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What is this black worm-like creature with a yellow underbelly
This was found in the Malay Peninsula around noon. Unfortunately it was doused in hot water by my grandmother.
Image below is after having been killed by hot water.

It is about 1.5cm-ish long. It was curled up for some time but it started to move when it was exposed to sunlight(before it was killed). According to my grandmother, she had seen these long ago and they would stick on trees and foam up when touched. It didn't seem to foam up after it was killed though.
What species is this and is it endangered?
Edit : I'm very sure it is a type of chiton now and that it has already been doccumented. I'm saying this because I saw a video on YouTube with an extremely similar creature. Although I am still not sure what species it is.

Any chance you have a photo of the other side. It looks to be a slug or perhaps a flatworm of some sort.

No, I did not take a picture of the other side unfortunately.


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Detection of primer dimer on RT-PCR?
I usually do RT-PCR test for covid-19. Curves for Patients and Positive CTRL mostly appeared at 20 to 25 Ct. Sometimes, there are some curves that emerge at the last 5 cycles. Some argue that they are probably primer dimer and should not interpret as positive. How primer dimers would appear on the amplification graph?

I assume you do a proper negative control, right?

Negative CTRL is double-deionized water.

If you're testing for diagnostic purposes, you should probably be using a kit with sequence-specific fluorescent probes, not an intercalating dye like SYBR. Primer-dimers won't show up as florescence in a probe based PCR, but they can reduce reaction efficiency, leading to later detection of your target. You should also consider running a negative specimen control, along with your water control, to screen for possible contamination events during extraction or sample prep.

This is a bit complicated from far away, but I will share a few thoughts on it. The occurence of primer dimers depends on the design of the primers (sometimes they are inevitable due to sequence limitations), but then they also show up in the negative controls.
If they are not present in the negative controls (meaning: never), I would not expect them to be present in the test reactions either. It is possible that you are getting very late unspecific DNA amplification from other sequences due to degrading etc. but this is also unlikely.
You could do a melting curve analysis to see what your product looks like. A pure product (even in the late phase of the PCR) should show up as a sharp and clearly defined peak, whereas primer dimers (and also the products of unspecific DNA amplification) have generally a much lower melting temperature and give a much broader peak. The figure (from here) illustrates this nicely.

You could also run your samples on a gel after the PCR and see what the product looks like. Product gives nice and clear bands, while byproducts are smaller and more diffuse.
It is not unlikely that you either tested people who have gone through an infection with SARS-CoV-2 and have only some virus left in their body or that the sample comes from people very early in their infection, when the detectable amount of virus has just gone over the threshold for detection. Assuming that the samples have been correctly taken (which is another possibility for error), I would collect a new sample from these individuals and test them again.

I would just add to this that most commercial PCR tests for Covid diagnosis use sequence-specific probes for detection, not intercalating dye. With a probe assay, you should not see fluorescence increase from primer dimers alone, because the probe should still have nothing to hybridize with. That said, most commercial kits also have a pre-defined cutoff cycle for amplification to be considered positive. The utility of these cutoffs can be debated, but if you're testing for diagnostic purposes, I would not recommend deviating from those specifications.

source: Stack Exchange

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

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Could the use of genetically engineered crops result in the population decline of other organisms?
Population decline of other organisms has been an ongoing phenomenon since man learned how to domesticate corps. Many people, including me, is curious if the use of genetically engineered grops result in the population decline of other organism.

Why do you think genetically engineered crops would cause a decline in some organisms?

Pretty much any human activity will benefit some organisms and hurt others. What "use" of genetically engineered crops interests you? What type of genetic engineering are you thinking about? What population(s) of other organisms are you interested in? What time span are you interested in?

Do you have any specific example in mind?

Genetically engineered crops are more resistant to pathogens, harsh conditions, etc. As such they have advantage over other plants in competition for resources, and thus may lead to dicrease in biodiversity. On the one hand, this is not new - any crop or animal is cultivated by human to disadvantage of its natural competitors - just thinkn of the fate suffered by weeds, or by the natural population of the areas cleared for crops. On the other hand, if the genetically modified crops are able to reproduce (which is not always the case by design), they can take over other plants even beyond the areas where they were planted. Finally, the diversity of the organisms feeding or parasitizing on the genetically modified crops declines as well, for obvious reasons.
As far as my experience goes, the issue of genetically modified crops is somewhat of a controversial subject - public fears them, while the scientists forcefully push back against these fears. Thus discussing the issue seriously is hard. Still, I would be glad to correct/complete or remove my answer, if somebody more knowledgeable in the crop science chimes in.

I believe you are mistaken. There is no inherent reason a genetically engineered crop (whatever that means in a given example) would be more or less resistant to "pathogens, harsh conditions, etc", and no inherent reason for it to "have advantage over other plants in competition for resources".  As you point out, "any crop or animal is cultivated by human to disadvantage of its natural competitors " - but that is because it is disadvantaged relative to its natural competitors, and needs human help.

Could you expand on why "Finally, the diversity of the organisms feeding or parasitizing on the genetically modified crops declines as well, for obvious reasons"? Any such reasons are not obvious to me. Remember, we are comparing "genetically engineered" crops with "normal" crops.

@Armand my understanding is that crops are genetically engineered to make them more productive - that includes making them more resistant to disease and parasites.

@Armand Non-engineered crops are indeed disadvantaged - this is precisely what I was pointing at. So humans use pesticides or clear a forest to make place for a field - all of which literally means exterminating lots of specimen, sometimes on massive scale.

Re "crops are genetically engineered to make them more productive "  Some are and some aren't, but it is always in a context.  In one situation, that may result in increased productivity and in another lowered productivity. For example, "disease resistance" typically has a resource or metabolic cost, so in the absence of significant presence of the given disease, the plant will perform more poorly than an unmodified one. Productivity etc depends on the individual plant's genome and the environment it is raised in, not on how its genome was generated.

Re: "So humans use pesticides or clear a forest to make place for a field " This has nothing to do with genetic engineering; it is done for "normal" crops as well.  "Genetic engineering" only refers to how a genome is generated, not to farming practices.

@Armand this is precisely the point I was making in my answer - that affecting biodiversity didn't begin with genetic engineering. I will think how to rewrite it in more understandable fashion... this discussion seems to be based on a lot of misunderstanding.

Genetic engineering is a process, not a product or end result.  Thus, it has no direct effect on "other organisms".
Humans have been modifying organisms for tens of thousands of years. We've developed multiple techniques to do so, including selective breeding, mutagenesis, grafting, interspecies hybrids, multiploidy, "genetic engineering" and so forth. Just as with producing books, the resulting product is evaluated on its own, not by what process produced it.
What matters with a book is the words it contains, not whether they were handwritten, block printed or even carved in stone. Similarly, what matters in an ecosystem are the organisms present (and their function, much determined by their genes) and the conditions they live in, not how those organisms were created.

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


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How many genes per 23 chromosomes in human genome?
It is estimated that humans have between 20,000 and 25,000 genes. Every person has two copies of each gene, one inherited from each parent.
There are 46 chromosomes, half from the mother, half from the father.
Does this mean that there are
a) approximately 20-25,000 genes on the 23 chromosomes inherited from the mother, and 20-25,000 genes on the 23 chromosomes inherited from the father, or
b) approximately 10-12,500 genes on the 23 chromosomes inherited from the mother, and 10-12,5000 genes on the 23 chromosomes inherited from the father?

Welcome to Biology.SE. This community has agreed that 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. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

I don't have the ability to do that, but you can Flag your post for moderator intervention and ask for this to be deleted (may not be possible with an answer) or closed. ——— Please also note that "homework" on this site includes "self learning", please follow the link in my first comment for details.

Answer A is correct!
The human genome has around 20,000 genes. In both, diploid and haploid chromosome-count, the gene-count stays the same; grown humans have 2 alleles per gene in most of their cells, which is considered 'diploid'. Gametes are haploid.
Willyard, C., Expanded human gene tally reignites debate. Nature, 2018. 558(7710): p. 354-355.

Please don't encourage posting of "homework" questions which do not show research efforts.

I did spend quite a lot of time searching for a clear answer to this question. I couldn't find one and that's why I posted the question here.

The aim of stack exchange is to develop an extended topic-related FAQ. I did not find this question here. As this is a natural question that I remember from my own study-years, I really don't care if this is homework; as long as it serves a purpose on the site / for google, it should always be accepted.

This isn't 'homework' by the way. I'm studying on my own, for myself. PS @KaPy3141 : thank you.


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How can animals that rely on SONAR not see color?
Humans can sense colors with acuity and can distinguish them because of the light of different spectrum that follows into their eyes. Not its also said that sound is different for different colors,
Wouldn't this mean that during echolocation , dolphins, Bats and other animals can see colors? Please explain

"its also said that sound is different for different colors" - said where and by whom?

@Bryan Krause https://en.m.wikipedia.org/wiki/Colors_of_noise#:~:text=Different%20colors%20of%20noise%20have%20significantly%20different%20properties.&text=Other%20color%20names%2C%20such%20as,of%20light%20with%20similar%20spectra.

That article has nothing to do with visual color except a modest analogy. Also has little to no relationship to echolocation sounds. "Noise" in this context isn't even necessarily related to any sort of sound, but rather to random patterns which can be in any sort of signal.

@Bryan Krause  oof yeah you're right I should've read it better, sorry

I’m voting to close this question because it is unclear and seems to based on a fundamental misunderstanding of a non-biological concept (color).

Color is a characteristic of visible electromagnetic spectrum, see the graph here. Electromagnetic means here that it has the same nature as radio-waves, X-rays, and gamma radiation, whereas visible refers to the region of spectrum - waves of frequencies ranging from TeraHertz to PetaHerz (i.e., from $10^{12}$ Hz to $10^{15}$ Hz). Specific colors essentially refer to sub-ranges of the visible spectral range (ordered as in a rainbow).
On the other hand, sound waves, used in echolocation, are waves of material compression/decompression in air, liquid or solid, and their frequencies rarely exceed one MegaHertz (that is $10^6$ Hz, i.e., $10^6$ oscillations per second). E.g., human ears distingushes sounds in the range from $20$ Hz to $20$ kHz, whereas animal sonars use ultrasound frequencies above the human hearing threshold - from $60$ kHz to $200$ kHz (see here).
To summarize: sonar and sound have nothing to do with color perception.

The question is based on a false premise.  Humans (and other animals) perceive color because they have sensors - in the case of humans, three types of cones - that respond to different frequencies of light.  "Color" is really a construct of the brain, as it interprets the intensities of the signals from the different receptors.
Sonar is more analogous to the rod visual system, used in low-light conditions where you can see things, but not distinguish their colors.
Of course an animal echolocation system (or a technological one) could potentially distinguish something analogous to color, by having receptors that respond to different sound frequencies.  But the sound reflection characteristics of objects would have nothing to do with their colors.  That is, a hard red surface would reflect sound differently than a soft red one.

Bats at least seem to have fairly sophisticated sense of texture, probably the best analog for "color vision" in this context. https://www.pnas.org/content/101/15/5670 for example

@Bryan Krause: Interesting!  I learned something new :-)


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What causes the distinct color change in matured leaves in some plants?
Maybe that color change is caused by lower chlorophyll concentration in younger leaves' cells, or chlorophyll a to b ratio differs between younger and older leaves. All I could find is that the chlorophyll a to b ratio in higher plants is 3:1, but there's little data if that ratio ever changes.
That color change is especially noticeable in conifers, but I've seen it in trees belonging to other divisions.

My guess would be that the structural metabolites and waxy cuticle that give these leaves rigidity and protect them from the elements can't be produced in these tips of new growth without stunting their development (note that the branch tip is still green and not yet woody). Conifers have some of the toughest cuticlular waxes in the plant world, and I know that a property of these waxes is that they change the apparent color characteristics of the leaves by reflecting or absorbing certain wavelengths of light (it's what makes the blue spruce blue).


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Flying Insect Identification
What insect is this?

Found in the UK, approximately 10mm-15mm in length.

That is clearly a mayfly (family: Ephemeroptera) — using that may help you find an answer for yourself. It would also be very helpful if you were to [edit] your post to include "as much information as possible on location/habitat, size/characteristics and behavior." (from the species-identification tag description) ——— In particular, what is the local environment is like and can you give more specific location information than "UK"?

if you want to learn more about this group of insects you can take a look here https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/ephemeroptera

That insect looks quite like a Mayfly, it's an ancient insect that belongs to the order Ephemeroptera. I'll go a step further and guess that species, that one there is most probably a Green drake, they aren't harmful at all as in they don't sting or bite but if a lot of dead mayflies pile up they can cause respiratory inflamations, asthma, hay fever that sort of stuff.
They're a vital part of the pond ecosystem. Here's a picture of a Green drake and it's quite similar to your picture. Credit to Missoulian Angler
I think some of the major reasons why it is a Mayfly are a s follows:-

The transparent wings are a minor giveaway.
The three tail filaments are a major giveaway.
Very short almost non-existent antennae

Welcome to Biology.SE! 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. ——— Thank you for taking the [tour], but you may also wish to consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!

There friend, added a picture.

Thank you for the update! Please provide a citation/source for the image you are using — images must be credited to their creators just like quotes are to their authors. This is generally considered good practice in scientific communication and will help other users understand by providing context. ——— In addition, it would be very helpful if you could describe the key features that allow you to be certain this is a mayfly and what makes you suspect a Green drake in particular. Thanks again!

There mate edited as you said I should, I think that should put me in the clear. Grateful for your sound advice


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Are dark skinned natives of Central America dark skinned due to the same genes as people of African heritage?
I'm trying to understand how strong the evolutionary pressure on genes for skin color happens to be. Was it fast enough that the humans that migrated through the Bering Strait had lighter skin color and evolved darker skin color again afterwards?
Do the genes that give natives living near the equator in central America exist in African populations as well or are they new genes, that were likely evolved in that Central America?

The equator actually runs through South America, not Central America, so you might say tropical regions, rather than equatorial.  Also, you need to specify whether you mean the current inhabitants of the region, or the pre-Columbian ones.  I would suspect that there has been quite a bit of admixture of African (and European) genes in the current population.


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Is there a term for non-DNA gene?
Initially, the term "gene" referred to abstract concept of inherited trait.
Currently this term was hijacked with molecular genetics and means a continuous sequence of nucleotides. However, it omits the fact that for a phenotypic trait to be inherited, sometimes there can be more than one sequence of nucleotides, and sometimes one sequence of nucleotides participate in the formation of more than one phenotypic trait.
Is there a single-word term describing non-DNA "Mendelian gene"?

Welcome to Biology.SE. How is any of what you are describing non-DNA? Please [edit] your post to be clearer and make sure you demonstrate that you've done the expected prior research. Please also take the [tour] and consult the [help] starting with [ask] a good question on this site and make changes to your post accordingly. Thanks!

@tyersome I replaced "sequence" to "continuous sequence". However, there are also phenotypic traits that even do not completely depend on DNA sequences, even if they conventionally claimed by the molecular geneticists to be derived from some continuous nucleotide sequence (which is nowadays called "gene"). For example, if the child will not learn language to a certain age, he will lack the phenotypic trait of speech. If he missing any of (non-continuous) nucleotide sequences responcible for development of vocal cords, he will also not be able to produce speech.

But what about Why genes in pieces?

@user268587 You seem to be referring to a polygenic trait, not a "non-DNA" trait (multiple genes affecting a single trait). The opposite, a pleiotropic gene, is where one gene affects multiple traits.

Epigenetic inheritance is one example, but it is not covering all the possibilities. https://en.wikipedia.org/wiki/Transgenerational_epigenetic_inheritance
I suggest reformulating the question in less controversial terms: less attacks on the established terminology, and more about non-genic inheritance.

Please remove the phrase “non-DNA” from your question. The only non-DNA genes are RNA genes in certain viruses, which is not what you mean. The nucleotide sequences you describe are DNA — by definition. Specific descriptive terminology is used for genes which encode subunits of a protein, both of which are required for a functional whole (1) or generate more than one product by differential splicing (2), but it only makes sense to answer your question in these terms if you transform it into something that makes sense. “Answer only well-asked questions” is a principle of this site.

@David I can use "DNA" here, because despite the fact that "RNA" also encodes genes in molecular biologist definition, all non-microscopic organisms with observable phenotypes are DNA-based, my question is fully understandable and the phrase "non-DNA" adds additional context to it in the sense that it asks about "non-nucleotide" gene.

You seem to be asking about DNA based phenomena (you wrote "sequence of nucleotides" twice), but then you say "non-DNA". This is at best confusing. Please edit your post to make your question clear. In addition, you give the impression that you may be unfamiliar with molecular genetics, so I encourage you to avail yourself of some of the introductory material available online. That may answer your question and will definitely help you ask a clearer question. ——— In addition, you may not like how the usage of "gene" has evolved, but that isn't a fight you can win ...

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

@tyersome I disagree. You give me impression that you may be unfamiliar with structuring of sentences so I encourage you to embrace yourself with grammatic and logic books. First, I do not wrote "sequence of nucleotides" twice. In the first example I wrote "more than one sequence", while in the second just "one sequence". Second, there is no fight. I doubt that you have seen me fighting against this trend of merging these ideas of a gene definition on a public debate. Rather there is a question if this term exist in the scientific community nowadays.

"Non-DNA gene" makes it sound like these https://en.wikipedia.org/wiki/Xeno_nucleic_acid  .

I think that what you are interested in is the original Johannsen definition of the gene as of 1909 (I translated this article, caveat emptor). Notably, Johannsen cautioned explicitly against reading too much into the abstraction of the gene, and instead insisted on reference to heritable phenomena that we would call traits or phenotypic characters, with the understanding that underneath that there is an unseen and unknowable "genotype", which can be inferred through the use of logic and statistics.
However, as you rightly point out, molecular genetics came along and changed things. At that point, many of the phenomena that Johannsen was interested in could be directly be related to genes in the sense of DNA sequences. The Central Dogma of molecular biology reorganized thinking along molecular gene-centric lines, which do have issues as you note.
However, the original Johannsen definition of the gene was never more than a a vague factor for helping genetic reasoning, no one has ever observed such a thing in the wild! There is a reason why no one speaks of genes in this way anymore, and it's because we now know a lot more about how complex molecular mechanisms that generate phenotype are. This is one of the good things that molecular biology gave us, even if you take issue with its reductive character.
If what you want is just a term that refers to a character which can be built of many genes (e.g. polygenic), or including e.g. epigenetic inputs, then "phenotype" or "trait" is perfectly good. But again, such things are subjective, and are limited by what humans can measure and observe.

The Cambridge Dictionary, CDC, and the NIH's institudes researching the human genome and cancer all agree that genes have 2 properties:

they are associated with heredity
they are a section of DNA translated into proteins

However, the Oxford Dictionary has an informal definition and formal definition. The informal definition refers to only to the first property and the technical definition refers to only the second. It also agrees with you on the etymology of the word.
It is clear to me that in the modern usage, gene refers to one factor in the inheritance of traits. The definition does not assume that no other factors of trait inheritance (e.g. DNA methylation, memes) exist. This differs from the early 20th century use of the word, which assumed that no other factors besides genes are responsible for inheritance, i.e. 'gene' was an inclusive term for all factors of inheritance.
To my knowledge, there is no single word in modern usage that has the same definition as 'gene' did in the early 20th century. The phrase 'factors of inheritance' is as close as I think you can get.
P.S. Technically detail, but not all continuous sequences of nucleotides in a strand of DNA are genes. Many sections of DNA serve structural purposes (e.g. centromeres, telomeres) or help regulate gene expression.

There are some exceptions to your (2): for example, some viruses encode their genes in RNA rather than DNA. More importantly, many genes are not translated into proteins -- their RNA transcript is the functional unit: for example ribosomal RNA genes or transfer RNA genes. Other parts of genes (such as promoters and introns) are either not transcribed or not translated, but help determine the transcribed or translated product.

Thus, a more complete version of your technical definition (2) above would be: "a distinct sequence of nucleotides forming part of a nucleic acid segment, the order of which determines the order of monomers in a polypeptide or nucleic acid molecule which a cell (or virus) may synthesize." (minor modification of Oxford Languages definition returned by Google)

Your right. What is interesting though is that of the 5 sources I had for definitions, only the Oxford Dictionary includes viral RNA as containing genes. The rest make explicit reference to DNA.

General dictionaries are a useful reference to the English language, and I would quote them on SE English language and usage, but they are hardly where one goes to discover the terminology used in specialist aspects of a subject. This is trivially obvious from definition 2, which ignores both RNA viruses and non-coding parts genes and mRNAs.


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Did or do these gigantic spiders really exist in Finland and/or Northern Europe?
In the year 2000, the newspapers in a small coastal town of Finland ("Hanko"; current population: ~8k) had some very disturbing reports of a couple who had just moved into a new rental apartment/house in the central part of the town, and there encountered these monstrous spiders that look like they come straight out of a horror movie. In fact, apparently, they are literally the kind of spiders used in the classic spider horror movie "Arachnophobia"...
Digging through old things recently, I encountered the saved newspaper pages and was shocked by just how large and disgusting they look. I must have repressed this whole thing for the last 21 years, since I first heard about it when it was current. From the oddly-worded Swedish-language report (clearly not written by somebody with perfect Swedish skills), it's not made clear whether the couple was "just" working on fixing the place up, or if they actually had already moved in and saw these monsters while they were there to sleep. But the basic point is that the spiders allegedly existed at all, and may well still exist...
The article also notes that these spiders were "common" in Denmark in the beginning of the 1900s, further creeping me out. My initial assumption and hope was that these spiders had miraculously survived in their undisturbed habitat for 50 years (the article also mentions that they were "last spotted" in the 1950s), and that they were not native to Europe at all, but simply had been accidentally shipped in a crate with exotic fruits or something from some tropical island somewhere back in the day, and had not spread but simply hung around in their little basement in a place which, somehow, just happened to not have any humans going there for all these years.
The article further mentions that some kind of professor had determined them to be Tegenari Atrica spiders. However, looking them up on Wikipedia, I got redirected to the disturbingly named article "giant house spider", where it's mentioned that these are:

among the largest spiders of Central and Northern Europe.

And:

original habitat consists mostly of caves, or dry forests where it is found under rocks, but it is a common spider in people's homes.

Source: https://en.wikipedia.org/wiki/Giant_house_spider
The map on that page suggests that they are all over Northern Europe... But if I ever saw such a spider, I could never again live in or visit that house and would need to have it burned to the ground and then salt spread all over the ground in the extended area so that nothing can ever grow or live there again. Not exaggerating.
I actually tried to contact the newspaper about this but haven't heard anything back so far. Hopefully, it was all completely fake and made up due to a shortage of "exciting" news, but if real, I'm not able to ever revisit that place (the town in general) out of fear of encountering further such spiders.
I'm having very serious trouble believing that people ever had these huge spiders "commonly" inside their living places, let alone these days. And I wonder what "common" means in the context; to me, it means that you regularly spot them on walls or walking across the street, etc. The Wikipedia article even mentions that they have started being spotted in some Eastern European countries in "the last few years", which is very bad news for me, and really makes me wonder what could possibly explain that.
I had to dig up the old scanner and scan the newspaper pages for this question:
Scan #1 (Swedish-language article with a photo): https://i.ibb.co/yy00H2b/1.jpg  (link broken)
Scan #2 (Swedish-language article, continued): https://i.ibb.co/DWfN3W1/2.jpg (link broken)
Scan #3 (Finnish-language article with the scariest photo): https://i.ibb.co/pW6gZMx/3.jpg (link broken)
I have not manipulated those photos in any way, but hopefully, the newspaper did... Maybe somebody wanted to show off their skills with Photoshop, the year being 2000? This is a place where I spent a lot of my childhood and we slept in all kinds of old houses there. I don't recall any monster spiders, but my skin starts crawling just thinking about the fact that I was sleeping quite near the area where the spiders were allegedly found... Although the exact street/address is frustratingly not mentioned in either article.
I almost get the feeling that this whole thing has been "hushed away" in order to not scare away tourists, rather than sensationalized. I would be very interested in hearing serious theories or even hard facts regarding this.

Re "hushing away", quite the contrary.  Promote a "Giant Spider Festival" to attract arachnophile tourists, as Scotland has done with Loch Ness.

@jamesqf I certainly hope that there are no arachnophiles...

Welcome to Biology.SE. Please take the [tour] and consult the [help] starting with [ask] for details on what is expected on this site and [edit] your post accordingly. In particular, please focus on a single biological question and eliminate the anti-spider ranting. You shouldn't expect a lot of sympathy for this irrational hatred here — spiders are an essential part of ecosystems and help control real pests like cockroaches (as well as being very interesting in their own right). I  suggest you find psychological help for your phobia (e.g. search for exposure therapy). Thanks!

@tyersome And I, in turn, suggest that you "find psychological help" for your insane love for these physical manifestations of pure evil.

@Dimitar: Alas, your hope is doomed to go unfulfilled, There's at least one web forum devoted to them: https://arachnoboards.com/  And while I'm not an actual arachnophile myself, I certainly like them for being the interesting and useful critters that they are.

I apologize if my comment came across as dismissive or insulting. As someone with more than my share of psychological issues, I have some understanding of how terrible a strong phobia can be. Unless you are massively exaggerating your feelings about spiders I imagine this must be a huge burden for you. My suggestion about looking into exposure therapy is not meant to belittle, but instead is done with the hope that you can find a way to make your life less stressful.

This is their size and demeanor (non-aggressive). And, yes, they are common and they tend to keep to themselves in their own spun funnel-webs: https://www.youtube.com/watch?v=Vy66QUsflKk

No and yes.
No - the articles are fear-mongering. I can see that without even being able to read a word of Suomi (Finnish) or Swedish.
In particular the Finnish article with the couple holding a picture of the spider. In this case the picture is a close-up picture of the spider that has then been expanded onto a largish photo (I would guess about 12 in/30 cm by 8 in/20 cm). In this picture you can see the texture of the cloth the spider is sitting on (seeing the texture would be unusual for a life-size photo) and a coin in the top left of the photo. I can't make out the coin denomination, but I doubt that they have a currency with approximately 8 cm (3 in) diameter coins - indeed the largest Finnish Makka was just over 3 cm (1.2 in), but this was only used between 1928 and 1939 (according to the linked Wikipedia page), so the coin is not likely to be that large. As you can see if you look at the photo, the diameter of the coin is about the length of the body, so at most the body will be about 1 inch, and the legs about twice that.
In the top-right of the same article is a photo that is much more realistic size - compared to the hand you can see that the body of the spider is about 1-finger width, so 1-2 cm or slightly less than 1 inch. If you then refer to the description part of the Wikipedia article you linked on the Giant House Spider (Eratigena atrica), you can see that the dimensions of the spider indicate body length of 18 mm (0.73 in) and a typical leg span of 45 mm (1.8 in) - so the hand picture is more realistic. They can have larger leg spans of up to 70 mm (3 in) apparently, but I have no idea how common this is.
However, the yes part is that: Yes, this type of spider does exist. They are widespread in Europe and parts of North America (introduced, but there are native Eratigena species in NA). They are mostly harmless and very unlikely to bite unless attacked. If they do bite, it will likely to only cause local pain with very little envenomation.
You are only likely to find them inside when it starts to get cold outside; as is the case for many animals, they try to find somewhere warm to live.
Note the spiders used in Arachnophobia were Avondale spiders (Delena cancerides) a harmless, but ugly looking, member of the Huntsman spider family, and a Tarantula species (I don't know which one, but there are quite a few species). Avondale spiders are from Australia and were introduced to Avondale in New Zealand, where they got their name, as they are apparently uncommon in Australia. Neither the Tarantula nor Avondale spiders are found natively in Europe.

After reading your answer, it makes perfect sense. I didn't even notice that the round thing in the corner was a coin, and indeed much larger than any coin used then (or now). It does indeed look like a scaled-up photo now. But even the "small" spider shown on the hand photo is still large enough to be quite horrible to me, although infinitely less so than the monster spider I imagined from that photo. I do feel a bit better now. Thanks (seriously).


text:
How can the recurrence risk ratio be calculated?
The recurrence risk ratio is calculated as follows:
$$ \lambda_s = \frac{\text{risk of sibling}}{\text{risk in population}}$$
where the risk of sibling refers to the risk that a sibling has to get the disease and the risk in population is the risk that the disease occurs in the population.
I do not understand how it is possible to calculate the numerator. I saw a video here that discusses how it's calculated for simple diseases that follow Mendel's laws. However, my lecturer was discussing this in the context of multifactorial traits.
How would we calculate the risk of the disease occurring in a sibling without simply forcing the parents to breed thousands of times?

If we look at web resources, what we will notice is that this ratio is not deployed at the family level but at the population level.
In other words, when we look at a population, we can ask:

What proportion of these people have the disease?

That is the denominator.
Taking that group of people, we can then ask:

Of those people that have the disease, what proportion of this affected group has a full sibling that also has the disease?

That is the numerator.
So if we have a population of 100 people, say 10 people have the disease. The denominator is then $0.1$. We might then observe that 4 of those cases are two pairs of siblings (and there are no other siblings). So
$$risk\ in\ sibling = Pr(sib\_has\_disease | person\_has\_disease) = \frac{4}{10} = 0.4$$
And thus
$$ \lambda_s = \frac{\text{risk of sibling}}{\text{risk in population}} \
= \frac{0.4}{0.1} = 4$$
It's worth pointing out that we are not controlling for environment or for pedigree or anything like that here. The null hypothesis of what $\lambda_s$ should be without any genetic risk is a complex function of prevalence and family structure (what if everyone is an only child, or the whole population is all siblings?). So it's not even clear how to interpret it, except to say that you might intuitively guess that a disease that strikes purely randomly might have $lambda_s = 1$. But I'm not even sure that that's true! All that this ratio is measuring is a rough estimate of how clustered the disease is within families within a population.


text:
Procedure of diagonal electrophoresis
I am learning protein sequencing and it seems that diagonal electrophoresis is a common method in the identification of disulphide bonds (S-S) exist between polypeptides in a protein.
Questions:

After horizontal electrophoresis, we need to cleave the S-S bond using performic acid. According to Wiki,

Its strong oxidizing properties are used for cleaving disulfide bonds in protein mapping.

However, from what I have learnt in SDS-PAGE, 2-mercaptoethanol OR dithiothreitol are commonly used for cleaving S-S bonds, may I ask why do we need to use formic acid specifically here?

the first electrophoresis is done horizontally and the second is done vertically (bottom to top). May I ask whether we can do it vertically then horizontally instead? It seems to me that it should be OK since there doesn't exist any disruption to the proteins but I would like to confirm.

Thank you.

You probably don’t need to oxidize the disulfide bonds rather than reduce them. Performic acid has the advantage that the oxidation products can’t spontaneously reform a disulfide bond whereas the reduction products from a thiolate reductant can. This may not be a significant issue in the actual application. Oxidation by performic acid also causes a significant mass change for the cysteine residues which can be useful for downstream mass spec. These oxidation products are also negatively charged which can increase mobility in PAGE and possibly aid separation.

@canadianer thanks for pointing out my mistake :) So can I say: performic acid oxidize the sulfur in cysteine residue, forming cystenic acid i.e. disulphide bond is cleaved. Moreover, this is the cause of 'significant mass change' (-SH --> -SOOH), which can be utilized by MS for easy determination of S-S bond (where B-ME and DTT cannot achieve this)? Thanks

ref: https://www.researchgate.net/profile/Tanea-Reed/publication/51828850/figure/fig11/AS:668669944279047@1536434746552/Cysteine-oxidation-at-neutral-pH-Cysteine-plays-an-important-role-in-the-regulation-of.png

This article states that complete oxidation of the cystine to cysteic acid occurs (SO3-), which is a molecular mass change of 48 u. With BME or DTT reduction, you are left with a thiol or thiolate.

Now I understand thank you very much

You’re welcome.

You probably don’t need to oxidize the disulfide bonds rather than reduce them. Performic acid has some potential advantages:

The oxidation products can’t spontaneously reform a disulfide bond whereas the reduction products from a thiolate reductant can.
Oxidation by performic acid causes a significant mass change for the cysteine residues which can be useful for downstream mass spec. This article states that complete oxidation of the cystine to cysteic acid occurs (-SO3-), which is a molecular mass change of 48 u. With BME or DTT reduction, you are left with a thiol or thiolate.
These oxidation products are also negatively charged which can increase mobility in PAGE and possibly aid separation.


text:
How do obligate carnivores not have nutrient deficiencies?
I know that if a human eats just meat without plants, they develop issues like scurvy. If my understanding of it is correct that there are nutrients not found in meat, then how do obligate carnivores not suffer from certain nutrient deficiencies?

To add to Bryans answer there are a few other issues.
mainly pickiness and brains.
Human can handle an all animal diet surprisingly well, look at the modern Mongolian nomad diet, which is exclusively animal based. One problem we see in modern humans in industrialized nations is they often avoid eating organ meats, eating only muscle tissue "meat" can easily lead to a nutrient deficiencies. Ask yourself when is the last time you sat down to a liver or kidney dinner. many vitamins are almost exclusively found in organ meats and not muscle tissue. So many times when people from first world countries end up on an all meat diet they end up with deficiencies because they are not eating the vitamin rich portions of the animal.
The other problem is humans have very big brains, and brains can't burn fat. They can only burn carbohydrates or protein. you may already see the problem, animal tissue is rather poor in carbohydrates. But, you say, they have lots of protein,  which is true, but humans along with many animals do not metabolize proteins well, doing so on a large scale leads to ketone and other toxic byproducts. Human brains demand so many calories that they burn thorough what little carbohydrates animal tissue have, very quickly forcing ketosis. So humans must burn far more protein than most other animals on a all animal diet even when lipids are available because carbohydrates are lacking.
Carnivores also have adaptations to better deal with ketones, they still produce a lot of ketones but have better methods for managing them, mostly better ways to excrete them. Most apes only eat small amounts of meat and rarely lack carbohydrates in their diet, have not needed this adaptation. This is true for most of human history and the exceptions are very noticeable. The Mongolians I mentioned earlier also eat a lot of milk and cheese which contain a decent amount of carbohydrates.

Humans are pretty unusual in their inability to synthesize vitamin C (in humans, scurvy is caused not just by a lack of dietary vitamin C but the important factor that we can't simply make our own).
Wikipedia lists just a few mammals as examples of those unable to synthesize vitamin C: simians, tarsiers, capybara, and guinea pig. None are obligate carnivores.
Humans, like the others on this list, have a gene for the L-gulonolactone oxidase necessary in the synthesis pathway for vitamin C, but it's non functional. It seems that either losing function of this gene provided some evolutionary benefit (without a cost if diet was a sufficient source at the time), or it simply didn't provide any benefit and so there was insufficient selective pressure for it to remain functional.


text:
I found this bug on my washer please help identify it
The bug was a light brown
It had like 4 legs and two antennas

Welcome to Biology.SE! For identification questions please [edit] your post to include the location (e.g. country and region — the more specific the better) where you observed this creature. The location can be an essential clue for identifications. ——— If possible clear, closeup photos of the creature from multiple angles would also be helpful. ——— Please see the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site as well as clicking on the species-identification tag for details. Thanks!

I live in northwestern Pennsylvania and I only got on picture but haven’t seen any more of them and oh boy I have been looking


text:
Virus lineage, strain, and relation to spike protein variants
On the CDC website we have virus lineage which appears to be constant for all cases presented, or am I reading that wrong? Then the different names and of those with different names, different spike proteins can be associated. Then in these two papers authors use the word strain and describe as so:
paper a)
SARS-CoV-2/human/Liverpool/REMRQ0001/2020
where they mention that they also test the D614G variant of the spike
paper b)
BetaCov/human/CHN/Beijing_IME-BJ05/2020
BetaCoV/Wuhan/IVDC-HB-01/2020|EPI_ISL_402119
How do I use the species information to determine what spike variants were used in the studies?

You can trace the first one back to the original paper. In general though, if you want to check specific sequences, look for the Genbank numbers, have a look on VIPRBRC and/or get a GISAID login (I think you need affiliation with a recognized organisation for this one). GISAID generally has the most sequences, but I'm too lazy to dig out my login and tell you if these ones are deposited. That being said that last one certainly is as the EPI_ISL # is GISAID format

Thank you, bob1. I am wondering whether the discrepancy in the results between paper a and paper b could be attributed to a variance in the spike protein, that's why I'm looking into this. Also, if this not out to not be the reason for the discrepancy, would the use of the pseudovirus in paper b potentially provide an explanation?

It is possible that it is the variant. For the last part, you should post it  as another question.


text:
Is there a resource that lists the quantity of active transposons for various species?
I read the thesis that transposons are a major factor in human aging. To study that thesis I want to see how the count of active transposons differs by species. Is there an existing database or study that lists active transposon count by species?

https://mobilednajournal.biomedcentral.com/articles/10.1186/s13100-019-0150-y

RepetDB (linked by Maximilian) and Dfam are both good databases for TE sequences and lineages, though I think determining which are active is a harder question, especially since TEs are highly polymorphic within a population.  A great place to start would be this recent review of eukaryotic transposable elements; see Fig 3, in particular, for a wonderful graphic giving the distribution and genome percentage of different TE classes across eukaryotes.

Also be aware that the 'density' of transposons can vary hugely within a species — one example is in maize, where high latitude cultivars are selected for smaller genome sizes (to allow shorter generation times) and consequently have fewer transposons.


text:
What is meant by “unique ligand” on the RCSB Protein Data Bank website?
I went to the https://www.rcsb.org/ site, and searched for some proteins. For each entry, “unique ligands” are listed.
I understand a ligand is a molecule or ion that binds to a metal atom. I don’t understand what a unique ligand is. Why is this important? What can we do with this information?

It is usually helpful to search the documentation of the site in question: https://www.rcsb.org/docs/general-help/identifiers-in-pdb (section "Small molecule Instance ID"). If the documentation doesn't answer your question, then you can post here and explain what is still confusing. Ideally, you would get in touch with the administrators of the database in question to ask about their database-specific terminology. (This term is only for their database, it is not a biological concept.)

@Maximilian Press , it doesnt mention "unique" ligand. I thought it was a biological concept hence my post.

"Small molecules such as ligands, ions, drugs, inhibitors, and individual residues (amino acids, nucleotides etc.) are found in PDB structures... For example, all ligands, water molecules, etc. nearest protein chain A will also be assigned to chain A, though each of these small molecules will have unique residue numbers. So all ligands, waters etc. near a protein with chain ID A will be assigned the same chain ID. However, each of these small molecules and ligands can be specifically located by using unique residue numbers.

Your understanding is incorrect. A ligand at its most basic is a molecule that binds to another molecule. There is no requirement for metal atoms whatsoever. In the context of RCSB (home of the Protein Data Bank) we are only concerned with ligands that bind to macromolecules, the structures of which are presented there — usually proteins. The following definition is in the Glossary on the RCSB site.

ligand - A molecule that binds specifically to another molecule (usually a protein or nucleic acid) to form a complex. A ligand can be another protein, but is often a small molecule.

I’ll assume a protein here.
Original Answer
Unfortunately that Glossary doesn’t explain their usage of “unique” in this context, perhaps because it may be a recent modification. However what it would appear to me to be is an aid to distinguishing those molecules that bind in a biologically significant manner to a protein, from those molecules — metal ions and molecules like glycerol — that only bind to the protein because they are present at a high concentration in the crystallization or other preparation medium. Such molecules are likely to be present in more than one copy, i.e. not unique.
Why not just say “biological ligand” rather than “unique ligand”? The fact that only a single molecule is present doesn’t prove it is biologically significant, and this information would seem generally to be absent from submission information (in my experience). The job of the curators of PDB is to describe rather than interpret.
Edit: 17 June 2021
After inspecting several entries it became evident that my original interpretation of “unique ligand” as “individual ligand” (with a suggestion of biological relevance is incorrect. There are examples of non-biological molecules, molecules present several times, and molecules occurring in different numbers in different identical subunits all listed as “unique ligands” (@canadianer also commented on this.) The bromide ions in protein 2RC3.pdb provides an example.
I wrote to support at RCSB Protein Data Bank and I would summarize the situation as:

Any non-polymer, non-water molecule in the structure is designated in
the RCSB interface (but not in the mmCIF data format) as a “unique
ligand”.

The support at RCSB tacitly acknowledged the unsatisfactory nature of this and stated in their reply that “We will re-visit the use of this term.”.
As the reply was from support, I feel that it is reasonable to quote from it, but thought it better to exclude the name of the actual contact.
In short, “unique ligand” means: each of the distinct small molecule entities present in the PDB entry (i.e. a “non-polymer entity” in mmCIF nomenclature).
The word “unique” is our attempt to describe what an entity means in a brief way.  We will re-visit the use of this term.
Please note that the data is very well described in mmCIF format (https://mmcif.wwpdb.org/; https://mmcif.wwpdb.org/dictionaries/mmcif_pdbx_v50.dic/Items/_entity.id.html).
For example, here is an excerpt of the mmCIF file for the 2RC3 entry:
_entity.id
_entity.type
_entity.src_method
_entity.pdbx_description
_entity.formula_weight
_entity.pdbx_number_of_molecules
_entity.pdbx_ec
_entity.pdbx_mutation
_entity.pdbx_fragment
_entity.details
1 polymer     man 'CBS domain'                      15169.631 4   ? ? ? ?
2 non-polymer syn 'BROMIDE ION'                     79.904    39  ? ? ? ?
3 non-polymer syn NICOTINAMIDE-ADENINE-DINUCLEOTIDE 663.425   4   ? ? ? ?
4 water       nat water                             18.015    710 ? ? ? ?
Lines 12 and 13 correspond to the 2 “unique ligands” shown on the structure summary page.

and then is a second message:
To clarify, entity is a chemically distinct part of an mmCIF entry.
For example, looking at entry 4hhb (https://www.rcsb.org/structure/4HHB), there are 2 "unique" protein chains OR 2 protein entities.  There are 2 copies of the alpha subunit (chains A and C; one entity) and 2 copies of the beta subunit (chains B and D; a second entity).

thank you so much for your explanation David. I have been searching everywhere since this post, read so much about ligands . but unique ligands yielded no results.

You are welcome. "Unique ligands" is not a set phrase, which is why you didn't find it — the PDB was just using "unique" as an adjective. Some years ago I looked through the PDB entries for 400 proteins to find ligands and had a terrible job finding which were "real" in the biological sense. Often you have to go to the original paper, and even then it may not be clear.

Any chance you can also explain what a unique branched monosaccharide is refering to? That yields no search results either :(

@HarshDua Again it sounds merely as if it is being used as a descriptive adjective. You need to provide context. Write a separate question, quoting the sentence in which it occurs, the source (name of the book or web link) and what you think it might mean. Then you will have played by the rules and I or someone else will surely be able to provide an answer.

But non-biologically significant “ligands” like glycerol are still listed in RCSB as unique ligands. I think unique ligands in this context is a list of all the small molecules that appear in the structure, but does not include multiple entries for multiple occurrences of the same molecule. This applies to both molecules that have a biological interaction with the protein and molecules which interact only as a result of the experiment.

@canadianer You are right that the situation is not as simple as I stated. Earlier today I was working on the PDB site and took a random protein with two “unique ligands” to post as an example. But… So I have contacted their support for clarification and will update my post when I hear back from them.

I have now (17.06.21) posted an edit to my original answer following correspondence with RCSB.


text:
How to estimate the scientific consensus or not about Hydroxychloroquine?
In several (political) discussions, I have been told that there are around 200 papers stating that the Hydroxychloroquine is successful in treating COVID-19...

Is this statement true?
How can we estimate coldly and reasonably the absence or not of scientific consensus about Hydroxychloroquine regarding COVID-19?

I'm not able to judge: I am not a virologist myself. But I have a modest statistical background that made me have extreme doubts about the behaviour of Dr Raoult: Answers to my statistical question in April 2020 https://stats.stackexchange.com/q/459501/2910 highlight those doubts.
Looking back in time, there are things that does not help the seriousness of RAOULT statements:
During January February and early March 2020;

in those times Dr. Raoult was mocking Coronavirus repeatedly , saying pandemics only exists in video games (I'm gonna a add a link to this one, it's just mind-blowing to see his carelessness)
Dr. Raoult was also joyfully repeating that Dr FAUCI was senile.

But:

there may be personal conflicts between FAUCI and RAOULT
there may be pharmaceutical conflicting interests. That already happened in the past in other economical fields... Yes that can exist sometimes, so that remains possible. In France, the Raoultmania and friends transforms this argument into: "Big Pharma" wants to bring down Dr. Raoult at all costs, he is the best virologist in the world, he is "the only one" real specialist.

So what to say to people saying that there are 200 scientific papers concluding that Hydroxychloroquine is effective: maybe there's a possibility to know how many papers are stating the contrary?
Any pointer is welcome. Even in my family it has sometimes become a political drama. I would like facts, or factual trends, or constructive conclusions based on clearly stated hypothesis.
I don't know where to start and it is important for me. And I clearly don't want to fall in the opinion-based trap.

As it is important for me, I'd really appreciate downvoter(s) to guide me on how to gather more scientific facts about my question, or how to refocus it. Any comment appreciated.

I don't speak for the downvoter(s), but your question (at least as currently written) seems to be off-topic for this site. Most of your post is about politics and the core of your question seems to be how to evaluate whether there is a scientific consensus about this subject. Unfortunately I don't see how that can be answered in a way that depends on facts rather than opinions — this contradicts one of the criteria for good questions mentioned in the [help], see for example [ask]. This is also more of a medical question rather than a biology question.

I think Skeptics.SE cover questions of "how much support is there really for this in the scientific literature".

This question is off-topic in my opinion in that it is not a question about biology or even medicine (that would be "is hydroxychoroquinine effective against covid?") but about reaching decisions and arguing with others. Both of these are in the realms of sociology and psychology. In life we all make decisions on incomplete data. I trust the scientific and medical institutions in advanced Western societies (Britain, the US, W. Europe) and so if they haven't rejected this I trust there is a good reason for it. I don't need to read 200 papers to make my decisions in life. cont.

cont. If you haven't come to the same conclusion of me I might have a low opinion of your decision making, but I need to ask myself why. What social influences have prevented you coming to what I consider the obvious conclusion. I am not going to argue with you because I realize it is a waste of time. Likewise, should you decide that hydroxychloroquine is snake oil, I don't reckon much for your chances of convincing your family unless they regard you as some sort of a guru on the subject.

Hardly, the question that's been asked seems to be entirely about plain fact.

@A.B. I understand your point of view about forwarding to Skeptics. However I doubt I might access the reading span of virologists. I have tried on Reddit but they don't take plain text question/statement on Covid subreddits that I know about.

If you don't have the time or inclination to develop the skills to evaluate scientific papers on your own, you pretty much have to take other peoples' word for it.  Even if you are not knowledgeable in a field, you can evaluate things like experimental design, data analysis, consideration of possible alternative explanations, etc. The infamous Turkish study involving measuring blood oxygenation before and after performing a surgery (with masks on) should certainly provide examples of poor experimental design.

@Armand But you can at least try to use your judgment about whose word you take for it - as the OP did by coming here.  Better to take the word of someone who's studied biology, and how to evaluate papers, than of a random person in a political argument.  (Good point that a lot of the most basic ways of evaluating a paper apply to lots of fields.  As bob1's answer says, one very important one to know in anything medical is sample size.)

Oh, and if the OP (or anyone else) is interested in learning more about why not all published scientific studies should be believed and how to recognise good ones, I recommend a recent book called "Science Fictions" by Stuart Ritchie.  Crammed with information and really entertaining - and unnerving, in places.

Not sure why this is getting upvoted. Whilst interesting, it's clearly offtopic as Tyersome and David have pointed out.

Skeptics.SE has been mentioned; note that there are already several questions there on this topic. This answer might be the most relevant.

Sientific debates are no deifferent than thsoe in real life or politics: there are may be people believing one side or the other, and on some occasions the debate may be distorted by the political and financial considerations involved. The level of the debates is however very different, and the debated points are much finer - I would not be surprized, if Mrs. Fauci and Raoult agree about the positive and negative sides of Hydroxichloriquine a lot more than their supporters/detractors. contd.

cont. It is instructive to read the recent tribune by a group of renowned scientists regarding the need for deeper investigation of the origins of Covid pandemics, to understand how it differs from peedling conspiracy theories: https://science.sciencemag.org/content/372/6543/694.1

Is "how does one assess the reliability of biology papers" really off-topic?  I'd have thought that bob1's answer would be very useful for a lot of other visitors.

@David Does the thoroughness of the answered question change your point of view? Would you have been able to reach such an explanation? I would not have been able to formulate such response. In your comment, to siplify, you say you trust medics etc... The huge problem here is that the Hydroxychloroquine debate has been thrown in the public debate during election campaign in France. And just like in the US with Fox News and Trump, there is a lot of Raoultmania on the right and far right. And that pleases a lot the inner "egomania" of Dr Raoult: it is a choice from him to move the debate there.

@David this is the reason why I asked for a clear, un-opinionated description of how to evaluate scientific consensus (so as to have trust in Science like you do), and how to reach a conclusion based on that. You have to understand that Raoult and friends propaganda says to people "look at all the science that says our treatment works, just look" - the same technique used by Trump during his Ukraine affairs, telling supporters "read the transcript", knowing nobody in the right-wing will read the transcript for real. That's the same technique. And it's not by chance they use the same technique.

@David you have to remember that Trump world-widely promoted Dr Raoult's treatment a few hours after the paper was released. 24h IIRC. I would be surprised if Trump was a daily reader of scientific papers.

This site deals with specific problems in biology. One such problem related to your concern might be "Is Hydroxychloroquine an effective treatment for Covid 19?", although I would think it more appropriate for SE Medical Sciences. But your question is really about the philosophy of science or of life — How do we distinguish between what is true and what is false, as individuals, as scientists — and hence is not on topic here. And of course, human judgement involves a heuristic approach, which doesn't always produce the right answer. There is no perfect approach, but there are sane ones.

@David thanks for your answer. Unless I did not pay enough attention, it is too bad you or someone-else did not ention SE Medical Sciences before. I was touchy about skeptics SE but your suggestion is right on spot. I share your point of view that it would have been much better there. I'd correct you on one point though: my question is about Virology, and how to estimate how/if a consensus is reached in Virology (Dr. Raoult says he is the best virologist in the world). I've suscribed to SE Medical Sciences, and if ever I have topics that are more appropriate there, I'd follow your indication.

The difficulty here is that these sorts of questions are hard to understand for non-scientists and the results difficult to interpret for non-scientists.
This will be long, and I will likely miss things while writing this, so anyone please feel free to weigh in and/or edit if you feel the need.
First some background about treatments and how we (scientists and medics) know they work or don't work:
In general for a drug to be assessed for its efficacy it needs to undergo something known as a clinical trial. These are studies that involve proper experimental design and have at least one testable hypothesis with results that can be interpreted statistically. Proper experimental design for these sorts of things is difficult and aims to ensure that any there are no biases in the data that may invalidate the results!
First off the trial should be controlled in some manner. Control in this context means a comparison group who receive something other than the treatment in question. This might be that the patients receive a different drug (of known efficacy or not) or a placebo. You can even compare different doses of a known efficacious drug (say you know it works a dose X, but you want to see if it works at 10-times that dose). You can also compare things like surgery with no surgery - sometimes by doing mock surgery as a placebo.
The treatment also has to be tested in a randomized manner (assigned to some participants on a random basis), you also need to make sure that neither the participants nor the people giving the drugs know which people are receiving the placebo and which the real drug(s) until after the results are in and have been fully analysed. This is a process known as blinding. There are quite a few different sorts of blinding. The one I described above is called double-blinding.
If you put all these things together you have what is known as a controlled randomized double-blinded study. These are often considered the most effective at determining the efficacy of treatments. Not all trials will meet these conditions - for example it would be very hard to double-blind a surgical trial as it would be hard to blind a surgeon as to whether they have done real surgery or not.
Next, clinical trials should also ideally involve lots of random participants from random populations so as to not introduce bias(es) (for example: don't sample just a few patients from your local hospital when you live in a high-wealth area and assume that your results are able to be generalized to the whole population). This means you should sample young, old, rich, poor, body types etc). There are a few exceptions to this rule - perhaps you want to examine the effect of a particular treatment on obesity (so you need obese people to start with) or perhaps a particular age-group, but that can be part of your experimental design so is less of a problem, but you still need to sample randomly within that group
However,in addition to all of the above, there are a few more conditions that should be met:
The next rule is that you need to sample large numbers of people - often in the several thousands. Smaller sample sizes may have larger (relative) biases (e.g. maybe, just by accident, 50% of the 60 patients in your trial were from a single family with a genetic mutation who all caught the bacterial infection you are studying at a family gathering - which could bias your results towards how that genetic mutation affects your treatment). Another issue is that small samples may not have enough statistical power to show minor effects. Proper experimental design will have determined the statistical power needed and how large the minimum sample size should be before the study is conducted. Large sample sizes also allow you to look at different groups within the study during analysis - perhaps your drug isn't effective in the population as a whole, but it is in those over age 70, or those with kidney disease or a missing left leg (very unlikely - but you wouldn't see this last unless you had a large enough sample size!).
A clinical trial should also be registered with a clinical trial register (e.g. The USA one) with open methodolgy and aims etc. outlined. As I write this, there are 5874 clinical trials on COVID-19 registered on the Clinicaltrials.gov website from all sorts of places around the world and looking at things from known treatments (e.g. remdesivir) to wearable smart devices.
Another requirement is that the results are reported in the literature (we are getting closer to your question here...). If they are a well designed study that meets all the above criteria and show a result of interest to the medical community, then it should have no problem with peer-review (where experts working in the field examine all aspects of the trial before the results get published) and will likely get published in a well established  and respected scientific or medical journal.
Thanks to @BenBolker for the following idea and paper:
To show you just how hard all of this is, there's a review paper in the British Medical Journal (BMJ, one of the top-ranked medical journals) with the title Drug treatments for covid-19: living systematic review and network meta-analysis. Link to article: here. What this paper aims to do is to look at many of the drug treatments for SARS-CoV-2 infection and aggregate data from all the published trials from the start of the pandemic through to February 2021. The abstract provides a summary of the data starting out with inclusion:

196 trials enrolling 76 767 patients were included; 111 (56.6%) trials and 35 098 (45.72%) patients are new from the previous iteration; 113 (57.7%) trials evaluating treatments with at least 100 patients or 20 events met the threshold for inclusion in the analyses.

This means out of the ~200 studies, just over half met the criteria of significance (for this analysis) - they excluded vaccination, nutrition, antibody-based therapies, supportive therapy and traditional therapies that included more than 1 active molecule.
As further evidence of how hard it is:
Figure 1 from the BMJ paper shows the triage process for the articles they looked at. It shows that they started out scanning 31,752 articles on COVID-19 and trimmed that down to 632 randomized trials, which were then examined closer and found that 343 of these weren't actually randomized or were excluded for other methodological problems, leaving 289 trials. These were then pruned to 206 for a bunch of reasons (duplicates, pre-print (so not verified), corrections, retractions etc.) leaving 196. A further 83 were excluded for not meeting criteria on size, lack of data, no outcomes reported or same-drug comparison (not controlled properly). Leaving 113 in total.
So if you take the 632 trials and are left with 113... that's only about 17%: less than 1 in 5 get it right!
Now, this is where it gets murky! What is a "good" journal? Well, that's a tale for another day, but there are many "scientific" journals that are neither scientific nor good. Many of them are listed on Beall's list, which is a list of publishers and journals known or suspected of being "pay for display" - essentially pay them money and they will publish your paper without doing the proper peer-review process, which science uses to determine if a study meets scientific standards and rejects those that don't.
Unfortunately, proper peer-review takes time - the journal gets a paper submitted to them. An editor reads and then rejects or sends out for peer-review. The reviewers then read the paper, write a report suggesting problems, fixes, questions etc - these then get communicated to the editor, who either rejects the paper or sends it back to the authors for amendments (may be needs more experiments, more statistics etc). The authors fix and then re-submit to the editor, who again reads and sees if the review has been addressed. The paper may then be sent out to the reviewers again, rejected (if concerns not addressed) or published. Generally this takes between 3 and 12 months.
With the current pandemic there has been a problem with this system of peer-review. Because of the urgency of the pandemic and the strain on resources, people have been submitting papers to journals for peer-review and posting them on "pre-print" servers (not peer-reviewed), where they are read and used, based on the information presented. Many journals also suspended peer-review because of the need to get information, especially about therapeutics, out to their audiences as quickly as possible. This resulted in some of the checks-and-balances that normally go on in the scientific field to be suspended and papers published that would not normally have passed peer-review.
We are now finally at the point where I can discuss Hydroxychloroquine (HCQ):
Hydroxychloroquine has been around for a long time and touted as a potential therapeutic for a number of diseases. It works well for rheumatoid arthritis, systemic lupus erythrematosis and as an anti-malaria drug. However, it has never been shown to be an antiviral in any form outside of the laboratory.
Initially reports of HCQ as a treatment for COVID came out in May 2020 (e.g. this British Medical Journal paper (an excellent journal). These were small trials which were some times randomized and generally non-blinded (AKA open-label), and showed variable effects. 6 out of 8 papers mentioned in the FDA revocation of emergency use for HCQ letter (see Table 1 on page 5. PDF!) show no effect, while 2 do, with the largest in terms of numbers of people (the BMJ one linked above) showing no effect. The ones that do show an effect are very small sample size
Based on the evidence presented in some of these studies and (I think, can't find publications) some laboratory data indicating that HCQ might be effective against SARS-CoV-2, the FDA issued an emergency use authorization (I also don't know if there was some political interference in this). At the same time the University of Oxford (UK) started recruiting for a large clinical trial of HCQ. This trial is known as the RECOVERY trial and is not just for HCQ, but a bunch of other drugs too. Currently they have recruited nearly 40,000 patients for their trials across multiple countries.
The results from the RECOVERY trial into HCQ were released in June 2020 (this is very very quick for a clinical trial, but then massive numbers of patients) with 11,000 patients tested in a randomized, controlled, double-blinded manner. The results were then published in New England Journal of Medicine (another excellent journal) and showed no effect of HCQ on any of the metrics recorded. Since then other trials, mostly smaller ones (~1000 patients) have been run by a bunch of people, none of which (to my knowledge) have found any effect of HCQ on SARS-CoV-2 infection.
Taken together, but heavily weighted towards the results of the RECOVERY trial, the data indicate that HCQ is not effective at all against SARS-CoV-2.
Edited to add: @Chris has commented with a link to a site that aims to look into the science behind medicine and some of the claims made around therapeutics and make it available for the layman. The link for hydroxychloroquine is here

You are right (as far as I followed this up): There is no proper trial (number of patients, controls etc.) which has found an effect of HCQ. Only the very early, methodically heavily flawed "studies" saw small effects. This should have been a massive warning sign on its own.

Wish I could upvote this twice!  It sounds as if the answer to the "200 papers" thing is that if there really were 200 papers in favour of HCQ, they were rubbish ones.  All scientific papers are not created equal and, sadly, there are a lot of rubbish ones about - just because something is stated in a "published paper" does not by itself mean it's reliable.

https://www.bmj.com/content/370/bmj.m2980 ("Drug treatments for covid-19: living systematic review and network meta-analysis") is a very good reference. Someone who felt like it could build an answer based on that resource ...

@BenBolker thanks. I've edited that in with some explanation about difficulty of doing trials correctly.

To add to your answer: The blog "Science based medicine" has a number of articles on this topic: https://sciencebasedmedicine.org/?s=hydroxychloroquine&category_name=&submit=Search

@Chris thanks for the link, that is a wonderful site, I am sure I will spend many an hour there shaking my head at the lack of science behind so much of the disinformation going around. I'll edit the link into my post.

@bob1 You will need time :-) And they have a lot of good articles on other topics as well.


text:
Does a vaccine reduce the contagion "efficiency"?
Note: I am specifically interested in the question in the context of COVID, but general information is welcome as well.
If someone vaccinated still catches the COVID, is their capacity to infect others smaller, the same, or higher compared to someone not vaccinated?
In other words, is there a relationship between the "efficiency" of infecting others and the fact that someone was vaccinated (but still got infected)?

Each individual case will be different, but in general it is useful to ask "why did the vaccinated person still catch the Covid disease?"
If they caught the disease because the vaccine had essentially no effect on them (for example, some immunocomprimised individuals who cannot generate an appropriate immune response), then they are likely to be at least as contagious as an unvaccinated individual. In fact, they may carry a higher viral load and be more infectious because of their underlying impaired immune response.
It's clear now that those who are vaccinated and successfully develop a targeted immune response against the covid virus (almost everyone for the two current mRNA vaccines), tend to have lower viral loads even if they are infected with the covid virus. This is presumably the reason why the incidence and severity of Covid disease is dramatically lower among vaccinees. The lower viral loads do indeed lessen the chance of infecting others with the covid virus, but do not completely eliminate it.

Thank you. What exactly does "virus load" mean? Is it an absolute number of the "amount of viruses" - that is there are fewer individual viruses, which all keep the same capacities of infection (so the lowered contagion is because of fewer viruses, and there are statistically less chances to get in contact with one), OR are the viruses "weakened" (possibly being as numerous as in a normal infection), so the lowered contagion would be because even if they get to the target, they are not as "powerful" as normally? (sorry for the non-technical terms)

@WoJ Your first answer is right -- virus load just means the number of virions (mature, infectious virus particles).  With the immune system responding well, fewer cells get infected, leading to lesser disease symptoms and also to reduced production of new virus particles.


text:
Is it possible for someone to be of no race?
I apologize if this is not the right forum to ask this question, but I don't know of any better forum to ask it. It is certainly possible for someone to have no religion, but is it possible to be of no race? That is, do "a-racial" people exist?

Race as we think about it today is entirely a social construct, developed to support and validate European colonialists' ideas and actions, and which has supported the very real experiences of race and racism to this day. The American Association of Physical Anthropologists' statement on Race and Racism, specifically the executive summary, puts it very well:

Race does not provide an accurate representation of human biological
variation. It was never accurate in the past, and it remains
inaccurate when referencing contemporary human populations. Humans are
not divided biologically into distinct continental types or racial
genetic clusters. Instead, the Western concept of race must be
understood as a classification system that emerged from, and in
support of, European colonialism, oppression, and discrimination. It
thus does not have its roots in biological reality, but in policies of
discrimination. Because of that, over the last five centuries, race
has become a social reality that structures societies and how we
experience the world. In this regard, race is real, as is racism, and
both have real biological consequences.
Humans share the vast majority (99.9%) of our DNA in common.
Individuals nevertheless exhibit substantial genetic and phenotypic
variability. Genome/environment interactions, local and regional
biological changes through time, and genetic exchange among
populations have produced the biological diversity we see in humans
today. Notably, variants are not distributed across our species in a
manner that maps clearly onto socially-recognized racial groups. This
is true even for aspects of human variation that we frequently
emphasize in discussions of race, such as facial features, skin color
and hair type. No group of people is, or ever has been, biologically
homogeneous or “pure.” Furthermore, human populations are not — and
never have been — biologically discrete, truly isolated, or fixed.
While race does not accurately represent the patterns of human
biological diversity, an abundance of scientific research demonstrates
that racism, prejudice against someone because of their race and a
belief in the inherent superiority and inferiority of different racial
groups, affects our biology, health, and well-being. This means that
race, while not a scientifically accurate biological concept, can have
important biological consequences because of the effects of racism.
The belief in races as a natural aspect of human biology and the
institutional and structural inequities (racism) that have emerged in
tandem with such beliefs in European colonial contexts are among the most
damaging elements in human societies.

Race, as a social construct and means for prejudice and oppression, is very real. However, biologically speaking, there is no such thing as race.

Race is partially a man made concept. The only scientific base for this term is genetic similarities among people of some race but they are just a result of very remote family relations. So the "a-racial" person and all his remote family members will be considered as part of one race until you reach other remote family members who are considered as part of another race.

This is a reasonable answer, but it is encouraged to provide sources or illustrative evidence.

I would instead write that race is a wholly man-made concept, given the lack of any scientific definition for a given race.

We can scientifically determine if someone is of African(sub-saharan African) origin or European(white) so we can't say it is wholly man-made. Saying that the idea of race was made up by European colonialists to validate their actions is just wrong and actually sound overly politically correct. The man-made part is how many people tend to define race by physical appearance alone, especially when it comes to skin color.

All concepts are made up by humans. The idea that colonists used race to justify their attitudes is not wrong historically, but it is irrelevant when we discuss biology. What matters is that the term race is so overloaded and compromised, that every time biologists discuss anything related,  they prefer to use less confusing terms, like genetic profile. Thus the questions that refer to just race sound either vague or provocative, at least in the West.

@Eleanor the problem is, we can't "scientifically determine" if someone is sub-Saharan African, for example. There is no one gene variant that is shared among all Africans. From my answer: "variants are not distributed across our species in a manner that maps clearly onto socially-recognized racial groups." "Dark skin" is not a clear phenotype, because not all sub-Saharan Africans have dark skin, and you can find quite dark skin in many other places on Earth. And where do you draw the line between light and dark? Race as a biological concept just doesn't make sense.

@MattDMo you say that there are no detectable genetic similarities among sub-saharan africans and other races?. There are many studies that tested the dna of old human remains and managed to find their origins/race. I don't think anyone consider all people with dark skin as one race and there are obvious differences in appearance between black Africans and non-African people with black skin.

@MattDMo I don’t disagree with your overall point but your statement is basically incorrect - it certainly is possible to tell whether someone is from sub-Saharan Africa just by genetics and with a very high degree of accuracy.


text:
Question about the use of Var. in different species
I just recently started studying Taxonomy and seem that I am the only one that got such question in the Internet...so pardon if this is a silly question...and my silly grammar because it is not my first language.
After genus we have species, sometimes subspecies and variety. For example, the Full Red Albino Guppy breed is named Poecilia reticulata var. "Full Red Albino" because it is one of the variety of guppies. But I was soon confused when it comes to succulents and dogs/cats.

Echeveria elegans 'Alba' is one of the variety of Encheveria elegans, why it is named so with the '' marks instead of Echeveria elegans var. "Alba"?
Dalmatians/Maine Coon are a breed of dog/cat under Canis familiaris/Felis catus, so they are actually varieties of the subspecies/species but I never see anyone naming them as Canis lupus familiaris var. "Dalmatian"/Felis catus var. "Maine Coon"?

I know there is no point of naming them so but I am just curious about if this is scientifically correct or I got the wrong concept. Thanks for reading till here.


text:
What is the point of calculating extinction coefficients of a protein without Cys residues?
ProtParam computes various physico-chemical properties that can be deduced from a protein sequence. One of these parameters are "Extinction coefficients". They provide two values. One value considers that all pairs of Cys residues form cystines. The other considers they are reduced.
What is the point of giving two values? Is it to provide the upper and lower bounds?

Cystine absorbs 280 nm light due to the disulfide bond (ε = 125 M-1cm-1) whereas cysteine does not (appreciably). Thus the extinction coefficient of a protein as a whole depends on the redox state of its cysteine residues. Cysteine residues in a protein may or may not form a disulfide bond and the sequence alone does not contain that information.
You can read about this in the ProtParam documentation.


text:
How are gene and DNA linked in this file?
So I am preparing some documents about Sar-Cov2 and I wanted to illustrate the "definition" of the virus with the DNA sequence. I found this sequence in GenBank.
Now I think I need  an explanation about what this sequence described exatly. From y research, I understood:

The first part of the text listed genes that had been identified in Sar-Cov2. Each gene would be responsible of a "feature" of the Sars-Cov2.
The second part, named "Origin" in the text, is the complete DNA sequence of the virus.

Now my question is: how is one gene from the first linked to the second part? Is there some sort of "stamp" that allows to say: "gene X starts at fifth letter in DNA sequence and ends at tenth"?
If yes, is the information in the text from GenBank (link above)?
Example of the pieces of the file:
First part
FEATURES             Location/Qualifiers
     source          1..29903
                     /organism="Severe acute respiratory syndrome coronavirus
                     2"
                     /mol_type="genomic RNA"
                     /isolate="Wuhan-Hu-1"
                     /host="Homo sapiens"
                     /db_xref="taxon:2697049"
                     /country="China"
                     /collection_date="Dec-2019"
     5'UTR           1..265
     gene            266..21555

[...]

Second part
ORIGIN
        1 attaaaggtt tataccttcc caggtaacaa accaaccaac tttcgatctc ttgtagatct
       61 gttctctaaa cgaactttaa aatctgtgtg gctgtcactc ggctgcatgc ttagtgcact
      121 cacgcagtat aattaataac taattactgt cgttgacagg acacgagtaa ctcgtctatc
      181 ttctgcaggc tgcttacggt ttcgtccgtg ttgcagccga tcatcagcac atctaggttt
      241 cgtccgggtg tgaccgaaag gtaagatgga gagccttgtc cctggtttca acgagaaaac
      301 acacgtccaa ctcagtttgc ctgttttaca ggttcgcgac gtgctcgtac gtggctttgg
[...]

Your question is, in my opinion, unsuited for this site for several reasons. First it is not self-contained — it requires one to read a document on an external site to understand. Second it is not sufficiently focused — it is, in effect asking for a complete explanation of a datafile format. Third, one could argue that this is not a problem in biology per se (although this is more debatable than my other objections). However, fourth, and most important, you show no evidence of trying to solve the problem yourself by using the extensive documentation on the NCBI website.

For the first reason: the linked document is a dna sequence. I cannot "say it in my own words" and reproducing it in the post is useless and decrease readability. Second: no, it is focused on the link between gene and DNA sequence. Third: yes, this could be an objection. Fourth: I went into some of this documentation, not all. I did not find something that lighten me about how gene are linked to dna sequence

I think it is not unreasonable to expect you to reproduce examples of the file in question. You obviously have identified the different pieces of the structure of the GenBank file. It would be simple enough to place that at the bottom of your question, if you don't like having it in the middle of the question.

In a GenBank format file, the first line of each feature entry gives the location of the feature in the sequence.  Consider, for example, the second feature in the linked file:

 5'UTR           1..265

This means that the 5' untranslated region of the viral genome is from bases 1 through 265.
Bases start counting with 1, so down below in the sequence after the ORIGIN, marker, this corresponds with the bases:
        1 attaaaggtt tataccttcc caggtaacaa accaaccaac tttcgatctc ttgtagatct
       61 gttctctaaa cgaactttaa aatctgtgtg gctgtcactc ggctgcatgc ttagtgcact
      121 cacgcagtat aattaataac taattactgt cgttgacagg acacgagtaa ctcgtctatc
      181 ttctgcaggc tgcttacggt ttcgtccgtg ttgcagccga tcatcagcac atctaggttt
      241 cgtccgggtg tgaccgaaag gtaag

Note also that "feature" means more than just genes, as in the case of this 5'UTR. Any identifiable region of interest in a sequence may be marked with a feature. Take a browse through the Sequence Ontology to see what other sorts of things are likely to be marked as features.

Thank you for your answer
How strong is the association made between the region of interest and the feature ? Is it made with a test (like supprres the zone and see how the feature evolved?)

@totalMongot You'll have to look at the article that produced the sequence to see how they identified features. Most of these features come from sequence analysis.


text:
What is prochromosome?
My textbook says that prochromosome is a false chromosome present in the nucleoid of prokaryotes.
I looked up Wikipedia and all over internet and this word is kinda sus. So I'm asking about it here. It doesn't seem legit. Wikipedia has just mentioned that the DNA like thing is present in nucleoid but never calls it prochromosome.

It would help a bit to get the exact quote from the text. That definition doesn't seem to agree with what I find when I research the term. For prokaryotes, I find the term here but it is poorly defined and does not agree with what you write. It is described as a "naked" chromosome that is only DNA, but that also doesn't make sense as bacterial chromosomes are bound by proteins. There is no page on wikipedia, as you note, supporting your "sus" designation.
There are current definitions available from online resources. It basically corresponds to condensed pieces of chromosomes (heterochromatin) that are apparent under a microscope under certain conditions. But it is not very well defined biologically, it is a name that humans give to something they see that they don't totally understand.
The term itself appears to be archaic. An early usage in reference to plant genetics is here. I think that it was probably a label that someone put on observations made microscopically before people knew what they were seeing. It looks to have become mostly outdated as cytology matured as a scientific field, here is an example quote from that paper:

Rosenberg (i8) was the first to show that the number of
prochromosomes is approximately the same as the number of
chromosomes. Prochromosomes have been considered as
structures identical with chromosomes (Malte, I3; Stout, 28;
Eichhorn, 2), as centers about which chromosomes form
during the prophases (Laibach, 9; Overton, 17; Rosenberg, 20) and as portions of chromosomes which persist through
the telophases (Heitz, 5; Gregoire, 3; Doutreligne, i). It
has also been considered that prochromosomes bear no direct
relation to chromosomes (Lundegardh, 12; Tischler, 30) or
that they are not directly concerned in the formation of
prophase chromosomes (Kuhn, 8). De Smet (24) stated
that prochromosomes may not be present in meristematic
nuclei.

This does not really correspond to any structure I can think of in the nucleus or nucleoid. It also doesn't correspond to the current heterochromatin definition.
Looking through search results, I am inclined to believe that the term as you have found it is an archaism that has somehow remained in some textbooks through bad editing. Very little current scholarly work is using the term. The scholarly work that does use it recently is using it in the more obscure cytological observational sense (heterochromatin), not in the prokaryotic sense that you have pointed to.
So it makes sense that you were confused given the inconsistent usage and the lack of current rigorous work on it. I would recommend sticking to recent scholarly work or definitions that come from traditional publishers (e.g. here). I would more or less entirely ignore question and answer sites that don't directly cite the scholarly literature.

Interphase chromatin can be divided into "chromosome territories" by chromosome painting probes.  It does seem like people a century ago without these probes may have been able to track these from telophase to prophase to a certain extent (see Figure 4).

@MikeSerfas I'm a little confused; the later reference has no reference to prochromosomes. Are you just speculating that well-known nuclear compartmentalizations are what such terms referred to? This seems uncontroversial, I guess, for the heterochromatic/eukaryotic definition of the term. But it doesn't seem to bear on the asker's question?

See Figure 2 / page 80, for example

@MikeSerfas The PLOS paper (the later reference) has only 1 figure? The other paper is relevant to eukaryotes but not prokaryotes.

Sorry - I had read "latter" for "later" in your comment.  The eukaryotic definition is by far the most prevalent.  Its extension to prokaryotes, however, is logical -- if a chromosome is defined only as a condensed, distinct structure, and "prochromosome" refers to the diffuse chromatin, then a bacterium should not be said to have a "chromosome" throughout its cell cycle, but rather a "prochromosome".  But I think that most people, rather sensibly, have not attempted to keep track of this distinction.  It relies on a uniform morphological distinction made in very different situations.

@MikeSerfas "...if a chromosome is defined only as a condensed, distinct structure, and "prochromosome" refers to the diffuse chromatin..." I guess that I find this a deeply confusing distinction (as do students apparently!). It really makes no sense once the chromosome is understood as anything other than a cytomorphological observation. But the bigger issue is that it doesn't even track with the present-day definition ("Heterochromatic blocks detected during interphase.") linked in my answer. According to that, only the most condensed regions should be prochromosomes (?am I crazy?).