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How are CheY, CheA, CheW, CheZ pronounced in speech?
This is a quick followup question to this question about proteins that play important roles in chemotaxis:
How does one pronounce the protein names "CheY", "CheW", etc., in English?  My guess would be that they're pronounced like "key why", "key double-u", etc.
(I want to refer to these proteins in a philosophy of science presentation, but don't have much background in molecular biology. I know about chemotaxis only from reading.)

That's certainly how I would pronounce them: you're abbreviating 'chemotaxis', so "key-Y' makes sense. You could probably get away with 'C-H-E-Y' or 'Chemotaxis-Y' but I'd use the first one. When they're unpronounceable spell it, otherwise say it if you can. There aren't official guidelines on gene symbol pronunciation, so you're on your own.

These are not English words that have any defined pronunciation. These are more like code-words. You can pronounce them as you want. For these proteins, I just pronounce them as if they were abbreviations and not acronyms.

@Resonating, WYSYWIG, these are answers, and the best answers possible, I suspect.  Each of your comments helped me.  You should post them as answers, so that I can upvote them.

Resonating, @WYSYWIG, these are answers, and the best answers possible, I suspect. Each of your comments helped me. You should post them as answers, so that I can upvote them.

As was mentioned in the comments, these are not real words and there is no authority on their pronunciation. Given that Che is an abbreviation of chemotaxis, I would pronounce it the same as key.


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Are cortical columns restricted to somatosensory cortical sections?
From this previous question, it seems like evidence for the minicolumn organisation of the neocortex seems to be primarily based off observations around the sensory parts of the cortex, such as the primary visual cortex and the barrel cortex. Have column-like organisation been observed in non-sensory regions of the neocortex?

Cortical columns (also called minicolumns) are not limited to the somatosensory cortex. As shown in this paper (which discusses how the miniucolumns change in response to aging), it is also present in the associative cortex.
However, it should be noted that "minicolumn" in this paper is defined as neurons that are close together and form a minimum spanning tree, as shown below.

Connectivity doesn't seem to be analysed, probably because connectivity information is really painful to collect, but I'm not sure given I'm an amateur when it comes to neuroscience.

source: Stack Exchange

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How does food preservatives effect salivary digestion?
What effects do common food preservatives have specifically on saliva?

First you'll have to provide evidence that preservatives do have an effect on saliva.

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How to calculate water pressure (Kpa/Mpa/PSI) with depth in the Biofloc fish farming?
Can you tell us a little bit about the water pressure (Kpa/Mpa/PSI) with depth in the Biofloc fish farming and the calculation of Kpa / PSI / Mpa so that one can understand which air pump machine should to buy.

this is not a biology question,here is how to calculate the pressure your air pump need to overcome https://www.engineeringtoolbox.com/hydrostatic-pressure-water-d_1632.html

I’m voting to close this question because it isn't about biology. Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

In round numbers fresh water is 2 ft for 1 psi. For example 50 ft depth requires 25 psi to barely push out an air bubble. There are other factors like resistance of an air diffuser ,etc.  If that is a little too "round" , use 0.866 psi for 2 ft . Fresh water = 62.4 pounds/cubic foot; a square ft is 144 square inches , so 62.4/144 = pounds/sq.in at one foot depth (0.433) . Then for salt water replace the fresh density with your salt density.

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Eradication of HIV
If the last person with AIDS dies, does that mean the disease/virus has been eradicated forever?
Since the disease can ever only be transmitted, shouldn't it be possible to completely remove it from the face of the earth?

are you suggesting to eliminate the potential sources for hiv,this sounds a little too extreme for my taste.

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, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have with references to reliable sources. ——— The US CDC is one potential source of information — many more can be found by searching for "disease eradication criteria". Thanks!

Sir my apologies if it sounded extreme, it was just a simple question in my head.

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Can elephants smell when they have water in their trunks?
For humans, humans cannot smell when they have water stuck in their noses. However, I am wondering if elephants can smell scents when they have water in their trunks, as they are designed to hold water.

Yes they can, as the G protein-coupled olfactory receptors detect presence of molecules and no receptors exist that are inhibited by competitive binding of water molecules.
Both you and an elephant can smell (with) water in the nose! Just try it! I am sure you can smell a difference between pure water and water with a tiny drop of perfume in it if you aspirate it though your nose!

But can elephants inhale while holding water in their trunks? That is the question; because airflow through the nose is necessary for olfaction. E.g., humans can't smell well when they have a blocked nose, people who have had their larynx removed can't smell well because they no longer breathe through their nose (see https://www.cancerresearchuk.org/about-cancer/laryngeal-cancer/living-with/stoma/life), etc.

When you say 'humans can not smell when they have water trapped in their noses', I believe you mean the loss of the sense of scent caused due to nasal congestion, which is due to inflammation, blocking the scent receptors in the nasal cavity (any mechanical blockage preventing odours from reaching the olfactory nerves can cause a loss of sense of smell. This blockage can be due to inflammatory processes like simple infections causing mucus plugs or nasal polyps(1)). Since the basic structure of the respiratory tract is similar in mammals, mucous plugs reduce scent sensitivity in elephants as well.
Olfaction occurs when odourants bind to specific sites on olfactory receptors located in the nasal cavity. They get into the nasal cavity when you breathe or sniff the air.

Molecules of odourants passing through the superior nasal concha of the nasal passages dissolve in the mucus that lines the superior portion of the cavity and are detected by olfactory receptors on the dendrites of the olfactory sensory neurons. This mucus acts as a solvent for odour molecules, flows constantly, and is replaced approximately every ten minutes.
...(2)

(Thanks to @Adhish for the above point.)
If the water itself has a scent, then, as @KaPy3141 pointed out, it can be distinguished because it is in contact with the olfactory receptors. Scent of anything else outside cannot be determined, because they do not reach the receptors.
Elephant lungs are attached directly to the diaphragm and chest wall, allowing them to create much greater "vacuum pressure" for sucking water through their long trunks, while drinking.(3) To open its mouth to breathe would cause the loss of the low pressure and the water column would expelled. So the water column must first be transferred to the mouth, then swallowed before breathing can recommence.(4) Thus, as far as respiration is concerned, they cannot breathe when the trunk contains a column of water, and, as a result, odourants cannot enter the nasal cavity, and elephants cannot smell in this case.
1-https://www.ncbi.nlm.nih.gov/books/NBK482152/
2-https://en.wikipedia.org/wiki/Olfaction
3-https://www.elephant.se/elephant_lungs.php?open=Elephant%20anatomy
4-https://www.quora.com/How-do-elephants-breathe-when-drinking-water

I am not familiar with elephant nasal anatomy, but this answer definitely needs corrections regarding human nasal anatomy and physiology. E.g., (a) mucus, far from being a barrier to olfaction, is ESSENTIAL for chemicals to dissolve and reach the olfactory epithelium. (b) Not everything in the nose is in contact with the olfactory epithelium, which is a localised structure far up in the roof of the nasal cavity. For a review of these topics, see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131780/

Also, the Quora website cannot be considered a reliable source of scientific knowledge. Most of their answers are opinion-based and do not cite any sources.

I agree with your opinion regarding Quora, but the lines I picked were from a well detailed, clear answer. I was looking for a logical explanation of a known fact, and Quora seemed to have it - so I used it. 'Most' of Quora is junk, not all. If there are still things that are not clarified yet, I would humbly delete the lines I borrowed, but that would just make the answer difficult to digest.

+1 for the edits. Also, I just came across this book (which can be previewed for free on Google): https://books.google.co.in/books?id=A3GFYySwY1cC. It talks of the vomeronasal organ, which has a role in olfaction in the elephant, particularly where pheromones are concerned. I'd recommend it, I found the text on pp 411–412 quite interesting.

Humans are not designed to have water inside their nose, so water doesn't get stuck there very naturally. Neither humans nor elephants can inhale new scents if they have their nose blocked by water or otherwise, but the olfactory cavity will still transmit some information to the brain even if the nasal passage is obstructed.
There isn't a lot of research on the subject online.

Oops, I accidentally clicked downvote and can't undo it now.

I think I'll be able to undo it if you make any edit, even if it's just a comma. You could also edit it to include information about the vomeronasal organ, a parallel olfaction system in the elephant (see https://books.google.co.in/books?id=A3GFYySwY1cC). And sorry for the mistaken click again.

oh it's ok. no worries.


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Myelinated vs Un-myelinated
If an axon is completely myelinated (doesn't even have Nodes of Ranvier), is it faster than an un-myelinated axon when conducting action potentials?

What do you think would happen in an axon without nodes of Ranvier?

The action potential would die out without any further stimulus, right?

Yes. So..what's the conduction velocity of something that doesn't conduct further?

Would the velocity be 0? And would that mean that the un-myelinated axon is faster?

Does it matter how fast a train is if it never gets to the destination? I wouldn't say the velocity is zero, it's meaningless.

Ok, thank you for explaining


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Arthropod identification request (a spider with no legs?)
My mother sent me a picture of a creature she encountered and couldn't identify. It looks kind of a like a spider - a mostly black body, about 1cm in size, with white specks - except without any visible legs. Apparently it was hanging from a thread, descending to the ground, and still moving.
I don't know a lot about arthropods, and, perhaps unsurprisingly, searching for "spider without legs" gives no useful results, so I'm at a loss.
This is in Northern Germany, mid-March. (The background is a cork floor.)

Any info on what this could be - and whether it's dangerous or not - would definitely help put her at ease.

ID chances are much higher if you photo the top side. Perhaps fiip him with a piece of card, that looks like it's feigning to be dead, trying to look like a stone.

This appears to be the underside of a walnut orbweaver:

These orbweaver spiders are not medically significant.
Spiders often lose their legs in wasp attacks. Some spider wasps will remove the legs and then try to bring the spider to its nest for larvae to feed on. Sometimes they drop their spider victims accidentally.
Some will simply deposit eggs into the spider and leave it there, letting the larvae grow inside the spider and feeding on it from the inside.. these ones don't usually remove the legs - they usually just paralyze the spider.
Spiders can lose their legs through various attacks, but they can also lose their legs in molting accidents... particularly if they are in the middle of a molt and then are aggressively interrupted.

This is a great answer, so interesting and informative! +1 (more if I could). Where did you find out about the... unseemly... wasp behavior? Do they also decapitate their prey? I'd like to read more. Thanks!

Thanks! Here is a video of a wasp removing legs... it says 'spider' but it appears to be a harvestman ("daddy long legs"): https://www.youtube.com/watch?v=NwPuhVS2RhE
But that's not a spider wasp... that one is just using it for meat. Here is a spider wasp, which will be using the spider to grow a larvae:
https://www.youtube.com/watch?v=rs_Q7S3Rxkk
and:
https://www.youtube.com/watch?v=9tfblWSdEHs
and here's one with the act of removing legs:
https://www.youtube.com/watch?v=BKZAsxHAV7w

@anongoodnurse Found another video of the full process (the hunt, the attack, leg removal, and carry-away): https://www.youtube.com/watch?v=a592T6KmwmU

BTW - I'm not convinced this was the fate of the spider. The question poser said it was descending down a silk line. I think @aliential is correct that it was probably feigning a dead pose. It looks like you can see some of the legs against the body (the hind leg on the abdomen and the tarsus/foot slightly covering the ventral white mark)

Thanks for the reply. Those videos... omg. Nature is really red in tooth (or mandible) and claw.  Your comments led me to explore and learn. I hope you're right about this spider's fate. I like spiders, especially orbs and jumping spiders.

Thanks so much for your answer! I'm not sure about it being a wasp attack as it's not yet wasp season (though it's fascinating that that can happen), but the species looks to be a perfect match. :)


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Arachnid identification request
Every so often I come across one of these (presumably) spiders, but haven't been able to find out what species it is.
It is black, ~7mm in length, has a long and narrow body and relatively short legs, and seems to be able to spin threads. I came across it indoors in South-Western Germany in early Summer. The closest match I could find is the Zebra jumping spider, but "mine" has no stripes. Could it be another species of jumping spider?
I realize the picture quality isn't great, but it's all I have:

Not a zebra jumping spider - but it is in the same family of jumping spiders.
It is a kind of ant-mimic jumping spider. Possible genuses (genera) are: Synageles, Myrmarachne, Leptorchestes, which are present in Europe.
Micaria is another genus in Europe but this does not look like one of those.
There are other similar-looking genera Peckhamia, Sarinda, Synemosyna, but these are mainly found in the Americas and not in Europe.
--
(EDIT) the most observed species in Germany from these genera are (in order):

Synageles venator
Leptorchestes berolinensis
Myrmarachne formicaria

(according to iNaturalist)

Thanks very much! I can't verify for sure, but Leptorchestes berolinensis looks like a very close match.


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Twin with one boy and one girl with single placenta
I am 27,male and just become father of twins.
One baby boy and one baby girl.
According to my wife’s medical report both of the babies were sharing a single placenta.
I am not an expert in medical science but through internet I have read that the twins will be either boy or girl.
So is it a rare case that I got a baby boy and a baby girl who were sharing a single placenta?
Just curious to know. If yes then what was the probability of this case?

First and foremost, congratulations!
Yes, it is extremely rare for dizygotic twins (two eggs/zygotes, fraternal) to share a single placenta. This is referred to as monochorionic (one placenta) dizigotic twins (MCDT). This is the rarest of all twins.
It was a well known occurrence in cattle, but until recently not recognized in humans. For this reason, articles you find online will often still state that twins with shared placentas are monozygotic (identical) twins. The rate is influenced by assisted reproductive technology (ART) e.g. IVF, which itself increases the rate of twin births. The exact rate is not known, but it is probably more common than estimated, as more testing is now being done on monochorionic twins.*
This happens because the two placentas happen to implant too closely to each other in the uterus, and sharing a relatively small space grow together to form one whole. The degree to which they grow together is variable.
Without IVF, twin birth (in the US) occurs in about 2% of births, so 1 in 50. Including IVF, twin births increase the total to about 3 in 50 births (numbers vary from country to country). In one study of 31 MCDTs, 87% followed assisted reproductive technology; only about 18% were conceived naturally. So, 18% of (2/100) is about 1 in 250 naturally conceived twin births. If ASR twins are included, it increases, but it's still uncommon.
*In one case, a pair of monochorionic twins were found to be dizigotic at 14 months of age after testing because the parents believed they were not identical.
Unusual Twinning Resulting in Chimerism: A Systematic Review on Monochorionic Dizygotic Twins
Chimerism in monochorionic dizygotic twins: Case study and review


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What are good techniques for determining direct maps of proteins?
I am looking for which techniques to explore to determine electron density maps (or Fourier maps) for a protein (possibly using an assumed model).
In particular, I want to avoid techniques that create difference maps like Fo - Fc, and I think this means I also want to avoid 2Fo - Fc or other types of "sigma_A" maps, which all (I think?) contain data indicating the difference/discrepancy between observed and modeled densities. I believe what I am referring to is a "direct map."
While I'm open to techniques that are informed by a candidate model, I don't want F_calc to show up in the actual output. Also, I'd like to reduce model bias as much as possible while still arriving at a direct map (assuming that is the correct nomenclature).
I've seen references to "Iterative OMIT" and various other "OMIT" maps, but could not determine whether those gave the output I'm looking for.
Ideally, I'd like to use techniques that are implemented in open-source libraries, though that may not be an absolute requirement.

The 2mFo-DFc map is considered to be least biased by the model. Reportedly, it was shown to be least biased in a paper from 1986.

Unrelatedly, I am not certain about it but should this be migrated to SO bioinformatics?

@marcin, I believe the 2mFo-DFc is still a difference map. Its values (if I understand it correctly) are not intended to be an image of the actual electron density.

@DavidR they are. 2-1 map looks like direct map, but is less biased. You can google to find various presentations (from lectures and MX workshops) that cover map types. Books such as Biomolecular Crystallography probably also cover it.


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Why does constant current in electrophoresis mean that the molecule moves at the same rate?
Two part question:
Part 1:
I have always learned that when running a SDS-PAGE current is what decideds how fast the macro molecules migrate.
However, if the force excerted on a molecule is equal to charge times electric field.

Then wouldn't the speed at which the protein migrates depend more on voltage then current? As the the electric field is a measure of Voltage across an area.
Also, does this change based on the type of electrophoresis? (specifically, Agarose/DNA, and native page)
Part 2:
How do you calculate the time it would take for a molecule to reach the end of a gel based on the length of the gel and either the voltage or current?

Related

Voltage is proportional to current, so it depends on both equally.  Constant current is safer though, since as the resistance drops, so does the power dumped into the circuit.

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Regarding the role of enzymes
Textbooks commonly state that the role of enzymes is to speed up a chemical rxn by lowering its activation energy.
However, I'm unsure what enzymes like helicase, DNA/RNA polymerase, and restriction enzymes have to do with lowering the activation energy. Isn't helicase's primary role, for instance, to unwind double-stranded DNA?

What is the problem with the enzymes you mention? They all catalyse chemical reactions which have activation energies. Those for polymerases should be self-evident. If you are unaware of the reaction catalysed by helicases, consult the relevant Wikipedia page, for example.

All reactions require an amount of energy to proceed called the activation energy. Enzymes lower that activation energy through various means. An example here is the unwinding of the double-stranded DNA requires breaking hydrogen bonds. Energy needs to be supplied for the reaction to proceed. The rate of the reaction can be  described by Arrhenius' equation

You can increase the rate of the reaction, or decreasing the activation energy. Enzymes are required to do that at physiological temperatures by lowering the activation energy, because increasing the temperature is usually not an option.
The enzymes you mentioned are no different.

Helicase also hydrolyzes ATP.

Your answer seems to me misleading. Whether a chemical reaction requires energy or releases it is irrelevant to the requirement for an enzyme. Both types of reaction have an activation energy barrier to overcome. What is pertinent is that it is a chemical reaction which helicase catalyses — as has been mentioned, one involving the hydrolysis of ATP.

Yes, an amount of energy is needed to overcome the activation barrier. Mentioning that helicase requiring ATP doesn't contribute anything to the answer.

Since some might not consider the breaking of hydrogen bonds in DNA to be a chemical reaction, it might not then be immediately obvious why helicase is considered an enzyme without accounting for its hydrolytic activity.

@canadianer — Strictly speaking I gather that it is a process in which chemical energy is converted into mechanical energy like other molecular motors. I’m not an expert on such, but it would seem to me that whatever the molecular details of this conversion, there must be an energy barrier for an enzyme to be required. However, if we throw out the nonsense about polymerases from the question, it may be worth considering helicases alone and in detail. As I have already said, I think this answer is bad as it suggests that an enzyme is needed because the process has a positive delta G.


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What differentiates diseases like Covid-19 and Polio from the common cold
Why are vaccines required for our body's immune system to destroy viruses that cause the likes of Covid-19 or Polio, while viruses that cause the common-cold are self-limiting (go away on their own)? What is so different about viruses that cause diseases requiring vaccines?

"..while viruses that cause the common-cold are self-limiting (go away on their own)" You heard of the human immune-system and antibodies - right? But to partially answer your question: Certain strains and their mutations are more 'contagious' and more 'viral' (have a higher virality) than others..

"Why are vaccines required for our body's immune system to destroy viruses"...no, vaccines are not 'required' for anything.  Most people infected with Covid 19 are recovering fine with no special medicine, so it is self-limiting in most people.

@swbarnes2 Thanks for the response! Sorry, you're right that a vaccine isn't necessary for the viruses. However, viruses that cause the common cold doesn't cause a pandemic, while the virus that causes Covid-19 does. With relation to the human's immune system, what can be attributed to that difference? I'm sorry if this question sounds silly...

It's not that polio &c don't "go away on their own" - or more accurately, are defeated by the immune system, it's that they cause lasting damage that persists even after the active infection is controlled.  The common cold just causes a bit of sneezing and runny nose, but the polio virus damages nerves.

There is not really an inherent difference between these viruses.  Polio is a run of the mill enterovirus - some of its closest relatives are "common colds", while others are less pleasant - see https://www.slideshare.net/TarekMahbubKhan/enteroviruses-and-polio for some examples.  Note that some "common cold" viruses have uncommon but nonetheless devastating polio like effects; a leading culprit for acute flaccid myelitis (polio-like paralysis) was the common cold enterovirus D68 ( https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(18)30094-X/fulltext but I haven't checked for updates lately).  But for that virus, damaging replication in nerve tissue is at most a rare complication rather than a frequent one.
Coronavirus has long been known for several strains of "common colds"; they were just not as frequently deadly.  Unfortunately, we did not see the "cold and flu season" as a demonstration of defenselessness against viral outbreaks, and did not use the opportunity to practice exterminating them.


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Question regarding the number of alleles
Why is it that in biology we often say that a gene has two alleles? When we analyze allele frequencies (e.g. using Hardy-Weinberg Equilibrium), formulas are often generalized for two alleles of a gene.
Given mutations, isn't it quite likely that a population will have more than two alleles for a gene?

The two-allele scenario is often used in genetics teaching because of its simplicity. However, quite a few genes have more than two alleles. Some examples that readily come to mind are:

The ABO gene in humans: This determines ABO blood group, and has six common alleles. Many more rare alleles have been described [1].
The human leukocyte antigen (HLA) genes: These are well-known for their allelic diversity. One of them, HLA-A, alone has over 6,000 alleles [2].

Reference

Seltsam A, Hallensleben M, Kollmann A, Blasczyk R. The nature of diversity and diversification at the ABO locus. Blood 2003; 102(8):3035–3042. https://doi.org/10.1182/blood-2003-03-0955
Robinson J, Halliwell JA, Hayhurst JD, et al. The IPD and IMGT/HLA database: allele variant databases. Nucleic Acids Research 2015; 43:D423-431. http://hla.alleles.org/nomenclature/stats.html

Depending at which level you are defining an allele. As @Adhish described, at the molecular level there is no theoretical limit on the number of alleles of a given gene. The presence or not of more than 2 alleles depends on evolutionary factors such as population size, fitness change, genetic drift, etc. Hardy-Weinberg Equilibrium with two alleles is easier to understand but is possible to extend the genotype predictions for multiple alleles in the equilibrium. Also remember that the Hardy-Weinberg Equilibrium is theoretical and requires assumptions that are never really met in nature, so is extremely hard for multi allele systems to ever reach the equilibrium.


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Movement of Common Jelly Fish
Among the different types of movements in the bodies of various organisms, the movement exhibited by jelly fishes are very unique and peculiar in some ways. I can't understand how to classify the type of movement for jelly fish.
Its movement is also similar to octopuses and squids, but they have proper propelling arms which they use to propel themselves forward. Whereas Jelly Fishes don't have such structres in them, then how are they producing such movements?
Also they outer structure (often known as "bell" or "hood") is made up of an external epidermis and an internal gastrodermis (containing nerves but no muscles) and their bodies are mostly water, so how are they able to produce such movements.

Welcome to the site! Questions without evidence of a search in an attempt to answer are off-topic. (E.g. did you google "how to jellyfish swim"?) Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to ask a good question.

I obviously did the research and I have noted my inferences in the description of my question. I also mentioned what I don't understand particularly and so I asked them as I didn't get any satisfied on Google. If there was a way to just get all the answers from the web then I wouldn't use this site. If I google how jelly fish swims? do you really think that will aswer my question, Put some thought into it. I didn't ask this doubt particularly here for no reason, if I just could have got my answers on Google.

Also it is a not a question about species identification or something, I don't know what kind of "evidence" I have to submit to ask a question on concept.

It's not obvious that you researched it because we see no sources. You must wonder what kind of Q&A site this is, being asked to show your search results; shouldn't we 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 (show a source + a quote); not a ton, but not nothing, either. Consider this kind of like a classroom, not a chat room. You'll get a (better) response with a better effort on your part.

Also, I googled "how do jellyfish swim" just to see what was out there, and my first hit answered the question. Usually with multicellular organisms like jellyfish, movement involves muscle tissue. There are lots of ways to move in the ocean, but clearly jellyfish propel themselves, so... muscle.


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Simulate merging of two ssDNA together
I have two .pdb files with two ssDNAs, which should form some specific shape when closed together. Is it possible to model/simulate this merging somehow?
I would preferably like to have a program that would take both .pdb files as input and return .pdb file of the combined molecule.

If the structures are relatively small (< 4 nt), you can use Chem3D (from PerkinElmer ChemOffice software): Load both of the PDB files and run an MM2 minimization task.
For more complex structures GROMACS or similar molecular dynamics tools are used.


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Infection induced immunity vs vaccine induced immunity
I'm of course concerned about COVID here, but my question is about viruses in general and mRNA vaccines. I'm reading reports including one by the government seeming to suggest that vaccine-induced immunity is more robust than one induced by contracting a virus itself.
Doesn't a vaccine trigger the immune system in the same way that a viral infection does? I would think it would be weaker in that it is only one protein factor rather than what would be found by a true infection. The vaccine also doesn't "fight back."
What am I missing here? Thanks.

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 (including related questions on this site), 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.

I'm not a biologist. I just want to be an informed proponent of vaccines. I just want to ask a question. I could go on for a paragraph about how the stack sites position themselves as places to get answers to questions but require too much from the askers. But I'll only say as an expert developer, I use stack overflow only as a last resort. It's more trouble than its worth most of the time. Thanks.

There are several factors at work here, and I don't think the relative importance has been determined with any certainty. In descending order of my own estimation of their importance, vaccine-induced immunity:

Stimulates the systemic immune system, rather than the mucosal,
Presents only antigens that will inactivate the virus when bound by
antibody,
and does not disrupt the immune system, which can result in a better response.

From a 2005 review on the mucosal immune system:

The mucous membranes covering the aerodigestive and the urogenital tracts as well as the eye conjunctiva, the inner ear and the ducts of all exocrine glands are endowed with powerful mechanical and chemical cleansing mechanisms that degrade and repel most foreign matter. In addition, a large and highly specialized innate and adaptive mucosal immune system protects these surfaces, and thereby also the body interior, against potential insults from the environment. In a healthy human adult, this local immune system contributes almost 80% of all immunocytes. These cells are accumulated in, or in transit between, various mucosa-associated lymphoid tissues (MALT), which together form the largest mammalian lymphoid organ system1.
The mucosal immune system has three main functions: (i) to protect the mucous membranes against colonization and invasion by potentially dangerous microbes that may be encountered, (ii) to prevent uptake of undegraded antigens including foreign proteins derived from ingested food, airborne matter and commensal microorganisms, and (iii) to prevent the development of potentially harmful immune responses to these antigens if they do reach the body interior. At variance with the systemic immune apparatus, which functions in a normally sterile milieu and often responds vigorously to invaders, the MALT guards organs that are replete with foreign matter. It follows that upon encountering this plethora of antigenic stimuli, the MALT must economically select appropriate effector mechanisms and regulate their intensity to avoid bystander tissue damage and immunological exhaustion.

So, by injecting a vaccine, it's expected we can provoke a more robust response than a natural infection that stays in the lungs. A few COVID cases result in high viremia (virus in the blood), but I don't know of any studies comparing viremia to duration of IgG levels, etc.
Regarding antigens; viruses have evolved ways to trick the immune system, e.g., presenting an antigen that is attractive to the immune system, but the virus can still function when it is bound by antibodies. In COVID, this is the post-fusion state of the spike protein itself. The mRNA vaccines, at least, include mutations that block the spike from transitioning to the post-fusion state.
And finally, successful viruses actively interfere with immune function. COVID has been found to induce immunodeficiency in recovered patients. This prevents the immune response to a natural infection from being as strong as you would expect, even though it is a more severe challenge to the immune system than a vaccination.

Thank you. I appreciate your answer and understood most of it.


text:
Why are bacterial genomes limited in size compared to eukaryotic ones?
I was looking at this graph that shows that the eukaryotic genome has "no size limit" whilst the bacterial one does. Unfortunately the graph has no reference but essentially the idea is that most bacterial genomes are in the roughly 10^5 - 10^7.5 base pair range whilst eukaryotic genomes can be anything from 10^7 t 10^12 base pairs long for example and there is a lot more variation in genome size.
I was wandering where this limit for bacteria comes from? Specifically is eukaryotic DNA packing more efficient in eukaryotes than in bacteria and therefore more genetic material can be safely carried? Or does this have more to do with evolutionary constraints on bacterial genome size with smaller genomes being selected for?


text:
Does your blood stop moving in between heart beats?
Does blood stop moving in between heart beats or does it move continuously?

Welcome Akshay. This is not simply a Q&A site, here we are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on, see our section on how to ask and see our homework-question policy. Enjoy the Stackexchange network.

I couldnt find the answer fairly simply on google, so i wrote one here, so that it exists on the web. Agreed the question looks like a homework query without prior investigation.

I think there is a difference whether you mean veins or arteries, and which ones.


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How does the cell-wall ultrastructure of gram negative bacteria justify it being unable to Sporulate?
The following is a quote from my Microbiology Lecture PPT: "Some gram positive bacteria but NEVER gram negative ones produce spores under harsh conditions".
It got me wondering why gram negative bacteria is "NEVER" involved in sporulation? At this level of which the argument has been presented, I deduce that the distinction should be in the cell-wall ultrastructure differences (gram positive vs gram negative). I do understand the ultra-structural differences between gram positive and gram negative bacteria but I cannot relate it to Sporulation, that is, how does the cell-wall ultrastructure of gram negative bacteria justify it being unable to Sporulate?
Before you mention it, yes I did approach my professor about it, and she, too, got interested to know about this and we are both on a quest to find an answer for such a seemingly interesting question.
Many thanks in advance!

What do you mean by "justify"?

Provides a scientifically plausible reasoning for why gram negative bacteria cannot sporulate with the reasoning being attributed to the cell wall ultra structural differences (vs. gram positive bacteria). Hope this helps. @BryanKrause

Endospore formation is probably unique to a single phylum (Firmicutes) and requires something like 80 different genes. Non-Firmicutes spore-formers (just a handful of Actinobacteria that I'm aware of) use a substantially different mechanism resulting in different spore structures lacking certain components essential to endospore formation. Seems like a bit of a stretch to assume the cell wall structure is the primary limitation.


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How does new species come into existence?
The only reason for the creation of new species that I found from the internet is geographical isolation. Are there any more reasons?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For this question, you can easily find good answers online and as such this question seems to fit this sites criteria for "homework". ——— Thank you for taking the [tour], but please also go through the help pages starting with [Ask] questions effectively on this site. Thanks!

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

A paper from Müller et al. proposes a molecular marker called a CBC, differences in which can be used to call two different species, even when closely related: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1950759/

In this study we are looking for a molecular classifier that might indicate that two organisms belong to different species. We are interested in an indicator hypothesis that is easy to work upon and additionally yields a certain probability that two organisms belong to distinct species. Compensatory base changes (CBCs) in the internal transcribed spacer 2 region (ITS2) of the nuclear rRNA cistron have been suggested as such a classifier.

Some mutation event that creates sufficiently different CBCs in a viable offspring capable of further reproduction, i.e., survives natural selection, would therefore lead to speciation, by this measure.

So, natural selection is another type of speciation. I understand.

Natural selection acts on organisms. Some organisms have deleterious mutations. Some have neutral mutations. Some have (more rarely) beneficial mutations. If mutants survive or thrive and (most importantly) reproduce, and if they carry sufficient and specific genetic changes, then those mutants could lead to what this method would term a new species.

This seems like a very specific answer to a very general question... I see it's been accepted but I'm worried that it's a bit misleading.

If it is misleading, you're welcome to provide another answer.

Drive-by downvoting is of no help to improving Stack Exchange, nor this subsite, generally. Clean up your act.


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Understanding the ECG waveform with respect to Lead Positions
I am really confused about the Representation of potential in an ECG graph.
First i will ask what is on the vertical axis? (I guess it is electrical potential in millivolts)
But again it changes for various positions and the graph takes a different shape. These are called Lead positions ( correct me if i am wrong )
I don't understand why the waveform changes for different Lead positions. Basically I do not understand how the ECG machine works in relation to what happens in the heart ( i.e. the action potentials from SA nodes and so on...)
This diagram shows what I meant.
How am I supposed to interpret the data if it is different depending on direction.
I will be grateful if someone can also provide some information on the cardinal directions in these cases.
Thanks!


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What happens if a lysosome is pierced and it's enzymes are made to get released
I am confused the results be same as it happens when lysosome gets damaged during some metabolic activity or different . If same  the cell will die by the actions of those hydrolytic enzymes slowly or immediately , I think the results might differ from the accidental case

Enzymes of lysosome are usually inactive and are activated only in low pH environments, so I guess, randomly puncturing a lysosome wouldn't affect the cell to any serious extent unless the cell is an acid secretory cell or It's membrane is easily permeable.


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Is there potential to modify GM crops to inhibit their reproduction with non-GM crops?
I've been reading on terminator gene sequences and was wondering whether the same technology could be applied to GM crops to prevent transgene flow. Turns out Monsanto had developed the technology but pledged not to use it in their crops, from what I gather because it would have forced farmers to keep purchasing new seeds from the company annually.
Thus my question is: how feasible is it to genetically modify GM crops so that their gametes produce healthy offspring when crossed with other GM crops, but produce lethal mutations to the embryo if crossed with a non-GM crop in order to eliminate the possibility of transgene flow?

I can imagine a couple of different ways to do it. One would be "terminator" seeds of the kind that you mention. Another might be a gene drive style system to make GM-wild hybrids sterile.
I would argue that it's feasible right now to use the GURT systems such as terminator seeds to prevent cross-breeding- after all, you'd just have to set up the genetic switch to respond to a stimulus that you can control, and once the seed grows feral without the right stimulus, it becomes sterile or non-viable (see figure from wikipedia).

The problem, as with any bioengineering, is that biology loves breaking rules and escaping from these kinds of systems in the wild under intense selective pressure.
This kind of mutational or epigenetic escape from the lethality system is probably rare enough to still make it worth it to Monsanto to develop the tech (especially when complemented with intellectual property legal instruments), but still plausible enough to freak out folks who don't like GM organisms.


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Can humans eat a greater variety of things than other omnivores?
One thing that I've always noted is that humans seem able to eat just about anything that isn't toxic (and many things that are). Even when compared to other omnivores, I have the impression that humans are capable of eating far more things without harm. Is this true?

I don't know about that.  My dog seems to eat anything I would (of course I don't give him things like chocolate, but he would eat it if I did), plus many things I would not, such as horse manure, hoof trimmings, long-dead critter bones...

Maybe so, but you COULD eat those things (disgusting, but that's all). On the other hand, your dog would actually get sick, and possibly die, from eating things such as; onion, garlic, chives, chocolate, macademia nuts, avocado, xylitol (sweetener), cherries, grapes/raisins... You get my point?

No, because even if I (as a typical human) could force myself to swallow many of the things that a dog happily eats, I would actually get sick, and possibly die, from eating them.  Sure, humans can safely eat some things that dogs can't, just as dogs can safely eat some things humans can't, but that is not saying that humans can safely eat more things.

@jamesqf Really? I know there are many things a dog eats that I would not like to eat, but I've not thought about them being "inedible" for me. Do you have a few examples?


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Why didn't more muscles evolve the endurance of heart muscle?
The heart is a muscle capable of both the quick contraction of white muscle cells, and also the endurance of red muscle cells. Why haven't more muscles in the body adapted the same combo of abilities? Is there a known weakness to the heart muscle? Excessive energy consumption, or something else?

Different strokes for different folks, as they used to say.

Our heart, diaphragm, and arterial muscles need to work 24/7. No other muscles even come close to that requirement, so they evolved in different ways. Always be wary of asking Why? when it comes to evolution.


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Are diplobacillus physically connected?
I know that a diplobacillus is a bacillus bacteria that has a buddy 'attached' to it.
What I haven't been able to determine is exactly how is it 'attached'? Are their cell membranes fused - are they even touching? If they aren't fused, what keeps them together? Also, does this make diplobacillus a multi cellular organism because there are multiple cells in this organism?

I couldn't find anything about diplobacilli, but I did find some information on Streptococcus pneumoniae, which has been extensively studied. S pneumoniae (R6 strain) normally occurs as diplococci. Electron micrographs—see here and here—show that the two cocci of a pair share a portion of cell wall. This is a result of incomplete separation during cell division. Also, mutations in peptidoglycan-hydrolysing enzymes have been shown to produce longer chains of cocci.
Presumably, something similar holds for diplobacilli.
Calling these bacteria 'multicellular' might be inappropriate, because multicellularity implies at least some division of labour: the cells perform different functions in a cooperative manner. Diplobacilli (such as Moraxella lacunata) or diplococci have not been shown to have such a division of labour, as far as I know.


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Using Nerve Conduction Studies to determine nerve regeneration
I was reading a paper investigating using MRI as a way to determine peripheral nerve regeneration: https://sci-hub.do/10.1016/j.expneurol.2009.10.012
They mention that

... nerve conduction studies are widely used but these studies are limited
only to the distal parts of peripheral nerves and not suitable to
measure regeneration early on and in response to proximal lesions
(Kimura, 1999). Furthermore,after complete axonal injury, particularly
as it relates to traumatic nerve injuries or proximal plexus lesions,
the distal portions of nerves are often inexcitable, which limits
electrodiagnostic testing's utility to assess the degree of
regeneration in proximal nerve trunks.

I understand this because normal nerve conduction studies wrap an electrode on your finger (where current goes in) and reads it down stream at your wrist.

I totally get why this wouldn't work if the injury occurred very high up at say the elbow, because the signal could not travel from your finger upwards since it's all degenerated.
However, what if we instead stimulated the nerve a bit above the elbow (maybe using a needle) and measured the signal downstream. We could move closer and closer until a signal was detected. This is where the nerve has regenerated to - thus this method CAN detect peripheral nerve regeneration. What is wrong with my reasoning?

I think that theoretically there's no fault in your reasoning. However, technically, to access the regenerating axon at the elbow level could be almost impossible. I also think that the labels in your draw should be: (in -> recording; out -> stimulation)

Remember that peripheral nerves come all the way from the spinal cord. When they write of

traumatic nerve injuries or proximal plexus lesions

they are talking about injuries to the trunk, nerves running more or less around the collarbone. They're not talking about elbow vs wrist. See for example https://en.wikipedia.org/wiki/Brachial_plexus and the image there from Gray's:

They're also not necessarily saying that it is physically impossible to do a nerve conduction study in these areas with traditional means, they are talking about practical matters and use in-practice, and their paper is touting their method using noninvasive imaging.

Great points but I don't see what's so impractical to stick a few pads on someone's collar bones? Is it that we would actually need to stick deep needles into the person?

@JohnHon Yeah the surface isn't anywhere near those nerves.


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Why do T cells have MHC II receptors?
I have seen the answer to this question which says that T cells do not express MHC II proteins which would make sense.
However, my textbook "The immune system" by Peter Parham disagrees. It says that T cells do gain MHC II receptors after activation.

*Activated T cells express MHC class II molecules, whereas resting T cells do not.

I cannot see why this is needed. MHC II molecules are for CD4 cells (helper T cells).
If the T cell presenting the antigen was a CD4 cell, then that seems useless, because this cell was already the one that could recognise this particular antigen - so why show it to others? The chance that another T cell that could recognise it too would be incredibly small no?
I guess I can see the merit of a CD8 T killer cell to show the antigen, as it could alert other CD4 T cells to come assist (although cytokines seem like a better method...)
So what is the purpose of T cells, in particular CD4, of showing MHC II proteins?

That's the description in my book which has the same image.
The book is: Janeway's Immunology (9th Edition)
Article discussing MHC Class II expression in humans:
https://doi.org/10.4049/jimmunol.168.2.763
Excerpt from the book:

The processing and presentation of pathogen-derived antigens has two
distinct purposes: inducing the development of armed effector T cells,
and triggering the effector functions of these armed cells at sites of
infection. MHC class I molecules bind peptides that are recognized by
CD8 T cells, and MHC class II molecules bind peptides that are
recognized by CD4 T cells, a pattern of recognition determined by
specific binding of the CD8 or CD4 molecules to the respective MHC
molecules (see Section 4-18). The importance of this specificity of
recognition lies in the different distributions of MHC class I and
class II molecules on cells throughout the body. Nearly all somatic
cells (except red blood cells) express MHC class I molecules.
Consequently, the CD8 T cell is primarily responsible for pathogen
surveillance and cytolysis of somatic cells. Also called cytotoxic T
cells, their function is to kill the cells they recognize. CD8 T cells
are therefore an important mechanism in eliminating sources of new
viral particles and bacteria that live only in the cytosol, and thus
freeing the host from infection.
By contrast, MHC class II molecules
are expressed primarily only on cells of the immune system, and
particularly by dendritic cells, macrophages, and B cells. Thymic
cortical epithelial cells and activated, but not naive, T cells can
express MHC class II molecules, which can also be induced on many
cells in response to the cytokine IFN-γ. Thus, CD4 T cells can
recognize their cognate antigens during their development in the
thymus, on a limited set of ‘professional’ antigen-presenting cells,
and on other somatic cells under specific inflammatory conditions.
Effector CD4 T cells comprise several subsets with different
activities that help eliminate the pathogens. Importantly, naive CD8
and CD4 T cells can become armed effector cells only after
encountering their cognate antigen once it has been processed and
presented by activated dendritic cells.

Unfortunately the most recent review specialized on this topic (I found) dates back to 2004, and it's pretty confusingly written, IMHO. The general gist of it appears to be that T cells can act as APC cells under some conditions (aka T-APC) and it was generally thought that this serves a down-regulatory function for T cells, e.g.

There is considerable evidence, dating as far back as
1978, in support of the notion that human activated
T cells can function as APC (so-called T-APC) and
thereby affect the activities of other T cells. [...]
Most reports show that MHC class II–mediated antigen
presentation by T-APCs provides downregulatory signals
by inducing either apoptosis or clonal anergy in activated
T cells or cytotoxicity in resting T cells.
This T-T presentation-induced anergy does not appear to
result from TCR ligation in the absence of costimulatory
molecules, because activated T cells themselves express
CD80 or CD86.

More recent work has found that trogocytosis is possible between T cells, i.e. they can pass each other peptide-bound MHC. In particular trogocytosis explains some mysteries in this area, such as how mouse CD8 T cells, which cannot express the MHC-II gene, themselves actually acquire such receptors on their surface.
One such recent paper proposes that such T-T interactions differentiate CD4 T cells into regulatory ones vs Th17 pro-inflammatory ones:

We investigate the functional outcome of T-T cell antigen presentation by CD4 T cells and find that the antigen-presenting T cells (Tpres) predominantly differentiate into regulatory T cells (Treg), whereas T cells that have been stimulated by Tpres cells predominantly differentiate into Th17 pro-inflammatory cells.

The introductory section of this 2021 paper contains a useful minireview of the directions of research  (some of them being apparently somewhat contradictory to each other, if more specific conditions of the experiments aren't taken into account)

Another important mechanism of intercellular communication within the immune system is trogocytosis (Joly and Hudrisier, 2003), where T cells and natural killer (NK) cells acquire micrometer-sized fragments of the APC membrane (Carlin et al., 2001; Vanherberghen et al., 2004). These fragments can contain immune-modulating membrane receptors such as killer inhibitory receptors and major histocompatibility complex (MHC) class I and II complexes. Previously it was shown that MHC-II vesicles are released by APCs and acquired by responding T cells (Arnold and Mannie, 1999; Patel et al., 1999). T cells also acquire peptide MHC (pMHC) complexes at the IS [immunological synapse] via a process that requires T cell receptor (TCR) internalization and TCR signaling (Huang et al., 1999; Hudrisier et al., 2001). In addition, they acquire CD80 and CD86, ligands of the co-stimulatory receptor CD28 (Hwang et al., 2000; Sabzevari et al., 2001). This could convert T cells into APCs. Both CD8 T cell-dendritic cell (DC) interactions and secondary T cell-T cell interactions are required to generate protective CD8 T cells (Gérard et al., 2013), and CD8 recall responses depend on CD8 T cells taking up MHC-II from DCs to present it to CD4 T cells and obtain their help (Romagnoli et al., 2013). In contrast, other results have suggested that pMHC acquisition by T cells may play an inhibitory role (Dhainaut and Moser, 2014). For instance, T cell antigen presentation to other T cells has been associated with the induction of anergy, apoptosis, and even tolerance (Chai et al., 1998; Mannie et al., 1996), and may represent a mechanism to limit clonal expansion (Tsang et al., 2003).

I believe in the article you provided it is stated that the function of MHC class II molecules on activated CD4+ T cells is still unclear. It is believed that these MHC class II molecules-presenting T cells have potential ability to act as antigen presenting cells and induce immune response by activating other T cells. They are also capable of inducing down-regulatory signals for immune response by inducing anergy in activated T cells and cytotoxic resting T cells. In addition, they have also been reported to transduce intracellular signals into T lymphocytes.


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Are antibodies labelled with fluorescence that have not attached to an antigen visible under light microsocopes?
I came across this thought while studying histology, what happens to fluorescence labelled antibodies that do not bind with an antigen, can we see them? or are antibodies activated upon antigen binding which in turn activates the Fc region to which the fluorescence molecule is attached.

By far the most common IHC protocol, in my experience, is using a primary antibody which binds to your target of interest, followed by a secondary antibody (which carries the fluorescent tag or labeling enzyme) to bind the primary antibody.
An example protocol from one manufacturer is found here:
https://www.rndsystems.com/resources/protocols/protocol-preparation-and-fluorescent-ihc-staining-paraffin-embedded-tissue
Summarizing:

Apply primary antibodies diluted in Incubation Buffer according to manufacturer’s instructions...

Wash slides 3 times for 15 minutes each in wash buffer.

Incubate with the NorthernLights™ secondary antibody diluted in Incubation Buffer according to the manufacturer’s instructions...

Wash slides 3 times for 15 minutes each in wash buffer.

The "wash" steps are intended to remove from the tissue any primary antibodies that are not bound and later any secondary antibodies that are not bound.
You may still get some residual background fluorescence either due to non-specific binding of the secondary antibody, or unbound primary antibody that isn't washed out (I believe in typical use the non-specific binding of the secondary antibody is going to be the most relevant contributor to background, but I don't know a good citation for that), but you use "blocking" steps to attempt to reduce non-specific binding, and the assumption is that anything remaining contributes to a fairly even background stain.
You can further use negative controls that omit the primary antibody to estimate non-specific binding of the secondary antibody and check for any unexpected partitioning that may contribute to an artifactual signal.

Oh wow! Beautiful! Thanks a bunch!


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How would it be possible to engineer cows to have more offspring?
Cows usually only give birth to one calf per year and only several in their lifetime. What would we have to genetically alter so they can have more offspring, more frequently. I read that their is a record for most births from one cow at once: 16. How could we possibly genetically engineer a cow to make this them give birth more frequently?

High potential of being unanswerable due the large number of physiological aspects likely to be involved and our lack of understanding of them.

With a couple of notable exceptions, the vast majority of agricultural "genetic engineering" is by selective breeding; the answer would typically be "continually mate cattle from lineages with high fecundity together". Little knowledge of biology beyond that is necessary.
However, you could also look for particular alleles involved in increased fecundity; here's a paper talking about one example:
Kamalludin, M. H., Garcia-Guerra, A., Wiltbank, M. C., & Kirkpatrick, B. W. (2018). Trio, a novel high fecundity allele: I. Transcriptome analysis of granulosa cells from carriers and noncarriers of a major gene for bovine ovulation rate. Biology of Reproduction, 98(3), 323-334.
If you wanted to raise a herd that had a high rate of this gene, again, you could use selective breeding alongside genotyping to propagate that particular allele.
It's a bit more complicated than just making lots of bovines, though; if you're doing this for agriculture, it's going to be quite important that the offspring have healthy development so they can be used for milk or meat. I'm not an expert in the field so I may be mistaken, but it doesn't seem like fecundity is a crucial limiting factor for cattle.


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What benefit do cardiomyocytes accrue by requiring calcium induced calcium release (relative to skeletal myocytes)?
According to 2 sources I've read, in contrast to skeletal myocytes, cardiac myocytes need calcium to diffuse in to result in contraction. One source says that they need large amounts of calcium to diffuse in through T-tubules as the cardiac sarcoplasmic reticulum is not as well developed as the skeletal sarcoplasmic reticulum, whereas the other source says that a small amount of calcium diffusing inwards is required to activate ryanodine receptor channels in the cardiac sarcoplasmic reticulum which then release large quantities of calcium which result in contraction. Regardless, what benefit do cardiac myocytes gain over skeletal muscles by being regulated by extracellular calcium? My best guess is that it helps prevent the possibility of tetany, but I am unsure.

It would be helpful to include specific links to the sources you refer to. You might also have more luck with the Medical Sciences Stack Exchange. https://medicalsciences.stackexchange.com/


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How can I measure rodent local field potentials (LFPs) with single electrodes (not tetrodes)?
We have platinum-iridium single microelectrodes lying around in the lab with 125/150µm tip diameters and I'd like to use one or two of them to measure hippocampal/brainstem LFPs. All the protocols I've found either use tetrodes or multi-electrode arrays. I understand that single electrodes are not ideal because of the noise, but is there a specific protocol I could use? I've been searching for a very long time. Am I missing something?

People measure with single electrodes all the time, you just have a very remote ground so what you measure is more like an "EEG". It's not a matter of protocol, it's a matter of physics. You can only measure what physics lets you measure.

@BryanKrause Sorry, I'm not sure I understand. I'm a little new to this. I understand that the signal between the recording electrode and ground gets subtracted. Are you suggesting that I need at least two electrodes in close proximity to measure LFPs? Could you clarify please?

You can place your ground as far away from your recording site, somewhere you don't expect any input to matter for your system. Typical choices are in the bath (in vitro or in vivo) or the animal's skin. Make sure you are recording in differential mode.

@RobertS The further away your ground, the less "local" your measurement is. In many cases like vkehayas says a reference/ground under the skin is considered suitable.


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Which anaerobic environments would exist without aerobic life?
All of the anaerobic environments I can think of are that way because a layer of aerobic life above them separates them from oxygen. If the aerobic life were removed, the anaerobic compartment would equilibriate with the partial pressures of the atmosphere, however slowly, and it would remain at equilibrium until competition between aerobic cells once again pushed the oxygen boundary to the top.
After the great oxygenation event, there was oxygen in the atmosphere but no layers of aerobic life to stop it from diffusing to the bottom of the ocean or deep underground. If there are anaerobic environments that exist independently of aerobic life, our anaerobic ancestors could have survived there until aerobic respiration or tolerance evolved. Otherwise aerobic tolerance would have had to have been present before the great oxygenation event for anything to survive at all.
Which is closer to the truth? (An environment that takes extremely long to equilibriate with the atmosphere, long enough for evolution to be fast in comparison, would count as isolated for the purposes of this question since it would serve as a reservoir of life from which aerobic respiration could emerge.)

well since most of the oxygen is made by aerobic life, anywhere they want.

A lot of chemicals would have buffered the oxidation event. Especially Fe2+ in water oxidising to Fe3+.

In the question body it says:

After the great oxygenation event, there was oxygen in the atmosphere but no layers of aerobic life to stop it from diffusing to the bottom of the ocean or deep underground.

This statement isn't justified, given that the Great Oxidation "Event" developed over one to two billion years. It took half a billion years for the atmospheric oxygen concentration to go from nil to around 3%.  This is a large amount of time for evolution to select organisms that can tolerate the presence of free oxygen at various levels.  There would be a wide range of environments with differing levels of oxygen, depending on many factors including distance from the oxygen emitters (cyanobacteria) and the nature of the intervening materials.  The atmospheric oxygen concentration remained at fairly stable levels of 2% to 4% for nearly a billion more years, giving more time for evolution of oxygen-tolerant and -consuming organisms to evolve. Thus, to the extent that anaerobic organisms depend on aerobic organisms to shield them from oxygen diffusion, there would have apparently been plenty of evolutionary time for that to occur.

Deep sea hydrothermal vents release reducing chemicals like sulfide ($S_2^-$) and ferrous iron ($Fe^{2+}$). These chemicals establish anaerobic conditions abiotically[1].
[1] "M. jannaschii uses sulfide (S2-) for growth and energy, which is good because sulfide is present in high levels in the vent fluid. It reacts with oxygen to establish anaerobic growth conditions for the archaea."


text:
Why and how do species diverge in the same region?
I want to begin by saying thatt I'm not a student of biology, so I apologize if this is an obvious question. My question is about species in general, but I'll be focusing on hominins since I'm more familiar with them.
I've been reading about human evolution, and it seems that at some point 3 different genera coexisted (Austrolopithecus, Paranthropus, and Homo) somewhat close to each other. My question is twofold:

Why did this three species diverge? One partial answer is specializing to a niche; e.g. the Paranthropus can eat less nutrient rich food, but there doesn't seem to be a concrete niche the Homo are filling compared to the Austrolopithecus. For some birds, it seems even less clear if they are filling a niche; e.g. sometimes just a couple of colors, feathers, or songs change.
How did they maintained the divergence? At least based on Homo Sapiens behavior with other relatives, I'd believe that these hominins wouldn't mind procreating with each other. It seems to me that they all live in a relatively small area, at least when considering that they are not sedentary and have hundred of thousands of years to move to cycle around all Africa, so I'd think there were plenty of opportunities to mix. Why didn't they mix until they got completely homogenized? Thinking of birds again, at least for those that don't have a very specialized mating ritual, I'd have expected all of them to mix so that there is at most one subspecies of bird per niche, but this is not at all the case.

There might be different reasons I guess. In general, there is a machanism for speciation in the same region, namely sympatric speciation. However, I doupt this is relevant for hominins. But, even if these species lived roughly in the same regions, there can become geographically isolated, for example by newly formed river, etc.


text:
Molecules, Targets and Isoforms
I have a question. Given a molecule A and two isoforms of a gene X, Y, and the knowledge that A targets X. Can I infere from this anything about whether A targets Y?
As a motivation think about Furosemide (= A) and SLC12A1, SLC12A2. From Drugbank I know that Furosemide targets SLC12A1, and from KEGG I know that Furosemide targets both genes. I wonder whether I can infer the KEGG knowledge already from the Drugbank knowledge...
Best,
Alex :)

The short answer is no.  What matters is whether the sequence and folding (if you are talking about binding of A to proteins instead of DNA) of each isoform of your gene still results in the binding of A.
I other words, A may bind to X. Y, an isoform of X may not have the same sequence that A likes to bind to. Or, in the case of proteins and A, Y may fold slightly differently, preventing accessibility of A to Y.


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Why do shed and brown poplar (Populus) leaves get an iridescent blueish colour when wet?
When the brown leaves of poplars shed on the ground stay for a while under wet conditions (e.g. like in a puddle), they become a fascinating iridescent blueish colour, which is best seen when light shines on it. I tried to look this up, but did not get any results... any ideas?


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Allometry of vision, can mice see their own fingers?
Looking around, I've found a lot of research on the allometry of visual acuity and vision at a distance, but not so much on vision close-up. As I understand it, the "near point" of vision is largely determined by the optical/focusing power (diopters) of the lens, which is itself determined by the refractive index and lens curvature (lensmaker's equation). Assuming the refractive index is constant, this implies smaller animals should have the more powerful vision (assuming smaller eyes) necessary to resolve something as close to their eyes as their own claws. Does measurement agree with this hypothesis? What is the scaling relationship? Is there a single one, or is it sensitive to eye type like acuity is?

Exciting question, and anticipations are largely met for mice (featured in title). Mice have a closer focal point than humans. As less than 2 cm they can likely see their fingers. Assumption on constant refractive index would require to further assume that viewing angles are different as numerical aperture changes. Mice having a more powerful vision system could be considered true.
Recent publication with measurements underlying above: https://doi.org/10.1364/BOE.3.000715
Generalization beyond mice would be interesting, but likely require control for other things such as habitats and whether predatory animals, ....


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What are these needle-like plants growing in the ground?
I was outside and noticed some strange, needle-like plants growing on the ground. I managed to search for "needlegrass" but couldn't find it.
Here is the photo taken on April 20, 2021 in Long Beach, California; these red circles point at what the strange plants look like:

What you have here is a Filaree/heron's bill/stork's bill (Erodium species). These are widespread in California, being plants of disturbed and unmanaged soils - farms, dunes, roadsides, etc.
Note that I'm not Californian, or even from North America, all I did was google "weed species california" (without the quotes) and hit the first link that looked reputable, then used a small bit of knowledge of plant forms (rosette in this case...) to follow the links inside - and found the species at the link I supplied.


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What are those berry-like plants in this photo?
I found this photo on a Flickr gallery and I have no idea what this plant is. Is it supposedly a type of berry or something?

I really think you should be giving full attribution to the owner of the flickr photo or gallery. Or at least a link to the source.

A google image search finds:
https://www.flickr.com/photos/15110103@N08/2044059567
which was taken in The Hague, Netherlands. And also identifies the tree.

Without knowing the geography of where the photo was taken, we could guess this is a European Mountain Ash (Sorbus aucuparia) which is fairly widespread in North America and Europe (but doesn't really grow in South America, Asia, Africa, Australia)..
You can look up this plant for information on the berries. They contain vitamin C, but don't have much other desirable properties.

There was no exact location on the Flickr page, so I couldn’t put the date.

@Kylethedownvotedisliker definitely an Sorbus tree, sometimes known as Rowan or Whitebeam. Pinnate leaves with serrations, red pome-like fruit in corymbs, very distinctive.


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What is the motivation behind the AAAAGCAUAU GACUAAAAAA of the mRNA SARS-CoV-2 vaccine when encoding its polyadenylated ending?
The very end of mRNA is polyadenylated as usual, but the BNT162b2 vaccine ends the following sequence, as denoted in this article:
                                     ****** ****
UAGCAAAAAA AAAAAAAAAA AAAAAAAAAA AAAAGCAUAU GACUAAAAAA AAAAAAAAAA
AAAAAAAAAA AAAAAAAAAA AAAAAAAAAA AAAAAAAAAA AAAAAAAAAA AAAA

This is 30 A’s, then a “10 nucleotide linker” (GCAUAUGACU), followed by another 70 A’s.
What is the reason for this design choice?

To enhance stability and translation efficiency according to {1}:

The 5′UTR (TEV) [8,21] and 3′ UTR (F-I) of this construct have been shown to enhance stability and translation efficiency, as has the 100-nucleotide poly(A) tail interrupted by a short linker (A30LA70, where L = GCAUAUGACU) [22]

References:

{1}
Stadler, C., Bähr-Mahmud, H., Celik, L. et al. Elimination of large tumors in mice by mRNA-encoded bispecific antibodies. Nat Med 23, 815–817 (2017). https://doi.org/10.1038/nm.4356 https://www.nature.com/articles/nm.4356
{21} Gallie, D.R., Tanguay, R.L. & Leathers, V. Gene 165, 233–238 (1995).
{22} Vallazza B, Petri S, Poleganov MA, Eberle F, Kuhn AN, Sahin U. Recombinant messenger RNA technology and its application in cancer immunotherapy, transcript replacement therapies, pluripotent stem cell induction, and beyond. Wiley Interdiscip Rev RNA. 2015 Sep-Oct;6(5):471-99. doi: 10.1002/wrna.1288. Epub 2015 Jun 9. PMID: 26061157. https://pubmed.ncbi.nlm.nih.gov/26061157/

It’s curious that, as far as I can see, reference 22 doesn’t mention linkers in the poly(A) tail at all.

@canadianer yes I got stuck there too… next steps is likely to email Stadler, C., Bähr-Mahmud, H., Celik, L. et al. They might have mixed up some references.

Patent referring to that linker: https://patents.google.com/patent/JP2018525410A/en


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Can arthropods rotate their joints?
I've been recently researching arthropod exoskeletons, and one thing I've seen more than once is that exoskeletons, due to how they work, only really allow for hinge joints. However, from seeing flies and mantises, I've more than once seen tilting or even rotation of the head. I've tried searching more, but all I found was how mantises are the only arthropods capable of rotating their heads, a process that I couldn't find an explanation for.
Essentially my question is: can arthropods in general rotate their joints or are mantises truly alone in their ability to have rotation with an exoskeleton as far as we know? While it's not the main goal of the question, I'd really appreciate an explanation on how exactly mantises achieve this rotation


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Are there any sources of the approximate width of azhdarchid wing limbs?
Are there any sources with approximate calculations on how wide the front limbs of azhdarchid pterosaurs, especially hatzegopteryx should/would be? I've been searching but most of what I've found were papers describing the length of certain bones, the closest I've found being certain descriptions of the humerus.

wingspan is approximately 12 meters, from the orginal descrption.
https://www.researchgate.net/publication/11313784_A_new_giant_pterosaur_with_a_robust_skull_from_the_Latest_Cretaceous_of_Romania
Your not getting anything more detailed than that becaue we don't have a complete wing, only a reconstructionf from parts of the wing bones. This is really common with very large animals, its just hard to get all of a large animal in the right conditions for preservation.
https://markwitton-com.blogspot.com/2017/01/new-paper-when-short-necked-giant.html
for anything more detailed your best bet is to take measurments from reconstruction images. they are created using the best anitomical knowledge available so they are the best you will get.


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is there a difference in meaning between the terms "bone architecture" and "bone structure"?
I'm wondering whether "bone architecture" and "bone structure" mean the same thing, or whether they refer to two different concepts.
In this article - http://rheumatology.oxfordjournals.org/content/48/suppl_4/iv3.full - bone microstructure and bone microarchitecture are mentioned in the abstract in a way which makes them sound like they are the same thing. Also, they seem to be used as synonyms in the rest of the article.
This website - http://www.doitpoms.ac.uk/tlplib/bones/structure.php - discusses cortical vs cancellous bone under "structure and composition of bone" while other sites often discuss the same thing under the heading "bone architecture".
So am I right in thinking that the architecture of bones and the structure of bones are synonyms and that either term can be used when referring to osteoporosis? Thanks.


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Epidermal layer and muscle wall of colon?
First of all,I wanted to ask that whether epidermis is present in colon ? And if yes than how is muscle wall present with respect to epidermis. Can anyone give me a pic that has both the epidermis and muscle wall of colon.

Is there a source that leads you to believe there is epidermis? Do you mean epidermis as in the outer layer of skin? Or are you thinking of epithelium?

Good question. The colon is lined by epithelial cells (as are all hollow organs). These particular epithelial cells are different from epidermal cells, which are another particular type of epithelial cells found in skin.
Epithelial cells are distinguished by the way they connect with each other using tight junctions to form a permeability layer between compartments.

In the colon, the purpose of the epithelial cells is to both to absorb water and to form a barrier between the luminal contents and the body.  They form the layer facing the lumen. The muscular layers of the colon, both the circular and the longitudinal, are further out from the lumen. You can see them in this histology slide:


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difference between trisomy and partial trisomy
Trisomy is having 3 chromosomes but then what is partial trisomy ?. I was reading about Patau syndrome and it is called trisomy 13 ( because instead of usual 2 chromosomes,it has 3 chromosomes). it was also wriiten that 20% cases are PARTIAL TRISOMIC...what is the meaning of partial trisomic?

I assume you checked Google first? The first result looks like it covers this (https://rarediseases.org/rare-diseases/chromosome-6-partial-trisomy-6q/) - are you asking for further explanation of some aspect of this?

no, actually i was reading from the slides given by my professor

Any organism with a partial polyploidy has got some tissues with a different number of chromosome set, unlike the rest of cell tissues.
These situations are often consequences of meiosis error and are more common in plants than in any other organism.

I think the OP's question is "What does it tell about the genetics of an individual if this individual has partial trisomy?". I don't think the question was "What are the health consequences of partial trisomy?" nor "How does partial trisomy comes to exist?"

Partial trisomy is just an example of a partial polyploidy. So actually I think my answer is short but straight to the point.


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What is the difference between a virus and virion
What is the difference between a virus and virion.  Correct me if i am wrong but i think that one can simply say that " virus outside a cell is called a virion" and that this stage is used to go from one cell to another

A quick google search of "virion" reveals the following: "the complete, infective form of a virus outside a host cell, with a core of RNA or DNA and a capsid."
This article is interesting too: http://www.virology.ws/2010/07/22/the-virus-and-the-virion/
Your definition is basically correct, but keep in mind that the viral particle itself never enters the host. It merely attaches to the host cell and inserts its genetic material.

@Astrolamb you're correct, except that whether the viral particle enters the host or not will depend on the virus.

Right, I'd forgotten about enveloped viruses. However, "the complete, infective form of a virus" which has an envelope includes said envelope, and since the envelope doesn't enter the cell, I argue that the capsid is not the entirety of the viral particle in that case. I suppose I'm arguing semantics at this point though :P


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What is the meaning of Sequestered germline?
What is the meaning of Sequestered germline. I understand the meaning of Sequestered in English but what is its meaning in context of germline.
For eg-"  female germ cells are Sequestered early in development ".


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Insects emerging from vertical tube
I found a vertical mud tube about the thickness of a pencil in my garden with a series of metallic green insects coming out of it. They came out when I pulled a weed but stopped when I stopped, as if the vibrations were scaring them out. I think they were bees, wasps, or flies. They were 1/2" long or a little longer and thin. Head, thorax, and abdomen were all shiny green, wings transparent. What are they?
I live near Philadelphia and it was in the upper 60s F today.

Did you happen to take a picture of them?

alas, no camera available

Mud tube, metallic green, bee-like - sounds like a mason bee to me.
There are several metallic green mason bees (Osmia spp.). As Wikipedia explains:

Mason bees are named for their habit of using mud or other “masonry”
  products in constructing their nests, which are made in naturally
  occurring gaps such as between cracks in stones or other small dark
  cavities; when available some species preferentially use hollow stems
  or holes in wood made by wood-boring insects.

One example here:

Photos at http://www.laspilitas.com/insects/megachilidae/osmia-mason-bee.html


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Fluorescent purple flowers?
Do some flowers fluoresce? Some deep purple Lobelias and larkspurs seem to glow and confuse my eyes in sunlight. It reminds me of those blue LED Christmas lights (they come in strings with other colors) - the blue ones only seem to be showing two colors at once.

Many flowers fluoresce under the influence of UV and white light. The compounds that fluoresce are called Betalains, and are either red/purple (betacyanins) or yellow (betaxanthins).
It is thought that this is a method of making the flowers more obvious to insect pollinators. However, there is some debate about whether the fluorescence contributes to this much compared to just the bright colours.

Fluorescence is a way of making brighter colors, though.  Ever looked at day-glow colors under UV light?  It's also common to fluorescent chemicals ("optical brighteners") in laundry detergents, in order to make colors (especially whites) appear brighter: https://en.wikipedia.org/wiki/Optical_brightener

@jamesqf - that's exactly the point of the papers linked in my second paragraph. It isn't known how much the fluorescence contributes to attractant for insects as the colours are already bright in the ranges that insects use. Fluorescence always puts out less energy than is put in because of the energy cost of the electron excitation step, so while those colours may be bright under UV alone, with the additional very bright white light spectrum, the fluorescence is somewhat lost.

We may be thinking about different things.  I'm not thinking of UV colors that are visible to some insects & birds, but of fluorescence absorbing the incident UV light and re-emitting some of the energy in the human-visible range.  Just as for instance day-glo orange is orange under inside lights (no UV), emits nearly the same shade of orange when you illuminate it with a UV light in the dark, and is really bright orange in sunlight because both oranges combine.

@jamesqf, no, that's what I am talking about too. The evidence for significantly brighter signals for plants emitting in the visible spectrum isn't there. It looks like <10% increase in brightness.

Hmm this seems irrelevant

@Harrychink what seems irrelevant? The question or the comments?

@bob1 the answer, as neither lobelias, nor larkspurs produce any betalains

@Harrychink The question specifically asks Do some flowers fluoresce? it's the first sentence. Yes, the question goes on to mention larkspur and Lobelia, but doesn't specifically ask about those. I should have noted that anthocyanins and anthocyanidins also fluoresce, but it isn't as strong as the betalains.


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Action Potential
I was wondering what exactly initiates an action potential? I understand that for depolarisation to occur, the membrane potential must first pass through the threshold potential, but what process leads to the membrane potential being raised to the threshold potential in the first place? I suppose this question would pertain more so to nerve cells since in muscle cells the membrane potential is raised due to the opening of nicotinic receptors and the influx of cations.

In addition to the duplicate which answers your question, I would note that a typical textbook progression introducing neuroscience is to go from resting membrane potential to excitable membranes (= action potentials) to synaptic transmission, so if you're learning from a textbook you may just need to keep going to the next chapter.


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Potassium Permeability in Cardiac Muscle Cells
From my research it seems as though there's a difference between cardiac and skeletal muscle cells in that during depolarisation, the permeability of potassium actually decreases for cardiac muscle cells. How does this occur? I imagine it would be due to the closure of potassium channels but if this is the case, then how is the inwards current of calcium balanced during the plateau phase?


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Identification of Secondary metabolites gene clusters in fungi
I am trying to identify secondary metabolites gene clusters specifically PKS from endophytes through PCR then sanger sequencing. Are there set of specific primers available or do I have to design my own?

What fungal species is it ? Are there primers in the literature designed by people who study the same secondary metabolites as you ?
What aspect of the gene clusters do you want to study ?


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Can someone identify this species of Protolophus?
I have posted my observation on iNaturalist, but so far this Harvestman has only been identified as genus, Protolophus. Here are three angles of the Harvestman in question, which has been observed in North Sacramento County, California.


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Is it possible to plant tardigrade DNA into a human? What would happen even if?
So I have been reading a WEBTOON (A distant sky) and the 2 mcs have tardigrade stem cells in them which gives them the abilities tardigrades have. I am aware that the story is obviously fictional, but I was wondering if it is possible? What would happen?

Welcome Pluto. Could you read the [ask] section of the [help] and [edit] to include more (much much more) specific details of what you're referring to in terms of the specific "genes", where and in what cells you'd transplant the "genes" and in what position on which chromosomes, and your own research into the topic. You could do worse than start with this paper: Extremotolerant tardigrade genome and improved radiotolerance of human cultured cells by tardigrade-unique protein

This is like asking what would happen if you put helicopter parts into a bicycle.

Well thank you Jim for answering properly unlike some

These are comments not answers. You're still expected to edit the question to show your own research as per the [ask].

Yes, parts of tardigrade DNA that code for specific proteins or abilities could potentially be isolated and inserted into human cells in vitro. Getting them into a living human is technically possible, but nothing like that has been done. This doesn't mean the process would result in any tardigrade-like effects in the human cells.
However, tardigrade survival is a complex system, not a single superpower gene. You can't just insert 'the tardigrade gene'. Multiple systems would need to be altered successfully for anything close to tardigrade-like resilience. Even if a tardigrade protein was successfully integrated into a human cell, we don't know what would happen because that protein will interact with the rest of our human biology.
As the comments indicate, this is entirely dependent on the specific gene you insert. There are many genes, and each can have a different effect. Many genes also need other systems or other genes to function properly. Also, inserting tardigrade stem cells into the body is different from inserting genes into human cells.


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Are humans unusual, compared to other animals, in not understanding the mechanics of sex instinctively?
To begin with a personal anecdote: there was a period in my childhood, which I can remember clearly, in which I was aware of sexual reproduction as a fact, but the mechanics of it remained a fascinating mystery. From conversations with friends - both at the time and later, recalling earlier times - and also from looking at popular culture, my experience seems pretty typical.
There are numerous instances from history of adults who were ignorant of sex to a degree which - from the perspective of our own time, where graphic content is ubiquitous and sex education mandatory - is quite baffling. A couple of royal examples:

Anne of Cleves seems to have believed, from a conversation with the Countess of Rutland in February 1640, that her husband kissing her goodnight was sufficient to impregnate her.
Louis XVI famously took seven years to consummate his marriage with Marie Antoinette. The rumours about there being an anatomical problem, i.e. phimosis, seem to have been discredited. Neither does there seem to have been any emotional barrier; the two always seemed to like each other, and eventually had four children together. But there was no consummation until Joseph II gave his brother-in-law some practical advice on the matter, after which he described Louis and Marie Antoinette as 'a couple of complete blunderers'.

Looking at the topic more systematically, this article summarises several scholarly sources. Said page discusses one book in particular called The Facts of Life: Creation of Sexual Knowledge in Britain 1650-1950 (1995) by Roy Porter and Leslie Hall. Although I have not read this book myself, the article I mentioned states:

Imagine a wedding night where neither party had any idea how the mechanics of sex functioned. Imagine a new bride so terrified of the “rude” action her husband tried to commit, she runs home to her parents and asks for an annulment the next day[...] These terrifying circumstances where women had no reproductive or sexual knowledge prior to real-life experience were all a reality, according to Roy Porter and Leslie Hall

So that's my case for humans lacking an instinctive understanding of the mechanics of sex. What about other animals? To the best of my knowledge, humans do seem to be unlike other mammals, at the very least. Any dog-owner can testify to the naturalness with which both male and female dogs play their respective parts. I remember a sheep farmer once telling me grimly that, in some breeds of sheep, it was a struggle to keep the male lambs from impregnating their mothers.
And what about other species of ape? With humans, there is a stock character in literature of the midwife/cunning woman/duenna/etc who advises the bride what to expect on her wedding night, and this character seems to have at least some basis in reality. There are also male equivalents to such a figure, e.g. the advice Joseph II gave to Louis XVI I mentioned above. Do we see any comparable roles being played among other species of ape? If so, could this be considered an example of epigenetic inheritance - analogous to the famous example of a rat mother licking her pups - and/or animal culture?

Absent sufficient sex education, teenagers get each other pregnant quite efficiently whether or not they intend to, suggesting they figure it out as well as any other animals. I question how you'd ask a dog, sheep, etc whether they understand the motions they're going through or are just following their instinctual programming.

only humans is weird societies that don't let children see adults have sex have this problem. humans learn about sex the way they learn about almost everything watching adults.

Giant pandas have been purported to benefit from instructional videos, but I found that to be not well attested when I looked for references for an answer.


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Are there ontologies for the description of the look of plants?
Are there existing ontologies for the description of the look of plants?
I am looking for something formally defined giving me at least or better more information like in descriptions:

They are mainly deciduous shrubs and trees, often with brush-like foliage, often spiny to deter grazing, and masses of small, pea-like yellow blooms which are sometimes fragrant.

which I took from https://en.wikipedia.org/wiki/Genista .
The use case is to be able to procedurally generate 3D models of them, which are not too far away from the reality as far as an ordinary person would notice.

Not a complete solution, but a lot of what I think you want can be done with L-systems.  See for instance "The Algorithmic Beauty of Plants" (Downloadable here: http://algorithmicbotany.org/papers/#abop ) See also various things to be found under the heading of Algorithmic Botany.

To transform an object in an ontology to an image of that object?  Sounds unlikely, I doubt that any botanical ontology is that developed and detailed.  It would be great if it worked.  Could be used to check the ontology.  The website https://www.ebi.ac.uk/ols/ontologies lists 251 biological ontologies.  There are several on specific plants or groups of plants (brassica, beet, oats) and several that might be more relevant to you: Plant Ontology, Plant Phenology Ontology, and Plant Trait Ontology,