hence can survive in bare minimum availability which is abundant on the floor itself. Personally i feel they should prefer locations like next to a cave entrance which is damp and dark and near the food.

But what do they eat?

They can infest the log if there is something for them to eat in there. If they can eat rotting wood then of course the log is made of food. But can they eat rotting wood?

They should eat loose parts rotting wood bark since they themselves can't bore into the hard wood which is water resistant, but once it is primarily infested with termites and degraded to a certain level they can infest deeper

Mostly they get sufficient amount from fallen leaves, they aren't as hungry as termites are for wood otherwise you would have seen libraries getting eaten in some really worse manner and it would have been so hard to get rid of them. Which concludes they are not voracious feeders

Where does it say in the references that they eat fallen leaves?

because there isn't anything else to eat on the lowest stratum of forest if we look by their preference of food, that they should be rich in cellulose and i don't see any other possibility here rather than leaves


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Simultaneous activation of myosin kinase (MLCK) and myosin phosphatase (MLCP)
Reading about smooth muscle cells, I stumbled upon this sentence in Guyton & Hall, Textbook of Medical Physiology (14th ed):

When the myosin kinase and myosin phosphatase enzymes are both strongly activated, the cycling frequency of the myosin heads and the velocity of contraction are great. Then, as activation of the enzymes decreases, the cycling frequency decreases but, at the same time, the deactivation of these enzymes allows the myosin heads to remain attached to the actin filament for a longer and longer proportion of the cycling period.

I'm having trouble reconciling this with myosin phosphatase's role. Elsewhere in the book it is stated that myosin phosphatase plays a role in smooth muscle contraction cessation, and that phosphorylated myosin (i.e. the product of myosin kinase) can, by itself, repeatedly attach to and detach from the thin filament and perform the cross-bridge cycles. As in, detachment of the myosin head from the actin filament does NOT require its dephosphorylation (via myosin phosphatase); and rather, the dephosphorylation only occurs when the cycling should stop altogether so that muscle relaxation occurs.
If this is true, then why would myosin phosphatase need to be 'strongly activated' (as per the quote above) so that the cycling frequency and velocity of contraction increases? Would that not actually reduce the cycling frequency? It seems to me that myosin kinase should be strongly activated and myosin phosphatase be strongly inhibited if the cycling frequency is to increase, but I'm probably misunderstanding something.
How does myosin phosphatase activation (or as the quoted part says, strong activation of both myosin kinase and myosin phosphatase) actually increase the cycling frequency?

Simply cutting the calcium level will not revert the mechanism in case of Vascular Smooth Muscles. Due to absence of Troponin in their sarcomere.
For the reaction to go forward as well as backward we are dependent on MLCK and MLCP both respectively and to shorten the time period(increase frequency) we need to raise the concentration of both.
Citation & Explanation
Unlike skeletal muscle, smooth muscle is phosphorylated during its activation, which creates a potential difficulty in that simply reducing calcium levels will not produce muscle relaxation.(Section:Mechanism Paragraph 3rd).
Citation: https://www.ncbi.nlm.nih.gov/books/NBK526125/
This is due to absence of troponin which is present in Cardiac Smooth Muscles and Skeletal Muscles but not in vascular smooth muscles.
Citation:https://pubmed.ncbi.nlm.nih.gov/12665242/
Citation:https://cvphysiology.com/Blood%20Pressure/BP026 (check paragraph 1 and the Image shown on the page)
Thank You

For the reaction to go forward as well as backward we are dependent on MLCK and MLCP both What is this 'reaction' that needs to go backwards? I don't understand what muscle relaxation has to do with the cycling frequency. Doesn't relaxation (via MLCP) happen AFTER the cycling is done? I'm asking about how increased MLCP activity is needed for the contraction itself (i.e. the cross-bridge power-stroke cycles that occur during the contraction), not why MLCP is required for contraction (and the entire cycling mechanism) to stop.

https://pubmed.ncbi.nlm.nih.gov/9887960/ this is the paper which you'll probably find the answer, i will post my updated answer after reading it.


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Maternal Effects
Does anyone know of a good review of non-human maternal effects, preferably the most recent? I'm looking for a breakdown of the most well-studied/least studied biotic and abiotic cues. Perhaps something more comprehensive than Bell & Hellmann (2019), with an emphasis on maternal effects as opposed to the more general "transgenerational plasticity".

Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer.

Maternal effects of what sort? I could suggest some social effects of neglect of children by working mothers, but I doubt that you had that in mind. If you define your problem clearly, An internet search will surely provide answers. Any opinions of what constitutes “good” here would be subjective — you need to make your own judgment.

Also did you tag predation and toxicology for a reason?

@user438383 Predation and toxicology are two possible environmental cues that can promote maternal effects (see linked paper, table 1). Others include temperature extremes, nutrition quality, in eutero hormone cascades.

@David I narrowed my question to non-human maternal effects. Regarding what kinds, I am interested in a contemporary review paper, so all possible kinds.

The word “effects” is meaningless scientifically without saying what is doing the affecting, and what is being affected. Questions here should be self-contained, and I certainly am not going to follow a link to find out what you are talking about. So let’s try again: “Maternal effects of ****** on ****”. You know what you have in mind, but you need to make it clear to us, because we do not.

@David I am unsure about your field as "biology" is extraordinarily broad. In evolutionary biology, the phrase "maternal effects" has a precise meaning. It is a subset of transgenerational phenotypic plasticity, and a considerable body of literature is associated with it.


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How many plant species would have existed immediately after the K-PG extinction?
Specifically, what is the best estimate for the minimum number of plant species during the aftermath and recovery period following the K-PG extinction event?
Do we have any idea how low that number got?

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

Good question.
The fossil record post Cretaceous-Paleogene boundary is much less clear than the animal fossil record. It's basically impossible to give a true value, since there's no way to determine the number of plant species either side of the event, due to the sporadic nature of plant fossilisation.
In contrast to the wide-scale extinctions that occurred in the animal Kingdom, no major plant groups became extinct across the boundary, and the damage primarily occurred at the species level. However, there is a very strong bias towards sites in North America as these are the ones which are the most well preserved.
This is a cross sectional map of the palynological diversity across the K-PG boundary from North Dakota (source).

The average extinction proportion of miospore taxa in North America is
around 30% (Nichols, 2002, Nichols and Johnson, 2008) and this is
synchronous with a significant drop in gross palynological diversity
(Fig. 5). An additional 20–30% of the miospore taxa underwent a
statistically significant decline in abundanceThe extinction magnitude
was apparently lower within New Zealand assemblages where 15% of
pollen and spores species disappeared


text:
Need assistance identifying palm-like tree
I need assistance identifying what type of palm-like tree we've been growing. My husband's Grandfather brought the original plant home in 1974 from Florida and we've been growing and repotting them for the last 25 years. The leaves are incredibly sharp. They are very hardy and survive Ohio winters living in the basement. We have had them grow up to 5 feet in height. They produce numerous new plants each year.

Not a palm, looks like a Dracaena. Do a search for Dracaena images and you'll find something close -- Lots of hybrids out there.

This is definitely not a palm species as these all have leaves either deeply divided or coming off as leaflets from a stalk.
I think this is a Yucca (Asparagaceae) species. Yucca and the very similar looking, and closely related Dracaena are very similar in appearance, both (depending on species and cultivar) often have sharp, spiky, inflexible leaves coming directly off a stem (i.e. no stalk).
In the case of Dracaena, the leaves fall off the stem leaving a diamond/triangular scar, but Yucca tend to retain the dead leaves and have the new leaves push through the dead ones.
Dracaena stem:

Image attribution: Auckland Museum, CC BY 4.0 https://creativecommons.org/licenses/by/4.0, via Wikimedia Commons
Yucca stem with dead leaves (note similar scar pattern):

Image attribution: Stan Shebs, CC BY-SA 3.0 https://creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons


text:
What are these stinkbug-like insects?
Lots of these insects appeared on a wall in my garden for about a week. I've never seen these before, and they behave like ants. They look like stink bugs and are 2-3mm long.
My search on google lens suggests Nysius Raphanus, but many sources say this species is limited to North America, and I live in south Italy. I think it could still belong to the Nysius genus, though.
Here are a couple of photos I took with my phone (sorry for the bad quality).

Thanks.

Please update with better quality up-close photo.

You are right and these are true bug (Heteroptera) larvae (see this answer on how to recognise them), although not of the familiy "stink bugs", but of the superfamily "seed bugs".
Determining true bug larvea to the species level is tricky and rarely done. But with some experience, it is possible to tell the families apart. Seed bug larvae have elongated, rather flat bodies of brownish colors (which camouflage them on the ground where most of them dwell). Often, they have a pointed nose (a long head) and relatively large eyes.
From their habitus, they could actually belong to the genus Nysius (you could compare with Fauna Europaea which species occur in your region).
But they could also be another species from the seed bug superfamily.
Moreover, identifying Nysius (and most other seed bug) species usually requires a microscopical inspection.

Interesting. Later I discovered that they were coming from and going to a mature Portulaca Oleracea lawn.


text:
Why am I losing much more vector than insert DNA during RE cloning?
I've been cloning some inserts into a lentiviral vector (pBOB backbone) by RE digestion and blunting ends with T4 DNA polymerase.
After these steps, I usually load the digested product onto 0.7% agarose gel to isolate the expedcted size fragments.
Unexpectedly, during agarose gel separation the bands from the lentiviral vector are much less intense compared to the insert ones.
Having exctracted the DNA from such a band, its amount is not sufficient to pursue the ligation process (I'm getting around 0.5 ng/ul of vector!).
I have already repeated the digestion three times and always get the same profile. I've also been checking the DNA amount after each cloning step (e.g. RE digestion, fill-in) and I notice that the lentiviral vector DNA amount is always half the insert DNA, which is always ok and in a sufficient amount to be ligated.
Having used the same reagents for either vector and insert DNA, I would actually exclude a technical issue, as I'm taking the impression that there's something wrong with the lentiviral DNA. Of note, it is a purchased plasmid from Addgene which I have already checked by RE digestion.
Do you have any idea of what's going on? Also, do you have any suggestions about how to fix the problem?
Thank you in advance for your kind help!

Welcome to the site. Can you please provide more details on your procedure - how (method) are you checking the DNA amount (concentration?). What site are you digesting at and how are you sure that the vector:insert molar ratios are correct? Gel extraction is notoriously low-return (generally <10% of input), so how much DNA are you loading onto the gel?

I have seen so many students getting stuck at cloning.
Alternative Strategies:

Linearize your vector with PCR (use polymerase with corrective activity like Pfu) using primers that face away from the insert site. This yields large amounts of blunt ended dsDNA. Extract from gel. Then get the insert in by blunt-end ligation.
Change the restriction enzyme using a mutagenesis kit to introduce another restriction site.
Change the restriction site (or homologous sequence for different cloning technique) by extending the insert and/or vector with PCR using primers with overhangs.
Switch to another cloning technology (TOPO cloning, LIC, SLIC, Gibson, Gateway).

Other suggestions:

NEB says: "CAUTION: Elevated temperatures, excessive amounts of enzyme, failure to supplement with dNTPs or long reaction times will result in recessed ends due to the 3´→ 5´ exonuclease activity of the enzyme."
If you have checked the vector with RE digestion it should be fine..? Did that check yield the same unexpected low yield pattern?
Sometimes it helps asking someone else to do the procedure for you. That way you can exclude an error on your end.
Sometimes the restriction enzyme/T4-pol is old. Buy new one.
NEB has a troubleshooting guide for cloning.


text:
Greyish spots behind a peach's stone, what could they be?
I'm sorry if it's a silly question, but what are those greyish spots behind the stone of this peach (or whatever this is)? What are they for? Are they safe to eat? The fruit is ok from the outside

it is some type of mold,you should probably not eat that one.

I concur, looks like it has a yeast or bacterial-infection - a very common thing in fruit.

Callus can develop inside peaches (https://www.tasteofhome.com/article/peach-callus-tissue/), between the mesocarp and the endocarp. Callus is edible and harmless. It's a tissue composed of unorganised parenchyma cells, which in turn are multi-purpose cells that can be found in a number of "soft" tissues with metabolic purposes including, but not limited to, the mesocarp and the endosperm. Callus' main purpose is to seal damaged tissues, see for instance:

this blogpost that explains the difference between mold and callus in a peach where there actually is a mold infection (which you should not eat)
its counterpart where there is no mold, but a considerable amount of callus (way more than you have there) was produced because the stone had split open; this one would be safe to eat, once you've ascertained that there is no mold, although callus may contain pieces of hard tissue from the stone.

Small quantities of callus can appear as leftovers form older and smaller lesions.

Which begs the question, how could that peach get "wounds" from inside?

A peach is not waterproof you know ;)


text:
What does "run" mean in DNA sequencing?
In "[Genomics: A Very Short Introduction]" by John Archibald, the author discusses the DNA sequencing:

In reality, most nuclear genomes are a mixture of unique sequences and short and long repeats of various kinds, and researchers have developed ways of dealing with the issue. One approach is to obtain sequences from both ends of the randomly selected DNA fragments (see Figure 6), and to have the algorithm keep track of these so-called ‘paired ends’ and the distance between them (which is known because the genomic DNA was size-selected prior to library construction and sequencing). This improves the chances of being able to anchor the sequence data from each DNA fragment onto the genome. It is also common to perform multiple sequencing runs using DNA that has been sheared to different sizes (e.g. 2, 10, and 50 Kbp); this makes paired-end data even more effective in overcoming the problems associated with repetitive DNA.

I don't have enough knowledge about this topic, and I'm not sure of the exact meaning of "run" in this context. Does it mean "performing the process of sequencing multiple times" or "generating multiple sequences"?

This is English not Biology. I suggest you abbreviate the question and transfer it to SE English Language Learners.

@david ‘run’ is a technical scientific term that’s used often, and asking about terminology is on topic here. Most importantly, this is likely to be useful to biologists, so I disagree with your suggestion.

@user438383 See Merriam-Webster Run noun "4 : a continuous period or series especially of things of identical or similar sort" with 7 examples, including ": a set of consecutive measurements, readings, or observations". The poster seems to be trying to use this site as a consultancy to help him reading a book, rather than asking questions about biology arising from it. I would encourage him to learn to save his own life.

It looks to me like that sentence should really read "It is common to prepare multiple sequencing libraries using DNA that has been sheared to different sizes". While you can run the same library over and over again, since one run is only a sampling of the library contents, it looks to me like the author is talking about combining information from libraries of different insert sizes as being more effective than resampling from one library with one target insert size.

Each run is simply each time a reaction/process is performed, though usually applied to something that is performed on a machine or device that does the "running" - so you could do quantitative PCR runs or run a gel.
Multiple runs would be repeated reactions/processes (in this case sequencing library preparation then run on the sequencing device).

DNA sequencing (e.g. Illumina dye sequencing) does not sequence all DNA available; it simply sequences a sample of what you provide, i.e. it "samples". Say you have a bag of 100 differently-colored ping pong balls, and you have a set procedure wherein you take out 50 balls at random and note down their color to understand the color distribution. You could do this "run" once, but you can get a better, more reliable look into your bag if you do a 50-ball-random-sampling multiple times! You do many "runs". That's why in research we use the phrase "multiple runs" when we have preset procedures.

^above is addendum to answer to help make it more intuitive, i make no comment on the actual answer, it's very good. +1


text:
Scientific terms for front-brain, mid-brain and back-brain
I am looking for a (semi-) scientific way of phrasing "front part of brain" (part 1), "middle part of brain" (part 2) and "back part of brain" (part 3) as denoted in the attached picture.
I would (VERY!) loosely define these parts as:

front: everything in front of the ventricles
mid: approximately at the same height as the ventricles
back: behind the ventricles

I need this to qualitatively describe some results I have.

Note that this is different than forebrain, midbrain and hindbrain (which is the main result that google comes up with when searching for this).
(edit) Additional context: I have a method that selects a certain background volume in the brain. These background volumes are then used to make a segmentation. The placement of these background volumes seems to correlate with whether or not the segmentation is "good" or "bad". "Good" segmentations seem to correlate with backgrounds placed in the "mid-brain". "Bad" segmentations seem to correlate with background volumes places elsewhere.

Welcome. What's the context of the terms? I mean, what do you wish to explain? Chances are big there are no established anatomical terms for what you wish to describe.

Since you are working with 3D data, why not segment them into lobes? You have 4: frontal (front), occipital (back), temporal (lateral middle) and parietal (top middle) lobes. If you really must have three only, group the middle two together.

You have sulci (singular: sulcus) as references which you can naturally use as topographical borders for segmentation.
You can also define your own regions, provided that they are universal. I see no reason why not to define your own regions. You can define the arm as ending at the wrist, or including the hand. It's all semantic, and what matters most is to be clear with your definitions, not inflexibly adhering to preconception. You can use any gyrus or sulcus to define your arbitrary areas, pick however you like, with the knowledge that it must be suitable across all your samples and not confound your data in the end:

thanks, this helps. I decided to do it based on lobe/part of lateral ventricle it is adjacent to.

Short Answer

Anteroventricular coronal segment

Paraventricular coronal segment

Posteroventricular coronal segment

Long Answer
As indicated by @AliceD in the comments, I'm not sure there are technical terms to describe these regions per se.

Of greatest issue is how imprecise you're describing their cutoffs. Without citing very specific brain region/anatomy demarcations, any chance for proper technical vocabulary is minimal. (even broad brain divisions have defined boundaries)

Although something specific/technical is not really appropriate given your imprecise approach, I think some sort of general regional approach could be adopted:
So, what you have drawn are three mostly arbitrary coronal segments of the brain (i.e., three regions divided by 2 frontal planes).

You could simply refer to them as the anterior, posterior, and middle coronal sections or segments.
Or, I suppose you could also say pre-ventricular, ventricular, and post-ventricular coronal segments to place them in the context of the ventricles.

Though, perhaps you could create even more precise affixed terms: anteroventricular, periventricular, and posteroventricular coronal sections.

though, perhaps paraventricular could also be used vs periventricular, since your middle segment extends beyond the immediate perimeter of the ventricles.

Again, the above is stated based solely on a broad application of these generalized affixable terms. I am not commenting on their appropriateness or possible conflict with any current usage of any of these terms to perhaps clinically refer to more specified regions.


text:
Does nature have a mechanism to turn charcoal back to usable carbon?
I have in past asked this about ash, but apart from ash most fires - whether natural or fires in stoves - leave a bunch of charcoal as well. When I was sifting old compost last year, I could identify the layers where the fire pit contents were dumped in - but not by ash, as it really mostly dissolved and disappeared, but by charcoal (and also nails sadly).
In those layers, there were chunks of charcoal as well as larger partly decomposed pieces of wood covered by charcoal.
So, since no wildfire is perfect to the point of burning all organic matter perfectly, what happens to the charcoal after wildfires - or to the charcoal that is dumped with ashes to composts and gardens? Carbon is extremely chemically stable unless you set it on fire, so is there anything that can oxidize it in nature?
If not, is the soil in places of common wildfires rich in pure carbon crystals from millennia of fires and regrowth?

https://www.natureworldnews.com/articles/51463/20220620/430-million-year-old-charcoal-deposits-oldest-wildfires.htm, https://www.sciencedirect.com/science/article/abs/pii/S1871174X20300172, https://pubs.acs.org/doi/10.1021/acs.energyfuels.1c01559. I would suggest researching "biochar".

Short answer - not really. Charcoal as almost pure carbon is fairly inert, not readily available and can remain in the environment almost indefinitely. This is evidenced by charcoal in rocks from the Silurian period (~440 million years ago). We also find evidence of forest fires in the form of charcoal in almost all time periods since this point.
I've personally picked charcoal out of buried soils that is at about 2000 years old from volcanic eruptions - admittedly there the top layers might well have been sterilized by the heat of the pyroclastic flows, so not a perfect analogy.
However we can identify domestic camp sites from Neanderthal and other early human species for the past ~160,000 years, mostly from ash and charcoal presence.
Edited to add: in the case of biochar and similar products, the charcoal is used to act as a reservoir for the nutrients (charcoal is really good at absorbing things a la activated charcoal), which can be taken up into the microstructure of the charcoal and released as the plant rootlets and/or mycorrhizae invade. The charcoal also provides a looseness to the soil allowing greater aeration, better drainage and allowing roots to penetrate to a greater depth. These all help plants to grow well.


text:
What bug is this in my closet
I keep finding these little insects on my clothes in the one corner of my closet. They seem to be a mm in length. I’ve never seen them walk and I’ve only seen one in any given time. I’ve never seen hairy projections so it makes me want to rule out carpet beetles since the photos online show some hair. Tonight I found one on my fabric headboard. They seem light brown with black stripes.  Thoroughly disgusted. [

Hairy projections are only really found on the larvae of the carpet beetles.
The adult beetles look like beetles - which this almost certainly is.
Probably varied carpet beetle

Image attribution: Staff of York Museums Trust, CC BY-SA 4.0 https://creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons