text:
Is a FoldScope microscope suitable for plant cytogenetics?
I have recently been getting more interested in amateur botany, and have some background in genetics and genomics (PhD+). I have used standard light and confocal microscopes but don't have much expertise in microscopy.
I often find myself wondering what the ploidy is of some plant that I'm looking at, as I know that this is a major life history feature and genetic variant in wild plants.
I was curious whether a cheap little scope like a foldscope would be an adequate microscopy instrument for looking at the cytogenetics of a (probably rather crudely prepared) plant sample, assuming that I can come up with a suitable home protocol. (I don't currently have access to lab space.)
I have found this question, but it doesn't really explain much about the required parameters for cytogenetic microscopy.
So:
1) What microscopy parameters need to be satisfied to do cytogenetics?
2) Does a foldscope meet them?
3) If not a foldscope, what other cheapo scope would work?

Foldscope has resolution of two microns, not enough for this purpose. Sorry no extra refs.

@PolypipeWrangler Can you comment on why? E.g. I found this: "...the size of an average condensed mitotic chromosome, which is about 6 by 0.7 microns..." That is in the same range, which might mean it's either easy, hard, or impossible, but I don't know because I don't have the background. To reiterate, what are the parameters necessary for the task?


text:
Parasympathetic effects on digestive tract - motility versus absorption
The parasympathetic nervous system's purpose is often referred to as "rest and digest." As part of this purpose, parasympathetic innervation increases motility in the digestive tract to move food through. However at the same time, slowing gastric motility and peristalsis is important for absorbing nutrients, which is accomplished by enterogastrones like secretin.
So on one hand, the PSNS promotes more motility to move things through the digestive tract. On the other, certain hormones are released in response to the presence of food that slow down motility for better absorption.

If one of the main purposes of the PSNS is to promote digestion (and thus I would subsequently think absorption), why does it cause increased motility, which gives less time for digestion and absorption?
Is it important during digestion to sometimes increase or decrease motility? If so, how does it related to the PSNS and SNS in terms of when either happens?

source: Stack Exchange

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

sort: votes


text:
Is it true that recanalisation of the vas deferens, if any, tends to happen soon after a vasectomy (less than 1 year), and if so, why?
https://doi.org/10.1016/s0140-6736(00)02436-3 "How reliable is a vasectomy? Long-term follow-up of vasectomised men":

Most episodes of recanalisation are believed to happen soon
after vasectomy, and the pregnancy rate after vasectomy is
about 1 in 2000. Delayed recanalisation after the first year is
uncommon, only isolated cases are reported and its true
frequency is unknown.

https://www.medicalnewstoday.com/articles/326737#vasectomy-reversal:

Most cases of recanalization happen within 12 weeks of the procedure.

Is it true that recanalisation of the vas deferens, if any, tends to happen soon after a vasectomy (less than 1 year), and if so, why?

This is a medical rather than a biological question as it relates to a surgical procedure. Try SE Medical Sciences.

@David Thanks, the recanalisation process is biological.

But your question does not ask about the biology of the process, but asks if it is true that it happens a specific time after a surgical procedure. It's up to you, but if I wanted an answer to a question like this I know where the most likely place to get an answer is.

Is it true that recanalisation of the vas deferens, if any, tends to happen soon after a vasectomy

Yes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7175481/:

Studies have shown that early recanalization usually occurs between 2 and 6 weeks post-vasectomy [9, 10].
Early failure, defined as a postoperative semen analysis showing persistent motile sperm, occurs in 1 in every 250 patients [6].
Late failure, defined as the rejoining of the severed ends of the vas deferens, occurs in 1 in every 2000 patients.

Note that the same article reports of a case of paternity that occurred seven years after a negative post-vasectomy semen analysis, which means that  recanalization can happen many years after a vasectomy, even though the odds are very low (<0.05% after 1 year).
Also, the risk of recanalization may depend on how the vasectomy was performed. For example, see:

How does the length of the vas deferens excised during vasectomy impact the risk of recanalization after a vasectomy?
Does the risk of recanalization increase if a person chooses an open-ended vasectomy (which closes only testicular end of the vas deferens)?

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


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What is the evolution metaphor about water flowing downhill?
As part of my biology undergrad degree, I took a course on the Origin of Species, where we read Darwin's book and also several other readings about the origins of evolution.
I recall that during this course we talked about a metaphor to the effect of "Like water flows downhill to fill every available lower spot, species evolve into every available niche," which really helped me understand Darwin's viewpoint on natural selection. But I cannot find this metaphor anywhere online.
What is the source for this metaphor? I don't recall it being in the Origin itself, but I could be wrong.

This metaphor looks to me dangerously close to circular reasoning: until some species evolves to have a certain behaviour which can be described as "filling the niche X", it would be impossible to even know that this niche is available. Also, the claim it makes is rather unfalsifiable: if on a continent B (unlike A) there are no species filling the niche X, it's impossible to say whether evolution will fill the niche one day, or the species on B are unable to evolve this way in principle. All in all, this doesn't look like a valuable metaphor, and certainly doesn't reflect Darwin's own views.

It sounds like you might be referring to Sewal Wright's fitness landscape analogy - https://en.wikipedia.org/wiki/Evolutionary_landscape


text:
How does the light-independent stage of photosynthesis get H+ ions?
From what I understand from my grade 11 biology:
During the light-dependent stage of photosynthesis, water molecules split, producing hydrogen and oxygen atoms. The oxygen atoms are basically “waste products” — used by mitochondria for respiration after being inhaled. These H+ ions are then taken by a hydrogen carrier (i.e. NADP+) to form NADPH (which is necessary for the light-independent stage). Where do these H+ ions suddenly just come from?
From what I’ve understood so far, the H+ ions are now “in” the NADPH.
I’m confused as to how in the light-independent stage, the carbon dioxide (CO2 molecules) can combine with the H+ ions to form glucose. I thought that these H+ ions had already got “converted” to form NADPH? Or is it something like only some of the H+ ions are necessary for NADP+ to form NADPH?

Summary
The question shows confusion about the purpose of the splitting of water in photosynthesis. Quoting from Berg et al., in the light reactions of photosynthesis

“Light is absorbed and the energy is used to drive electrons from
water to generate NADPH and to drive protons across a membrane. These
protons return through ATP synthase to make ATP.”

The useful product of splitting water is energy.
There is no problem in the provision of hydrogen ions for biochemical reactions as such — they are available from the dissociation of water.
Explanation

The diagram above, summarizing the light reactions may be helpful, although it conceals detail and introduces the complexity of energy generation. It shows the (thalkaloid) membrane separating the location of the reduction of NADP+ (outside) from where water is split (inside).

The important product of the reaction of light photons with water is excited electrons. The chemical products are relatively unimportant — certainly for oxygen, and the only importance of the hydrogen ions produced is their location within the thalkaloid, lowering the pH.

The initial fate of the hydrogen atom is complex, and there a many intermediates to which the excited electron is transferred before, ultimately to NADP+:

NADP+ + H+ + 2e– → NADPH

It is important to realize that the energy is used to reduce NAD to NADPH, that NADPH can be regarded as a special type of ‘high-energy compound’ — not a general one like ATP, but one that can specifically drive the reduction of carbon backbones needed in synthesis.
The misapprehension is that there the hydrogen ions for the above reaction are those produced in the splitting of water, or that there is in general any problem in obtaining hydrogen ions for biochemical reactions. Biology exists in an aqueous environment, and water dissociates into hydrogen and hydroxyl ions.

H2O ⇌ H+ + OH–

So hydrogen ions are irrelevant to the reduction reactions involved in the conversion of carbon dioxide to carbohydrates in the light-independent reactions of photosynthesis (they are actually produced in NADPH reductions.). It is NADPH that is supplying the hydrogen component of the carbohydrates.
ATP
The diagram also brings in a complexity that needs a book chapter to explain: the hydrogen ion gradient generated between the inside and outside of the thalkaloid space provides the energy to phosphorylate ADP to ATP. The ATP is relevant to the light-independent reactions of photosynthesis in that it ultimately provides the energy for formation of the carbon–carbon bonds.


text:
Why do the two sexes have different reproductive costs and capabilities?
Is there an evolutionary explanation that shows why the reproductive costs are mostly on the female sex?
And therefore, why do males can potentially have more offspring?
Does that happen to create more competition in sexual selection?

I may have misunderstood your question, but there is no theory why usually reproductive costs are on the female, as this is a fact. Females have usually larger (and fewer) reproductive cells (gametes), they frequently have to carry the embryo until birth, and sometimes they have to attend to the offspring during the first stages of their lives. To put it very simple, females are stuck with their offspring from the moment of conception until they are born - sometimes even longer - while males generally can mate with many females in a short period of time, potentially having much more offspring.
A consequence of this is that, usually, females are choosy (they want good mates), whereas males just try to mate as much as possible. Female choosiness generates sexual competition, as females prefer to mate with males having certain characteristics that hint to a superior genotypes/phenotype that may be passed to their prole (e.g. beautiful plumage, social status, size of the wallet). Sometimes the costs of attending offspring after birth are higher than the costs associated with reproduction alone. In some of these cases, we may observe unusual behaviors, e.g. male-only parental care and choosy males.
This is a very broad and complex topic and a short answer here cannot cover all of it. John Maynard Smith developed the game theory approach most commonly used to investigate the consequences of different pay-offs for the two sexes and to explore how these can influence the behavior of the parents. Moreover, this topic is also covered in many behavioral biology textbooks. I have had very positive experiences with Krebs & Davis Behavioural Ecology (ISBN-13: 978-0865427310), which I would recommend.
Hope to have clarified some of your doubts.
Cheers,
Emilio

Thank you very much for this answer! Unfortunately I don't have a very strong education in biology so I apologise for being unclear. In the question I was specifically referring to pregnancy and calories investment in giving birth(and maternal care as well). I guess the main evolutionary advantage that enabled sexual reproduction to evolve in this way lies in the competitiveness it generates among males (another reason may be reduced costs and easier reproduction). I will definitely check out those books! Thanks!

I would say that sexual reproduction has the big advantage of DNA recombination. Then, how sexual reproduction is actually carried out, it varies a lot even just inside the animal kingdom. One sex needs to give more resources to the embryo just from a cellular physiological point if view. Largest Investments cause competition in the other sex, which does not necessarily means females choose the best partner. For instance, an optimal choice is conditional to the environment and specific situation. I would thus be cautious interpreting sexual selection as evolutionary advantageous in general.

Within a two-sex species, there are roughly three possible evolutionary strategies for reproductive investment:
Sex A and Sex B invest equally.
Sex A invests more than Sex B.
Sex B invests more than Sex A.
The last two are practically equivalent if you don't project your assumptions about differences between the sexes.
So the only alternative to different reproductive investments is equal reproductive investments. That option is not stable since sex A can invest 10% less at only 5% (assuming a linear relationship between investment and reproductive success, which is not accurate) reduced viability since the partner is not investing more yet. This means sex A can use the saved energy to reproduce with 10% more partners. This is a constant evolutionary pressure, so eventually one sex will invest a lot less than the other.
The other sex will probably not invest 5% less too, since that drops offspring viability by another 5% meaning they gain 10% more partners at the cost of 10% less offspring. There is no advantage here, so there is no evolutionary pressure. Alternatively, they could invest 5% more leading to 5% more reproductive success. This also gives no advantage.
The only reason for any sex to increase investment is if the reproductive success gets so low that it it is worth a larger investment to keep reproducing. There is no reason to assume the investment will primarily come from the smaller investing sex, so that won't change the difference in investments.


text:
Why do humans need pillow to sleep better?
As far as I know, no animal sleeps with a pillow/support under their heads. Why then do we need to keep a pillow?

Many, many animals make beddings and nests. Not unique to humans at all.

Yes agreed. But specifically do they have to use a support for their necks?

humans can sleep fine without pillows.

Our cat does it all the time ;-)

This is because the pillows keep the head align with body making it easier for the spine to maintain its natural curve. It reduces the tension in the lower dorsal region of neck. Many animals are found to be using pillow like substitutes for the same reason.

Which animals  .?

@YasirSadiq mamals in general use pilows most often their front legs/paws humans too putting our arm under our head while we sleep.


text:
Can anyone identify these mushrooms?
Found in the Dolomites, Italy

in a wooden fence:

The first one is dyer's polypore or rusty gilled polypore.
https://en.wikipedia.org/wiki/Gloeophyllum_sepiarium
The second one looks a bit like orange peel fungus, although it could be something different.
https://www.wildfooduk.com/mushroom-guide/orange-peel-fungus/

Thank you! The second one is really similar to an orange peel fungus, unfortunately I did not take more photo that might have helped with identification...


text:
how to estimate phylogeny without using DNA sequences?
I am new to bioinformatics, I am reading ‘Analysis of Phylogenetics Second Edition and Evolution with R’ from Emmanuel Paradis.
I can create phylogeny from DNA sequences, by first calculating the distances and then using (ie nj() function).
My question is: if instead of DNA I have trait data (ie height and weight of species), how can I estimate a phylogeny? (is the same process valid? somehow calculate distances and pass that to nj()?)

You want to make a phylogeny with only two non-independant data points per species?

let's say I have 20 data points for weight and length, and 3 or 4 species, is it doable? (I am curious how, either using R or paper...)

Morphological taxonomies are typically based on presence or absence of different anatomical traits. While you could technically calculate a phylogeny based on size and weight, it seems unlikely to produce an accurate or valid phylogeny. Sometimes distantly related species have similar body sizes (raccoons and opossums). In other cases, related species might have dramatically different sizes. For example, the round-eared elephant shrew (Macroscelides micus) resembles a small mouse (weighing around 28g), but it is more closely related to elephants than rodents.

https://www.khanacademy.org/science/biology/her/tree-of-life/a/building-an-evolutionary-tree


text:
What does the decline of serum antibodies after infection mean for B cell immunity, exactly?
About a month ago there was a small media blip about a report in the New England Journal of Medicine that neutralizing antibodies to SARS-CoV-2 decline significantly within a matter of months. Published op-eds ranged from "a vaccine won't work, why God WHY" to "actually this isn't that weird, stop freaking out." Some key details from the articles I read at the time:

We still got T-cell immunity, and there are some signs this could last longer for COVID-19
Antibodies decline as infections clear for other illnesses.
Remaining memory B cells are (usually) primed to churn out more antibodies upon reinfection.
Nevertheless, the decline of antibodies is less protective and raises concerns of decay of immunity (an opinion in the original report)

I want to ask about the B cell side of this in order to better understand the somewhat conflicting messages and opinions.

If memory B cells worked as advertised, how would serum antibody levels even be a measure of immunity? It would seem that antibodies dropping to negligible levels wouldn't matter if your memory B cells can make them on demand.
Is there some benefit to having antibodies in your blood independent of your memory B cell function? Is it somehow quicker or vital to prevent reinfection or recurrence of serious illness?

The decline in serum antibody level after vaccination means the level of spike protein specific T cells declines, in another word, the virus is eliminated [1]. When the vaccine introduced a viral particle or mRNA into the cell, SARS-CoV-2-specific CDH4+ T cells recognize 2 variant spike proteins, helping B cells to secrete antibodies and activating cytotoxic T cells to destroy the infected cells [2]. After infected cells are destroyed, antibody level will gradually decline because the virus is eliminated from the body [3]. But this doesn't necessarily mean an absence of immune memory because

Memory T and B cells remain, however, and maintain a heightened ability to mount a response to a recurrence of infection with the same pathogen.

Otherwise, it's wasteful to have antibodies synthesized and maintained independent of B cells function.
References:

Cox, R.J., Brokstad, K.A. Not just antibodies: B cells and T cells mediate immunity to COVID-19. Nat Rev Immunol 20, 581–582 (2020). https://doi.org/10.1038/s41577-020-00436-4

Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Helper T Cells and Lymphocyte Activation. Available from: https://www.ncbi.nlm.nih.gov/books/NBK26827/

Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: The Immune System in Health and Disease. 5th edition. New York: Garland Science; 2001. Immunological memory. Available from: https://www.ncbi.nlm.nih.gov/books/NBK27158/

First sentence: "B cells", not "T cells"?


text:
Where can I download a list of all plant species of the world?
Where can I download a complete list or dataset of every plant species in the world?

If you download the tree of life 85mb file, it's updated often, although it contains all species of all living things. there are probably resources related to that, and sub sections with the different supergroups and kingdoms.

This website claims to contain all the plant species we know of (and also contains some statistics on the state of their collection). Keep in mind that there are many species that have yet to be found or assessed correctly. The world is a big place.
http://www.theplantlist.org

A web-crawler may assist in downloading the information for yourself - from this site :)

web-crawling, web scraping, maybe on kaggle there is a list too :)

@Andrew Interestingly, there is an option to download either your search result or per-family data in CSV format - for later machine processing

Fantastic, that is even better.


text:
What websites biologists use to check what new plant or animal species have been discovered in the world?
What are the databases or websites that biologists use to check what new plants or animals have been found in the world? The service should list the location of the discovery, time of discovery, image of the new species, the name of the discoverer and other vital information

“The service should list…”. Is this an invitation to tender?


text:
Is this question about limiting factors answerable?
This is from a Singapore-Cambridge GCE O-level Biology exam (a national exam for 16-year-olds). The exam board maintains that the question is "correct and accurate"—but isn't there a typo in option C?

Here's my argument:

Merely increasing the light intensity at either Points 1 or 2 speeds up photosynthesis, but varying the light intensity at Points 3 and 4 doesn't.
Therefore, light intensity is limiting photosynthesis at only Points 1 & 2.

At Point 3, merely doubling the $\ce{CO2}$ concentration speeds up photosynthesis; on the other hand, the graph shows no evidence that varying the $\ce{CO2}$ concentrations at Points 1, 2 or 4 speeds up photosynthesis.
Therefore, $\ce{CO2}$ concentration is limiting photosynthesis conclusively at only Point 3.

As this is a data-inference question, all the four answer choices are invalid deductions.
(Asserting that $\ce{CO2}$ concentration is a limiting factor at Point 4 requires assuming that raising $\ce{CO2}$ concentration beyond 0.08% continues speeding up photosynthesis.)
Excluding Point 4 from Option C will render this question finally answerable.

With your logic wouldn't that also mean that point 3 requires assuming that decreasing the carbon dioxide concentration would decrease photosynthesis rate? In statistics when you want to test if one parameter affects another it's sufficient to test a high and a low point.

@Cell No--because it stands to reason that $\ce{CO2}$ concentration is limiting photosynthesis in a given setup if varying it (in either direction) speeds up photosynthesis.

You misunderstand. It could be the case that a third curve exists at 0.02% carbon dioxide that begins to plateau at point 1. Also "rate limiting" could mean slow down too.

@Cell $\ce{CO2}$ concentration is said to be limiting photosynthesis in a given setup as long as increasing (or decreasing, for that matter) it there speeds up photosynthesis.  In other words, the fact that increasing $\ce{CO2}$ at point 3 increases photosynthesis is sufficient to assert that $\ce{CO2}$ is a limiting factor there -- regardless of whether decreasing $\ce{CO2}$ there increases or decreases photosynthesis.

So, why do you think that logic doesn't apply at point 4?

@tyersome The graph displays no faster photosynthesis than at point 4.

I think your thinking is fine, but you're being a bit pedantic about it. I don't think there is any typo.
The purpose of the question is for you to understand that there are two limiting factors here: light and CO2.
You can identify points in the graph where light is limiting because there is a slope with increasing light, and you can identify points in the graph where CO2 is limiting because light no longer increases the rate, and that the plateau level changes with different CO2 levels.
Yes, you are right, there could be other yet-unrevealed-to-you limiting factors here, but there is nothing in the graph to show this. You would need to see another set of lines where increasing CO2 further does not change the plateau level, and/or where the shape changes.
Chalk it up to Occam's razor. Without further information besides what is on this graph, if I asked you to draw your prediction about what the line would look like at 0.12% CO2, you should draw another line that follows the other and then plateaus at a third, higher level.

Without knowing that the optimal $CO_2$ concentration is above $0.08%,$ one might guess that at point $4,$ $CO_2$ is a limiting factor, but one can't be certain. 2. At room temperature, the optimal $CO_2$ concentration for photosynthesis is actually $0.10%.$ So, a $0.12%: CO_2$ graph would be no higher than—in fact, the same graph as—a $0.10% :CO_2$ graph.

@ryang There is no data in the graph supporting any limiting factors besides CO2 and light.


text:
Please help ID this possible fish skull
Found on the shoreline of a tributary of the upper part of the Chesapeake bay in Maryland:

More pictures here
ichthyology??

I suspect you're going to need better pictures from multiple angles to have a chance at an answer; from this view it isn't even clear you have a skull.

I don't disagree. I'm having trouble posting pics....it is definitely a skull. I will create a link to the other pics. Thanks for responding.! Please look if you have time. I have been collecting mammal skulls for quite some time & I am stumped.

Here is the link to more pictures.  Any opinions are greatly appreciated.  It's driving me nuts                                https://photos.app.goo.gl/Cg8t4Ttsde4oDDDg7

I think that's ichtyology because it's probably a fish, the comment says herpetology,

Similar to this https://biology.stackexchange.com/questions/74087/what-type-of-bird-skull-is-this

Thanks for your input

I've fixed your image link — in the future you should be able to avoid this kind of problem by entering each link on a separate line.  ———— I recommend uploading some more of your pictures — questions with clear images from multiple angles are more likely to get useful feedback! ——— To me this looks like it might be part of a turtle skeleton rather than a fish skull, but that's really just a guess.

yes an ichtyology forum is not suitable for fish IDs cos ichtyos dont know that kinda thing as well as this forum does.


text:
Use of restriction endonucleases to analyse Variable Number Tandem Repeats (VNTRs)
The textbook I’m using states that “Ends of VNTR have conserved sequences. These can easily be cut by restriction endonucleases.”
But restriction endonucleases cleave palindromic sequences. Does this mean that the repeated DNA and conserved sequences together form a palindromic sequence?

The general situation regarding using restriction endonucleases to analyse Variable Number Tandem Repeats can be explained with (as well as without) reference to the illustration below.

The original region of DNA in which the insertion occurs will in general be complex (rather than repeated) and conserved to a reasonable extent among H. sapiens. The complex conserved sequence is represented by a gradient of colour in the upper part of the diagram so that the point at which the original copy of the repeat inserted can be identified in different individuals (or alleles), A, B and C, where, for the sake of argument, two, three and four copies have been generated.
The individual repeat unit is relatively short (typically 10–100 bp), so it is relatively easy to find conserved sites for at least one commercially-available restriction endonuclease on either side of the original insertion, but not within the repeat.
The mathematics of this reasoning are quite simple, and I provide exercises on my University website. However, as an example, consider a 4-base pair sequence that is the target for a restriction enzyme. It need not be palindromic, but as most Type I restriction endonucleases are, let’s choose GGCC. The chance of finding this in any tetra-nucleotide is 1 in 256 (4x4x4x4), or, in other words, it should occur in any 256 bp stretch of DNA. (Of course this is just an average of what may be a normal distribution, and overall base composition will affect the actual frequency.)
The net result will be that it will be possible to generate fragments of an overall size such that the flanking regions are not so large that they make it difficult to distinguish differences reflecting different numbers of repeats.
And today?
The polymerase chain reaction (PCR) might well be used instead of restriction endonuclease digestion as, given that the DNA sequence of the region has been determined, one could choose appropriate positions in the flanking regions to generate DNA fragments for analysis. See, e.g. Richie et al. (1999).

The edited question is much closer to what I actually wanted to ask. And the exercises you provided are very useful as well. Thank you so much!!

You are welcome. Although written a few years ago, it is gratifying when students find them useful.


text:
Can someone identify these fungi?
Found them in Gujarat, India.
Found growing among potted plants

This may be Clitocyte odora commonly known as aniseed toadstool.

They can be found growing in small groups along the side of tree roots.

it is widespread in the temperate zones, occurring in Asia, Europe, and North America

Young specimens have a light blue texture on the cap which fades to grey in age. The gills and stem are white with no ring.

Reference

If there is a white skirt it is probably a verdigris argaric:
https://en.wikipedia.org/wiki/Stropharia_aeruginosa


text:
Question about the basilar membrane mechanics (cochlea)
I am reading about the mechanics of the basilar membrane in the inner ear.
In various publications, it is said that, at a specific position on the basilar membrane,
the outer hair cells are activated by the amount of basilar membrane displacement
while the IHC are activated by its velocity.
As far as I know each position on the basilar membrane vibrates at a characteristic
frequency. Given that the to-and-fro movements have the same frequency at all sound intensities, isn't the velocity be directly proportional to the membrane displacement?
If that is the case, does this mean that the activation curve is steeper at higher frequencies?

Only the inner hair cells are stimulated by the movement of the basilar membrane. The outer hair cells are active elements that contract and elongate in response to sound, in a way not fully understood, but no doubt helping increase sensitivity and likely also frequency resolution of the hearing.


text:
Can anyone identify this object?

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

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

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

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

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

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

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

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


text:
What is the adjective for PHAGE?
if the adjective of the noun BACTERIUM is 'bacterial' and that of VIRUS is 'viral', what is the adjective for (BACTERIO)PHAGE? Is 'phagial' accepted?
Thank you

Bacteriophages are viruses so what's wrong with viral?

@Cell "Bacteriophages"!? Not to be a grammar-nazi, but bacteriophage is an unchanging irregular noun. The plural of bacteriophage is bacteriophage. The plural of phage is phage.

@MikeyC If it's good enough to be acceptable on Nature's educational website, it's good enough for me: https://www.nature.com/scitable/definition/bacteriophage-phage-293/#:~:text=A%20bacteriophage%20is%20a%20type,surrounded%20by%20a%20protein%20structure Not to mention it is also found in published work: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109452/

Have you done a Google search for "phagial"? You might try and see what you find. (And there is no need to use capitals. On the internet that is considered to be shouting.)

can you give a context in which you want to use it?

The context would be: "there were 32 phagous species in our samples". (as opposed to 50 bacterial and 12 viral species).

@Cell. I learned something today. Thanks for supporting your usage. It seems both are acceptable. The invariant form was just drilled into me for 5 years of undergrad and 6 years of grad school. Seriously, my PhD advisor would interrupt a research talk to correct something like that.

It is bacteriophagous as given in wiktionary.

From bacterio- (“bacteria”) + -phagous (“eating”).

Reference

This is what I found by googling it and hence shared with the reference. Why downvote then?

I didn't downvote, but this would seem to me to be an adjective modifying "virus" (e.g. a phage is a "bacteriophagous virus") rather than an adjective modifying something associated with a phage "phagial(?) population growth", "phagial(?) biochemistry", etc.)

I downvoted this answer for 2 reasons: (1) a search for "bacteriophagous" on PubMed yields very few results (only 25), and (2) from the context of those results, "bacteriophagous" means a "bacteria-eating" or "bacteria-engulfing"; not bacteriophage-like.

In the literature, it's most common to see hyphenated compound adjectives, like "phage-mediated," "phage-dependent," or "phage-encoded" where "bacterial" or "viral" might be analogous. For example, "Phage‐mediated selection and the evolution and maintenance of restriction‐modification."
Sometimes "phage" seems to be used as a standalone adjective, like in "Phage antibodies: filamentous phage displaying antibody variable domains." Although I'm not sure that it would be correct to use "bacterial antibodies" or "viral antibodies" in this case, so maybe that one is an anomaly.
I would suggest following one of these trends, unless you want to do a lot of explaining to reviewers.

so something like "pagial/phagous species" should become phage-species, right?

In that case, you would probably not use the hyphen. There's some discussion of naming conventions in this article on PubMed, and they do use the phrase "phage species." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5408676/.

I read the article, but the space is related to naming the phage itself, not the adjective for phage...

I only referenced it to give you an example of how "phage species" might be used appropriately. Sorry for the confusion.

I asked the author of that paper and she replied: "I have never in my career heard anyone use the terms phagial or phagous." Probably "phage-species" of "phage species" is the more accepted way, 'phage' being (I presume) a modifier more than a real adjective.

From the University of Wyoming (courtesy Prof. Suess) I got: "I would go with phagial.   Following the Latin ending for viral, bacterial: -ial - (Latin: a suffix that forms English adjectives from Latin adjectives ending with -is or -ius with meanings about "pertaining to, relating to", or "characterized by")"


text:
Can you eat more calories than the body can store?
I believe I have read that if the body takes in too many certain nutrients/vitamins, the body simply excretes them.
How does this behave with calories? If I have a daily consumption of exactly 2,000 calories, would the body gain more weight if I took 6,000 calories in one day or if I took 2,500 calories over 8 days?
I know that excess calories can be stored by the body, but is there a point where the body can't keep up and excrete the rest?

you will run into the issue of eating more than the body can digest first.

Even if you only eat chocolate or something similar? For example, I have a bar of chocolate here that has ~550 calories per 100 grams. There would be 4,000 extra calories 'only' 700 grams of chocolate. But I think that there are also things that have much more than that.

After googling I found out that Macadamia Nuts has 718 calories per 100 grams. Thats even more.

As @John already pointed out, efficiency of digestion can be assumed to decrease in case of extreme uptake of excessive calories. (diarrhea)
In terms of the excretory system: Proteins are generally strongly retained by the kidneys, while glucose famously could leave the body through urine (diabetes) but should be taken up by your cells under normal circumstances. Fats, as carried by transporter proteins, should not be excreeted either. So I don't think you would excrete many calories.
Also I remember some papers stating, that short-term excessive caloric uptake is correlated with down-regulation of glucose transporters to your brain, while prolonged uptake of excessive calories (more than around 3-7 days) leads to changes in the brain-barriers permeability properties. It was observed that this change in permeability has long-term fatalistic effects: It will cause hippocampal damage and in turn further cause high caloric intake as a behavioral change due to reduced internal cues that depend on the hippocampus.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6381074/


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Identification: creepy dangling spiderthing
Can anyone identify this creepy mess dangling from the cieling of my garage on a few strands of spidersilk? The thing is 5cm.

Should I burn down my garage and move to another country (Currently Belgium)?

I think I found it now. Have a look at this:
https://fireflyafrica.blogspot.com/2009/03/rain-spider-nest.html
it features a nest, large ("tennis ball" sized), hanging from threads, and they claim it is a "rain spider" nest, but rain spiders do not seem to span Belgium.
I am not familiar with what a 'Rain spider' is, so looking it up,'rain spider' is a genus of the Huntsman spider family, and there are huntsman spiders in Belgium. But huntsman spiders are known to carry their own (small pouch) egg sacs.
Looking up "rain spider nest" finds many photos similar to yours. But I cannot find any that live in Belgium or Europe.
This is probably on the right path, and you can try searching for various cousins or other relatives of the 'rain spider' that might be in Belgium.

Well, it's more pingpong ball sized, so I think it'll be the egg sack of a rather ambitious Tegenaria

Stored prey? for a couple of years?


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Could DNA replication fail in the far future?
Assuming that all environmental conditions on Earth remain the same in distant future, the tendency of nature to increase entropy would cause the chemistry and the mechanism of DNA replication to create more and more "errors".
Could these errors accumulate over time for all life, resulting in failure of replication by means known today, bringing life as we know it to extinction?
In other words, will life eventually fail to continue reproducing due to the inability to maintain its inherent state of non-equilibrium?

Hi Dennis, you've misunderstood entropy and the second law of thermodynamics. Increased entropy doesn't create more genetic mutations.

Also, the "errors" do exist, they are basically what drives evolution and what made life what it currently is.

@Andrew is not what makes this errors appear. Replication and protein synthesis are chemical proceses, and they increase the entropy. The more errors in replication, the more chemical reactions, then the more entropy.

What i say @Alexlok, is that over time, the amount of errors could make imposible the appearence of new feasible organisms, because there would be more and more chunks of useless DNA. This would happen in the very long term.  My thinking is that replication seems like a continuous chemical process, but it can't last forever. or can it?

DNA replication won't possible in the heat death of the universe, but any creaters and planets will have disappeared long before that.

The principle that entropy (disorder) must increase is true for a closed system. An organism, however, is not a closed system; it obtains energy from outside itself and with that energy can maintain order. This is referred to as negative entropy; see the Wikipedia article on Entropy and Life.

Well said. Living organisms have been creating order from disorganized stardust for billions of years, so the premise that entropy is generally increasing among living creatures is false.

But the cost is that universe entropy increases, thats what i was refering to.

Assuming that all environmental conditions on earth remain the same in
distant future, the tendency of nature to increase entropy would cause
the chemistry and the mechanism of DNA replication to create more and
more "errors". Could these errors accumulate over time for all life,

An accumulation of errors in replication over time can certainly be assumed and observed. However, these errors -also called evolution- are generally not related to entropy.
Entropy, as a statistical concept (Boltzmann), describes the population of different states, like heads or tail in a coin-flip. If you toss 100 coins, the outcome of 50 heads would correspond to the maximum entropy, while 0 or 100 heads would be the lowest possible entropy. Boltzmann also describes that higher temperatures equalize the population of different states. Too high and too low entropy would both mean death.

resulting in
failure of replication by means known today, bringing life as we know
it to extinction?> In other words, will life eventually fail to continue reproducing due
to the inability to maintain its inherent state of non-equilibrium?

If an error leads to a decreased probability of reproduction, it dies out and will not accumulate. On the other hand, in the rare instances that the error actually increases the probability of reproduction, it has a high chance to accumulate. So in general, accumulation of errors would increase the ability of reproduction.
Not being able to maintain the correct state of entropy definitely is fatal and is the natural end of life when you grow old.


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Empirical Measurements of Barr Body Ratio
'Both X-chromosomes in a female have an equal chance of becomes a Barr body in each cell.' Every source I can find on Barr bodies claims this and I can think of no reason for why it may be wrong. What I want to know is if anyone has empirically tested this. Has anyone ever taken a model organism, measured the distribution of Barr bodies, and calculated exactly how far the result is from the 1:1 ratio that the theory predicts? Has anyone ever tested the Null Hypothesis of this statement, or has it just been accepted based on the theory alone?

Generally in science, accepted theories are not simply based on a presumption of accuracy just because it sounds right. While I don't have the citations you're looking for (this would be a good place to start looking), I'm certain it's based on strong empirical evidence, not guessing.

That is why I asked my question. Considering how wide-spread this claim is, there should be empirical evidence, but as far as I can tell there is none.

Did you start looking through the PubMed search I linked to? You can reverse-sort it by date published and start looking at the oldest papers first, as they're the ones most likely to have direct citations of the original work.


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Why are fatty acids synthesized in two carbon units?
Why does long-chain fatty acid synthesis involve the two-carbon precursor, malonyl CoA, rather than the one-carbon acetyl CoA (or even a three-carbon precursor).
Is this because fatty acids with an even number of carbons are somehow ‘better’ than those with an odd number, or does it reflect some aspect of the chemistry involved?

@kmm I do not think this question is about evolution except in the most tangential sense. There is a tendency of people to bring evolution into questions which just relate to functional utility. In this case there is no evidence that there were ever organisms that had a one-carbon pathway of fatty acid synthesis, so the question of a selective advantage does not come into play. In an effort to make people keep things simple, I have edited the question removing all references to evolution, and distilling it to its essentials, which now seem capable of a factual answer.

Thanks for the edit! The new question is pretty much what I'm interested in knowing about!

@kmm I did give the answer a read and I learnt something new, but it didn't help me exactly with what I wanted to know, thanks for providing the link though!

@David Now it seems more appropriate for chemistry.SE, as it is about biochem and not biology.

@kmm It is totally on-topic here as it is about biochemical pathways and metabolism, which are (molecular) biological concepts, not about chemistry per se. You will find dozens of questions in this category on the site. Please withdraw your close vote, I am in the process of answering. You will see my answer is about metabolic strategies, not pure chemistry.

The answer to this question lies in the chemistry of fatty acid synthesis — specifically the chemical energetics of the reactions. For those new to the biochemistry there is a basic concept that must be understood: that a reaction can occur spontaneously only if it involves a negative change in Gibbs Free Energy. This is discussed, among other places, in my answer to another question.
As regards long-chain fatty acid synthesis, the answer can be found in Section 22.4 of Berg et al. Biochemistry some of which I summarize here.
The reactants in fatty acid synthesis are linked to a protein during the cycle of reactions — acyl-carrier protein, ACP:
malonyl CoA + ACP ⇌ malonyl ACP + CoA
The first condensation reaction of a malonyl constituent in the elongation cycle of reactions is shown below.

The key point to note is that in this step the malonyl carboxylic acid
group is released as carbon dioxide with a substantial decrease in
free energy that makes the reaction favourable. Without it the
reaction would not proceed, which is why the synthesis of acetoacetyl
ACP from two molecules of acetyl ACP does not occur.

It is worth adding that this free energy is ultimately derived from ATP, which is needed to drive the reaction in which malonyl CoA is formed from acetyl CoA and carbon dioxide.


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Hepatitis Lab diagnosis based on serology
HBcAg which can't be detected in serum can be detected in hepatocytes , why is it so that they become detectable in hepatocytes?

HBcAg is capsuled by HBsAg and therefore can't be detected, while within the cells it's still free (before assembly of the virus).
The test checks for presence of antibodies (IgM) against HBcAg. It does not try to detect HBsAg anyways.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC154683/


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Has anyone yet figured out how sensory signals for eyes and ears are encoded by our organ into electrical signals?
The most obvious way to give sight to blind and hearing to deaf is to give them a replacement organ for these. In order to do that we would need to understand how our eyes and ears encode sensory information into electrical signals which then go into the brain. My question is, how close are to understand this mechanism at this time?

I don't understand your question -- My confusion is reflected in the responses to your post; Bryan Krause's quite excellent comment below delves into implant world, while some answers allude to normal physiology. I think this is because the post's body and title don't match -- they reflect the ambiguity in the question. In other words, like Bryan suggests -- current prosthetics don't treat hearing loss or blindness by reproducing normal physiological processes.

See what I want to know is, do we understand exactly how the vision is converted into electrical signals and how to interpret those signals? I am an electronic engineer myself and have studied a few communication protocols. My question arose during my contemplation of how we encode information in electronic systems.

Well, do we know it 'exactly'... no. But we do know a lot. But the visual system is large and complex. From physical stimulus to 'interpretation', as you say you wish to learn, is a lot to ask for. It spans the full range from sensation to perception to association - impossible to capture in a single answer. Dependent on your background knowledge, it may take a full uni course to even just understand the very basics I reckon.

I am only curious to know to what extent we can create an artificial eye that behaves like the real one at the present time

That answer to that Q is very simple - we can't :) Bryan has abstracted that below. I've worked with folks with retinal implants - while promising, it's not even close to normal vision.

I think the encoding is quite well understood, and in fact there are artifical cochleas available for deaf people: https://en.wikipedia.org/wiki/Cochlear_implant
For retina replacements, I think the hurdle is establishing the connections from any device to the nerve.  There are roughly 120 million rods and 6 million cones in the human eye. (Per Wikipedia: https://en.wikipedia.org/wiki/Photoreceptor_cell )  These connect to about 1.2 million optic nerves, so making the proper connections would seem to be a non-trivial matter.

Cochlear implants work by stimulating the nerves that normally innervate the hair cells. They give very low resolution - only about 20 total sites over the entire frequency spectrum. It would be just as much a hurdle to connect to the 30,000 auditory nerve fibers. However, there is enough redundancy in speech that the 30,000 -> 20 mapping is enough to resolve some speech from one talker (some other cues for direction and resolving multiple talkers are much more difficult). You can do the same thing in the retina, the problem is that you don't get much useful vision out of that low resolution.

See also: https://en.wikipedia.org/wiki/Visual_prosthesis

@Bryan Krause: I'd disagree that it's just as much of a hurdle. 20 into 30,000 nerves is rather easier than 20 into a million.  The problem is that hearing is linear, while sight is two dimensional, so for equivalent resolution you need to square the number of sensors/connections.

Even 20x20 pixels isn't much. It's less about 2D and more about temporal vs spatial resolution; it's a lot easier to put temporal information into one channel than it is for spatial. Paul Bach-y-Rita did make a tongue stimulation device for vision ( https://en.wikipedia.org/wiki/Brainport ) that gives about that 20x20 resolution. It's enough to help not bump into stuff but you aren't going to read. The rest of the information is conveyed with pre-processing rather than trying to render an actual image.

In general I would say a lot is known:
Seeing starts with the photo-receptors. See "signal transduction" section of the Wiki:
Signal transduction works though rhodopsin and subsequent closing and opening of ion channels.
Then the signal is transferred from the optic nerve to the brain.
Hearing works though hair cells and mechanotransduction.


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What specific markers does a Covid-19 PCR test look for?
I've done a search and can't find anything as to what specifically makes a Covid-19 positive that identifies it as unique. I would expect to see something like this:
https://madridge.org/journals-admin/uploads/fulltext/MJV/images/mjv-118-t002a.gif
or
https://i.stack.imgur.com/423Ay.jpg
Instead I find this:
https://communitymedicine4asses.files.wordpress.com/2020/05/2020-05-07-17_38_07-covid-19-testing-what-you-should-know.png?w=624
and
https://myrepublica.nagariknetwork.com/uploads/media/PCR_20200513092900.jpg

The SARS-CoV-2 diagnostic tests that are currently in use, both serological and nasal swab, are binary tests - they either are positive or negative, like a pregnancy test. They do not (yet) report viral titre, like the first image you linked, or look at restriction enzyme "gene fingerprinting" patterns, like the second. They simply tell you if either a part of the virus is in the sample (RNA or capsid protein in the two nasal swab tests) or if your immune system has seen enough of the virus to mount an antibody-mediated immune response (the IgM/IgG blood tests).
It's worth pointing out that all of the current tests in the US are available under emergency use authorizations from the FDA, meaning they haven't gone through the usual (and time-consuming) process of full qualification and validation. That type of work needs to be done in order to develop quantitative testing ("You have a viral titre of X, compared to an average range of Y through Z."), which will likely appear in the coming months and years as the proper development work is done to support their validity.

Thank you for your answer. If I'm reading it correctly, it's not know what specific markers make a test positive, it just pops up positive?

@JohnSmith It depends on the specific test, each is designed differently.

@JohnSmith the markers are known, that's how the test is developed. For example, for the PCR test, primers are chosen for a specific unique region of SARS-CoV-2 RNA that doesn't exist in any other organism, and that fragment is amplified in the reaction. The binary answer is whether or not something amplified in a particular reaction. A quantitative answer would be something like a qPCR test where a standard curve is generated and you can then back-calculate the starting concentration of RNA. [...]

[...] For the antibody test, for example, they use a recombinant protein from the virus's capsid/envelope and run a biochemical reaction that changes color if any human IgG or IgM binds to it - it's based on the same principles as a capture ELISA. The nasal swab virus surface protein detection test is also ELISA-based, but in a different configuration. The point is that in all three cases, all of the components of the tests are known and well-characterized, but the answer they give is either yes or no - present or absent. Does that help?

To my knowledge, all of the PCR-based tests that have been authorized for diagnostics use fluorescently labeled reporter probes specific to the the SARS-COV-2 viral genome. In real-time PCR, the intensity of this fluorescent signal is measured (spoiler alert) in real time, after each amplification cycle. The fluorescent signal increases with the amount of the target sequence present in a reaction. If the signal exceeds a certain baseline threshold before a certain number of PCR cycles, the test is considered positive for that target. It really is as simple as that, but a lot of work goes in on the development and validation of these threshold cutoffs to ensure they are sufficient for sensitive detection.
What identifies the readout as unique to this virus is the design of the probes and the primer sets that go with them. These are designed to be highly specific to a given target, and are validated in silico against existing sequence databases, and also empirically against closely related organisms, or just against other things that might be present in a specimen. They should also target conserved regions of the genome that are unlikely to mutate. Most of the tests I have seen use at least two different SARS-CoV-2-specific probe targets, and at least one amplification control (often targeting a conserved human gene) to ensure that the reaction enzymes are functioning properly. But the specific regions of the genome that are targeted can vary between different tests.
Using real-time PCR saves clinical lab techs the time and effort of making gels and running the amplified PCR products out on the gel, like those in the second example you posted. This not only improves the turnaround time for testing results, but saves countless work hours for the clinical labs processing these tests, especially when you consider the scale of how many tests are being processed right now.
As with any nucleic acid test, a positive result can only indicate if the target is (or was) present. It does not provide information to clinicians about whether it is actively replicating or even infectious. But in general, this kind of testing is highly sensitive and specific when properly designed and validated.


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From what kind of insect might these eggs be
Does anybody know what kind of insect might have laid these eggs:
The photo was taken a few days ago in Limburg, Belgium near a pasture with some goats.

Those are likely moth eggs... moths have a tendency to attach their eggs on metal screens that you might have in your windows or doors.
Here is a video of a moth laying eggs on glass:
https://www.youtube.com/watch?v=L2zf1J8CZdg
Here is a video of a moth laying eggs on a metal screen:
https://www.youtube.com/watch?v=qKHReVNAMYw
Here are photos of eggs on a wire fence, believed to be moth eggs:
https://www.whatsthatbug.com/2013/09/19/possibly-moth-eggs-deer-fence/
And another example of moth eggs on a metal wire:
https://hardtocomebylifestyle.wordpress.com/2014/08/31/moth-eggs/


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Auto-immune problems if immature B-cells released if bone marrow bone is fractured?
A fracture of a bone containing bone marrow with B-cells not yet taught to not recognize self-antigen, if the bone is fractured, can those cells get released and cause problems?

Most likely not, because immature cells require other signals from the marrow to survive, so "spilled" cells likely wouldn't last long.

Thanks good answer, sounds evolutionarilly probable.


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Why there is unusually big leaves on a single tree branch
I have a freshly planted katsura tree - in general it has leaves that are 1-2 inches in diameter.

But one single branch has grown disproportionally longer than others and leaves on this branch are up to 4 inches in diameter

Why is that? Should I trim it?

I'm not sure we can answer the bit about whether or not you should trim it (there is a landscape/gardening beta here which may be better). But what kind of 'why' answer are you looking for? One which explains it in terms of physiology / evolution / biochemistry / environment interaction?

With many plants, including Katsura, the juvenile foliage is different from the mature foliage. With Katsura the juvenile foliage has larger leaves.

The rest of new leaves are about the same size and structure as older leaves. Also no other branch has grew up THAT much - they added maybe a few inches but this one added 2 feet. I'm curios what may be the cause.


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Chiasmata and Adaptation
We know that during the crossing over of meiosis II, some portions of the paternal chromosome recombine with the maternal chromosome along the  chiasmata. And the number of chiasmata varies.
My question is this: If the crossing over is responsible for genetic variation, then does the number of chiasmata increase in the same chromosome in the same species for the sake of the species' survival? And if so, what factors contribute towards increasing that number?

Welcome to SE Biology! A note - selection virtually never occurs at the level of the species - it is almost always occurs at the level of an individual organism (or gene). So your question might be better framed if you ask about how crossing over might affect the fitness of an individual rather than how it might affect 'the survival of the species'.

The number of recombination events (chiasmata) varies dramatically from species to species.
It is also unlikely that this number has any universal relationship to selection, though for specific cases it has been shown that selection can change recombination frequency.
For some more information about the processes controlling this in present-day species and the inferred mechanisms driving among-species variation in recombination frequency, you might see this paper.


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are there examples of research harmed by the binary vs. non binary genders discussions?
As a base for my question, here is a link to an article from nature.com: https://www.nature.com/articles/d41586-020-00502-w
In the article, the following paragraph is relevant:

The researchers noticed that male participants’ typical immune
response to infection differed from that of female participants, which
could explain the more severe disease often observed in men. (Nature
recognizes that sex and gender are neither binary nor fixed.)

Obviously the researchers, studying immune response difference between sexes, made two categories: Male and Female.
Then the Nature article, trying to fit with the times wrote that they recognize that sex and genders are not binary, and if they really believed it themselves, they'd probably not publish research as it would be based on a model they say they don't believe in.
My question is: are there known examples where research has been openly discredited (in a publication, or through a public speech on the media) because it is based on the binary definition of sexes and therefore 'not inclusive'?
(for reference I believe Humans are XX or XY and that's it, so this may bias the question / terms I used)

Interesting though your question may be, it is not a question about a biology in the terms of SE Biology, in that it is a question about social influences on scientific practice and publishing, rather than a biological problem. For that reason I have voted to close.

@David, I understand the improper fit. Can you think of another site where the question might be a good fit since I'd like it to be seen by people in the biology field.

Sorry, but I only do hard question and answer sites like Stack Overflow, this and English Language. I happen to subscribe to Nature and noticed the editorial intervention you refer to, but at my age I avoid political discussion with people I do not know. Certainly I prefer to keep this site on topic — I can provoke antagonism easily enough without meaning to just doing that.

I think your logic is a little flawed here. Just because a classification system is not universally binary or fixed (few biological concepts are) doesn't make it useless. If it did, we would have abandon species classifications long ago.
Philosophy or politics would probably be more appropriate stacks for this question.

@Thomas I would possibly recommend dropping the political terminology (i.e. "political correctness") if you want to engage with biologist on this matter, most of whom (like David said) are quite politics adverse.

@4galaxy7, point taken; I'll edit it. Maybe Philosophy is a good place, but I was looking for real examples where this would be an issue in research and I'm afraid Philosophy would be a good place for a debate, but I wouldn't get the answer I'm looking for. With Philosophy, you end up with more questions than when you start usually :D

Your statement that "Humans are XX or XY and that's it" is false. Humans can be XXY, XYY, XXX, XO, and others. Gender and sex are biologically not binary.

I think that you will find that the opposite is the case more often.
First of all, a premise that XX vs. XY has some kind of fundamental truth (which really is a premise of this question) is simply incorrect. There are a wide variety of karyotypes of the sex chromosomes, and these do not line up well with common notions of sex.
Using the XX vs. XY heuristic, and trying to fit e.g. intersex people into it, leads to positively incorrect and unnecessary therapies and surgeries in medical practice. A strong devotion to an XX vs. XY binary simply writes off something like 10% of the population, who are biologically neither male nor female according to that criterion.
Fausto-Sterling's book Sexing the Body was my introduction to this topic, though I am certain that there are more recent works.
So, on the contrary, you are more likely to find instances of people who don't fit the binary being harmed by the binary than people who do fit the binary being harmed by "woke" verbiage.

Very interesting answer. I asked the question as a part of a debate with friends and now I feel like I learned something worth reading a lot more about. Thanks!

@Thomas lovely to hear that. Thanks for taking it seriously- we're all here to learn!


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With the 5$ covid19 test - an antigen test - , would trials (most likely) be independent?
Actual question
What would typically cause antigen tests to give a false positive or false negative and would these causes be typically independent (if we run the test twice it won't automatically fail twice) or would such tests typically fail in the same manner and thus consistently give the same result for the same person? Or is this completely different from antigen test to antigen test and nothing can be said in general?
I hope this question is narrow enough, and I totally accept an answer of 'nothing can be said in general'.
Background
Abbott’s BinaxNOW was recently approved by the FDA. These are the false positives and false negatives rates given by Abbott:

Abbott says that the test correctly diagnoses a coronavirus infection 97.1 percent of the time, and correctly returns a negative result 98.5 percent of the time.

Therefore, the probability that one has the disease given that they test positive is - if I didn't make a naive mistake in my application of Bayes theorem and assuming 1% of the population currently has it - only 39%. This obviously is... pretty bad.
The useful thing about Bayes theorem though is that we can also calculate the chance of actually having Covid19 if we take the test twice assuming that both trials are independent (97%).

Your interpretation with Bayes therom is likely on point, and this is a problem with broad testing of populations with low underlying rates. It's easy to find scenarios where are test is returning more false positives than true positives, even with what seems like a good specificity values around 99%. My intuition tells me that this might not be independent, and that retesting a false positive would yield similar result, since a false positive is likely the result of non-specific binding to similar antibody. But they say that immunology is the place where intuition goes to die.

I don't know enough immunology to answer the question properly, but here's a cool article that goes through the numbers and talks about when it's useful vs. when it's harmful (https://blogs.sciencemag.org/pipeline/archives/2020/08/27/thoughts-on-a-new-coronavirus-test-and-on-testing)


text:
Cancer in cardiac cells
We were recently taught that  cancer occurs only in those cells which undergo cell division so, cancer is not possible in cardiac cells and neurons.
But we know that till a certain age our heart grows in size so that means it goes under cell division. So doesn't that mean that cancer can also occur in heart cells?

Though very rare, primary cardiac tumours do exist.
Most of the 1° cardiac tumours are benign, malignancy occurence is pretty much low.
Give it a read—
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3113129/

As the other answer has already stated, there are cases of heart cancer. Just to expand on that answer further, according to this article, the rate of heart tumors is a mere 1.38 in 100,000 people per year and of that only around 10% are malignant (truly cancerous tumors) in nature. Just to put this into perspective of how low of a rate this is, the overall rate of cancer in the U.S. for both men and women combined is 352.2 per 100,000.[source]
Doing some rudimentary calculations, if the rate of malignant tumors is one tenth of 1.38 in 100,000, that means the rate of heart cancer is around 0.14 per 100,000! Just to add to how rare this is, the Mayo Clinic on average only sees around one case of heart cancer per year.[source]
Also, to clarify your statement about what types of cells can have cancer, it is not only dividing cells that can have cancer (even though the majority of cancer originates from cells undergoing a lot of cell division such as the skin and GI tract). While cell division by its nature causes a vast number of the mutations which would potentially lead to cancer, other environmental factors such as toxins and radiation could cause also cause similar mutations in cells that might not even be dividing.


text:
What is this insect, is it a butterfly?
I am not sure if this is the good place: I am wondering what sort of insect is in this picture. It is approximately 10 millimeters long and 15 wide with the wings.

I have found one of them each day for one week, in my flat, near the coast of France. Tonight I found three of them at the same time. I am wondering if they are dangerous/damaging....
Thanks in advance for any help

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Looks more like a moth than a butterfly to me


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Why PCR primers don't amplify beyond the target region?
I have been doing PCR for a while. I spared a bit of time to look it up but could not find an answer. So, for sanger sequencing, if we have a primer, it can amplify about 800-1000 bp. But, if you design a set of primers (forward and reverse) for PCR it will just amplify the target region. How does DNA synthesis from the forward primer stop when it reaches the point where the reverse primer is? How does the other primer which is binding to a different strand can stop the DNA synthesis in a complementary strand?

They don't stop replication. It's just that you replicate your dna in a number of cycles, let's say 30. after which you'll have a approximatly 10^6 molecules of the amplified region and only a few longer strands.
If you draw it out you'll see that your region of interest quickly start to dominate.
original strand
----/  /----ppp-------------------------/  /--
----/  /-----------------------qqq------/  /--

after one cycle
----/  /----ppp-------------------------/  /--
            -------------------qqq------/  /--

----/  /----ppp-------------------
----/  /-----------------------qqq------/  /--

after two cycles
----/  /----ppp-------------------------/  /--
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq------/  /--

----/  /----ppp-------------------
----/  /-----------------------qqq------/  /--

----/  /----ppp-------------------
            -------------------qqq

after three cycles
----/  /----ppp-------------------------/  /--
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq------/  /--

----/  /----ppp-------------------
            -------------------qqq

----/  /----ppp-------------------
----/  /-----------------------qqq------/  /--

----/  /----ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

after four cycles
----/  /----ppp-------------------------/  /--
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq------/  /--

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq------/  /--

----/  /----ppp-------------------
            -------------------qqq

----/  /----ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

----/  /----ppp-------------------
            -------------------qqq------/  /--

----/  /----ppp-------------------
----/  /-----------------------qqq------/  /--

----/  /----ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

            ppp-------------------
            -------------------qqq

etc.

How does DNA synthesis from the forward primer stop when it reaches the point where the reverse primer is?

Briefly, it doesn't. You get a lot of single-stranded long pieces of DNA (step 1 here, notice the overhang ends). But the exponential part of PCR only amplified common overlapping regions in these long single strands, also known as your target region between Fwd and Rev primers (step 3)

src


text:
Using serotonin for relief from allergies
When someone suffers from an allergy, due some allergens they are given drugs like anti-histamine, adrenaline or serotonin. How does serotonin affects the body to give a relieve from the action of allergents?
What is the physiology behind this?

Welcome to the Biology commmunity. Please improve your question by citing sources of the information used (in particular, that serotonin is useful in relieving allergies).

Also, please mention in your question body what attempts you made to answer it yourself. This will enable users to post helpful answers.


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Killing enveloped viruses with soap

Unlike non-enveloped viruses, enveloped viruses can be killed with soap, alcohol, etc. Why?

Why does just having an envelope make it susceptible to soap and alcohol?

(+1) Re: "Why does just having an envelope makes it susceptible to soap and alcohol?": We often describe humans as "two-legged" and cats as "four-legged", but in the parallel universe where humans are "handed" and cats are "non-handed", someone is asking why "just having hands" makes humans so much more susceptible to loss of balance.

different but related: How exactly does alcohol solution kill or neutralize viruses?

@Alex Reynolds do you know how soap and alcohol affect other viruses and or bacteria? does it make sense to only use soap or is a good alcoholic desinfectant still better?

If the CDC can still be trusted any longer, it indicates that washing your hands with soap and water is a good way to stay healthy and avoid a number of bugs, and that it does better at that job than alcohol-based hand sanitizer: https://www.cdc.gov/handwashing/show-me-the-science-hand-sanitizer.html

Soap molecules are amphiphilic. This means those molecules have parts which are hydrophilic (water-loving, or "polar") and parts which are hydrophobic (water-avoiding, or "non-polar").
Fat molecules are non-polar. They avoid water. This is why a mixture of oil and water will separate into layers. In this mix, oil molecules prefer to hang around other oil molecules, and water molecules prefer to hang around other water molecules. Soap "likes" both oil and water, so it can be used for cleaning, by helping dissolve this mixture. (For a similar reason, this is why vinegar is used to dissolve or emulsify oil in salad dressings. Vinegar — acetic acid — is amphiphilic and likes both water and oil.)
The coat of an enveloped virus is made up of layer of phospholipid molecules and proteins. Phospholipid molecules are similar to detergents, made up of polar and non-polar ends. These lipids arrange themselves into a two-layered sandwich called a "bilayer". The polar ends of this sandwich are the "bread", while the fatty non-polar ends are the "filling".
Detergents can help disturb this by pulling or dissolving out phospholipids from the virus coat to form micelles, tiny bubbles of fat and soap that can be washed away. This puts holes in the virus coat and helps dissolve it.
The insides of the enveloped virus particle cannot infect directly and must rely on its envelope to get into and infect a cell, so breaking down the coat inactivates (or "kills") the virus.
Alcohols are also amphiphilic. There are many different alcohols, but they all have a hydroxy group at one end, which is polar, and a saturated or partially-saturated carbon chain on the other end, which is non-polar. Like detergents, this amphiphilic property allows an alcohol — at a sufficient concentration — to disturb and break down the virus envelope phospholipid bilayer, inactivating it.
Non-enveloped viruses lack this phospholipid bilayer coating and are instead protected by a protein capsid. The proteins in a capsid will not dissolve with detergents, but they can be attacked with other disinfectants that chemically denature the proteins. Examples of such disinfectants are chlorine (bleach), iodine, peroxides, etc.
Just as soap can put holes into the phospholipid coating around enveloped viruses, destabilizing them, denaturing agents change the structure of proteins that protect non-enveloped viruses, also destabilizing the capsid. If the capsid proteins are damaged sufficiently, the virus particle is not able to infect a cell and so is deactivated.

Great answer, but a minor organic chemistry quibble - alcohols are defined by having a hydroxy group attached to a saturated $\alpha$-carbon, but further down the chain, any existing carbons don't necessarily need to be completely saturated.

Small correction: enveloped viruses also have a capsid.

Feel free to add a better answer to How exactly does alcohol solution kill or neutralize viruses? or we can consider closing that as duplicate of this question. I find this answer much more informative, and you've covered alcohol here to some extent.

I don't mind; whatever you prefer.


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Can any glider incapable of powered flight strike its prey by descending on it?
TLDR
I was not able to find the precise definitions of “true flight“, “sustained flight“ and “gliding“, that are often used on Wikipedia.  My layman’s understanding is that true flight is the same as “powered flight” and means the animal can utilise muscles to generate life force that exceeds its weight under a wide range of air flow conditions. That is, it does not need upward air currents such as thermals
By contrast, gliding is defined here as:

falling at an angle less than 45° from the horizontal with lift from adapted aerofoil membranes

You are welcome to suggest more correct definitions.
Question
Can any animal that glides but is incapable of true flight (of course hawks may glide) descend upon its prey?
I am aware of this question not being very well defined, since animals such as sugar gliders can jump on their prey and  perhaps utilise a tiny amount of lift to prolong their jump. It is difficult to rigorously separate this from gliding. Let’s require that the animal glides a distance more than 10 times its length from a height more than 10 times its height.
Inconclusive information
Bats
Don’t count because they are capable of powered flight. But they can do it.
Sugar gliders
Can “leap out to catch flying insects“ (source), but that’s all I found.
Flying squirrels
“harvest fruits, nuts, fungi, and birds' eggs”(source), so they may not even prey.
Colugos
Appear to be strictly vegetarian (source).

Sure, but it would be very situational. True flight = powered flight = sustained flight (although an albatross soaring the waves indefinitely could be technically be sustained but does not follow the spirit of the term).


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How can tooth enamel feel pain when drilled by a dentist?
Enamel has no nerves, so theoretically a tooth should not feel any pain when a dentist bores into it. Yet still we use anesthetics...
Maybe it’s dentin's fault? It apparently has some tubes filled with liquid and the tooth's nerves can feel this liquid's movement. So, maybe, the closer the dentist gets to dentin (especially if he/she touches it), the more pain is felt? By the way of vibrations from the boring tool?

I was wondering about this from the opposite direction, actually. I always refuse local anesthetic for simple dental work, because I never feel anything and I hate having my mouth numb. So I'm curious if other people's teeth are somehow more sensitive than mine!

@Glenn Willen Definitely! How a local anaesthesia is going to work, how much time it will take to numb the area does depend on an individual. There are people who are resistant to a type of local anaesthesia, eg lignocaine. In those, other types are used. Whereas many people are allergic to one of the components of local anaesthesia. Also if there is lot of inflammation then it takes time plus more dosage of local anaesthesia is required to come into action. So it depends on lots of factors.

Whether an individual wants to have an anaesthetic injection or he/may will resist that pain, purely depends on him/her.

Where I am, the dentists use a range from "No need for anesthesia here" over "Probably no need for anesthesia" to "This will hurt - would you like to get anesthesia" and "You need anesthesia". Sometimes also: "if the nerve is not yet dead, you'll need anesthesia"

@cbeleites unhappy with SX but I am sure, that must be working fine. They must be accurate in their probabilities!

@Ojasvi: they don't need to be - they express uncertainty in the intermediate variations ;-). Their repertoire also has suggestions like "would you like to try without".

@cbeleitesunhappywithSX I had a root canal near a live nerve last year taking long enough to require multiple sets of anaesthetics. They were not an option and it still hurt a lot more than the anaesthetics could hide. I'd been wondering why that was, but the answer explains it quite well. If your gum is sub-par (like mine), there's dentin exposed that really doesn't like the procedure.

@cbeleitesunhappywithSX Agreed! That maybe because of toxic effects of local anaesthesia and some patients are scared of the 'injection'!

@Mast if it was a root canal then,  below the dentin, pulp must have been exposed and severely infected. Pulp has neurovascular supply. Now generally giving local anaesthesia, the pain doesn't happen, but in your case infection would be so much that the effect of anaesthesia would be very less or your tooth might be less sensitive.

Yes you are right. It is the dentin.
Enamel has got no nerves.
So when the dentist use his/her instrument, initially there is no pain (if the enamel is intact).
The next layer is dentin. As you said, dentin has got dentinal tubules containing dentinal fluid.
Whenever there is any stimulus which has not yet reached the pulp, but may have reached the dentin, eg of stimulus in the form of pressure, temperature change, sweet food, sour food etc, cause the fluid to move or get displaced. The displacement of dentinal fluid stimulates nerve endings in the pulp and hence generates a pain/ sensitivity response to your brain.

Reference

Reference

There are three main theories of dentine hypersensitivity:
Direct Innervation (DI) Theory
Odontoblast Receptor (OR) Theory
Fluid Movement/Hydrodynamic Theory

The Hydrodynamic or Fluid Movement theory is one of the main theories in dentistry to explain the mechanism by which a tooth perceives the sensation of pain. It is currently the most widely accepted theory used to explain tooth sensitivity.

Reference
Now the drilling causes heat generation, even though little, due to the coolant, plus pressure and hence causes the fluid to displace and hence pain. This pain usually ends after the treatment.
Hence anaesthesia is required.
Hope I have answered your question :)

Very nice images too, I wouldn't be able to find them myself!

The heat generated by grinding is critical. Being very old ,my first ( painful) dental experiences were with the old belt drive drills = hot=painful . When the water turbine drills came along it was a whole new world ; Novocaine shots were unnecessary for drilling..

@blacksmith37 Oh! I didn't know about the belt drive drills. With their low speeds and without water coolant they must be very painful plus dangerous for the tooth also! In the current scenario yes, the increased speed handpieces with a water coolant are used, but if the tooth is very infected then they do cause quite significant pain as the dentin thickness in those cases is very less. And hence anaesthesia is required. Interestingly, these days lasers too are used which are not at all traumatic for the patient as well as the tooth.

I was always told that tooth structure was like a stack of straws on their side. Now, finally, I'm getting the picture. Great answer, thanks!

@uhoh well, enamel does have a kinda stack of straws like structure. It has got enamel rods which are arranged vertically and obliquely!

More generally, the same can be said of sensory nerves anywhere in the body. You don't have to physically touch a living nerve cell in order to stimulate it: Touching/stressing/heating/cooling nearby tissue causes the tissue to release chemical signals that stimulate nerve endings which can be, in some cases, up to several mm away from the site.


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Are sizes of potatoes normally distributed?
I'm currently researching the variability of sizes of potatoes when all of the potatoes in question have been harvested from a single field. One question keeps coming up in my statistical analyses: Under normal circumstances, are the sizes of potatoes - within a single field - normally distributed? (Please feel free to define the weasel words "normal circumstances" in the most helpful way you can imagine.)
Human height is often given as one of those classic examples of a normally distributed phenomenon. The little that I know about plant biology suggests that the central limit theorem applies just as much to potatoes as to the human body: the lengths of potato tubers and the lengths of human bones should have similarly-shaped distributions. But is that correct?

A bit of context to my original question: what I'm trying to do is to take the mean and standard deviation of my data and then, using the 68-95-99 rule, construct a series of confidence intervals, which I can then test or refine by looking at other data sets. Obviously, no real data set is going to conform perfectly to a model; I just need to know that, in principle, potato sizes are normally distributed enough that my method for drawing up confidence intervals isn't hopelessly misguided.

There seems to be some misunderstanding of the central limit theorem (CLT). CLT emphatically does NOT say that all variables in nature are normally distributed. Rather, it says that the sample means are normally distributed (approximately) when sample size is large.

The only way to find out whether the sizes of potatoes or human beings are normally distributed is empirical measurement.

@Adhish Forgive me if I didn't express myself as clearly as I might have done. I did not claim that, because of the CLT, all natural phenomena are normally distributed; I merely suggested that, because sizes are normally distributed in humans, it is plausible that they might also be normally distributed in potatoes.

@Adhish 'The only way to find out whether the sizes of potatoes or human beings are normally distributed is empirical measurement.' I was hoping that someone would point me to some empirical research on the topic. That's why I asked the question.

If you have data from your potatoes of one field, can't you answer empirically what the size distribution is from your own data?

@BryanKrause I have to emphasise that I'm not a professional statistician, but the data from the one field I've had a chance to examine properly do seem to be normally distributed: they're clustered symmetrically around the mean. But it's not a classic bell curve, and I'm anxious about seeing only what I want to see. If someone could point me to a paper that said something like, "Potato sizes generally follow X distribution", that would save me a lot of weeping and gnashing of teeth.

@Adhish as far as I know, since height is the average of many QTLs it is normally distributed since it becomes a distribution of the means of these genes. I use this alot so I'd like to be corrected on this if I'm wrong

Most statistical comparisons are comparisons of AVERAGE1 versus AVERAGE2, versus etc. It is the averages that are normally distributed.

@Hachiloni That seems to be a valid approach, but I'd still say it depends on the trait in question. What is valid for height may not be valid for other quantitative traits. (See https://www.genetics.org/content/204/3/1281 for a discussion on non-normal quantitative traits.) I guess a lot would also depend on how much of a deviation from normality one is willing to tolerate.

Not an answer, but you might want to reconsider what a normally distributed variable means and why you want to know it, since height seems to deviate significantly https://stats.stackexchange.com/questions/360254/why-does-the-distribution-of-height-follow-normal-distribution. Also https://stats.stackexchange.com/questions/2492/is-normality-testing-essentially-useless

It is important to keep in mind that the normal distribution is a model. George Box had something so say about models. You should also carefully consider why you care about the distribution of potato size. You might be looking at the wrong thing here (e.g., in regression analysis you'd care about the conditional distribution only) or be able to remove this assumption (non-parametric statistics comes to mind).

Thank you to everyone for contributing your brain power to this surprisingly tricky question. I've just added some context to my original post which might simplify things a bit.

If your sample is not too small, you could use bootstrap to derive CIs for the mean, no distribution assumption needed.

Empirical observation (growing potatos in my garden) suggests not.  From any mature plant (that is, when the tops die back) I will get several large ones about the size you'd find in a store, several smaller ones that might go as "baby" potatos, and a bunch that are marble to pea size.  Presumably commercial growers sort out the small ones before sending the rest to market.

@TomHosker if you are only trying to calculate CI for the mean of the potato size in the field AND you have enough samples (usually 30) you can assume the mean size of the potato is distributed normally. There are methods to find the best distribution fitting your sample and than you can calculate CI.

According to Evaluation of the Effect of Density on Potato Yield and Tuber Size Distribution potato tuber size was estimated using a normal distribution but they are not normally distributed
They found that a Weibull distribution with specific parameters estimated better than a normal distribution.
In fact you should not expect a normal distribution because there are no potatoes of negative size  As such you expect a gamma distribution.  The Weibull distribution is in the same family of distributions.
But in many cases the normal distribution is used since the probability of a negative number is negligigble.
Does this mean that potato sizes are still the result of many factors? It would seem so

The link to "this article" for me yields "access denied".  Perhaps a bit more explicit citation would be good.

StackExchange answers should stand on their own; other references are great and are even required in many cases here at Biology.SE, but people need to be able to read your answer and understand it by itself, too.

@BryanKrause could you elaborate? I don't know where to elaborate more. One good article states they are not normally distributed and cites others that say the smae. I edited for the name of the article per mgkrebbs comment

i added more explanatory text with a reference.

I'm on the cusp of accepting this answer. I've just added some context - hopefully helpful - to the end of my question. If you could make a brief comment on that, then I'll give you the green tick.

As a side note: I'm not convinced by your claim that 'you should not expect a normal distribution because there are no potatoes of negative size'. There are plenty of normally distributed phenomena which never take negative values. Am I misunderstanding something here?

If you are looking for the CI of the mean and you sample n >30 you can assume the mean is normally distributed per CLT which is different from the distribution of the potatoes. I added another link explaining why the normal distribution is used for only positive vallues. In short, the probability of a negative is so low that it is ignored


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How can the layperson test whether a UVC light sold as "germicidal" is a fake or probably the correct wavelength?
Are there simple ways to test whether a light is likely short wave / UV-C, or at least whether it is probably a fake?
Real Example:
2 lights are allegedly germicidal and supposedly emit germicidal 254nm radiation.

Light 1 darkens transition glasses and emits the smell of chlorine / ozone.
Light 2 does neither but appears much brighter than Light 1.

Does the ozone smell of Light 1 entail that it at least emits radiation within the UVC band?
Assuming the glasses do darken outdoors and do darken in response to Light 1, given that they do not darken with Light 2, is it safe to conclude Light 2 emits no UV at all?

I’m voting to close this question because it isn't about biology — please consult the [tour], [ask], and other [help] pages for details.

@tyersome will this question be a better fit on one of the other SE sites,if so it should be migrated.i think the question is important to get answered as there is a lot of fake gemicidal lamps on the market and we are in a pandemic at the moment.i do not disagree wit this question beeing a poor fit here on biology but what are the alternatives.

@trondhansen — If I had a good suggestion I would have made it — since this seems to be fundamentally an optics question there might be a place for it in physics. However I'm not familiar with that site, but since this is a "how do I do this at home" question rather than one about fundamentals of science I'm skeptical whether it would be a good fit there. I think there is also a site about DIY/home repairs. Finding the right site is ultimately the responsibility of the poster. Also note that there is no guarantee that there will be a SE site for any particular question!

Sometimes Physics SE is very helpful, but not always. I think if you have a little patience and the question is closed and then migrated by a moderator, there's a good chance it will receive an answer, though I don't know if it will be helpful.

FYI: a "blacklight" LED will darken transition glasses (Don't ask me how I know!)

Transitions lenses darken with exposure to UV-A light, so they do not indicate whether a bulb is emitting UV-C or not.

You can do the banana test to identify if it is real or fake.
Get a green banana and cover parts of it with a sticker you now need to expose the banana with the uv light for about one hour,the green banana will get brown/yellow at the exposed part and stay green under the sticker if the uv-c light is genuine..
It is best to do this in a dark room and the banana can not be in a plastic bag or any covering as this might stop the uv-c light.
The uv source needs to be close to the banana for this to work.
If the color of the green banana stay the same after the test your uv-c light is fake.
Never look directly at the uv-c light and do not shine the light on your bare skin.
source https://www.reddit.com/r/BigCliveDotCom/comments/gj9ymb/uvc_the_green_banana_test/

Re, "Never look directly at the uv-c light." UV-C exposure will hurt your eyes alright, but it doesn't matter whether you "look at" the light or not. The UV-C rays will never reach your retinas. All of the damage will be superficial. Don't expose any part of your body to UV-C if you can avoid it, and also, don't breathe the ozone.