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Why aren't the antibodies in the mother's milk digested by the infant's digestive system?
Why aren't the antibodies in the mother's milk digested by the infant's digestive system?
Enzymes like pepsin have been found to be present in infant's digestive system(1). Though the pH in the stomach of infants is high(The gastric pH of neonates between 2 and 13 days increases from 3.5 to 5-7 for 2 h after ingestion of human milk)(2) activity of pepsin like enzymes from mother's milk itself or infant's stomach is appreciable(1). Moreover tryspin function in infant's intestine is equal to the level in adults by the age of one month(3). Many more proteases are also seen in both mother's milk and in infant's digestive system(1). If this is the case why are antibodies present in mothers milk not digested by the infant?
I have two hypotheses regarding this

Glycoproteins by their nature cannot be digested by the enzymes in infant.
Antibodies are present in such large amounts that many of them are undigested by chance.

I have no idea whether either of these are true. Any ideas will be appreciated.
References:
(1)Thérèse A. Holton et al. Following the Digestion of Milk Proteins from Mother to Baby.Journal of Proteome Research 2014, 13 (12), 5777-5783
(2)Mason, S. Some aspects of gastric function in the newborn Arch. Dis. Child. 1962, 37 (194), 387-390
(3)Lebenthal E, Lee PC. Development of functional responses in human exocrine pancreas. Pediatrics. 1980, 66(4), 556-560

Demers-Mathieu et al. 1 used ELISA to quantify immunoglobulin concentrations from milk after 2 hours of digestion in the stomachs of preterm-delivered and term-delivered infants.  From the abstract:

Total IgA concentration decreased by 60% from human milk to the preterm infant stomach and decreased by 48% in the term infant stomach. Total IgM and IgG concentrations decreased by 33% and 77%, respectively, from human milk to the term infant stomach but were stable in the preterm infant stomach.

The authors note that the infants enrolled in this study had a variety of medical conditions, but "no overt gastrointestinal tract issues or other medical conditions that have been associated with an effect on gastric emptying or digestion capacity." Two hours of digestion was chosen to ensure recovery of sample from the stomach while maximizing digestion time, per the gastric emptying times observed in Siegel et al. 2
So, it appears that term infants are digesting antibodies from their mothers, but a substantial portion of immunoglobulins remain intact.  Weaver et al. 3 report IgA concentrations between 0.311 and 1.247 g/L across 1600 breast milk samples, with negative correlations to maternal age and parity.
Taking the median IgA concentration of 0.708 g/L, a 48% reduction gives 0.368 g/L post-digestion.  Dewey et al. 4 report that 3 month-old infants consume 818 mL of breast milk (assuming 1 g/mL) per day, on average, which suggests that ~300 mg IgA are available to the infant intestine from daily breast milk consumption.  If the adult human gut produces 40 to 60 mg IgA per kg body weight per day 5, then ~300 mg IgA is in the ballpark of what a 6 kg infant would need to phenocopy the IgA concentration of an adult gut, assuming limited immunoglobulin production by infants themselves.
So, it seems like hypothesis #2 is close to the truth, at least for highly abundant antibodies like immunoglobulins:

Antibodies are present in such large amounts that many of them are undigested by chance.

Demers-Mathieu V, Underwood MA, Beverly RL, Nielsen SD, Dallas DC. Comparison of Human Milk Immunoglobulin Survival during Gastric Digestion between Preterm and Term Infants. Nutrients. 2018 May 17;10(5):631.
Siegel M, Lebenthal E, Topper W, Krantz B, Li PK. Gastric emptying in prematures of isocaloric feedings with differing osmolalities. Pediatr Res. 1982;16(2):141-147.
Weaver LT, Arthur HM, Bunn JE, Thomas JE. Human milk IgA concentrations during the first year of lactation. Arch Dis Child. 1998 Mar;78(3):235-9.
Dewey KG, Heinig MJ, Nommsen LA, Lonnerdal B. Maternal versus infant factors related to breast milk intake and residual milk volume: the DARLING study. Pediatrics. 1991;87(6):829-837.
Jacob Campbell, James Berry, Yu Liang. Chapter 71 - Anatomy and Physiology of the Small Intestine, Editor: Charles J. Yeo, Shackelford's Surgery of the Alimentary Tract (Eighth Edition). [via ScienceDirect]

Thank you for the great answer. Have any such studies been conducted on adults? i.e.if an adult was given a proportional amount of antibodies through ingestion would they be able to digest all of it?

I’m not sure. If you post your comment as a new question, you might get an answer.


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How is boiling oil tolerated by some people?
There are people who can withstand exposure to extreme heat with no apparent side effects. One such person is Kann Trichan, a Thai street vendor who dips his bare hands in hot oil. An old TV show featured another person who, as a child, was found touching a red-hot hotplate. On the show, he was filmed holding a piece of food in a deep fryer for tens of seconds, and his hand showed no visible change when it was removed, not even surface redness.

Is science any closer to explaining the phenomenon?
Although there are no visible ill effects, are there any that might be developing (eg. a risk of cancer due to DNA damage)?
Why is blistering not occurring? What specifically triggers blistering, and how might it be being suppressed in these people?

For some of these cases, look into the leidenfrost effect (https://en.wikipedia.org/wiki/Leidenfrost_effect). people can literally touch molten metal for a fraction of a second and it's find simply because of the moisture in our hands providing a protective barrier when super heated.

In a biology forum, you may be asking about a biology question by proxy, though what we'll really be getting at is that one must first correctly apply a healthy amount of scientific thinking to questions about any observations. This is more a discussion on  science and skepticism rather than a mechanism in biology, but I will humor you briefly.

Is science any closer to explaining the phenomenon?

Why yes, in almost all of such extraordinary feats of inhuman ability, you are seeing fraud and quackery.
There are a great many 'phenomenal' people and feats who appear in Guinness record books and on TV programs and on YouTube videos, performing amazing and unbelievable feats. Very often these involve the presence of an 'expert' making sure everything is kosher, a science professor standing by, making sure there is no trickery and that the experiment is controlled. We've seen this plenty of times, with homeopathy demonstrations, extrasensory perception, free energy devices, wireless power transfer at a distance, conducting, storing or generating copious amounts of electricity from within their bodies (e.g. Battery Man), the list goes on.
Unfortunately, there a few things that tend to go wrong upon presentation to the audience at the very end:

The shows edit out much of the scrutiny or discussion of possible confounding factors. The oil may have bubbled to indicate it's boiling, but did we measure its temperature with a thermometer? Was the hand covered in a heat-resistant gel or a layer of insulating water which doesn't mix with oil and provides temporary heat resistance? Was the hand a prosthetic?
Expertise is faked by an accomplice who poses as an authority. Alternatively, an authority fails to spot the trick. You can convince many persons by virtue of a proxy; this is very human tendency that is quite easy to exploit.
Relatedly, with clever tricks, illusionists are often better candidates for spotting cheats than most scientists. This is well-understood among illusionists; 'trained folks' tend to think in certain ways and the exploitation of their expectations or predictions can proceed more easily. Analogously, visual artists may be better trained to spot fakery in videos than your average scientist (e.g. Captain Disillusion?). This is the artful aspect of deception, and no one individual can be said to be immune from professional quacks at all times; there are myriad ways to overcome a single individual's scrutiny.

There are plenty more possible explanations, I only touch on the obvious ones. Certainly many more probable explanations than exposed human skin not reacting to boiling oil upon prolonged exposure.
Rather disappointingly, in almost every single case, performers who achieve extraordinary and inhuman feats are charlatans. A rather simple answer!

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In plant cells, is water stored only in the vacuole?
In the turgor of plant cells, is water stored only in the vacuole or can it be stored in the cytoplasm and the other cellular organs too?

One of the properties of "storoge" is that in can be filled or empied when needed. Contents of cytoplasm and all organelles are aqueous solutions so all of them contain quite some water. However, thease solutions need to maintain precise concentration of many solutes in order to facilitate proper enviroment for various biological processes. Therefore, radical changes in amount of water in cytoplasm would be detrimental to life of the cell. Vacuole is not as sensitive and it can expand or shrink and act as a sort of water availibility buffer for the rest of the cell.

The cytoplasm of the cell is 80% water$^1$. All organelles contain water because all enzymatic activities inside the cell require water. However vacuoles are generally said to store water because they generally make up 30% to 80%$^2$ of the plant cell.
Thus the cytoplasm, vacuole and all other organelles contain water and contribute to the cells water potential and turgor pressure.
References:
1.Wikipedia cytoplasm
2.Wikipedia vacuole

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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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Why do doctors reccommend vegetable oils in high cholesterol and cardiovascular disease?
As there is high cholesterol in body why the patient need more fats and why the doctors are recommending it
Transcribed:

Vegetable oils are rich in polyunsaturated fatty acids (PUFA). The fatty acids present in such oils have more than one double bonds. Doctors recommend such oils to patients suffering from high blood cholesterol or cardiovascular diseases. This helps in lowering the cholesterol level in blood. When vegetable oils are hydrogenated, the unsaturated fatty acids become saturated and the oil changes to solid fat (vanaspati and margarine).

source please it will improve your question.

The subtext of the textbook excerpt quoted above is that when people are eating vegetable oil, they are not eating other fat sources. Saturated fats increase LDL levels, and unsaturated fats do not.
A C Beynen, M B Katan, Why do polyunsaturated fatty acids lower serum cholesterol?, The American Journal of Clinical Nutrition, Volume 42, Issue 3, September 1985, Pages 560–563.

Replacement of saturated by polyunsaturated fatty acids in the diet may lower serum very low-density and low-density lipoprotein concentrations because the liver preferentially converts polyunsaturated fatty acids into ketone bodies instead of into very low-density lipoprotein triglycerides. Thus unlike saturated fatty acids, polyunsaturated fatty acids are transported to the tissues for oxidation without leaving a trail of lipoprotein remnants in the form of low-density lipoproteins.


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Can I relocate bird's nest?
Doing a deck project and found a bird's nest.  Can I safely move it in order to continue working?

Think they'll fledge soon?
This is in New Jersey.

You can move it but the parents will likely not return to it or care for the chicks.  If they are nearly ready to leave the nest, perhaps you might wait a bit until that happens.
I'd say put things back the way they were and keep an eye on the nest.  If the parents don't return there is nothing more you can do.

I think they will be gone in not much longer than one week.

This same thing happened to us only we found eggs and not birds. We decided to leave it and wait for the birds to do their thing.
It doesn't look like you would have to wait too long on that one but probably not what you were hoping for.

Welcome to Biology.SE! While anecdotes are potentially interesting, answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and would be more appropriate as a comment. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!


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Spider Identification in Miami, FL
These two spiders were found at the Fairchild Gardens in Miami, FL.
What spiders are these?

Please [edit] to separate this into two questions and include size estimates for both species. Please also consult the "species-identification" tag (click on the tag I added to your post) for more information on how to best ask this kind of question. Thanks!

The second one is called the golden silk spider commonly found in forests.

@JossieCalderon If you are certain about that post it as an answer. It's OK to answer your own question.

@aminabzz Terrible moderating removed it. This answer is hidden. This answer was deleted and converted to a comment last month by AliceD♦

@AliceD terrible.


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Expected number of times a mosquito bites (per night)?
Imagine you are sleeping alone in your bedroom and there is a (female) mosquito in the room wanting to feed on your blood. I read here the mosquito will try to keep biting and feeding on you until its belly is full.
Question: What are the expected number of times the mosquito will bite you if you do not actively avoid it? (For example, in the case you were sleeping). However, I imagine this might vary with the mosquito species.
In particular, I am thinking about strategies aiming for minimizing the number of the mosquito bites: would it be feasible to let the mosquito bite you once and suck your blood until becoming fully feed?

as far as i know mosquitos bite only once,if they get disturbed before they are full they will not bite again.

@trondhansen Best to answer in a supported answer rather than a comment.

@BryanKrause i know too little about mosquitos to make an answer,my comment is more an asumption about mosquitos not taking the risk again if they got some blood the fist time.

Your answer is here: https://www.google.com/search?q=how+many+times+do+moskitoes+bite There is no limit to the number of mosquito bites one of the insects can inflict. A female mosquito will continue to bite and feed on blood until she is full. After they have consumed enough blood, the mosquito will rest for a couple of days (usually between 2-3) before laying her eggs.

@com.prehensible That is not the answer to my question. The number of times a mosquito bites a sleeping person (or a person actively not avoiding the bites) will typically follow some distribution; I am asking about the expected value of this distribution (and possibly its standard deviation). However, I understand probably this has not been studied.

There are many variables to your question then... 3000 species of mosquitoes, dozens commonly drink human blood. A sleeping person, what are they wearing, what are they covering up? how much the person stirs if they are bitten? What time of night bitten,,, deep sleep? That is the science you want, human physiology of stirring in response to bites. mostly she will find a spot with enough bloodflow to fill up, and only sting  once. thats why no research is that general.

quote:... In particular, I am thinking about strategies aiming for minimizing the number of the mosquito bites: would it be feasible to let the mosquito bite you once and suck your blood until becoming fully feed? ... it does answer your question in particular.

@com.prehensible mostly she will find a spot with enough bloodflow to fill up, and only sting once. could you provide some source for this? (And maybe write it in an answer)

No. I just linked the NYT science post on it, check the google search to find references yourself: It is also possible that some blood types are not as easily thinned by the anticoagulant in the mosquito’s saliva, so the mosquito has to make more tries to get a satisfying meal. Another factor may be...

From a couple of species (Culex quinquefasciatus, Anopheles gambiae) I rear and feed in laboratory, I can tell that if the female is not disturbed, she will bite only once, untill her belly if full, as you said.
So the best to minimize the number of bites (and to get rid of the disturbing mosquito noise while trying to sleep!!) is to let you be bitten once to be alright the rest of the night. This is easier to say than to achieve, but this should be the best, provided on:

filling all the largest holes of your room to be sure that mosquitoes cannot enter (use mosquito nets!)
switching off the main light to encourage the mosquito to come quickly (for night species). The mosquito will be attracted to your breath, then to your heat at close proximity.
offer the back of your arm where the skin is the thinnest, that may be less scratchy
after the bite, you can put some water gently on the bite to avoid any body response against mosquito saliva, but don't touch it otherwise you may elicit  the scratching feeling.

Then, you should sleep peacefully for the rest of the night, except if a mosquito gang is around.

Nice answer haha Though I tend to go with the more destructive alternative: eradicate the little monster (at the cost of losing my sleep).


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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.

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


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Why is sheep erythrocyte lysis considered as classical complement activation pathway, and rabbit as alternative one?
Any suggestions are highly appreciated.

Unfortunately I can not add "Complement" as a tag.

The sheep erythrocyte lysis you mention actually involves sensitised erythrocytes, i.e. erythrocytes already coated with antibodies. Antigen-antibody complexes are well-known for their activation of the classical complement pathway.
In fact, rabbit erythrocytes coated with antibodies also activate the classical complement pathway$^1$. Thus, sheep erythrocytes are not special in this regard.
The difference comes when we incubate only erythrocytes—devoid of any sensitising antibodies—with serum containing complement factors. In this situation, erythrocytes from the rabbit, but not those from the sheep, are lysed by alternate complement activation. Why is there such a difference?
Fearon and Austen$^2$ showed that this is due to a protective effect of the rabbit erythrocyte membrane on C3b. Normally, C3b is inhibited by factor I and  factor H in serum. This effect is lost with rabbit (but not sheep) erythrocytes, which explains the difference in complement-mediated lysis.

Journal articles cited:

Dijk HV, Rademaker PM, Willers JMN. Estimation of classical pathway of mouse complement activity by use of sensitized rabbit erythrocytes. Journal of Immunological Methods. 1980 Dec 22;39(3):257–268. https://doi.org/10.1016/0022-1759(80)90060-5
Fearon DT, Austen KF. Activation of the alternative complement pathway with rabbit erythrocytes by circumvention of the regulatory action of endogenous control proteins. Journal of Experimental Medicine. 1997 Jul 1;146(1):22–33. https://doi.org/10.1084/jem.146.1.22

That is a fantastic answer. Thank you Adhish Sethi.

@Andrew You're most welcome. :)

@Adhish, thank you for the answer.

The complement system is an innate immune response which has three pathways - as shown in the image below.
The breakdown of red blood cells assesses the functional capacity of the complement system. This experiment is titled: "Total complement activity", "CH50" or "CH100". Is this what you're referencing?
Hemolysis of sheep red blood cells occurs via the classical complement pathway.

More information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4360204/

thank you for your contribution.


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Will obligate aerobic bacteria die if placed in a buffer solution even in the presence of oxygen?
The electron transport chain in aerobic bacteria functions by pumping H+ out of the cell to establish a concentration gradient.
So if the bacteria are placed in a buffer solution having pH equal to the cytosolic pH of the bacteria, will they still be able to establish the required concentration gradient? Will the increase in pH of cytosol(due to loss of H+) alone be enough to drive ATP synthesis even in the absence of a pH change in the medium? i.e.Will obligate aerobic bacteria die if placed in a buffer solution even in the presence of oxygen?

Answer
No. There is ample evidence that:

Most non-extremophilic bacteria grow over a broad range of external pH values, from 5.5 – 9.0, and maintain a cytoplasmic pH that lies within the narrow range of pH 7.4 – 7.8.

The explanation for this is another matter, but, before discussing that question there are two points of possible misunderstanding in the question that require a note of clarification.
Clarifications

What the electron transport chain establishes is an electrochemical proton gradient, or proton-motive force (PMF). This consists of two components§: the hydrogen ion concentration difference, ΔpH, and the electric potential gradient, Δψ.

The source referenced in the question shows hydrogen ions being pumped from the cytoplasm, across a membrane, to a space labelled “outside”, which, according to the figure legend represents hydrogen ions “pumped out of the cell”. This is incorrect. The hydrogen ions are pumped into the space between the inner and outer membranes of gram-negative bacteria, or the space between the inner membrane and cell wall of gram-positive bacteria. It cannot necessarily be assumed that this space has the same pH as the external milieu.

How is the proton motive force maintained?
A possible explanation of why a constant or, more striking, alkaline pH does not destroy the proton motive force relates to the two-component nature of the latter. Bacteria appear to be able to compensate for any decrease (or even inhibition) of either ΔpH or Δψ by a reciprocal increase in the other (Bakker and Mangerich,1961). One mechanism that illustrates how this can be achieved in certain cases is the use of an alternative terminal oxidase, cytochrome bd:

Cytochrome bd generates a PMF by transmembrane charge separation, but
does so without being a proton pump.

However there is a complex set of anion co-transporters involved in cytoplasmic pH homeostasis which may influence the membrane potential. The situation is neither simple nor, as yet, completely resolved, as far as I am aware (but it’s not my field).

§ The treatment of electric potential gradient, Δψ, tends to be downplayed in biochemistry text books. This may be because the generation of a hydrogen ion gradient is easier to understand than that of a membrane potential, or because the texts deal with the latter in sections on nervous tissue. There is a quantitative treatment of the free energy changes involved in Chapter 18 of Berg et al. online.

Does the electric potential gradient Δψ refer to the potential gradient due to all ions including H+ ?

@trinitrotoluene — Δψ is the potential gradient resulting from the membrane polarization. It has nothing to do with the ions in solution, save for any role their transport across the membrane may have had in producing this. I am not the best person to explain this further — electrophysiology is something I never studied and scares me rather. The ΔpH is easier to understand, which is one of the reasons text books focus on it. I have added a reference to Berg in my answer, where this is considered from a bioenergetics standpoint.

OK thank you, I'll try looking into it myself


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What is this larva/insect?
What is this larva/insect that I saw crawling on one of my books?

It moves by wriggling motion and seems to be able to retract it's head(?) when disturbed. It is about 8mm long.
Location: Chennai, TamilNadu, South India

Does this answer your question? Identify this smooth-cocoon worm from Southern India

@tyersome While the question is the same I'm not satisfied with the answer given. The larva mentioned in the answer has a white body. This one has alternating white and black stripes. Moreover this larva has two small protruding structures that arise from its head while the one in the answer doesn't. I would like to know the exact species of this larva. If they are just different developmental stages of the same larve then please correct me.


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Why are some parts of an rRNA structure diagram not labelled?
I've been looking at this structure diagram of the 16S rRNA and have been wondering why some parts of the diagrams have labelled base pairs while other parts are just lines and dots. I'm new to this field of science and am an undergraduate biologist just getting into reading this sort of scientific literature out of pure curiosity.

The diagram is a composite of all 16S RNA structures.
It has a summary with it that explains all.
"16S rRNA secondary structure, showing conserved parts for Prokaryotes (IUPAC letters) and amongst Archea/Bacteria (asterisks) all others as dots. Adapted (in SVG!) from Woese Bacterial evolution 1987"
The base pairs that are marked with A,U,C,G are present in all Prokaryotes studied so far.
The lines are base pair links (A-U and C-G)
There are a couple of lines that are pointers from the reference numbers e.g at 700 and 750


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Can there be traits which aren't possible objects of selection, e.g. beneath a "threshold of genetic noise"?
Is it possible that there are traits that might not be possible objects of the selection because of highly sensitive dependence on genotypes? The context of my thought came when I was having a discussion, more philosophical/political, with someone who was asserting individual characters (e.g. being good or bad) are innate in some sense. My impression is that, to whatever extent genetic determination of observable personality is the case, it'd be a highly complex phenomenon that could depend on many genes, and such matters are very much up in the air. This led me to thinking more abstractly about whether there could be such a thing as a trait that depended on so many genes-- to make it simple, let's say the entire genome-- and depended on in in a way that made it essentially a random trait.
For example, let's say there's a trait T, and we are looking at a creature that has a genome of only three base pairs, and to make it simple let's suppose the genetic code was binary, 1s and 0s (so eight possible genomes). So 100 represented an entire genome for whatever this is. And suppose that T was completely determined by genome (or else, that probability of T was determined by genome), and that the trait T was distributed over genomes such that T={000,110,101,011} and not T={100,010,001,111}. Visually, one could picture the genomes as corners on the unit cube in three dimensions, and T has been distributed so that any two corners separated by a single edge are opposite with respect to T, or, equivalently, that any two corners that can be connected by a minimum of two edges are of the same class with respect to T.
If there is no copying error in genomes then we can have selection for T; for instance, we can have pressure that favors one of the four genomes that cause T. But suppose there is always some random genetic error when a new individual is made. Say, for instance, the third spot is always randomly 1 or 0 with probability .5, and that there's no reducing the genetic randomness below this threshold. Then it seems impossible for there to be selective pressure for or against T, for any non-random distribution on the first two digits still just moves probability around genomes that give a net 50% probability of T being instantiated or not, because in the way I've assigned T, it is statistically independent of the value of any particular (or even any two) genes.
In essence, the trait is so very sensitive to changes in genome-- changing any single gene completely changes the trait-- that whether or not it is instantiated is swings back and forth with any random genetic changes. This is reminiscent of chaos in classical mechanics; some systems are simply so sensitive to underlying conditions that they are no subject to control and prediction in the fullest sense (though that doesn't mean they have to be fully random like the thing I've made here). Just on this basis a phenomenon like this seems formally possible, but my question, as someone who doesn't actually know the field, is whether it's in fact a known or theorized phenomenon, and if so what it would be called. Do there exist, or is it possible there exist, traits that are so sensitive to changes in genome that they can't be objects of selection because they fall under some barrier of genetic "noise," or perhaps things that at least start to look like that on a spectrum? Or are genomes always more "continuous" than this, so that, for pretty much everything, a small change in genotype leads to a small change in phenotype? If that were the case for some reason, then I think what I'm describing couldn't happen.
My apologies if my question is amateurish and my use of the language isn't quite right; I've never posted here before, and I'm a mathematician who's only just beginning to go back and self-educate on chemical and biological sciences, and this was a random thought I had while brushing my teeth, and didn't have the vocabulary to successfully search for and recognize answers.

some people suggest that the entire genome does affect certain traits and these traits are still the target of selection: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5536862/

Don't want to get too down into the weeds here, I think you are making things rather complicated (thus someone else's downvote), but here are a few notes:

I would recommend looking up epistasis, which is a fundamental concept in genetics. (https://en.wikipedia.org/wiki/Epistasis). There are many ways in which a trait can be non-responsive to selection, one way is complex epistasis, which can have an effect on selection similar to what you say, in the case of (for example) sign epistasis.

Another way a trait can be not affected by selection is just not being important - if the selection coefficient (https://en.wikipedia.org/wiki/Selection_coefficient) is smaller than the inverse of the population size, selection will not work.

When I was first learning to code I made a toy model of a genotype:phenotype map here that can simulate both cases I think: https://github.com/maximilianpress/teaching_code/blob/master/EvoSim.r. It won't win any prizes but it illustrates the issue rather clearly IMO.

I would suggest reading a bit and maybe playing with the toy model to think about this more.


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Deliberately choosing one nostril to breathe through
James Nestor, on pp. 41-42 of his book Breath: the New Science of a Lost Art, claims the following.

The right nostril is a gas pedal. When you're inhaling primarily through this channel, circulation speeds up, your body gets hotter, and cortisol levels, blood pressue, and heart rate all increase. This happens because breathing through the right side of the nose activates the sympathetic nervous system, the "fight or flight" mechanism that puts the body in a more elevated state of alertness and readiness. Breathing through the right nostril will also feed more blood to the opposite hemisphere of the brain, specificially to the prefrontal cortex, which has been associated with logical decisions, language, and computing.

Inhaling through the left nostril has the opposite effect: it works as a kind of brake system to the right nostril's accelerator. The left nostril is more deeply connected to the parasympathetic nervous system, the rest-and-relax side that lowers temperature and blood pressue, cools the body, and reduces anxiety.

... Our bodies operate most efficiently in a state of balance, pivoting between action and relaxation, daydreaming and reasoned thought. This balance is influenced by the nasal cycle, and may even be controlled by it. It's a balance that can also be gamed.

A question on this site describes we only breathe out of one nostril at a time: at any given time, one of our nasal cavities will be more open than the other, and this switches back and forth every couple hours. For the most part, we are unaware of this. (At any rate, I was!)
I am very curious about Nestor's claim that the balance can be gamed. It seems that one could prepare effectively for a math exam by practicing right-nostril breathing, or for sleep by practicing left-nostril breathing. Is this the case?

“Breathe on me breath of God”. Notice the difference in spelling which reflects the difference in pronunciation.

I ve never heard any citations stating a basis of research on which side nostril causes what mental states, so the research is probably lacking. Wim hoff stuff conversely does have evidence.

A quick search shows that there is evidence that nostril breathing influences the autonomic nervous system, but currently not much evidence that right vs left nostril breathing influence different states.

Any kind of higher awareness of breathing is likely to improve mental abilities, for one it gives free divers the ability to dive a lot longer, and Wim Hof uses it to stay consciou s and submerged in ice water for 112 minutes, which wasn't believed to be humanly possible previously. It must be difficult to tell the difference of a breathing exercise versus an alternate nostrile breathing exercise.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681046/
Assessment of the Effects of Pranayama/Alternate Nostril Breathing on the Parasympathetic Nervous System in Young Adults
Result and Conclusion: This study showed that the parasympathetic tone was enhanced appreciably in the participants. The observations of this study suggest that the yogic exercise of A.N.B. influences the parasympathetic nervous system significantly.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978938/
Slow Yogic Breathing Through Right and Left Nostril Influences Sympathovagal Balance, Heart Rate Variability, and Cardiovascular Risks in Young Adults
Short-term practice of LNB improves vagal tone, increases HRV, and promotes cardiovascular health of medical students. Practice of RNB increases sympathetic tone and could jeopardize cardiovascular health.

There seems to be some evidence that this works.

note the sample sizes, n=30 which makes the conclusions of the study very weak at best, the differences are equally miniscule (and swamped by the margins of error). this is just bad applications of statistics in the guise of a preliminary study.


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If calcium ions and cholesterols are found on the surface of the skin, would it be possible for Vitamin D to be synthesised on the skin?
Calcium ions are abundantly found in the extracellular space of the stratum corneum area, the top most layer of the skin (Skin Barrier and Calcium; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5929942/). Isn't it very probable that it can also be found on the surface? Calcium ions are also actively involved in regulating the water gradient of the stratum cornuem. However, they may be easily washed off from the surface of the skin through the regular use of water and surfactants. Plus, the use or over-use of moisturizers also interfere with natural sebum production and the Calcium ion gradient of the stratum corneum ( The Changes of Epidermal Calcium Gradient and Transitional Cells after Prolonged Occlusion Following Tape Stripping in the Murine Epidermis; https://www.sciencedirect.com/science/article/pii/S0022202X15405603) If calcium is found on the surface of the skin, and sebum plus intercelular lipids (which also eventually make their way to the surface of the skin and mix with sebum and sweat to form the acid mantle) contain cholesterol, wouldn't it be possible then Vitamin D could be synthesised on the skin through irradiation?

Welcome to SE Biology. Please finish the Tour. My first reaction to your question was "What is this all about?". You provide no context to your question. Why are you asking a hypothetical question about a tissue, the structure and metabolism of which is very specialized? One is suspicious that you are engaging in an argument with someone and are trying to get support for a point of view. Is your question any more than will the conversion of 7-dehydrocholesterol to cholecalciferol by UV occur in vitro? Tell us why you want to know.

Long ago I read that vitamin D is made on the skin and absorbed. Not an answer because I have no idea where I read it.


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What is this lightning-fast tiny spider?
Saw this spider as I was taking a shower. It moves really fast. This I noticed when it moved away (from the center of this splendid pattern) to repair its web.
Location: West Bengal, India.
It appears to be almost 1.5 cm in length.

Many web-dwelling spiders are lightning-quick in their own web (even if they are slow/clumsy walkers outside of their web) so that doesn't help in identification.
Hard to tell from the photo, but it appears to be Cyclosa ginnaga
A better image of the specimen would help identify.
edit after comment:
Here is a gallery of observations (currently 50 of them) of cyclosa ginnaga: https://inaturalist.ca/observations?place_id=any&subview=grid&taxon_id=360502
All those observations were made in South-East Asia or Australia.
You could also look at Cyclosa Insulana with similar range:
https://inaturalist.ca/taxa/560706-Cyclosa-insulana/browse_photos?quality_grade=any
But I think the length of abdomen in your photo more closely resembles C.ginnaga, and also the observations of C.ginnaga more consistently show a spiral in the thick webbing while C.insulana tends to be more random.
And here is a breakdown of the cyclosa genus broken down into specific species if you want to browse other possibilities:
https://inaturalist.ca/taxa/127360-Cyclosa/browse_photos?quality_grade=any&grouping=taxon_id

Welcome to SE Biology. This answer would be improved by a picture of Cyclosa ginnaga.


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What kind of soil-dwelling flying insect is this?
In the UK. They are roughly 1.5mm long, appear to crawl much more than fly, and seem to live in the soil of indoor potted plants. They are fast and tiny, so apologies for very shallow DOF. The first is on an aloe, the second is on a pot. They really like the soil around some capsicum plants.

Those look to me like fungus gnats. If you're looking to get rid of them, I've heard that putting a layer of rice hulls on top of the soil keeps them from reproducing. From what little I've read my identification doesn't go much deeper than superfamily, taxonomically, but it's a least a common name to work from.

Some kind of Sciarid does seem plausible, thanks!

Agreed that we're looking at a Sciarid ("Dark-winged" or "Black" fungus gnat, depending on the side of the Atlantic), in which case going deeper won't be possible without dissection and slide-mounting (see here for an abstract of the most recent Palaearctic monograph; it might be possible to download it for free from researchgate.net [look for the author Menzel], but use will require fluency in German).


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Are “tremors” and “ tetanic contractions” the same thing?
Do these two expressions have the same meaning?
1- Tetanic contractions in the skeletal muscles
2- Rythmic shaking of the hands
(These two expressions are supposed to be two symptoms of Parkinson’s disease ,however I am told that this is repetition)

I think both for the purpose of convincing your instructors, and for the purpose of asking a well-researched SE question, it would be better if you started with trying to make your case. Why do you think they should be considered distinct? What have you learned about these symptoms yourself? Telling a test grader "these should be considered distinct!" is less convincing than "these should be considered distinct because A, B, C, D". I worry that giving you an answer here that you use to debate a test grade is similar to doing homework for you.

I really appreciate your point of view and admit I have to do better research . But I wish you would at least answer this question :  do you consider them distinct?

No, I won't, for the reasons I've stated.

Tetanic contractions and tremor are different phenomena.
Tetanic contraction (or tetanus) refers to sustained contraction of a muscle subjected to high-frequency stimulation. With this high frequency, a new contraction begins before the previous one has ended. Thus the contractions get 'summed up'. You could see this interesting video for a demonstration.
Tremor is an involuntary shivering movement which is caused by alternating contractions of opposing muscle groups. The causes are many, ranging from physiologic tremor to degenerative disorders of the nervous system (such as Parkinson disease).
Note that tetanic contractions are not a symptom of Parkinson disease. In fact they are not a symptom of anything at all, inasmuch as they are a physiological property of isolated muscle. Tremor, on the other hand, is a phenomenon seen in muscle groups, and is one of the core symptoms of Parkinson disease.

What about “rythmic muscle contractions” ? As it is stated here  (https://g.co/kgs/Pvd27p) as a symptom.

@user261947 The Google page is probably referring to myoclonus, which is sometimes seen in Parkinson disease.


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Tree-pest coevolution
Many trees first reproduce decades after germination.  Many pests of trees reproduce in under a year.  It would seem that the pests have an advantage in the evolutionary arms-race, as they can evolve a means of attack far faster than the tree can evolve a defense (cf. Does an increased reproduction/mortality rate provide an evolutionary advantage?).
I once read a speculation that trees might mitigate this by varying the genetics (or perhaps only epigenetics?) of different branches within an individual.  The branches that do better produce more seeds.  The seeds produced by a branch carry information specific to the branch.  This means evolution (or the epigenetic equivalent) happens at the level of the organ, not the individual.
Is there any research supporting this speculation?  If it has been refuted, how do trees compete effectively in the arms-race?


text:
Do DNA viroids exist?
Viroids are described as short circular ssRNA with no protein coating.
Are there any analogous infectious particles that contain DNA instead of RNA?
If DNA viroids do not exist, is there an obvious reason for this?

The definition on the Wikipedia page you recite uses the language 'no protein coating' as opposed to 'protein coating'.
A protein coating would make it a virus.
No protein-coating would make it a Viroid.
As far as we know DNA Viroids do not exist. But this is an advancing field of research and it depends on what structure of genetic material you are referring too.
The general different types of genetic material include - but are not limited to:
Single-stranded DNA (ssDNA),
Double-stranded DNA (dsDNA),
Single-stranded RNA (ssRNA),
and double-stranded RNA (dsRNA).
There is more information on Classes I and II DNA viruses here:
https://www.ncbi.nlm.nih.gov/books/NBK21523/
If there were no DNA viruses without a protein coating - what is the reason?
Viroids only infect plant cells.
It may be that Viroids route of entry via microscopic junctions between plant cells (Plasmodesmata) are only large enough to fit single stranded genetic material. Therefore allowing ssDNA and ssRNA, but not dsDNA and dsRNA to act as plant cell infectious agents.

Welcome to SE Biology. I think, as a non-native speaker, you are on shaky ground criticizing the use of the word "particle" by the poster. The definition from Oxford Languages is "a minute portion of matter", which in no way implies a container. I would delete your first two paragraphs. Also questionable is your remark "it depends what you mean by DNA". DNA is unambiguous. The strandedness and cicularity of DNA may vary, but it is all DNA, and it is clear that the poster wishes to know whether an entity composed only of DNA with no associated protein can exist as an infectious agent.

@David thank you for your response. I made your changes. I hope we can get on in the future here at SE.


text:
Plant with purple/white/yellow flower
This plant popped up as a volunteer in a flower box in Winnipeg, Manitoba.
It is roughly 6-inches tall by 6-inches wide.
What is it?

The plant is Convolvulus tricolor, the dwarf morning-glory. It belongs to the family Convolvulaceae.Blue, white, red and pink flowering cultivars of this plant are available$^1$. It is a annual/perennial growing to 0.3 m (1ft) by 0.2 m (0ft 8in) at a medium rate$^2$.

Image source
References:

Plantasm

PFAF database


text:
Firstly, Spider ID? Also possible relation to ~100+ serious bite reactions in past 1-2yrs
Might have been occuring since day 1 in new residence about 2 years ago. Bites are painful to touch, when fresh, very odd sort of void filled with black stuff under skin which regularly shows fang type trackmarks.(golf ball size swelling, pussing, twin &/or parallel punctures wounds, black(necrotic?) Substance under hardened skin cap as healing, long term healing) Spider found in nightstand drawer, maybe stranded in bottom of SS can cooler.
I have many pics of the live spider in a jar. Thankyou...;)>!

Please add information such as size of spider and your geographical location. Clearer pictures of the spider would also help.

Thank you for reply... I am located at Northern border of 54121 zip code, I'll transfer it to a better container than old mason jar and try for better pics... was having issues uploading here,

Will confirm and post better pics asap, ... but body appears to be ~15mm and leg spread in standard stance ~35mm. I'm not sure, but it may have shrunk a little after spending the last few days in an empty jar.  I will say that thing is very aware and has great sight through that distorted glass, it tracks and follows me around the room from 10-15 feet away even after 2 days of ignorance to it...

https://drive.google.com/folderview?id=1By0VjOmEnhSb-zVieAbHfEjwVg2jpnYf

The link above has a dozen of the best pics

Holy fk 100 bites sounds like a spider drive thru.

It is a wolf spider. It grows from about 1cm to 5cm long. Wolf spiders are usually gray with brown to dark gray markings. It does not spin webs, instead it actively hunts it's prey. Wolf spiders are agile, robust and have excellent eyesight$^1$. That is why you have noticed that it is quite aware of your movements.
Hogna radiata:

Alopecosa Kochi:

The bite of this spider leaves prominent marks$^2$.

In severe cases, the surrounding area may develop redness, swelling, and even ulcers that spread beyond just the bite location. Allergic reactions may cause even more severe symptoms in some people$^2$.

Since the wolf spider is not poisonous its bite can be treated by cleaning the area with soap and water and then placing a bandage over it$^2$.
Note:
I am unable to identify the exact genus of the spider. I believe it could be Hogna or Alopecia. Someone more knowledgeable could inform me.
References:
1.Wikepedia
2.Healthline

That is what I was leaning towards too, it's not identical to any pictures I can find but it's closed of course a lot of the other ones are close to each other being different spiders too.   I don't understand why I'm getting consistently bitten over such a long period of time, all seasons.  Some bites are much worse than others, but fang marks and spread are pretty consistant. But doesn't seem like nesting type, more territorial, I would guess.  I bomb the place three times w/ double doses: doesn't seem to have much effect, not permanent one for sure. I've added bite pics to drive link

@CustomCreations I am not experienced enough to know the answers to these questions. Hopefully someone else will give a solution to your issue.


text:
How can I search through literature databases for words containing a * when the asterisk is read as syntax and not part of a query?
I'm exploring the literature on microRNA, where it is common for the less utilised strand of the miRNA duplex to be referred to as the miRNA* strand.
However, I am experiencing some issue searching for literature sources, as the databases I use for my searches (Web of Science, Google Scholar) utilise an asterisk as part of the search syntax rather than part of the query itself. This leads to any search for "miRNA*" yielding every paper on miRNA in general.
I am getting by for now using alternate search terms and other papers references, however it would be excellent if someone knows how to tell these databases that the asterisk is part of the query and not syntax.

Regarding Google Scholar this answer  should be relevant. Regarding WoS, this support document. In short: no luck.

I have not tried this (and it isn't really my field), but it should be possible to save search results to a file with a tool like this https://www.seoquake.com/index.html to give you a file of URLs.  Then you could search for "miRNA", save those results, then write a program to check those sites for "miRNA*" using something like wget and grep.  One of the programming sites might get you better info, since it's more a programming/web use question than specific to biology.


text:
Are all antibodies against a common antigen identical?
I understand that when some antigen (e.g., virus, bacteria, etc.) is recognized in the body, antibodies specific to this antigen are produced that, in turn, bind to the antigen and effectively neutralize them as a potential threat to the organism.
Are all the antibodies that are produced against a specific antigen necessarily identical?  Either within a single organism (e.g., a single person), or between different organisms (e.g., between different people, different species, etc.)?  If two people get sick with the same disease, develop antibodies, and recover, are these antibodies the same?  If a human and some other animal get sick with the same disease, will the antibodies each develop match?
Key to the operation of the antibodies is their specific recognition/binding of the antigen.  I assume that the structure and composition of the antibody is tuned to bind to specific exposed moieties on the antigen.  I can imagine that there are many different potential binding sites on the antigen to target and many possible combinations of ways to recognize those sites by the antibodies.  I would think that it would be a remarkable coincidence (highly unlikely) if separate organisms both, independently, happened to develop the same “molecular strategy” for recognizing a particular antigen.  This outcome seems to be implied in this question,
How are antibodies specific for a disease detected in the blood if everybody produces a different antibody for the same antigen?

Alright, there are two major questions:
(a) Are all the antibodies that are produced against a specific antigen necessarily identical?
Not in most cases. Antigens can either be monovalent or polyvalent, meaning that they can either have one epitope or various different epitopes (an epitope is the site of the antigen that binds to a T-cell receptor or a B-cell receptor). Most antigens are polyvalent, which implies that a single antigen may interact with several different T and B cell lineages. Each B cell lineage is only able to produce and export one type of antibody. Because the antigen will interact with different lineages, it will promote the production of different types of antibodies. These multiple antibodies produced against one antigen are called polyclonal antibodies, since they arise from multiple clonal lineages. When the antigen only has one kind of epitope, it will induce the production of only one type of antibody, which are called monoclonal antibodies, because they arise from only one clonal lineage.
(b) Do the antibodies produced against a certain antigen differ between members of the same species or between species?
Yes, in both cases. There is an important genetic variability surrounding immunoglobulins and T cell receptors.
Reference: Karp, G. (2009). Molecular and Cellular Biology: Methods and Concepts. Wiley. New York.


text:
Can ACE2 receptors be syntesized?
I read that there are labs that can produces the spikes of the coronavirus. I wonder can they also synthesize ACE2 receptors or parts of them? If yes, can they be used as drugs?

It seems like Alex Reynolds gave a good answer when you asked a similar question: https://biology.stackexchange.com/a/93416/52196

You might spellcheck your title.

The Wuhan institue of virology Discovery paper transfected the ACE2 gene (from human, bats, mice) to HeLa cells making those transfected with human-ACE2 susceptible to SARS-CoV-2, thus proving the virus relies on this receptor for entry. Transfection means synthesizing the DNA gene in a plasmid form then adding lipofectamine to force entry into the cytoplasm then nucleus, the corresponding protein is synthesized by ribosomes and gets expressed on the cell's surface (due to a signal peptide)

The drugs you are referring to are called receptor mimics or peptide inhibitors.  Yes, molecular mimics for human ACE2 can and have been synthesized.  Binding of these mimics to coronavirus spike proteins leads to sequestration or inactivation of viral particles.

Relevant literature:
Romano M, Ruggiero A, Squeglia F, Berisio R. An engineered stable mini-protein to plug SARS-Cov-2 Spikes. bioRxiv. 2020.
Han Y and Král P. Computational Design of ACE2-Based Peptide Inhibitors of SARS-CoV-2. ACS Nano. 2020;14(4): 5143-5147.
Walls AC, Xiong X, Park YJ, et al. Unexpected Receptor Functional Mimicry Elucidates Activation of Coronavirus Fusion. Cell. 2019;176(5):1026-1039.e15.

Thank you very much for the exhaustive answer. Can these be effective drugs against covid and eliminate it? Are there clinical trials on the run? I see the articles are from very recent.

I'm not sure if any of the proposed drugs are currently in trials -- I'll be sure to update my answer if I find out.


text:
What specie of flying insect is this?
The insect pictured below just flown into my room. I live in Central Europe (Poland), it is about evening now. The thing is about 1,5 cm in length (not sure about this, I was too focused on driving it out). Its white stripe on abdomen seemed to be translucent. What is this insect?

It's a pellucid fly, a species of hover fly. scientific name: Volucella pellucens
https://www.naturespot.org.uk/species/pellucid-fly

Thanks. But isn't Gemeine waldschwebfliege a German name? I am not a biologist, but I thought those scientific names are always Latin-based.

my bad, I don't know why but my webpage translated the species scientific name into german which has never happened before so I didn't notice. I just changed it to its latin scientific name. .


text:
Is a corpse more flexible than a living person?
I read that the majority of humans have the muscular-skeletal potential to perform the splits that you see many gymnasts perform.  The reason a living person with no flexibility training can not achieve the splits is because the person's central nervous system (CNS) automatically constricts the muscle fibers of the legs when the legs move beyond the person's normal range of motion.  I read that this automatic CNS response is called the stretch reflex, and it is the CNS's way to protect the body from performing potentially dangerous movements.
So my question is: does this mean a body with a non-functioning CNS is very flexible?  For example, if I could not perform splits while I was alive, could someone position my corpse into the splits before the event of rigor mortis?

According to the science in this article: healthunify.com/why-cant-everybody-cant-do-a-split/, not really. Flexibility such as splits are only possible by lengthening the skeletal muscle fibers (in the case of splits, this includes the hamstring and iliopsoas). Which means that splits aren't solely dependent on how your CNS functions.
Furthermore, with death eventually comes rigor mortis where due to the body's chemical changes after death (lack of ATP production etc... https://biologydictionary.net/rigor-mortis/), the body becomes rigid which makes it even more difficult for a dead person to do splits than a live one without seriously damaging the dead person's body/muscles.


text:
Why is there no herd immunity against common cold coronaviruses?
In discussions of herd immunity against SARS-CoV-2 the underlying assumption usually appears to be that the virus basically stops spreading once a sufficient percentage of the population has overcome an infection.
My understanding is that this approach does not work for the seasonal flu, for instance, because the flu virus mutates too quickly. Since coronaviruses do not mutate so quickly, herd immunity "can work" for them.
Question: Given how long common cold coronaviruses have been spreading in the human population, why does there not appear to be herd immunity against the common cold coronaviruses? To what extend can we expect herd immunity to SARS-CoV-2 if there is no herd immunity against common cold coronaviruses?

The following review has extensive answers to the complex of this question. They also include MERS and SARS-Cov-1 in their discussion, as there is good data on them.
Huang et al., A systematic review of antibody mediated immunity to coronaviruses: antibody kinetics, correlates of protection, and association of antibody responses with severity of disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217088/
The best data comes from challenge experiments which, with common-cold CoV, are not ethically problematic. They write:

Several studies exposed volunteers to two challenges of virus, some months apart. Reed re-challenged 6 volunteers who had been experimentally infected 8–12 months previously(ref.9). On the first challenge, all 6 developed symptoms and detectable viruses and 5 of 6 experienced significant rise in titer. In the second, 0/6 experienced illness, detectable virus or significant rise in titer. Callow et al re-challenged volunteers with the same dose of coronavirus, one year apart(ref.8). Of 9 volunteers who were infected in the first exposure, 6 (67%) were infected in the second exposure. However, none of these individuals developed respiratory illness symptoms and they experienced a mean duration of detectable virus of 2 days compared to a mean of 5.6 in the initial challenge.

So, reinfection can occur even after 1 year with HCoV 229E, and this does not support the idea of herd immunity against that virus.
Note however that it is not known to date if, when reinfected after some years, you will also shed active 229E virus. If not, this would be just as good as neutralizing immunity and would support herd immunity.


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Public fermentation/cell cultivation database?
I am wondering if there are any large collections of fermentation or cell cultivation data publicly available.
I am interested in all cell types used within industrial biotech and biopharma, especially the most common ones, e.g. CHO, yeast, e.coli, bacillus, lactis.
I am interested in this from a process understanding point of view. So I am very interested in the conditions throughout (pH, nutrients, dissolved oxygen, media comp, turbidity, etc.) as a time series. If manual (offline) measurements are made, CFU, amount of metabolite produced, etc. they would also be incredibly interesting to have.
I have looked around without luck.
I guess the 'perfect' database probably doesn't exist, but I haven't been able to find anything.
So I would really appreciate help finding any dataset on fermentation data, even if it doesn't have all that I am looking for.

I found this article: Bio-Ferment A Database on Bioreactor and Fermentation from 2011, but I cannot find the actual database.

What kind of data are you seeking? Growth conditions? OD? Something metabolic?

What kinds of cells? Yeast, human, bacterial? What do "online" and "offline" mean? What kinds of fermentation? What is the readout- metabolite production, cell density, biomass?

@tyersome I am especially looking for growth conditions and OD. I have re-phrased the question so that it is hopefully more informative.

@MaximilianPress online means that the measurements are made continually - e.g. a probe sitting in the tank. Offline is when someone manually takes a sample and makes the measurement outside the tank.


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If the Brain can store as much information as a billion hard disks why cant i memorize a single word document of random letters?
I read a lot of articles on this and all seem to agree that the brain storage in neural connections is tremendous but that doesnt explain why we forget things so easily and have such a modest memory in our subjective lives and we use much humbler devices to store information, i specifically wanna know if we can really store this information but the problem is we cant acces them as efficiently as a computer can or the whole process of storing this information is different than a hard disk on a computer.
None of the articles i have read make any comments addressing this question.
Links to relevant information on memory processing and storage will be appreciated.

I think your question is based on a false premise. How do you know you can't? Have you tried? People can memorize apparently random information e.g. >10⁵ digits of pi ...

Some people can but the statistics is of the regular human brain what stopping everyone from doing that(and 10^5 is also almost nothing compared to a computer storage)

The brain is trained to remember patterns and predictable associations. Randomness is the absence of patterns, so it's the exact opposite of what the human brain is for. A human can remember random numbers to about 67,890, which is the world record digits of Pi. That's about 20 pages of irrational numbers. Some people can remember 20 pages of word documents.
To memorize random numbers, the brain has to join colors, places, objects, people, animals, onto the randomness and construct a story to which the randomness can correspond to. It gives an idea of what the human brain is very good at memorizing, which is real-world phenomena through experience.
The human brain actually predicts what it has seen before it knows: It represents an expected object, personality or event from imagination (for example if you see a rabbit/cat beside the road and it turns out to be a bag). New objects like a page of random letters are compared to previous patterns of sensory input.
There are regions of the brain which are especially designed for tesks which are more like computer-memory, especially the task of geographic memory used for path-finding, food sources, which is called the hippocampi, which taxi drivers have very developed.
A computer actually uses man-made tools to do the memorization. A computer can't design a hard disk or a memory module, the computer uses human memorization tools, which humans can use too if you change the rules of the game a bit... they can use pen and paper... in that sense humans and computers are equal, with the computers being subservient to the humans.

Our brains usually make associations to different words including images, sounds, emotions, etc... which help reinforce the neurological patterns required to memorize sentences, etc...
To remember something, it must also be repeatedly 're-thought' to strengthen the memory. Eventually with enough conscious and subconscious repetition of a thought, these neural networks for that memory will move to the hippocampus where long term memory is stored.
memorizing 'random letters' doesn't seem to have much of a use. Making connections to these different letters will help give them meaning that your brain can hold on to allowing you to hopefully (with enough practice) memorize the whol word document.
There are however people (some considered savants) who have an ability called hyperthymesia which forces them to be able to remember everything that they have experienced in their lives.
This article: https://www.psychologytoday.com/us/blog/defining-memories/201706/why-we-forget discusses in great detail why we forget and I strongly suggest you read it (I find it very interesting).

I'd just like to add that, in addition to what has already been said, it can be a lot harder for the brain to memorize information that it doesn't find useful or relevant. As someone with ADHD, this is a common issue for me. I find it significantly more difficult to not just pay attention to, but remember information on topics that I don't find intellectually stimulating. I believe this has in large part to do with the way my brain filters out information that it deems unnecessary to remember. After all, why waste precious mental storage space on a word document of random letters? It is still possible to commit that kind of arbitrary information to memory, though, as we've seen from people who've managed to memorize thousands of digits of pi, but that takes a lot of practice and dedication, as the human brain was never really designed for such a task.


text:
How does the human eye generate spikes?
Disclaimer: I have an academic background in computer vision but not biological vision.
Background: Classical computer vision is concerned with images from cameras that have a fixed exposure time for all pixels. During this exposure time, each pixel is essentially counting photons. This photon count then translates to a bitmap (usually 8 bits per pixel for monochrome cameras) which can be displayed on monitors.
However, the human/vertebrates brain does (afaik) not operate on integers or floating point values but spikes. Consequently, the brain must convert light to spikes for further processing.
Biologically inspired machine vision:
Let me quickly present you the simplified working principle of two major approaches of biologically inspired machine vision. They are the inspiration for this question.

Event Camera: The event camera has independent pixels that respond to changes in their logarithmic intensity $L = \log(I)$ ("brightness"). An event/spike is triggered at a certain pixel as soon as the brightness increment since the last event at the pixel reaches a threshold.
Formally, let $e_k = (\mathbf{x}_k, t_k, p_k)$ be the event at pixel $\mathbf{x}_k=(x_k, y_k)$ at time $t_k$ with polarity $p_k\in\{+1, -1\}$ as the sign of the brightness change. Then an event $e_k$ is triggered if
$$
L(\mathbf{x}_k, t_k) - L(\mathbf{x}_k, t_k - \Delta t_k) = p_k C
$$,
where $C>0$ and $\Delta t_k$ is the time elapsed since the last event at the same pixel. C is the contrast sensitivity and determines how much the brightness has to change to trigger an event/spike. This introduction is adapted from section 2.4 of this survey. For a more visual explanation see this introductory video.

Consequence of this working priciple: This camera only generates output when there is motion in the scene. Furthermore, it is not possible to reconstruct the actual intensity given spikes/events of an event camera. This is because the camera only generates output at intensity differences (it is a differential sensor).

Spike Camera: This camera also has independent pixel much like the event camera. However, each pixel integrates luminance intensity over time and emits a spike whenever a threshold is reached. This means that it essentially emits spikes to a rate proportional to the light intensity. More formally, let $I(t)$ be the intensity of a pixel at time $t$. Then a spike is generated at that pixel when
$$
\int_0^tI(\tau)\text{d}\tau\geq \phi
$$,
where $\phi$ is a threshold. More details are given in section 2.1 of this paper. Also have a look at the supplementary video for a visual impression.

Consequence of this working principle: Intensity is conveyed via rates of spikes. This rate is proportional to the measured photocurrent. Thus it is possible to reconstruct the true intensity at a pixel. Unlike the event camera, this camera also generates spikes when the scene is static.
My question: Can the spike generation mechanism of vertebrates vision be explained with these working principles? If not, is there another spike generation model that can be formulated mathematically?
Why I am asking this question: Literature regarding both cameras argue with biological inspiration but I have not found any evidence that either one of those approaches actually mimic the working principle of vertebrates' eyes. Any pointer to publications are welcome.

Are you acquainted with Carver Mead's work on bio-inspired, "neuromorphic systems" such as CCD sensors and the like?

I am aware of his pioneering works in neuromorphic systems but have not read his publications in depth because it is out of my field a bit.


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What is the smallest visual unit perceptible to the human eye, like a pixel? (esp. in visual static)
If you close your eyes, you can often see visual static, where individual pixel-like things are much more visible than with the more smooth, crisp images one gets with open eyes. This led me to wonder a few things:

Is there a name for this unit, like "pixel"?

What is the biological correspondent? A single rod or cone or something?

Are the individual pixel-like things making up the static noise the same underlying mechanism (and size) as the smallest perceptible units of vision one gets when actually looking at something? I suppose this is related to visual acuity. I've read that the cause of static is suspected to be excitation of neurons, but that's not what I'm asking.

Thank you.

The analogy between the human visual system and electronic screens does not go very far. While an electronic display can be described as the sum of individual pixels, what the human eye sees cannot be described as the 'sum' of inputs from all the rods and cones. The inputs from one cell interact with those from other cells at various levels: retina, lateral geniculate nucleus, visual cortex. Plus, there is interaction with neurons from other brain areas. This processing creates a complex 'image' very different from that of an electronic screen.

The human eye has two types of sensors that become stimulated when wavelengths of visible light (photons) hit the pigments in these sensors. They are known as 'rods' and 'cones'. Rods detect the brightness of light, cones detect the color. There are three different cones in the human eye: red, green and blue. Each cone reacts to the corresponding waves of light. When they are stimulated due to their corresponding wavelengths, they send a signal that travels through the optic nerve to the visual cortex at the occipital lobe.
individual cones don't have different levels of stimulation and always send the same frequency, it's the lack of the stimulation of other cone types that causes certain colors to appear.
in short:

signal or photon of the appropriate wavelength I suppose.
rods for brightness, cones for color.
probably not since the cones are microscopic and tightly packed, too close and too small to see what each cone is literally receiving. The moving static you're seeing is called phosphenes and is comprised of the inherent electrical charges the retina produces both during resting state and with the eyes open. they're just easier to notice when your eyes are closed. Try covering your eyes and you may get static just like when you close your eyes.

The electrical charges get sent to the visual cortex. that's where your brain processes the image. Here's an diagram of how the rods and cones send their electrical signals to the optic nerve (the optic nerve is the [4] label).

Here's a diagram of how those signals travel to the visual cortex:

Thank you. So a phosphene is a single pixel-like light? What would be the path from this electrical charge to a person's awareness of the light? The charge activates a single rod (or very small clump) and then travels down a nerve to the visual cortex or something? And each rod would have its own nerve line?

"So phosphene is a single pixel-like light?" It's a phenomena that causes your rods and cones to still send signals even when the eyes are closed, the rods and cones (or arguably the gangion cells) are the real 'pixels'. I made edits to the answer so that you see the pathways. Multiple rods can cones can be joined to one bipolar cell and multiple bipolar cells can join to one ganglion cell meaning that multiple rods and cones can send a signal through one pathway. to the visual cortex.

ganglion cells could be argued as the pixels since they send the signals to the visual cortex. The rods and cones just depict what the pixel will display (e.g. brightness and/or color of each pixel)

Thank you. This clears things up for me. A very informative answer!


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Can I use fluorophore conjugated antibody as neutralizing antibody?
I need to order a neutralizing antibody to block a protein of interest.
The pure grade functioning antibody (no conjugates) is substantially more expensive than the fluorophore conjugatated ones.
Can I achieve the same by using let's say Ab conjugated with APC/PE as a neutralizing antibody compared to the pure functioning grade ones?
Any insight would be great.

In short, yes, most likely.  When an antibody binds to the antigen at a region (epitope) that is needed for the antigen's activity then the activity is reduced ("neutralized").  The (proper) labeling of an antibody will usually not affect which epitopes it binds to, and so it will work OK (but it may have lower titer than the unlabeled antibody).  As always, there may be some exceptions to this.


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How to find the origin of each Single Nucleotide Variants (SNV) in child when having variant call data for both parents?
I am working with a trio (Mom, Dad, Child). I have variant call data for all three. Now I want to know each SNV in the child comes from which parent?
Is there any tool that could help me to achieve this goal?
Many thanks,
Vahid.

I think this is more suited to the Bioinformatics beta. If the post is migrated there, I can help you, as long as you give more information on the kind of data you are working with. Note, there is a plugin called parental-origin in bcftools which does what you need.

If a SNP is present in a child it is also present in at least one of the parents (except for de novo mutations which are fairly rare). So just check which parent has which polymorphism. For a question like that you would write a script yourself to check that.


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Why do we anthromorphize evolution and genes and nature?
Books sometimes says things "Our genes want us to have as many children as possible", or "Evolution
wants the fittest to survive". But genes are not conscious entities who can want things. So, why do we anthromorphize genes, evolution, and nature? I apologize if this question is not appropriate for this stack exchange. Perhaps it can be moved to an appropriate stack exchange if it is.

I’m voting to close this question because it is off-topic for this site. This question is about language or possibly psychology rather than about biology. It also seems likely to generate opinions rather than answers based on facts.

Then, can it be moved to psychology stack exchange?

Teachers often use metaphors or other story-telling devices to explain abstract concepts in more familiar terms to help information land with a broad audience. It's common in other natural sciences like chemistry, physics, and even mathematics. Maybe try asking https://academia.stackexchange.com

Things we can't see but want to believe in often are described using metaphors for things we can see and understand. Computers are a good example; they're new so they're entirely metaphoric: file, key, screen, message, program, ... are all metaphors of humans, things humans make and use, and the functions humans use them for. Metaphors are pretty much all we've got -- read Lakoff and Johnson and consider the alternative.

Just to help OP out, this is related to a really interesting concept called agential thinking in evolutionary biology. It can sometimes be a surprisingly valid and helpful metaphorical heuristic, and sometimes deeply misleading. A great book on the topic is Agents and Goals in Evolution by Samir Okasha


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Does thimerosal have some of the same mechanism of action as sodium benzoate?
I noticed that thimerosal's molecular structure is basically just sodium benzoate with an attached chain that includes a mercury atom.
Sodium Benzoate

Thimerosal

The Wikipedia article for thimerosal only mentions the oligodynamic effect (biocidal effect of the mercury).  However it doesn't explain the oligodynamic effect very thoroughly:

The metals react with thiol (-SH) or amine (-NH(1,2,3)) groups of proteins,

I read that sodium benzoate works by being absorbed into microbes and lowering their pH.  Thimerosal is also an anion - can it also be absorbed into microbes and disrupt their pH? Or is it unable to pass through the same channels as sodium benzoate?  If it is absorbed is the pH effect insignificant compared to the oligodynamic effect?


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Are earthworms edible?
Just that. It seemed weird for me not to find anything on Google. But I still think that they might be edible.

Strange, for me google returns thousands of good results for edible earthworms.

Asking whether something is edible is tricky business. You can get caloric value out of a lot of things without being poisoned, like grass, or random leaves and flowers. This doesn’t necessarily make them “edible”. It depends on the bar you set, and more logically how desperate you are for food

@mgkrebbs did my search in Spanish, found nothing, did again in English after your comment, found something. Interesting XD

they are notoriously unpalatable, but they are not especially noxious. it's also opinion based, because eating 1 is probably manageable and 5 of them will probably give someone unaccustomed indigestion/dysentery which would leave them less healthy that they were before. just a guess. they are full of earth and fermenting leaf matter.

@com.prehensible I guess that some preparation as with snails must be done in order to be able to actually eat them.

@com.prehensible I guess that some preparation as with snails must be done in order to be able to actually eat them.

Yes, they’re edible and even eaten in some places.
https://culinarylore.com/food-science:are-earthworms-edible/


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State of extracted DNA
A well-known and commonly-done experiment is to extract DNA from strawberries or other fruit by first mashing the fruit of choice, adding the mush to a mixture of water, salt, and detergent, and then adding isopropanol. DNA then precipitates out.
How intact is the DNA obtained from this experiment? Does the experiment introduce breaks or other forms of DNA damage? Is the DNA intact enough to be sequenced and for one to be able to identify what organism it came from?

For many sequencing methodologies, DNA fragmentation is actually necessary.

Yes, normal DNA extraction protocols fragment genomic DNA.  In my experience, extracted DNA tends to have a size distribution on the order of 10 - 20 kilobase pairs (kbp), independent of the protocol and source organism (assuming a chromosome size >> 20 kbp).  This seems to be corroborated by what I can find online -- see the gel below from Successful tips of DNA extraction and PCR of plants for beginners

Figure 1. Agarose gel electrophoresis of DNA samples extracted from horticultural plants. M, molecular weight marker. Modified from Kasajima et al. (2013)

as well as this gel from ThermoFisher

Genomic DNA purified with the Genomic DNA Purification Kit
Agarose gel (0.7%) electrophoresis analysis of undigested (odd lane numbers) and EcoRI digested (even lane numbers) DNA samples.
M – Lambda DNA/HindIII Marker [top band is 23130 bp]
1, 2 – human blood
3, 4 – human lymphocytes
5, 6 – human placenta
7, 8 – mouse liver
9, 10 – Hedera helix
11, 12 – Haemophilus influenzae
13, 14 – E.coli ER2267
15, 16 – Bacillus subtilis

The consistent size of extracted genomic DNA across organisms is a physical constraint rather than a genetic one.  When unwound and unprotected by the cell and nuclear envelopes, chromosomes are subject to the shearing forces of pipetting and vortexing.  Consider a mile-long length of high-test fishing line.  Coiled in the box or around a reel, the line is strong and stable.  If you laid the line out end-to-end, however, there would be many places along its length where the line gets snagged, knotted, and torn.
As hinted by canadianer, DNA fragmentation is necessary for most sequencing methods (specifically whole-genome shotgun sequencing, not sequencing of specific PCR amplicons).  As an example, Illumina sequencing platforms generally require libraries with fragment size distributions between 300 and 600 bp, and fragments larger than 1000 bp are sequenced inefficiently.  So, after DNA extraction, additional steps are required to further reduce the average DNA fragment size prior to sequencing adapter ligation.  The most common method of genomic DNA fragmentation for short-read sequencing is sonication, though enzymatic methods are also used in some kits.
Recently, long-read sequencing technologies have been developed to overcome the difficulty of assembling short reads.  Nanopore platforms can sequence DNA fragments that are 100s of kbp long.  To prepare these extremely long libraries, special care must be taken to not shear the DNA during extraction.  The Journal of Visualized Experiments provides a good guide on how to extract and process high-molecular-weight DNA:
Gong, L., Wong, C. H., Idol, J., Ngan, C. Y., Wei, C. L. Ultra-long Read Sequencing for Whole Genomic DNA Analysis. J. Vis. Exp. (145), e58954, doi:10.3791/58954 (2019).


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Why largest cats so much larger than canids?
It is striking to me that there is no dog-like creature larger than a wolf while there are at least two species, tigers and lions, many (at least twice and probably 3 or 4) times the size of the largest wolves. I would guess it has something to do with hunting style, packs vs individual hunters although lions do sometimes attack in groups. I am not saying I would like one to exist, but why is there nothing like a 400-500 pound wolf?


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What are these black masses floating on my pool?
I've been cleaning them for some time. At first I thought it was some kind of synthetic material, but when I took one with my fingers it disintegrated into filaments. I placed another under my usb microscope and they appear to be an aggregate of green tubular bodies.

They grow (appear) from one day to another, only 1-2mm diameter. My best guess is that they are some kind of algae, but I'm lost to find exactly what. I live in the south of Spain, the pool is treated with chlorine, in a well illuminated zone. There are no other algae growing, and the area is urbanized.

I was looking in the wrong kingdom. After much searching I asked myself: are those eggs? Silly me, of course they are. I should have thought it from the start. Mosquitoes plant their eggs on water over night. I was confused because in the past I've never seen the eggs, only the larvae and the pupae in the water. So, that's what I have every morning floating in my pool, groups of mosquito eggs.
http://animalia-life.club/other/mosquito-eggs.html


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How do animals contain and dispose of bacterial endotoxins (lipopolysaccharides)?
Gram negative bacteria naturally release endotoxins which are lipopolysaccharide molecules. These molecules are toxic to many eukaryote cells, including macrophages. My question is how animal organisms locate, isolate, contain these toxic molecules. For example, if a lipopolysaccharide attaches to a macrophage, thus neutralizing it, does this actually kill the macrophage or just render it inert? In any case, the ineffective macrophage must now be removed as waste. How does that occur?
In the Wikipedia article on endotoxin it reads "Normal human blood serum contains anti-LOS antibodies..." without further describing them. I find this statement strange because normally when I think of antibodies, I think of them attacking cells or organisms, not individual molecules like lipopolysaccharides. What are these anti-LOS antibodies and how do they function?

There are a lot of questions in this post. I went ahead and answered what I read as the central question, but you should consider making separate posts for your other questions re: macrophage killing, dead macrophage clearance, anti-LOS antibodies, etc.

There are too many questions embeded here to cover in a single answer. I'll summarize and answer what I interpret to be the "central" question.

How do animals A) locate, B) isolate, and C) contain/eliminate bacterial endotoxins?

LPS in the blood stream is rapidly bound by LPS-binding protein (LBP) and localized to the liver for detoxification and excretion (1).
A) LBP recognizes and binds the Lipid-A region of the LPS molecule (2),
B) At this point LPS is released from bacterial cell membrane and sequestered into complexes with high-density lipoprotein (HDL). This is also the stage at which free LPS can activate CD14+ monocytes, triggering an acute inflammation response (3). However, additional HDL reduces monocyte activation, suggesting that these complexes inactivate LPS by "isolating" it from CD14 (4).
C) Finally, the LPS-HDL complex is taken up by the liver, either into Kupffer Cells (~25%) or liver sinusoidal endothelial cells (~75%), where enzymatic inactivation of LPS occurs either by dephosphorylation of the phosphates or deacetylation of the primary acyl components of lipid A (5)
Given the hydrophobic characteristics of LPS lipid-A and the fact that it's processed in the liver, I suspect that LPS and its metabolites are eliminated from the body via excretion into the bile ducts, but I haven't found a reference in the literature to confirm that suspicion.
References:

Wassenaar and Zimmermann, Eur J Microbiol Immunol. 2018 Sep 28; 8(3): 63–69.
Tobias et al., J Biol Chem. 1989 Jun 25;264(18):10867-71.
Vesy et al., Infect Immun. 2000 May; 68(5): 2410–2417.
Flegel et al, Infect Immun. 1989 Jul; 57(7): 2237–2245.
Yao et al. J Immunol. 2016 Sep 15; 197(6): 2390–2399.


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Examples of species whose extinct common ancestor is well documented?
If we follow the ascendence line of two closely related species we can build a
"Theoretical" common ancestor, whose characteristics were inherited with few differences by the offspring.
         _______ species 1
Ancestor/
        \_______ species 2

Are there examples of extinct ancestors that we can be almost 100% sure they correspond to the ascendant of the two distinct species?
Are these examples well documented with fossils and the inherited traits well understood?

Not with fossils.
Very very few organisms ever fossilize and most of the organisms tissues are not represented in fossils. Less than 0.01% of all animal SPECIES have left a single fossil and most of those have not been found yet.
Because of how incomplete the fossil record is we can never say a species is definitively part of a lineage. in fact the basic assumption in paleontology is that you never have a direct ancestor (individual or lineage) and extraordinary evidence would be needed to demonstrate otherwise.
Only direct observations or high genetic sampling would allow something to be considered definitively a common ancestor at the species level. Now we do have this for some species. We also have fossil localities with really high resolution making common ancestors highly likely, but never definitive.
Part of the issue is also defining species, the definition for species used in paleontology is very different than the one used in say population genetic. Species are nota real things but a human category stuck onto what is basically a continuous spectrum, it only works because most of the spectrum is dead. There is no concrete point at which two groups are definitively separate species. Its a bit like trying to define the exact cut off between two colors. Some groups of biologists favor definitions which increase the number of species others ones that decrease it, and both work because for the actual practice of biology whether two closely related populations are or are not separate species really does not matter.

This phenomenon appears to be called "pseudoextinction", with dinosaurs as the classic example of an ancestor (of modern avians). We know tons and tons about dinosaurs and avians, such that we can be pretty damn sure that modern avians are the descendants of dinosaurs.
Granted, almost by definition no fossil evidence could yield conclusive evidence of such a relationship, as the fossil is just a fossil.
For example, I am not sure that anyone could point to a specific dinosaur and say "this is probably the ancestor of modern avians A and B." Though I could be wrong about that.


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Identify arthropod with many legs in Mumbai
Can someone please identify this ~5 cm long arthropod? I've been finding one of these every 2-3 days inside my apartment ever since rainy season started here in Mumbai (June).
The bulb portion is its head. The arthropod is capable of climbing walls.
Thanks.

Video of the worm (shot while brooming the floor. Hence the dirt)
https://i.stack.imgur.com/AB16p.jpg
By the way, I've seen it 6 times in the last 2-3 weeks. Except once when I saw it on the bathroom floor, all other instances were during night time. So perhaps this is some sort of a nocturnal creature?

It looks like a centipede. Can you confirm how does it move?

I've edited my post with a video link. Please check.

Welcome to Biology.SE! In the future please [edit] your post to include all essential information (e.g. size in this case) — comments are ephemeral and so should not be used to covey information important for understanding or answering the question. Also note that this is almost certainly a millipede rather than a worm. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I'm pretty sure It's a millipede from the Julida order, that includes 750 species distributed in the northern hemisphere.
https://en.m.wikipedia.org/wiki/Julida


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Identification of the bug on the curry leaf- Delhi, India

I found this bug on my curry leaf in early morning. Which bug is this?
Size- 1-2 cm
Habitat- Delhi, India.
The bug was on one of the curry leaf of the curry plant pot in my residential balcony
Time- 7:00 am

Identifications questions should also include an estimate of the size of the organism and as much habitat information as possible. Please [edit] your post to include this essential information. ——— Please also consider taking the [tour] and going through the help pages starting with [Ask] questions effectively on this site. Thanks!

@tyresome I have edited. Thanks for your advice!

You're welcome! That looks like what is commonly known as a shield or stink bug (a large and very diverse group of beetles) . If you don't get a more specific answer you might try submitting your observation to a site like iNaturalist, which specializes in species identifications.


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How do anticholinesterase pesticides kill nematodes?
Compounds that inhibit the enzyme acetylcholinesterase are commonly used as pesticides. In animals with centralized respiratory systems controlled by the nervous system, poisoning with an anticholinesterase would lead to death due to respiratory arrest. I presume that, in insects, the inhibition of AChE would lead to closing of the spiracles necessary for respiration
However, nematodes and other worms rely on diffusion of gasses for respiration and do not have respiratory systems controlled by a nervous system, so how would inhibition of AChE by agents such as aldicarb kill them, especially if the pesticide in question happens to be a reversible inhibitor?

Cholinesterase inhibitors and plant-pathogenic nematodes
While it is true that cholinesterase inhibition does not affect gas exchange in nematodes, it does produce other effects by paralysing motor activity:

Inhibition of larval hatching

Reduced movement to new roots

Impairment of root invasion and feeding

Impairment of copulation

Acetylcholine also has a role in sensory neurotransmission in nematodes, which could further contribute to the toxic effects.
Thus cholinesterase inhibitors do not directly kill nematodes, but only slow down their growth and reproduction. This is why some prefer to use the term 'nematostatic' over 'nematicidal' for these compounds.
Effects on vertebrate pathogens
Pyrantel is a cholinesterase inhibitor used to treat intestinal nematode infections in man and other mammals. Little is known about how exactly it works, except that it causes spastic paralysis of the worms. Possibly, it impairs feeding and reproduction (like its counterparts in plant pathogenic nematodes).

References and further reading:

Wright DJ. Nematicides: modes of action and new approaches to chemical control. In Zuckerman BM, Rohde RA, editors. Plant parasitic nematodes. Vol. 3. New York: Academic Press; 1981. p. 421-449. Link to publisher site.
Martin RJ, Robertson AP. Mode of action of levamisole and pyrantel, anthelmintic resistance, E153 and Q57. Parasitology. 2007 Aug 1;134(8):1093–1104. https://doi.org/10.1017/S0031182007000029

In nematodes, Acetylcholine is the main excitatory neurotransmitter at neuromuscular junctions. Large amount of nervous system cells in Caenorhabditis elegans secrete acetylcholine for Cholinergic neuromuscular transmission.
Cholinergic transmission is involved in various physiological processes in many C. elegans, such as locomotion, egg laying, feeding, and male mating.
So acetylcholinesterase which is an enzyme responsible for hydrolysis and inactivation of acetylcholine plays an essential role in regulation of cholinergic transmission.  Thus inhibitors of this enzyme can act as nematocide.
Reference:
http://www.wormbook.org/chapters/www_acetylcholine/acetylcholine.html#:~:text=Acetylcholine%20is%20the%20major%20excitatory,elegans%20nervous%20system%20release%20acetylcholine.
https://pubmed.ncbi.nlm.nih.gov/16569291/#:~:text=Acetylcholine%20is%20the%20major%20excitatory,for%20regulation%20of%20cholinergic%20transmission.


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What is the minimum atmospheric pressure at which bees can live/thrive?
Bees are amazing little critters. (Gosh, they're cute.) But what if we colonize Mars and start terraforming it? At what point will bees (and other insects) be able to live/thrive in that environment?
Obviously, there need to reasonable conditions:

total atmospheric pressure
partial O2 pressure and general atmospheric composition
no toxins
flowers to pollinate and get nectar from
a wider ecosystem to thrive in

For now I'm just wondering: What atmospheric environment do bees need to live on Mars?

Perhaps we should give them little space suits?

Yeah they're cute alright. I'm not an expert on this topic. However maybe this article with too many ads for its own good (https://www.dailymail.co.uk/sciencetech/article-2552098/Bees-scale-MOUNT-EVEREST-Insects-fly-altitudes-air-kill-human.html) might help a bit in understanding how change in atmospheric pressure can affect bees and also show's how awesome they are!

Also, insects used to be much bigger in the past and scientists believe this is because of the higher concentration of oxygen in our atmosphere during prehistoric times (https://www.nationalgeographic.com/news/2011/8/110808-ancient-insects-bugs-giants-oxygen-animals-science/). Imagine what that would look like!

They need a temperature over 0°C for starters. Insects thrive in mild temperatures, and Mars I fear is pretty cold (-65°C and lower). If we were to colonize Mars it would requiere to build indoor habitats to replicate Earth conditions, not only pressure but temperature, oxygen and humidity).


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For how long viruses survive in non-air moisture environments?
On the Internet there are plenty of information that viruses don't live long after they were exposed to air, after they starting to dry out.
But it's hard to find an information on how long viruses can survive in wet non-alive environments at a room temperature like food, oils, soap.
I understand that it varies from virus to virus, but there may be maximal (for the most survivable ones) or average values.

Depends on the virus. They have PH, and temperature requirements that can't be disrupted. If completely disrupted then the virus denatures causing it to no longer have the effect it had.

@Ark Lomas thanks for info. I know it depends on the virus, but there must be maximal (for the most survivable ones) or average values.