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Do wolves mate with siblings?
I have just watched a "documentary" on a female wolf raising her cubs in the Alps. I found various aspects of the programme less than convincing, but one in particular puzzled me. The alpha male of the pack is killed, and his eldest son takes over as alpha. Whilst the alpha female remains with her dying mate, the programme stated she could not rejoin her pack, as her place had been taken by her daughter. This would mean a brother-sister mating - the female became pregnant very soon - which I find highly unlikely, although perhaps not impossible.
Wikipedia simply states:

Wolves are monogamous, mated pairs usually remaining together for life. Should one of the pair die, another mate is found quickly. With wolves in the wild, inbreeding does not occur where outbreeding is possible.

Wondering if there are any wolf experts on here?
https://en.wikipedia.org/wiki/Wolf

Do you have a link to this "documentary"?

@MattDMo - yes, it's this one, it does say it was "dramatised", which was fairly obvious, but still wondering how true to the facts it was. Thanks.  "BBC Two - The Snow Wolf: A Winter's Tale" https://www.bbc.co.uk/programmes/b0bwqdbg

I'm in the US, so unfortunately I can't watch the program. Usually the BBC is pretty good about trying to get the facts right, but seeing as they heavily emphasize the "dramatised" part, they may have played fast and loose with a few key details. OTOH, I'm an immunologist, not a wolf expert, so I can't really answer your main question. I hope it was at least a good show.

@MattDMo - thanks for looking, anyway. I have a feeling I've seen it before, but the last showing had a disclaimer at the end, saying it was filmed using a variety of wild and captive wolves. That disclaimer was not shown this time, if it was the same programme. But, yes, the scenery and film work were spectacular!

Mating with siblings or incestuous relationships (breeding within blood relatives) enhances the chance of expression of disadvantageous characteristics (mostly recessive alleles). Therefore, natural selection for complex animals occurred in such a way they avoid close relation mating. Wolves are no different. One study by Smith et al. 1997 with the samples from 16 wolf pairs showed that wolves rarely mate with their close relatives. However, inbreeding does happen on infrequent occasions. For example, a pair of wolves migrated to Isle Royale through an ice bridge in 1948. They are the first wolf pair on the island (founder population). The ice bridge doesn't happen again. Through the help of inbreeding (population bottleneck), the pack survived, and the population became 50 individuals [Inbreeding Causes Isle Royale Wolf Population Crash]. However, genetic diseases started expressing, and morphological deformity became very common in that wolf population. Therefore it is clear that nature support variation by avoiding inbreeding. And though billions of years of permutations combinations, biological organisms avoid inbreeding in ideal conditions.

Thank you, a very informative answer. I do  know most animals - including humans - avoid incestuous mating, although it is not unknown. Being more comfortable and with history, I know that brother-sister mating is thought to be responsible for the end of Tutankhamen's line, with two stil-born infants found in his  tomb. I did just find the email whole scenario in the programme unlikely.

I am not a wolf expert, unfortunately, but was able to find an article focused on just this question with grey wolf packs (1). The article studies relatedness via microsatellite locations in the DNA of mated pairs, and found that incest is seemingly avoided when possible, which supports your Wikipedia finding. Another article on Ethiopian wolves came to similar conclusions- wolves avoid inbreeding where possible, and resort to extra-pack matings when necessary (2).
Reference: (1) Smith, Deborah, et al. "Is incest common in gray wolf packs?." Behavioral Ecology 8.4 (1997): 384-391.
(2) Sillero-Zubiri, Claudio, Dada Gottelli, and David W. Macdonald. "Male philopatry, extra-pack copulations and inbreeding avoidance in Ethiopian wolves (Canis simensis)." Behavioral Ecology and Sociobiology 38.5 (1996): 331-340.

wow! Great find, thank you :-)


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Is there a single protostomate common ancestor that has pseudocoelomate structure?
I think about 15 years ago I saw a new classification system that placed Plathyhelminthes worms with Annelids and Mollusks into a superphylum (or other systematic clade) Lophotrochozoa,  while Nematode worms were grouped with Arthropods into a clade Ecdysozoa.  This would suggest that Arthropods and Annelids did not have a common coelomate or pseudocoelomate ancestor (in the past believed to be a nematode), or that if they did, then flatworms evolved FROM the pseudocoelomate ancestor.  What are the current views of the characteristics of the Protostomate progenitor?  It looks like Roundworms may have diverged from a flatworm like ancestor, and then given rise to current roundworms and Arthropods, while Annelids and Mollusks may have arisen independently from a flatworm ancestor.  It would violate something I was taught in evolution (as a loose rule) that you don't usually call features like a coelem "homlogous" if they arose independently which would be the case for the Mollusk/Annelid Coelem and the Arthropod coelem.  Of course, it is possible since the genetic changes that allowed both coelom may have existed for some other purpose prior to divergence, but been activated by other similar evolutionary phenomenon, or if a gene became deactivate (for example, if a gene were deactivated in mammals making scales for instead of hair those scales would still bear homology with reptile scales.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614230/

https://www.cell.com/current-biology/comments/S0960-9822(17)31033-3

source: Stack Exchange

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

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Can I use the Winkler method as a way to measure the rate of photosynthesis?
I want to make an investigation where I measure how the color of light affects the rate of photosynthesis.
The idea is to put an Elodea plant in a test tube and shine with different color of light during time. I want to measure the dissolved oxygen in the beaker every minute for 5 minutes for different colors. As I have no access to a dissolved oxygen sensor I thought I could take out different samples of water every minute and separate them in bottles to conduct the Winkler method on each one. Hence, calculating the mg/L of dissolved oxygen and make a line of best fit for each color.
Is this a functioning idea? Could I get feedback?

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


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Effects of high extracellular fluid calcium ion concentration - what's the reason behind it?
The Guyton and Hall Textbook of Medical Physiology, p. 76, says:

For example, a high extracellular fluid calcium ion concentration decreases membrane permeability to sodium ions and simultaneously reduces excitability.

Why does this hold?
Naively, a high extracellular concentration of calcium ions should facilitate their flow through the calcium channels. Since the flow contributes to the action potential, the neurons should actually become hyperexcitable in the such a situation.
This post suggests that a high extracellular concentration of calcium increases the extracellular potential, thus causing hyperpolarization of the cell. However, this doesn't make too much sense either because, then, a high extracellular concentration of Na+ would also decrease the excitability in a similar way.
Note: this question is related to this one but I'm rather expanding it.

Can you provide some more context on the quote? The part you've included starts "for example" so presumably there is more content there of what this is an example of...


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Strange Onion and i don't know what it's
Today i cutting my onion and i saw so many verbs like this in it.  I searched about it through google lens and manually also but unable to find the reason of this. I doubt is it serious case ?

What you have there is the unripe flowering parts of an onion that's bolted, this can occur if the weather's been hot:

Copyright through: Greensideup.ie 2021, fair usage.
This would be more what it's like when the flowers open:

Copyright through: asergeev.com 2021, fair usage.
As you see, they come in a variety of colours, the ones in my garden are purple and red. They're edible and tasty in salads.

Ok so my one is also safe and it's normal.  Right ?

Assuming that what you had in the first place was an onion, then yes. But to be sure, check out hyacinths, they can look similar. Be assured that only the onion family (inc. garlic, chives, ornamental onions) smell like themselves. If it whiffs like an onion, then it's safe to eat. If it's an ornamental onion, it's safe, but not as tasty. @AmitMittal

Ohkey , thank you so much for all the details


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Is there any species of mammals where males can feed the offspring with milk?
It seems to me that an evolutionary path where not only females, but also males could feed the offsprings is entirely plausible: the males anyway have niples, so it is easy for the offsprings to confuse them for female nipples, and depending on hormonal background, some males are even capable to produce fluids with milk glands (even some humans). So, such capacity in males theoretically could improve survival chance. Also, this would somewhat relieve the females who contribute a lot of resources to the offsprings during pregnancy while the males in some species do essentially nothing except insemenation and/or fighting between themselves, thus wasting resources.
Given these speculations, if there is no such species with this trait, what is explanation for this?

It's not easy to give a definitive answer ("...what is explanation for this?") for a reason something doesn't exist. Why don't we have 31% O2 in the atmosphere instead of 21? What's the reason twins don't occur more often than they do? Since flight is a good escape tactic, why did only one mammal develop true flight? The number of such questions are endless. The reason is, it is what is (evolution.)

Does this answer your question? Why do some bad traits evolve, and good ones don't?

In the large fruit-eating bats Dyacopterus spadiceus and Pteropus capistratus the males are known to lactate. Wikipedia has an article on male lactation which mentions these species.  However, as discussed in an article by Kunz and Hosken (1), it is unclear why the males of these species lactate.  The biology and normal life history of these species is not well known, and apparently there are no reports of males actually suckling young bats.  Kunz and Hosken discuss ways in which the male lactation in these bats might be adaptive even if no or little nutrition is provided to the young by the male.
(1): Kunz, T.H. and Hosken, D.J., 2009. Male lactation: why, why not and is it care?. Trends in Ecology & Evolution, 24(2), pp.80-85; [PDF]

As @mgkrebbs mentioned in their answer, Dyacopterus spadiceus and Pteropus capistratus are the males speciees known to lactate. The Wikipedia link also mentions one more species - goats (Gómez et.al., 1999). In fact, male lactation has been observed in a few domesticated animals, including cats and guinea pigs but on rare occasion though it's not yet clear what is the mechanism to produce milk..
Moreover, Jennifer A Brunton and Thomas H Kunz of Boston University and their colleagues who studied the fruit bats in the Krau Game Reserve in Malaysia, suspect that the mammary glands of these bats contain an enzyme that converts testosterone into oestrogen -- a hormone that excites milk secretion. (source)


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Bacteria with daily bimodal energy cycle
Many years ago (about 20) I was told the following story by someone who was in field of biology that at some point there was a rift between researchers of some biological organism, that they were divided on if it consumed A and produced B as the by product of the process or reverse or maybe it consumed C and D was the by product.
The divide was so severe that it was a cause of conflicts in the said circles and heated exchanges in conferences.
The issue was resolved when someone noted that holders of A to B were day workers and C to D were night workers, and that the organism is question (bacteria?) behaved one way during day and then the other during night.
I am a programmer and apologies for being so abstract but that is all I remembered/understood from the story.
My question is :
A) If this is a (possibly) true story?
and
B)What might be the organism in the story be and if there might be any links to any related articles?
Please feel free to edit this to make more biology friendly as I have no idea about the proper terms to use to describe the possible story that I heard.

The key term I think you're looking for is bacterial Circadian Rhythms? Most evidence of this comes from studies of photosynthetic Cyanobacteria (which makes a lot of sense) and more recently from host-associated bacteria. This recent ASM article talks about circadian rhythms in different types of bacteria, with links to the primary literature. No mention of anything like the story you shared, but I'm pretty intrigued by it, and would love to find out more.


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Is there any possibility at all, that anything, bacteria, viruses, etc, can survive the plastic recycling process used for food and drink plastics?
The Question
-    Is there any possibility at all, that anything, bacteria, viruses, etc, can survive the plastic recycling process used for food and drink plastics ?

Since I notice that some bacteria ? viruses ? survive on undersea volcanic vents, or other extremely hot places on earth.

I am not wanting to put that industry on any disrepute. I wonder if bioplastics ( made from plants ) could be used for food and drink plastics or even for computers.

I did some research into this topic, and definitely could not answer it.

I assume that even if anything could survive the plastic recycling process, it would not be anything that could transfer and reside in the human body .

I have put the second part of my question, into another question  An experiment to confirm if anything can survive the plastic recycling process, and, if it could transfer itself into the food/drink, or human body?

Could you show us the results of your prior investigations as per the [help], which you may remember being reminded the previous occasion that you asked this question. Also focus it a bit, the part about bioplastic computers seems to be a different topic.

I was thinking of removing that part about bioplastics and computers, however, it helps to show alternative plastics when looking at this subject from a greater distance

I have now added a second part to the question, asking what would be an experiment to confirm if this is possible - If anyone can indicate if or not that should be posted as a separate question ?

Please take the [tour] and read [ask] from the [help]. You need to limit yourself to one question per question - this post has at least three. Also, "I did some research into this topic, and definitely could not answer it" is not acceptable as a prior research attempt. Tell us what you looked for, what you did learn, and where exactly you are stuck and need help.

Prions can survive higher temperatures than those required to melt plastics. They cannot be sterilized or cooked away (the temperatures and times required aren't really cooking anymore).
https://dwr.virginia.gov/wildlife/diseases/cwd/what-are-prions/
https://deq.nd.gov/publications/AQ/documents/Chronic_Wasting_Disease_Burn.pdf

That's a good answer, I have no qualifications in this area so I didn't know about that one. I wonder if there are any types of spores ( en.wikipedia.org/wiki/Spore ) that can survive these temperatures

Please add references to support your claims.

@MattDMo Isn't this common knowledge? Fine I'll get you references.


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Is Signal Transduction Unidirectional from the Stimuli to the Final Receptor?
I wonder if signal transduction in biological systems including visual, olfactory, tactile or any other biological system, is unidirectional. Suppose that $X_i$ is the $ith$ cell in the signal transduction pathway and $X_{i+1}$ is the next cell down the pathway. To be more clear let me rephrase my question. Suppose that,
$X_i \rightarrow X_{i+1}$
means that the signal is sent from $X_i$ to $X_{i+1}$ and,
$X_i \rightleftharpoons X_{i+1}$
means that the signal is being sent both from $X_i$ to $X_{i+1}$ and vice versa but the signal amplitude in the $X_i$ to $X_{i+1}$ direction is larger so on average we can say that effectively the signal is being transmitted from $X_i$ to $X_{i+1}$. Which one of these cases is true for biological systems? Or can both occur depending on the system?
The question might not be a very good one because I don't have any background in biology. I would appreciate any answer or guidance. Thanks in advance.

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please also try to focus your question (this is very broad) as this can involve chemical (e.g. hormones) and electrical signals. Please take the [tour] and consult the [help] starting with [ask] for details.

No.
I'll just use one example, the retina, for a proof by contradiction.
In the retina, the principle "forward"/unidirectional pathway would be from photoceptor cells (rods/cones) to bipolar cells (BC) to retinal ganglion cells (RGCs/GCs). RGCs are the projection neurons whose axons make up the optic nerve from eye to the rest of the brain.
However, there are other cell types in the retina as well that convey information horizontally and in reciprocal/feedback directions. Here are some examples depicted in a review paper:
(image from Demb & Singer 2015)

In (a), on the left, you see connectivity between a bipolar cell (BC) and an amacrine cell (AC), a type of interneuron in the retina. The AC is excited by the BC but also inhibits the BC; this is not unidirectional. In the middle, you see a horizontal connection between two BCs through an AC. On the right, you see another horizontal connection among BCs, in this case BCs of different types, through an AC.
Horizontal and feedback connectivity patterns are ubiquitous in the mammalian nervous system; you'll find them everywhere you look, so it's not reasonable to expect signal transduction to be unidirectional.
I'll add that it is not straightforward to determine the "strength" of signals in the nervous system, especially when inhibition is involved. For only excitatory connections, you might measure the excitatory potential (voltage change) at the cell body as a measure of "strength", but this is complicated because this strength depends on lots of other things: you can have nonlinear interactions in dendrites such that multiple signals sum linearly, sublinearly, or supralinearly; the rate of presynaptic activation matters, so even a "strong" synapse may not be particularly influential if the presynaptic neuron rarely fires, etc.
For inhibition, it's even more complicated, because many inhibitory potentials involve shunting and may not affect the membrane potential at the soma at all unless they are paired with an excitatory input. It's possible to have an inhibitory input so strong that a cell can effectively never fire, and yet the effect of that inhibitory input alone has no detectable influence on the cell's voltage, it merely provides a shunt that fixes the membrane potential at that voltage.
Demb, J. B., & Singer, J. H. (2015). Functional circuitry of the retina. Annual review of vision science, 1, 263-289.


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How can I decrease the generation time of Drosophila melanogaster?
I have a gene deletion strain of Drosophila melanogaster made with CRIPR/Cas9, and now I have to clean the background of this strain (TM6C balancer background) by making backcrosses with wild type. Normally, it takes 12 days for the entire life cycle at 25°C.
How can I decrease the generation time of Drosophila melanogaster?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site. Adding sources/citations and telling us where you've already looked  would help make it clear that you've satisfied this requirement. Please take the [tour] and consult the [help] starting with [ask] for details. ——— Also, which "life stage", or do you mean lifecycle? Finally, please don't use bold text in excess — it doesn't add anything.

I've edited your post to (I hope) be a bit clearer. Please make sure I've not altered your intended meaning and if you like any of the wording I used please [edit] your title accordingly. ——— Also it would be good if you could mention whether there are any known environmental sensitivities due to your deletion (and tell us what you deleted unless that is secret). If for example your strain was heat sensitive, that would rule out trying growth at increased temperature.

The Bloomington Drosophila Stock Center has a lot of information on Drosophila stock propagation. Their Working with Drosophila Stocks guide includes the following excerpt:

The frequency with which new subcultures need to be established depends on the health and fecundity of the genotype, the temperature at which it is raised, and the density of the cultures. Temperature has a large effect on the rate of Drosophila development. Generation time (from egg to adult) is approximately: 7 days at 29°C, 9 days at 25°C, 11 days at 22°C, 19 days at 18°C.

So, try keeping your flies at 29°C.

Thank you very much。 I try it.

@WiKC — If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered. Once you have >= 15 reputation points, you may also upvote the answer if you wish. There is no obligation to do either.

@tyersome thanks for the edit, I misread the question

You're welcome!


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how to extract garlic fructan?
can anyone tell me a not complicated way to extract fructans from garlic (i have access to highschool lab). I need this to be able to make an experiment on garlic extract and just fructan from garlic prebiotic activity

It seems that the basic method is just a water extraction - soak some powder from your garlic in water for a period of time. Ideally you would determine experimentally the optimal time and temperature for this using a quantitative method (e.g. HPLC or a biochemical assay of some sort), but you probably don't have access to those.
Here's an example of the method from this paper1

Water extraction procedure
Conventional solvent extraction was carried out in a water bath (model WB/0B7-45, Memmert Company, Schwabach, Germany). Ten gram of Serish root powder was suspended with distilled water under treated condition shown in Table 1. The suspension was then filtered through muslin cloth to remove the insoluble residues. The extracted slurry was centrifuged at 4,500 × g for 10 min to collect the supernatant. The resulting solution was diluted with water to obtain a 1 % solution and kept at 4 °C until the day of experiment.

Edited to add:
Note that this won't just get the fructans out, it will get any soluble components including sugars, water soluble proteins, polysaccharides etc - hence the need to quantitate the fructan component to be scientifically accurate. Ideally for proper fructan isolation you would also need to extract the fructan, which I think you could do with a FPLC via ion exchange chromatography. But this is also very unlikely to be part of your high-school's equipment.
1 Pourfarzad et al, J Food Sci Technol. 2015 May; 52(5): 2657–2667.


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Was the KT asteroid a dinosaur killer or just a large animal killer?
The KT extinction event is well-known as the demise of the dinosaurs. But today we have about 10000 bird, 11000 non-avian reptiles, and 5000 mammal species. That means almost 50% of reptile species are dinosaurs and mammals are a distant third, which is still pretty good! In fact, birds refilled empty niches left behind by the extinction event as did mammals and other reptiles. So was the asteroid really a dinosaur killer?
Consider the ratio of dinosaurs:reptiles:mammal species from the Jurassic to today. I see broadly thee possibilities:

It was much more biased, such as 4:2:1, in the Jurassic era, with the asteroid evening things out.
It was similar to today, but the asteroid initially hit dinosaurs exceptionally hard, leaving it as perhaps 0.25:2:1 after which bird speciation brought it back to 2:2:1. Note that birds are very deep within Dinosauria, with every other branch extinct.
The asteroid didn't change the proportions very much, but wiped out almost every large species as most extinctions do. The pruning of the dinosaurs was more spectacular due to a small number of large species in the fossil record, but in terms of total species counts they were hit no (more) harder than other vertebrates.

(2) is the classic "dinosaur killer" we know and love, while (3) means we should instead think of the asteroid as killing off giants and leaving the meek to inherit the Earth. Is there reasonably strong evidence as to which scenario unfolded?

I think small fossils are relatively rare because they are more likely to degrade, be scavenged etc. I can't find any evidence, but at the time of the KT debate I don't know how many small species (say <2-3 kg) were known, so the demise might have seemed more dramatic.


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Is there an evolutionary advantage to bees to becoming docile when exposed to smoke?
I have not seen other research on this on line, it occurred to me though that this physiological behavior / stimulus-response of bees (calm down when exposed to smoke) might be a subject for original research, and understanding how benefits of this behavior may be applicable to human group psychology as well is another possible avenue of research.
An initial thought, perhaps the colony would better weather forest fires docile and hunkered down in a hive/ground/tree than reacting aggressively, or it may be a matter of another mechanism piggybacked on this response to sensory stimuli that is beneficial to the colony...or worker bee.
I'm just throwing this question out there, in the event that there is a theory or "answer".

There has been research done on this, and it's easy to find. Have you googled, "Why does smoke make bees docile"? If you have, please edit your question to improve it, because I can't see any application for it to human behavior.

You also might wonder what kind of Q&A site this is, getting such feedback. Aren't we supposed to just answer your question? Actually, no. We're expected to help if we so choose. We're scientists or people interested in science, a lot of us teach, practice, or research some aspect of Biology. We expect some meaningful degree of research; not a ton, but not nothing, either. Biology students need to learn how to find information. Consider this kind of like a classroom, not a chat room. You'll get a better response to your question with a better effort.


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How to align more than 2 sequences with Needleman-Wunsch?
I have a DNA sequence of a protein and around 1200 zinc finger target sequences. These zinc finger target sequences are 9 bp long, resulting in BLASTn not finding them in the sequence. Needleman-Wunsch does find them, however, I can only search/align the DNA protein sequence with 1 zinc finger at a time. Is there a way to do this simultaneous (serial or parallel, computational time is not a big problem) for all 1200 zinc fingers and have the result in a table as with BLAST?

Could you clarify please. 1. Do you want a multiple sequence alignment with your protein and 1200 zinc fingers all aligned, or do you want to find out which of the 1200 zinc fingers align? 2. Do you really mean zinc fingers? This term is usually employed for the protein motif that binds zinc through non-adjacent Cys and His residues. A 9bp sequence could only encode three amino acids.

Also: by "Needleman-Wunsch" what do you mean? Are you using a specific software tool?

Welcome to Biology.SE. I’m voting to close this question because it lacks clarity and doesn't seem to be about a biological mechanism or process. This question might be a better fit for [Bioinformatics.SE], but please do not crosspost, instead request migration after reading that sites help. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site for details.

@MaximilianPress — NW is a specific algorithm for global pairwise alignment and has an entry in Wikipedia, as I imagine you are aware. I therefore don’t understand what you are getting at in your comment, as the particular implementations wouldn’t seem relevant. And, of course, it is the wrong tool here — Smith-Waterman local alignment is more appropriate.

@David different software can have different parameters which control execution. Possibly a simple change of parameters would get the OP what they wanted out of "NW", depending on the tool, their inputs, etc. It does not seem to be an algorithmic problem as many algorithms might get them more or less the right answer (SW being another example that might work as you say, or my simple-minded suggestion below). Rather, they don't like the outputs and mode of execution of the tools they're using.

@MaximilianPress — I don't really follow you, but it hardly matters because it is not clear to me what the poster is asking, and as he has ignored requests for clarification I suggest the question is best ignored (and closed).

(I assume that by "DNA protein" you mean "coding DNA".)
"I can only search/align the sequence with 1 zinc finger at a time" - does this mean that you have not found out a way to do so, or that you desire to proceed in this fashion? I think that it is the first, based on the title of your question, but it is not at all clear what you are looking to do.
If you want to locate specific 9bp motifs in your sequence, then I can suggest this small piece of code that I wrote that looks for exact matches of specific sequences, that outputs a BLAST-like table. It is slow relative to BLASTN but it does not use the short-match-ignoring heuristics that BLASTN relies upon so it may be helpful.
The code was written in response to this bioinformatics SE question, which seems somewhat similar to your question here.
Note that you will have to input each expected 9bp query against the reference sequence in the form of a FASTA file.

So, I shot myself in the foot a bit by posting this question before the holidays. Sorry for not responding in a better fashion. Thank you for your answer, that will certainly help me further!


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How do viruses/bacteria survive in extremely cold conditions?
So, recently, i watched a video, it was about a anthrax outbreak in Siberia.
The cause, supposedly were reindeer carcasses, infected by anthrax. Due to the thawing ice they resurfaced, and that lead to a outbreak.
So, i was wondering, how do viruses/bacteria manage to survive in extremely cold weather conditions?
I already did check Google and Youtube (in multiple languages), had a look into the book "Purves Biology" for answers, yet i did not find something specific enough to answer my question.

Anthrax is caused by the bacterium Bacillus anthracis, which is a spore-former. https://en.wikipedia.org/wiki/Endospore

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

Does not answer the question properly. I was wondering how bacteria or viruses generally manage to survive in such cold conditions. You only told me about how Bacillus anthracis survives in the cold. But what about other bacteria, do they survive differently than this virus? Or are "endospores" the general approach to survive these conditions? And what about viruses, do they do the same?

Thank you for adding more detail — however, unless you confine you question to anthrax your question is too broad. Bacteria  have been evolving for billions of years and there can be no universal answer that covers all of them — for example many of them won't survive freezing. Likewise viruses have probably been around for just as long (or possibly even longer) and whether they should be thought of as "alive" is debatable.


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Is the fin of ray-finned fish live tissue or more similar to scales?
In ray-finned fishes, are what exactly are the fins made of? Is it modified skin, dead tissue like scale or nail on humans, or something completely different? Can the fin heal?

In teleosts, the fin skeleton is made of structures called lepidotrichia and actinotrichia, whereas homologue structures called ceratotrichia are found in the fins of the chondrichties. These are covered by living skin.
Lepidotrichia are calcified, segmented and branched bone-like rays that extend along the whole length of the fin, shaping it. Actinotrichia are mostly made of collagen and are found at the distal end of the ray, where they provide flexible support to the fin edge1.
Fins are able to regenerate, and this capability has been studied in a few different teleosts2,3,4.
References:

I. Durán, M. Marí-Beffa, J.A. Santamaría, J. Becerra, L. Santos-Ruiz,
Actinotrichia collagens and their role in fin formation, Developmental Biology, Volume 354, Issue 1, 2011, DOI: 10.1016/j.ydbio.2011.03.014.
J. BECERRA, L. C. U. JUNQUEIRA, I. J. BECHARA, G. S. MONTES, Regeneration of Fin Rays in Teleosts: A Histochemical, Radioautographic, and Ultrastructural Study, Archives of Histology and Cytology, 1996, Volume 59, Issue 1, DOI: 10.1679/aohc.59.15
Norman E. Kemp, Jae Ho Park, Regeneration of lepidotrichia and actinotrichia in the tailfin of the teleost Tilapia mossambica,
Developmental Biology, Volume 22, Issue 2, 1970, DOI: 10.1016/0012-1606(70)90157-0.
Uemoto, T., Abe, G. & Tamura, K. Regrowth of zebrafish caudal fin regeneration is determined by the amputated length. Sci Rep 10, 649 (2020). DOI: 10.1038/s41598-020-57533-6


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

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

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

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


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Why do some hard-shelled seeds need hot water in order to germinate, when planted artificially?
Some plant species, such as Mimosa pudica, have hard-shelled seeds. I have tried to plant them from seeds a few times in my life, in Hong Kong.
I know that what follows is just an anecdote, but I hope it illustrates my point.
The first time I tried to plant M. pudica, I simply dumped the seeds in moist soil, in summer. They didn't germinate. So my grandma told me that I have to soak the seeds in boiling hot water. I didn't believe her at first, but my first batch didn't germinate so I thought I might as well try. So I put a second batch of seeds in a glass and dumped scorching hot water on them. Lo and behold, a few days later, this second batch started germinating.
Why is it that when planting these plants artificially, we have to use hot water? How would they manage to grow in the wild? (I do see them in the wild.) The soil temperature in Hong Kong is nowhere past 40 degrees Celsius, even in summer, according to the estimates in this article: https://doi.org/10.1016/j.enbuild.2011.09.026
What am I missing?


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What is the connection between LDL, liver, and saturated fat?
I've been trying to learn about cholesterol, lipoproteins, and fats, but unfortunately, there is an ocean of confusing information on the internet. I don't have any solid background in biology, so this is kind of making my head spin.
I know that Low Density Lipoprotein (LDL) and High Density Lipoprotein (HDL) are carriers of cholesterol in blood. LDL carries cholesterol from the liver to the tissues while HDL takes cholesterol from the blood to the liver.
How does saturated fat increase the cholesterol level in the blood?
Some sites explain that saturated fat affects the LDL receptors on the liver, which inhibits the liver's ability to receive and break down excess cholesterol in the blood. But LDL is supposed to carry cholesterol from the liver to other tissues. So why should the liver have LDL receptors in the first place? If saturated fat affected the HDL receptors on the liver, then that would have made sense, right? But many sites say saturated fat increases LDL cholesterol in the blood.
What is it that I'm missing here?

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users. ——— Please also tell us where you've looked for answers — for example by providing citations (to reliable sources) for the background you've provided.

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

I can’t. General normal fat metabolism involving liver, adipose and other tissues, and triglyceride synthesis and transport as lipoproteins is more than enough for me. How diet might distort that and affect cholesterol deposition in arteries is not something I know anything about, and is difficult because it is observational rather than a question of fundamental mechanistic design. Cave men didn’t suffer from arteriosclerosis. You might try asking on SE Medical Sciences.

I think I understand the picture somewhat now. The liver synthesizes both VLDL and cholesterol. Cholesterol is packed (along with triglycerides) in VLDL and send to tissues through the blood. As tissues absorb triglycerides from the VLDL, it changes to IDL and then to LDL. LDL continues to transport cholesterol to tissues across the body. But when there is excess LDL cholesterol in the blood, it comes back and is received by the LDL receptors in the liver. Meanwhile, the liver also synthesizes another lipoprotein called HDL. HDL travels to the cells across the body and receive excess cholesterol from the peripheral tissues, and take it back to the liver for breaking it down.

Welcome Curiouser. Whilst you may be correct (personally, I'm not familiar with this), your answer could be improved by references to  a reliable source which confirms your explanation. Answers without references risk being downvoted or deleted in extreme cases.

Saturated fat does not increase serum cholesterol. I know you can find lots of studies that say otherwise, but its basically a myth that has been propagated since the 1960s, like claiming that the human genome has 24 chromosomes (yes they used to say that). All of the studies I have seen claiming such things are "observational" studies with no controls. A lot of these studies are just BS generated by nutritionists trying to justify why you shouldn't eat eggs and other crazy things.
The intestines are impervious to sterols which have to be digested into more fundamental packages such as phospholipids before they can be transported across that boundary. Phospholipids are not processed by the liver, nor are they a component of serum cholesterol. Virtually all serum cholesterol is directly synthesized in the liver from fructose. This is easily proven (and has been proven) by guinea pig studies. If you feed a guinea pig a carbohydrate free diet which is heavy in saturated fats, their serum cholesterol drops to very low levels. Conversely, if you feed a guinea pig a high-fructose diet, they will develop high serum cholesterol levels. This is strong experimental evidence that serum cholesterol is almost purely dependent on carbohydrates and on fructose in particular (a carbohydrate derivative).

Please add references supporting your assertions. As currently written this comes across as excessively opinionated. In addition, I'm confused by you claiming that sterols are "digested" into phospholipids — this suggests that phospholipids are a component of sterols, which is not correct. Finally, since guinea pigs are not humans, it would be great if you could indicate why those results are relevant (with citations).

@tyersome https://onlinelibrary.wiley.com/doi/full/10.1111/eci.12161 To claim that guinea pigs metabolize dietary cholesterol in a different way than humans or other mammals I think is a specious argument.

I think if you were to reread my comment you will see I made no such claim — I am aware that there is evidence supporting guinea pigs being a good model for human cholesterol metabolism, but that is not known to everyone. I'm trying to make constructive suggestions — please respond by making edits to your post rather than posting links in the comments.

your answer is contrary to the most reliable hospitals, medical universities and dietary associations in the world such as the harvard heath school, mayo clinic and the American Heart Association. But your criticism of observational studies as evidence is spot on, a lot of laymen have been misguided by these studies' findings


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Can viruses infect adipose cells?
Can viruses infect adipose cells or tissue?

What do you mean by ‘store’ viruses?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site. We are also not a research service for debunking vague nonsense from fiction. Please [edit] your question to: 1) be clear, focused, and specific; and 2) tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

basically can virus get into a fat cell?

long story short- a longer story would be appreciated

Research demonstrated that viruses including HIV virus can find sanctuary in adipose tissue cells.
Earlier studies showed that interactions between immune cells and adipocytes, specifically perinodal adipocytes, promote immune activation and adipose inflammation,suggesting adipocyte regulation of HIV replication and pathogenesis.
Adipose tissue is categorized as mainly subcutaneous or visceral depots, with other minor depots uniquely associated with critical tissues and organs such as lymph nodes (perinodal fat) and the heart (pericardial and epicardial fat). Adipose tissue contains mature adipocytes and stromal-vascular-fraction cells (AT-SVF cells) which includes preadipocytes, mesenchymal stem cells, and immune cells, and this cellular composition changes significantly during disease and metabolic disorders, most notably obesity.
Murine models demonstrated migration of immune cells into adipose tissue to become major regulators of adipocyte function and metabolism, and studies of healthy and diseased humans further showed significant accumulation of immune cells. Additionally, virion-free circulating HIV proteins such as vpr, nef, and tat were shown to mediate detrimental effects on adipose tissue health and systemic metabolism.
So yes, the viruses can "live" and "reside" inside adipose tissue and regulate that environment to their own benefit.


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How to interpret this statement on missing heritability
I'm currently studying a behavioral genetic course, but still, I feel that I'm lacking many basic concepts.
A particular topic I don't understand is missing heritability.
Here's an example regarding the genetics of schizophrenia, this is what is stated in my course material: "GWAS studies have identified 240 genes associated with this disorder, but these only explain less than 10% of heritability, the missing heritability for schizophrenia is around 90%".
What does it mean that 90% of heritability is missing?
I'd like to understand the math behind this concept but I don't care if this statement is actually true, I don't know where this data came from.
PS
I know how heritability is generally defined in a narrow and broad sense.

Can you please clarify what you are asking: it seems clear from what you wrote that missing = unexplained (by known genetic factors). Does that help or is there some more subtle question that I'm missing?

Still unclear. Let's say you have a $ h^2 = 0.5 $. What exactly does it mean 90% is unexplained? How do you obtain 0.45 as a value for this missing heritability?

@Mirko It means that if we knew the effects of every SNP, we could make a predictor explaining 50% of the variance. But right now, we only can explain 0.10*50% = 5% of the variance with our current predictors.

Missing heritability refers to the fact that while we make heritability estimates using e.g. midparent regression, we can't actually find gene variants whose effects we can add up to the amount of heritability we think we should find.
This is in spite of the fact that we have sufficient statistical power that we should have found such gene variants given how many people we have genotypes and phenotypes for. (Under the normal assumption that they have effects at least somewhat independent of the environment or of other genes, and that we are actually observing the relevant genetic variation.)
As an allegory, let's say we have a bucket of apples. There are 20 apples in the bucket. I know that I picked one apple, and my friend Jane picked one apple, but I don't know where the other 18 apples came from, even though I have been watching the bucket and I should have seen anyone else put apples in there.
People are getting very clever with machine learning models that try to relax various assumptions and incorporate extra data to detect weaker effects.
At an extreme, people have resorted to arguments that literally everything in the genome contributes to every trait, the so-called omnigenic model. In this case they leverage gene expression data as a covariate to add information to models, since you will probably never have enough power to find all of those individual associations/interactions. I am unsure if this has gained much traction in the years since.
Perhaps more promising (IMO, I am not sure that anyone agrees with me) is that people are starting to incorporate more different kinds of variants (not just relatively common single nucleotide variants). There is perhaps some evidence that these sometimes rarer but more dramatic variants might explain more variance.


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Can some bacteria eat soap molecules in soapy water rather than get killed by it? How do they hang on to their surface lipids? Evolutionary advantage?
In my Chemistry SE question Quantifying soapiness; there's pH, pKa and pO2, is there a p_soap or p_surfactance? I explained that when I am too lazy or too much in a hurry to do my dishes right away I leave them full of soapy water so that stuff doesn't grow in/on the remainder of the food.
I was "yelled at" for not doing my dishes, yes even in Stack Exchange I get yelled at for not doing the dishes!
One reason forwarded in comments is that there is (or may be) bacteria that can eat soap molecules.
Is this true?
How do they not die in soapy water from having their precious membrane lipids removed?
Is it just a question of the level of soapiness being sufficiently low? Do they have unusually robust surface lipids or hang on to them more tightly?
Question(s):

Can some bacteria eat soap molecules in soapy water rather than get killed by it?
If so, how do they hang on to their surface lipids?
If so, did this offer some evolutionary advantage? ("bonus points")

Detergents are not disinfectants. They can kill bacteria but they aren't really designed to. They're designed to wash stuff away. Soaking dishes is probably better than leaving them dry and will probably slow the growth of many things, but it doesn't mean it's going to sterilize anything that is soaking in it. "How do they not die in soapy water from having their precious membrane lipids removed?" It might be false to assume they all have membrane lipids to remove.

The traditional, 1000's of years old soaps (sodium or potassium salts of fatty acids, used at least as early as ancient Egypt) are perfectly eddible not only for bacteria, but for mammals as well. Ever had your dog eat your soap?
Well, they may be too much alkaline for anyone's taste (or homeostatic equilibrium), but this can be compensated or in some cases lived with. The soaps used in the household or for hygiene purposes are never alkaline enough to burn your skin, so they are safe-ish for microorganisms as well.
Given enough water, these substance pretty much hydrolyse by themselves. The thin, barely visible layer the soap leaves over the water surface is pretty much the pure acid (the sodium ions are happy to dissolve to the bulk of water).
Other detergents (sulfonates, phosphates, etc...) have different compositions, but their common characteristic is the large non-polar part of their molecule that is still separable as a fatty acid. Om-nom-nom. The polar part of the molecule may be itself useful for microorganisms in one way or another (e.g. phosphates are of particular interest because they fertilize the open water bodies and algae grows more than it is acceptable).
Major detergent markets (EU, USA) even require biodegradability of the household detergents. The economy of scale means that you will get biodegradable detergents even outside of these markets. Nothing stops bacteria from starting biodegradation right in your kitchen sink (the osmotic pressure may slow them down, but only that much).

On the other hand, these microorganisms that can eat detergents cannot be really blamed for being pathogen for humans. If you are really lazy, leaving the dishes soaked can even help you do them later. The only real problems are the messy look, the smell and your life choices.

What happens to the microorganism's precious lipids? Given enough concentration of the detergent, the lipid layer will decompose. This is (one of the mechanisms of) how your skin dries when you do too much dishes. On the other hand, the outer cellular borders are not only lipids. There are proteins, glycans and other things that together with lipids make the cell not so much vulnerable.
The main factor one may expect to act on microorganisms subjected to common detergents is the osmotic pressure. The cells simply lose water. This slows down all the processes inside.

"...soaps used in the household or for hygiene purposes are never alkaline enough to burn your skin, so they are safe-ish for microorganisms as well." I don't believe that this is so conclusive. If I spill a jar of pickle juice or gin on my skin it is not burned, partly because my outer layer of skin is already dead, yet most bacteria will not survive those. Your answer is interesting but it has a lot of speculation and inference and zero supporting links. Can you support at least some of the most critical assertions of your answer somehow? Thanks!


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What are these little insects in that I found in my greenhouse?
I found these little (3-4mm) insects in my indoor greenhouse where I propagate Begonia from leaf cuttings.
They are slowly walking around on the soil and don't seem to be particularly interested in the plants. When I disturb them they start running around quite fast.
The (unfortunately low quality) pictures show some individuals that I managed to move into a test tube.
location: Switzerland.
the insects immediately make themselves drop when you try to lift them up with a piece of paper.

 Short answer
I think this could possibly be the nymph of some sort of cockroach.
 Long answer
I initially thought these were aphids of some type due to their pear-like body shapes and the small pair of upright projections coming off their backsides (possibly cornicles?).

However, zooming into some of your more-detailed specimens in the 2nd photo immediately made me questions this:
Your specimen appears to lack a prominent cauda sticking off the center of their backside; further, they appear to have some sort of palps around the mouth and a fairly hypognathus head -- all of these characteristics are inconsistent with any aphids I know.
Lack of a furcula (among other details) rules out springtails.
Your specimens appear to have filiform antennae, which doesn't preclude aphids or many other insect orders including beetles, roaches, and orthopterans (e.g., grasshoppers).
Your one specimen appears to have a prominent posterior femur (upper part of leg), suggesting these insects may be good jumpers. However, it could be that the enlarged region is in fact a coxa or that other enlarged femurs are simply less apparent from your photo. Regardless, given the enlarged leg and your observed running behavior, I'd guess these are cursorial legs adapted for -- in fact -- running! [See here for more on legs].

Running vs jumping rules out orthoptera nymphs of any kind.

Given the head type, body shape, mouth parts, rear projections (likely cerci not cornicles), and rear leg anatomy, I suppose this is some sort of cockroach (Blattodea) nymph.
Here is an example:

 Ectobius pallidus - young nymph (<3mm) ; Source: JungleDragon
Due to the poor quality of the photo, I think I'll stop here. You'll have to explore possible species based on your ability to ascertain in-person detail.

Alternatively, someone else might know a more specific group/species and/or may propose another order of insect all together. We'll see..

I'll consider updating if you provide additional detail.

 Also, I'm going to pitch the informative Insects information page from NC State University: https://content.ces.ncsu.edu/extension-gardener-handbook/4-insects

It's just great to read such an analytical answer to my question. Thank you!

@ert22 thanks! Glad I could help. Would you say your specimens looked anything like the photo I include? (i.e., am I close?? :p -- the photos really make it hard to tell!)


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What is the risk of permanent brain damage and/or long term cognitive effects from a single exposure to extreme altitude?
I have read some of the papers on the subject of the permanent brain damage induced by high to extreme altitude (5000m-8000m) climbing. The evidence seems contradictory. One paper (Fayed 2006) found significant post expedition MRI findings including white matter hyperintensities but this finding seemingly is in doubt for lower altitudes where studies other than this one have only picked up more temporary changes (usually in white matter fraction). The evidence for 8000m+ climbs seems clearer, in that it is clearly more damaging.
I would consequently be interested in any views based on the available evidence of the risk of permanent damage of a single 'normal' sojourn to 5000m to 7000m if acclimatisation profile is reasonable and HAPE / HACE do not obviously manifest.
The brain is evidently highly sensitive to hypoxia and there is some well evidenced impact on cognition whilst at high altitudes but do mountaineers exposed to these sub 8000m altitudes risk longer term damage?
Some relevant papers:
Fayed et al 2006 paper that was extensively picked up in the media but did not do pre expedition MRI: https://www.semanticscholar.org/paper/Evidence-of-brain-damage-after-high-altitude-by-of-Fayed-Modrego/f182e5c8a73b505e66e50bcb671ee8cf86c0f6f5
Fan et al paper on reversible abnormalities https://www.nature.com/articles/srep33596
Kotke et al paper finding limited evidence of structural damage (Morphological Brain Changes after Climbing to Extreme Altitudes--A Prospective Cohort Study) https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0141097
Dr Peter Hackett study on Denali - https://www.boulderweekly.com/adventure/this-is-your-brain-this-is-your-brain-at-altitude/

Your references aren't contradictory. The papers you cited (and others) all show the risk of permanent brain injury is obvious. (The Nature article showed persistent changes.)The pre-/post-HA MRIs study supports the Nature study. Brain changes at lower altitudes were observed in the late 1890's and in Fayed's later papers. The answer is most likely "high"). But does this brain damage manifest in permanently diminished post-climb capacities? That would be my question.

I do think the evidence is unclear e.g. Kottke et al (up to 7000m). No white matter hyperintensities nor grey matter atrophy but a decrease in brain WM fraction. Foster et al 2015 (3 weeks at 5000m) observed a GM reduction, while WM was unchanged.
Zhang et al (6200m): "disturbances mainly in cerebral WM, showing compromised fiber microstructural integrity".
Hackett study detailed here (https://www.boulderweekly.com/adventure/this-is-your-brain-this-is-your-brain-at-altitude/) found increased WM volume and subcortical climbers in 6% of climbers of Denali (6300m); the rest normal on MRI

So one paper found a decrease in grey matter but no decrease in white matter. Other papers found a decrease in white matter but no decrease in grey matter. Some papers found largely normal MRIs except when obvious severe AMS developed. Some papers found certain cognitive functions (e.g. motor or memory) had been affected, others found nothing. Is neuroscience always like this?!

@Anothercanary Yes, science with small samples is always like this. Those results need not be contradictory as they seem.

From my limited reading of the literature, it seems fairly clear - even with the small sample sizes - that permanent brain changes (call it damage if you will) do occur at lower altitudes, especially in novices. Do they occur in everyone in the same way? No. Do they matter? You'd need longitudinal studies (neuropsychiatric evaluations at intervals for years) to answer that. The longer the study, the more confounding issues result, muddying the conclusions. @BryanKrause, you're a neuroscientist, no? am I missing something?

Thanks, that makes sense. It's a shame there is no definitive view as it makes individual decision making about HA trips difficult as you're missing one side of the risk-reward equation. This study hypothesises: "There may be various reasons for these inconsistencies: different high-altitude experiences of climbers, manifestation of neurological disturbances during or after the expedition, [or] the use of different MRI techniques." https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1468-1331.2008.02243.x


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What does Guyton mean by "the ratio must be grater than one" when it comes to the safety factor to start an action potential?
AllorNothing Principle. Once an action potential has been elicited at any point on the membrane of a normal fiber, the depolarization process travels over the entire membrane if conditions are right, but it does not travel at all if conditions are not right. This principle is called the all-or-nothing principle, and it applies to all normal excit- able tissues.
Occasionally, the action potential reaches a point on the membrane at which it does not generate sufficient voltage to stimulate the next area of the mem- brane. When this situation occurs, the spread of depolar- ization stops. Therefore, for continued propagation of an impulse to occur, the ratio of action potential to threshold for excitation must at all times be greater than 1. This “greater than 1” requirement is called the safety factor for propagation."
What he means with "1" is he talking about milivolts? What are the values of the ratio he mentions.
Source of Info: Guyton & Hall Medical Physiology textbook

Welcome to Biology StackExchange! Ratio of two identical quantities has no units because both quantities have the same units, which then cancel each other. For example: if the action potential is $60;\rm mV$ above the resting potential, and the threshold potential is $15;\rm mV$ above the resting potential, then their ratio is $60;\rm mV/15;\rm mV = 4$.

Thank you very much!

The two quantities of concern are "threshold" and "peak voltage" (both relative to resting potential).
If the ratio "peak voltage"/"threshold" is less than one, then that means peak voltage is less than threshold, which by definition of threshold means an action potential will not propagate.
If the ratio is exactly = 1 then the peak voltage exactly equals threshold. This is a precarious situation: any little randomness in the system would mean the action potential could fail to propagate. That's why they're calling the ratio a "safety factor": if the ratio is, say, "2", then the depolarization is twice what you need to propagate and you could say this is quite safe. If it's 1.01 then there's a little margin built in but it's still likely you could see a failure to propagate.
For an analogy most people encounter in daily life now, let's think of the charge on your cell phone battery in the numerator and the charge you use in a day in the denominator. If the ratio "charge available"/"charge used" is less than one, your cell phone won't make it through the whole day without dying. If the ratio is 2/1 then most days you'll end the day with around 50% left; you could say you have a safety factor of 2 and if you use more than expected some days you'll still be okay.

Thank you very much! super clear!


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Why are nerves blocked even though potassium channels are not blocked?
One could read "Local anesthetics produce a very slight, virtually insignificant,
decrease in potassium (K+) conductance through
the nerve membrane." At Handbook of Local Anesthesia 7th edition by Stanley Malamed.
If potassium ion diffusion is not blocked, that means that there is still an ionic current which means electricity production and most important, the production of a magnetic field, which I assume is what depolarizes adjacent parts of the membrane, why this potassium ion current is not enough to start an action potential? Do the voltage generated by sodium and potassium ions must be add up in order to trigger an action potential?

In general, action potentials are initiated by an inflow of Na+ that depolarizes the neuron. Only after that, K+ channels open up that re-polarize the membrane potential to get the neuron back in business for a next action potential. In a way, the K+ channels open only at the tail end of the action potential, Na+ leads the potential change (Fig. 1). Here is a link to a credible chapter on the action potential that describes it all in more detail.
Note that K+ channels mediating action potentials are mainly voltage gated, meaning they start opening only when the membrane potential depolarizes. The same goes for the Na+ channels; they need an initial depolarization of the cell membrane due to neurotransmitter release to start opening. It has nothing to do with electromagnetic fields.
Anesthetics work in a variety of ways, so to answer any question on the relation between anesthetics and K+ channel kinetics, more information is necessary, but I think the matter is already cleared up by this answer.

Fig. 1. Channel dynamics during action potential generation. source: Idaho University

Thank you very much! I really appreciate it!

@Quique - no worries. If this is the answer you are looking for, please accept to let others know you found your answer

I don't know much about the effects of anesthetics, but I have taught basic nerve function at university level, so I hope I can help a little with that part.
Potassium flow does not start an action potential - on the contrary, increased potassium flow makes it harder to depolarize the membrane and initiate an action potential.
A brief explanation on membrane potentials and action potentials:
During rest the flow of potassium is much higher than the flow of sodium (and also chloride) and hence the membrane potential is driven towards the Nernst potential for potassium. The resting potential is often somewhere between - 40 to - 80 mV depending on cell type. To initiate an action potential the membrane potential needs to depolarize enough to exceed the threshold for opening voltage-gated sodium channels. The ion flow across the membrane will then be dominated by sodium and the membrane potential then moves towards the Nernst potential for sodium (which is positive, maybe 40-50 mV). These voltage-gated sodium channels will then close shortly after and then stay closed for some refractory period where they can't open, which brings the membrane potential back to the resting potential, because the flow will then again become dominated by potassium flow. There are also voltage-gated potassium channels in the membrane that open with a slight delay compared to the voltage-gated sodium channels. The opening of these potassium channels result in a faster return to the resting potential after the peak of each action potential.
Regarding your question on a small (but insignificant) decrease in potassium conductance:
Decreased potassium flow will bring the membrane potential further away from the Nernst potential for potassium and closer to the Nernst potential for sodium, i.e. causes a slight depolarization, which makes it slightly easier for the membrane potential to exceed the threshold for opening voltage-gated sodium channels and initiate an action potential. If the flow of potassium is completely blocked, the membrane potential would be determined by the relative permeability of chloride and sodium.
The Goldman equation is the key to understanding membrane potentials, and relative permeability changes between the potassium, chloride and sodium ions (and in some cases calcium ions) is what drives an action potential.
Neuroscience by Purves et al is a good resource on all of this.


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Does positive electricity run through neurons in the exact same way as it runs through copper?
Does positive electricity moves in the exact same way as electric current moves through copper,silver and gold? From what I understand, electricity propagation in neurons is not linear as it is in a wire but rather in a cross-sectional way, moving forward little by little depolarizing the adjacent part ot the axon untill it gets to its destination.This is because the neuron cell membrane is made mainly by fat, and fat is consider an insulator. Besides, this is not an electric current but rather an ionic current, so atoms cannot move the way electrons do.
https://www.youtube.com/watch?v=RNdvrkolW0M

Does this answer your question? Please search the site before asking a question. There's tons of information already here

@AliceD In other words, it is a polarization wave that propagates with a speed of sound in water (since it involves actual liquid flow). Whereas in copper we have a plasma wave, which propagates with the speed close to the speed of light.

@AliceD, I am not asking about the action potential in general, I am asking about the way charges move in the nerve fiber, and if they move just like they move in copper. I thought it was a specific question. Thank you for your reply.

@Roger Vadim Thank you very much!, I have done some research on this topic but I cannot understand the exact difference between a plasma wave and a polarization wave. Would you mind to clarify please?


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What is this large long-legged orange and black insect?
Around and inch long. 6 legs, bigger than a wasp, and orange and black. Found near the coast in the woods in South Carolina.

Welcome to Biology.SE. Please [edit] to include an estimate (in cm or inches) of the size (length) of your bug. Larger than a wasp isn't very precise, especially since there are many different types of wasp! Clearer photos (ideally from multiple angles) would also be helpful. Also note that "is this dangerous" is open to interpretation — I'm going to edit your post to better fit this site's standards, make additional changes as you see fit. Please take the [tour] and consult the [help] starting with [ask] for details.

Thank you! I’m just learning about this website! I will try to upload more pictures although I didn’t want to get too close.

You're welcome. This is almost certainly not especially dangerous to you. One way to avoid a painful bite while getting a sharp close-up would be trapping it in a sealable container and putting in the fridge for ... try 10 min and work up until it is very sluggish ... happy 'hunting'. Alternatively if you have a clear non-distorting container that could also work.

From these photos, the main features to go on are the dorsal black and red markings, the coloured bands on the legs, the white dots on the abdomen, and the shape of the body. These features does match well with this species, which is common in southern North America:
Milkweed Assassin Bug
(Zelus longipes)
The bite from this species is supposed to be very painful.

While not a threat to humans, if not handled properly, a Zelus longipes bite can cause a burning sensation with swelling that may last for several days.
https://entnemdept.ufl.edu/creatures/beneficial/bugs/zelus_longipes.htm

Additional resources:
https://www.insectidentification.org/insect-description.php?identification=Milkweed-Assassin-Bug
https://www.thoughtco.com/red-and-black-bugs-4138391

I agree, but this is close to a link-only answer. Answers (and questions) are supposed to be self-sufficient (not require following external links, especially since those can (and do) break making the post much less useful. Please [edit] to explain why your identification is correct, including a discussion of key features that led you to this conclusion and supporting references or at least validated (as well as public domain & properly attributed) images.

(+1) Thanks for the edits!

I agree. I have edited the post, which hopefully made it more useful.

Hi @Michael. welcome to BIO.SE! We appreciate the answers and quick involvement over the last 2 weeks. Willingness to edit and improve posts is a huge bonus -- thanks!! My only suggestion to you is that when answering questions (especially [tag:species-identification] Q's) that you avoid citing non-reputable sources. There are so many misidentified organisms (especially insects, plants, and fungi) all over the internet, that we want to avoid sending people to these sources. I think your ThoughtCo piece is decent and relevant in this case, but certainly be mindful moving forward. Thanks!

Thanks for the welcome and friendly advice. It is much appreciated.


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Sexual devolpment and sexual organs in humans
In an anatomy book from a friend studying medicine (Netter's book), I looked at some elements of sexual development in embryos. From a developmental stance, we can draw some analogous organs that correspond to the same organ earlier in development:
For example:

Clitoris <=> Penis
Scrotum <=> Vulva

In this book, there is not much more. Yet, I was wondering whether we could find the counterpart of any organs in the reproductive systems of each sex. There wasn't for example any counterpart described in this book for vagina in males, or for prostate in females.
Has someone any reference to give that list the most counterpart we can find between both sexes?

Have you looked at this answer to a related post?


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How do the anti-D antibodies help prevent Hemolytic Disease of the Newborn? And why do they not act like the maternal antibodies?
I understand that this question has been asked a few times in the past, but the answers there didn't really explain to me why the Anti-D antibodies we introduce are able to prevent the hemolysis of foetal RBCs, and why they aren't identical to maternal antibodies.
As I understand it, HDN is caused when, after the first pregnancy, the mother's body makes antibodies to the D antigen of an Rh+ve foetus, and in subsequent pregnancies, these antibodies cross the placenta and destroy the foetal RBCs.
How do the exogenous anti-D antibodies help prevent this?
Regarding what I didn't understand:
Why is the administration of exogenous Anti-D not harmful to the foetus?

This is exactly what the makers of RhoGAM suggest, saying that the amount of antibody administered at 28 weeks into the pregnancy is sufficient to block any Rh antigen on Red Blood Cells that escape into the mother's blood, but insufficient to cross the placenta and be a problem. At this time the child will be large enough that any RhoGAM that does cross the placenta will not kill enough Red Blood Cells to harm the child.

I thought that the problem was the maternal antibodies crossing the placenta, how does blocking antigens of foetal RBCS leaking into maternal blood help? Isn't it the leaking of maternal blood into the foetus which lets the Anti-D antibodies attack the D-antigen and cause erythroblastosis?
And either way, don't the maternal antibodies do the same thing as RhoGAM, i.e. attaching to the D antigens?

If other questions relate to yours, or other references you've read elsewhere on the internet, it's helpful if you cite and link to these answers and explain what they've said and where you are stuck exactly.

Thanks, edited.


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Interactive molecular machinery visualisation software?
If I want to manually feed mRNA through a ribosome to actually see what happens step by step which software can I use to do that?
I'd like to be able to see changes in geometry and orientation at an atomic level. Maybe this doesn't exist yet, I don't know!

Welcome to SE Biology. We try to clarify questions before answering to avoid ambiguity. Your request for software for molecular visualization assumes that the necessary data input exists. This would presumably be in the form of atomic coordinates for all successive states involved in peptide bond formation of the same ribosomal machinery. Do you realize why such data are not available? If your objective is to understand the molecular interactions at each step in protein synthesis, what is wrong with original papers and standard molecular visualization of their data?

Hello thanks for the welcome. Well it sounds like I'm being too greedy and what I'm looking for doesn't exist. The atomic structure of the ribosome has been available for over 2 decades now so in answer to your question, no, I don't understand why a few successive states have not yet been recorded. The question comes from a desire to interact with and visualise molecular machinery at an atomic level, I wish to visualise the sequence of mechanical steps that happen in for example translation because visualising something is understanding something.

As you may know, one has to trap all the ribosomes in a particular state to be able to get the coords by X-ray or EM. This generally means using particular modified reagents or inhibitors. Using these techniques, we certainly have snapshots of several stages of protein synthesis — however half a dozen snapshots do not make a movie. I am sure some of the molecular viewers that take PDB coordinates allow one to align and load different structures in sequence — I imagine that you are familiar with them. If you like I can look out what different stage structures and  associated stuff is available.

I was imagining that if such a program exists it would rely heavily on modelling and simulation and not necessarily move through a sequence of perfect images. We can find so many animations nowadays and while not perfect they do a good job of giving us the general idea however I wish to go a little deeper. I have 2 jobs and I'm a student so reading through multiple papers, viewing static PDB files and trying to imagine the changes in positions and bonds all in my head seems too difficult and inefficient. I will try to create my own solution! Thank you for your help!


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What is the significance of an adjuvant to traffic vaccine antigen directly to draining lymph nodes without diffusing into the systemic circulation?
I found the following sentence in the this paper- Safety and immunogenicity of an inactivated SARS-CoV-2 vaccine, BBV152: a double-blind, randomised, phase 1 trial

An imidazoquinoline molecule, which is a toll-like receptor (TLR) 7/8 agonist, has been used to stimulate cell-mediated responses. Algel-IMDG (an imidazoquinoline molecule chemisorbed on alum [Algel]) has been designed to traffic vaccine antigen directly to draining lymph nodes without diffusing into the systemic circulation.

My question is- what is the significance of trafficking vaccine antigen to draining lymph nodes? What will be the consequence if the vaccine diffuses into systemic circulation?

This paper, Controlling timing and location in vaccines, explains the concept in detail. The TL:DR version is that immune response is affected by the amount of antigen that reaches lymphatic tissue, that is, the tissue where the cells ultimately determining antibody production reside.
With a "non-lymph node-targeting adjuvant" vaccine given intramuscularly, the antigen in the vaccine must diffuse through more tissue, essentially with less reaching lymphatic tissue. With a targeted vaccine, more antigen goes directly where it's most effective, thus hopefully improving immune response.

As antigen availability plays a deterministic role in the strength and type of B cell and T cell responses induced by immunization, optimizing targeting of vaccines to lymph nodes and prolonging antigen availability over an optimal temporal window become key parameters shaping the immune response. As illustrated by recent studies, these are not just “nice to have” features, but can determine the difference between a vaccine inducing neutralizing antibodies or not.

Another theoretical benefit of targeted vaccines is that lower levels of antigen are required to produce the same response, meaning more vaccines can be made from the same amount of antigenic material.
The paper also nicely describes the benefits of nucleic acid vaccines (e.g. the mRNA vaccine).


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Is the use of DNA SNPs vs amino acid variations in the description to detail the absence or presence of a consequent amino acid variation?
Studying Schizophrenia and reading some papers discussing polymorphisms in the 5HT-2A receptor gene (HTR2A). Specifically, the authors mention A-1438G, T102C, his452tyr.
Was his452tyr not described as A-1438G and T102C, in terms of a DNA SNP, because the variations in A-1438G and T102C do not give rise to a different amino acid? Histidine is coded by CAU, CAC, and tyrosine by UAU, UAC. The first position in the mRNA sequence accounts for the variance, and hence the first position in the DNA sequence. In other words, it could have been described as G-1354A (if I did that right U->A and C->G and (452*3)-2 to give the 1 position). Or is this typically a matter of original author preference, or perhaps for amino acids that would significantly change the protein?


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Why do blobfish become bloated when they are brought to the surface?
There are several things that can happen to deep sea creatures that are brought up to the surface, but none of them explain why the blobfish becomes deformed. Blobfish don't have swim bladders, so that can't explain it. I'm pretty sure water isn't compressible enough to noticeably expand from the decompression. Wikipedia wasn't able to answer my question.

"Yes they do" referred to the article and the wiki answering the question. The linked post indicated "the bends". The Wikipedia page specifically states: "The popular impression of the blobfish as bulbous and gelatinous is partially an artifact of the decompression damage done to specimens when they are brought to the surface from the extreme depths" - i.e. it's in all the tissues that dissolved gas comes out within the cells and between them (as in the bends).

Blobfish don't have swim bladders, they also don't have a lot of other things we associate with surface animals, like much of a skeleton or many muscles. This is fine under the extreme pressure they live in, the pressure alone provides much of the bodies support, but on the surface tissues that are nice and rigid at depth become soft and droopy.
Also water may not be very compressible but that does not mean they do not subject the tissues containing them to pressure, especially when there a drastic difference in pressure, especially when you consider that that water at depth is almost 20 degrees colder than surface temperatures. Then you also have osmotic effects since the osmotic balance at 1000m down will be different than the surface, their tissue may well take on water as they are raised to the surface.
Finally and most importantly, it is not just water that is compressed, gasses like oxygen and CO2 are also present in their tissues (and in sea water), which can most definitely expand, this is why rapid decompression kills humans so often, dissolved gasses within tissues outgas. The bends are not your lungs over inflating, it is dissolved gasses in your tissue suddenly not being dissolved.
Sources:
Cossins, A. R., & Macdonald, A. G. (1989). The adaptation of biological membranes to temperature and pressure: fish from the deep and cold. Journal of bioenergetics and biomembranes, 21(1), 115-135.

Tokranov, A. M., & Orlov, A. M. (2007). Some biological features of rare and poorly-studied sculpins (Cottidae, Hemitripteridae, Psychrolutidae) in the Pacific waters off the Northern Kuril Islands and Southeastern Kamchatka, Russian Federation. Raffles Bull Zool, 2007, 187-98.

Pflugrath, B. D., Boys, C. A., & Cathers, B. (2018). Predicting hydraulic structure-induced barotrauma in Australian fish species. Marine and Freshwater Research, 69(12), 1954-1961.
Brown, R. S., Walker, R. W., & Stephenson, J. R. (2015). A preliminary assessment of barotrauma injuries and acclimation studies for three fish species (No. PNNL-24720). Pacific Northwest National Lab.(PNNL), Richland, WA (United States).


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Translating either rs number or genomic position to either a residue in the DNA or in the amino acid sequence
Studying Schizophrenia and reading some papers discussing polymorphisms in the 5HT-2A receptor gene (HTR2A). Specifically, the authors mention A-1438G, T102C, his452tyr. How does one best take processed genetic data, such as on 23andMe, or the entire raw data with Nebula to determine which variants are carried? 23andMe allows access to raw data and you can search for the gene by HTR2A where there is a list of rs markers such as rs9595552 and rs17069218 and their genomic positions 47407430 and 47408350, respectively. How do I take A-1438G, T102C, his452tyr and relate them to either the rs number or genomic position? Supposing they aren't on the list and I get a whole-genome sequencing done by Nebula, how would I go about finding these residues? I know that HTR2A is on chromosome 13q14-21. I understand the first part 'chromosome 13', but not the rest. Nor do I understand how I would go about navigating the raw genomic data.
Edit:
Luckily, I was able to use Google to track down these relationships.
rs6313 = T102C
rs6311 = A1438G
rs6314 = his452tyr
when I looked to the data on 23andMe, online it yielded:
rs6313 = T102C ; A or G ; AA
rs6311 = A1438G
rs6314 = his452tyr ; G or A ; GG
I was able to download the complete raw data and search the text file for the middle one yielding:
rs6313 = T102C ; A or G ; AA
rs6311 = A1438G ; TT
rs6314 = his452tyr ; G or A ; GG
Now the last one appears apparent. We are clearly discussing the amino acid sequence. Histidine (H) has two possible codons, CAU and CAC. Tyrosine has two possible codons, UAU and UAC. Meaning that the variation lies in the first position, with a G in the DNA yielding histidine and an A giving tyrosine. So G or A is what we are looking for in the DNA sequence from 23andMe and all is well.
If we then try and apply this same process to the other two polymorphisms, assuming they are amino acids and not nucleotides, it doesn't work.
alanine(A): GCU, GCC, GCA, GCG
glycine(G): GGU, GGC, GGA, GGG
threonine(T): ACU, ACC, ACA, ACG
cysteine(C): UGU, UGC
For alanine/glycine, the nucleotide variation would be occurring in the second position, G/C. Yet the 23andMe data says genotype is TT. Therefore I believe it is correct to assume A/G is referring to nucleotides in the DNA.
The same would apply for threonine and cysteine, for two out of three of the nucleotides must be the same and this is not the case. Assuming instead they are nucleotides is compatible with the data from 23andMe; A or G and AA.
That being said, I am aware that the promotor does not always lie at the beginning of a gene, but I do not know where else it can lie. Can it lie at the end? A-1438G is in the promoter, T102C in exonI, and his452tyr in exonIII. Converting his452tyr we have (452*3-2=1354) G-1354A. Putting them in order: exonI T102C, exonIII G-1354A, promoter A-1438G. Does this sound correct?

I'm not exactly sure what you're asking for, perhaps you could structure your question a little better. But searching for your gene at dbSNP seems like a good start. That lists you all gene variants currently mapped to the specific gene. Example: https://www.ncbi.nlm.nih.gov/snp/?term=HTR2A. After searching you can also click Varview to view the genome position of the gene and all its variants.

If you go to the gene at Genbank you will see that the gene has a few variants, which are based on differing intron/exon boundaries. The 13q... is the position based on karyotype analysis. You can relate this to straight genome positions to some extent, but you would need to determine the start codon and the intron/exon boundaries for your encoded protein.
There are a few possibilities:

The positions are amino-acid substitutions - They are related to the genomic sequence by the coding position starting with the start codon ATG (Met) and working from there. In this case it would be Alanine to Glycine at amino-acid 1438 of the protein sequence. However, if you look at the CDS regions and go to the linked proteins (/protein_id=NP_XXXXXXXX) you will see that there are only 430ish amino-acids in the sequence. The His425Tyr is certainly an amino-acid substitution of this sort, the others might not be.
The positions are raw coding positions. A highly conserved single base substitution at the designated site. This would be for the coding sequence only. You would take the exons only and count bases from the A of the start ATG.

I've not tried to access the 23-and-me data, so I don't know how it works, but the genomic position will be starting from the first base in chromosome 1 and counting up I think. Generally data of this sort will be analysed using a specific set of tools in a bioinformatics system.

Thank you for your answer, bob1. I updated the original post if you can check my work that would be helpful. I may have to update the post in the future if there is an instance where Google does not yield a rs number for the polymorphism in question.


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Does specific immunity affect the incubation period of viruses?
My interest was inspired by the observed variation in incubation times for different strains of Covid-19, however I ask the question in the broader sense as it seems hard to find an answer in general.
Does the presence of immunity affect the duration of incubation period? I would have thought the body's ready ability to identify and defend against a virus may mean that it is identified sooner following infection. But I can't find evidence to confirm or refute this idea. Would really appreciate any thoughts!
Thanks

Sorry - I'm not sure on the question here - once a virus enters a cell it will replicate at approx the same rate no matter whether there is an immune response. Immune response could prevent infection/limit infection, but won't affect replication kinetics.

I feel contradiction: if there is "incubation" there is bound to be "no immunity".

@bob1 It was a question of what is really happening during incubation. During incubation the virus is replicating undetected, but at some point it becomes detected and is no longer in the incubation phase. So I'm curious whether having a better immunity to a particular virus would result in a quicker detection in this phase, therefore shortening the incubation phase. Thanks for your answer

@PeterBernhard that's not true at all. The evidence is all around you - people who have been vaccinated are still getting sick with the omicron variant. Granted, not as sick as with other well-publicized strains, but sick nonetheless. The same thing happens with delta, to a lesser extent. So clearly, people with (good) immunity can still have virus incubation and eventually illness.

@MattDMo Thanks to your comment I now feel better ... with the question that seems to have incubated on me, just as your comment seems to have.
I will delete that expression of my feelings up above, as it hurts. Sure, me too, I have been misunderstood:  it's in your parenthesis, what I was up to, i.e. how can you use the word well - immunity - if incubation is evidence for its failure which is non existence. That is a debate on words and definition. Maybe more, though. (What is: symptomless infection) I feel understood. Still, I will delete my comment. I always did agree with all you say.

@MattDMo Amending my comment with the help of your comment I would say that the phrasing of the question "specific immunity" makes you think - first guess - of a kind of immunity that is effectiv (again, your parenthesis, to me are of importance).
The phrasing does not immediately let youknow what the point is: does specific immunity as a very good immunity shorten or prolong incubation  in cases that you list, i.e. in cases of break through infection, vaccine failure. That word vaccine failure does not go well with "specific immunity" in a head line. I still insist, but will delete.

The wording of the question does not seem convey what it is about: If there is enhanced, "specific" immunity, the incubation period of a  break through infection (vaccine failure might be  some inappropriate term) should be prolonged

as with specific immunity which is good ammunition the fight should last longer before it is lost and incubation becomes "success".
By intuition, the answer should run: yes, immunity affects the incubation period, the more  specific and thus the better the immunity the longer the fight, the longer the breakin' the immunity, the longer the  incubation time.

Does this question also refer to "symptomless infection"? I think it is important to be clear about definition of word: can there be spoken of "incubation" if there will never by any "symptoms"? Interestingly, your question is of practical relevance: thanks to vaccination people might either prolong their being infective to some indefinite point in the future - good to know -- and, counterintuitively, it is not at all trivially clear that (specific) immunity does not shorten the incubation - "period" :-) Seriously: it does not occur easily that good immunity just cannot shorten incubation.

You refer to "symptomless infection", too?  Can there be spoken of "incubation" if there will never by any "symptoms" (two terms mutually defined)? Of practical relevance: Thanks to vaccination people might either prolong their becoming infective to some indefinite point in the future - good to know.
It is not at all trivially clear that (specific) immunity does not SHORTEN - just cannot -  the incubation - "period" :-) Seriously: it does not occur easily that good, specific immunity just cannot shorten incubation time. @Bob: no "influence" of immunity on "virus as is"?

@PeterBernhard, I think you need to have a good look at the role of immunity in infection. Good immunity means infection is limited in some way. This will not prolong their being infective indefinitely. Either the virus will enter the cell and replicate, or it will not enter and no infection results. Replication kinetics of the virus are key. Good immunity results in lower levels of infection because virus that exits the cell will be absorbed by the immune response faster and to greater levels than with poor immunity. Not longer infection!

@PeterBernhard In fact, it is the other way around: Prior immunity shortens the observed incubation period. See my (now edited) answer to the question.

There are two effects that can shorten the observed incubation period in presence of prior partial immunity

Symptoms are caused mainly by the reaction of the body, not by the virus itself. When there is some prior immunity, the immune response kicks in faster, leading to an earlier onset of symptoms. This effect is genuine.
When the infection proceeds somewhat slowly, it may be completely terminated by the immune response without any symptoms occurring. This effect cuts off the long tail of slow infections, leading to a shorter average incubation period.

EDIT: Not a publication but a Twitter thread by a renowned scientist (Micheal Mina) confirming shortening of incubation period by immunity.