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Coronavirus and temperatures
An article on bioRxiv, Evaluation of heating and chemical protocols for inactivating SARS-CoV-2, recommends certain treatments to inactivate SARS-Cov-2 for lab work.
The abstract notes: "Although heating protocol consisting of 92°C-15min was more effective rather than 56°C-30min and 60°C-60min to achieve 6-log reduction, it is not amenable for molecular detection on respiratory specimens because of important decrease of detectable RNA copies in the treated sample vs untreated sample."
Do I understand correctly that 56C/30min is broadly as effective as 60C/60min? Given that 56C from previous research seems to be more effective than 22C, I would have expected 60C to require less time to achieve a similar effect to 56C. Especially with 92C/15min being more effective still, though more disruptive.
I'm curious what the explanation may be why effectivity might drop between 56 and 92C. Or why I may be misunderstanding the temperature/time scales. Please keep it simple. Thank you.

They only tested 3 heat treatment regimens: 56C/30min, 60C/60min, 92C/15min (6 if you consider the "with BSA" and "without BSA", but only 3 combinations of temperature and time). They didn't measure the time required at certain temperatures to get to a certain level of inactivation. It seems they chose some of these particular protocols because they have been recommended in the past for other viruses.
They don't really have sensitive enough data to compare the 56C/30min to the 60C/60min or really enough to do any sort of statistical comparison whatsoever (as far as I can tell they only tested a single sample of each); yes, you can say they were roughly as effective, but it would be a leap to say 56C is the same as 60C.

Thank you.
Does anyone know or a have an idea why 60C/60m levels off at an effectiveness comparable to 56C/30m?

@user345360 In 2 of the tests they ran (one at each temp) they got no detectable virus. In the other one they got a small amount. That's not enough information to make any conclusions about things "leveling off". The temperatures aren't that different, the time isn't that different. At best they might be able to detect a 10-fold change, and even then not be too certain about it.


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What is the pH of cytosol? And plastids?
My teacher ask this question, and I answered 7 to 7.4, but she said it's wrong.
I read a lot and found the same answer (wikipedia)
I'm here asking for confirmation of this and the pH inside & outside of the tilakoidal membrane.

What kind of plastid and which part(s) of the plastid? The wikipedia article on chloroplasts contains relevant information ...

Thanks, that is kindly useful. Now, I just need a litle more confirmation.

The optimum cytoplasmic pH for performing physiological activities in
plant cells is a neutral pH of around 7.2 to 7.4.
The pH of apoplastic space outside plasma membrane and vacuolar pH is
acidic ranging between 5 to 7.
The thylakoid lumen is more fluctuating which varies during light /
dark cycles and is highly acidic.
The mitochondrial compartment and chloroplast maintains a basic
conditions of about pH 8 for optimization of biochemical reactions
occurring in these two particular compartments.

(Via: https://www.frontiersin.org/articles/10.3389/fpls.2017.02079/full#:~:text=Plastid%20stromal%20pH%20could%20only,cytosolic%20pH%20(around%207.3).

source: Stack Exchange

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

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Examples of things that are undefined in terms of living and non-living
I'm putting together a class on basic biology for kids and I will discuss living and non-living.
I'm looking for examples of things which are undefined in terms of living and non-living, if there are any.
People expect viruses to be alive but they are defined as non-living. Other examples of things that go against intuition are also welcome. Or things which were once classified one way and later redefined.
I couldn't find anything online.

Viruses are not undefined - they are seen as non-living.

@Chris: Most people who study viruses consider them to be living organisms. Many consider bacterial plasmids to be alive, along with other transmissable genetic elements.

Does this answer your question? Is there any definition of life which makes viruses undeterminable?

relevant xkcd: Alive or Not

@user1136 Haha :)

People expect viruses to be alive but they are defined as non-living.

This is actually one of the most widespread misconceptions I see. I think it's just one of those interesting but dubious factoids that spreads around in dinner party conversations. There certainly are some who take that position. But, after 11+ years of formal university education in biology, I can't think of a single professor or colleague who firmly embraced the position that viruses are non-living. Most (including myself) have been firmly in the camp that viruses are, in fact, alive. And the rest are more-or-less agnostic or ambivalent on the topic.
There's an intesting mini-debate between experts on the subject found here, I'll share this quote from one of the participants below because I think it's on point.

"In many ways whether viruses are living or non-living entities is a moot philosophical point."

There isn't one single, universally accepted definition of life. So ultimately, the answer to whether viruses are living or not will depend on ones chosen definition, and that's the case with most other controversial things.
However, viruses are unquestionably classified as biological replicators. There's a review on that topic (found here). It also includes discussions of other replicators which some experts also think of as living entities (but many don't). Examples include certain genetic elements like plasmid and integrons.
One notable exception that I didn't see mentioned in that review is prions. The first virology professor I ever had strongly advocated definitions of life that were inclusive of prions, but I haven't found that position quite as common among other academics. I'm a bit more agnostic on the prion debate, because it's hard to find prion-inclusive definitions of life that arean't also inclusive of something like an inorganic crystal.
The problem is that scientists like consistent definitions that don't have lots of exceptions, or require us to split existing categories. Between viruses, plasmids, and prions, there's a lot to talk about in terms of what characteristics they share with other life forms and what they lack that makes some question their classification. It's also interesting to consider whether any of the attributes common to living things occur in silico (or if they could in the future).

It's kind of contradictory that you use dismissing language such as "widespread misconception" and "dubious factoid", but then cite a debate article because to whom is the paper targeted to if not to experts with opposing view points? And calling it a moot point because there is no universal agreement is counterproductive as there aren't many thoughts that are universally agreed upon. It's like saying studying phylogeny is pointless because my next door neighbour believes in creationism.

Also your post puts a lot of emphasis on replication although it's not a key necessary trait of living things. A yeast cell with a temperature sensitive allele of a telomere capping protein will arrest permanently in stationary phase at a restrictive temperature unable to divide. Humans can become sterile in their lifetime. Both of those are incapable of reproducing, yet are unambiguously living things. Conversely if the vegetative yeast cell or the human completely lack metabolic activity they are unambiguously dead. Metabolism is a more important criterion.

@Cell. It is a widespread misconception that viruses are non-living, not becuase it's false, but because it isn't settled fact (which is how it was framed in the question above). I never implied that sterile humans weren't alive, I merely referenced one classification encompassing viruses and other biological entities. I'd happily reply to your critiques point-by-point, but I don't think the comments are an appropriate place for it. If you find my answer factually inaccurate, please specify where and I'll try to fix it. If you find it incomplete, consider writing your own.

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


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De novo mutation selectivity
I was recently reading about genetic diseases and came to understand that many of them are caused by de novo mutations in the prezygotic or early embryonic stages of the life cycle of the organism. Most chromosomal aneuplodies resulting in well known genetic diseases such as the downs syndrome caused by trisomy of chromosome 21 are caused due to de novo mutations.
However the thing that I didn't clearly understand was the reason for some de novo defects being more prevalent than others. For example the trisomy of chromosome 21 causing downs syndrome is relatively more common than the trisomy of the other chromosomes. Why are some aneuploidies such as trisomy 21 replicated independently in many different individuals (are more prone to occur) than others?

Questions for clarification: Is trisomy 21 actually more common than other aneuploidies? Or, are other trisomys or monosomies more likely to result in a non-viable pregnancy or spontaneous miscarriage? My suspicion is the latter, but I haven't done the research to back it up yet.

Edit: I am only addressing aneuploidies as those are the examples given. Other classes of mutation have distinct mechanisms, so I would split those out into another question if you are interested.
Chromosomal abnormalities occur more frequently when it is hard for cells to do meiosis and mitosis properly with a chromosome, or when the chromosome is more prone to "break" for some other reason.
The cell relies on certain architectural features (centromeres) to segregate chromosomes properly during mitosis. When segregation goes wrong, then you find aneuploidy much of the time. Chromosomes have other features such as telomeres and satellite DNA that can lead to chromosome fusion errors by different mechanisms. For example, yeast cells that have aberrant telomeres lead to high rates of aneuploidy.
Different chromosomes of the same genome have some variation in structure, repeat content, and other features that may predispose to aneuploidy formation or otherwise. These can include the quality and functionality of features such as centromeres and telomeres; these can vary even for the same chromosome across the lifespan of an organism.
For example in yeast, people have observed quite dramatic differences in the occurrence of spontaneous aneuploidy between different chromosomes (see figure 1). Yeast cells are much more robust to chromosomal variation than humans as they do not have a complex developmental cycle. However, aneuploidy of chromosomes with certain genes does seem to be selected against in that paper. There also appear to be dependencies in which the aneuploidy tolerance of one chromosome depends on the karyotype state of some other chromosome. "In other words, CIN [chromosomal instability] does not appear to be caused by some general property of being aneuploid per se but rather by determinants associated with specific aneuploid karyotypes."

Figure 1.
Experiments in the muntjac (a mammal) seem to show that the different chromosomes segregate more or less effectively based on centromere size (Figure 2).

Figure 2.
Human chromosomes have quite different rates of aneuploidy formation (see Table 1), so yes there is a bias. This is most markedly a bias in which acrocentric chromosomes and the shorter chromosomes have a somewhat elevated rate of aneuploidy (Table 2, same paper). So having an acrocentric architecture may make a chromosome more difficult to segregate.
When you ask about trisomy 21, note that chromosome 21 is acrocentric in humans. Thus, aneuploidies occur for chr21 at a somewhat higher rate.
However, commenter @MikeyC has a good point that there is a bit of ascertainment bias in how we find aneuploidies. Many aneuploidies are embryonic lethal and spontaneously abort; chr21 trisomy on the other hand yields living babies with noticeable features of their aneuploidy, so we know a lot about it and see it a lot. This seems to agree with the yeast data.
So there are multiple contributing factors. There is some variation in how chromosomes give rise to aneuploidy, but we also need to consider the means by which we observe aneuploidies in evaluating those molecular mechanisms.


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Is there any small animal that can jump over a meter high/long?
By small, let's say less than 5 cm body length. I always thought that grasshoppers were the highest absolute jumpers in this class but the highest jump according to this article is 0.7 m...

no animal smaller than 5 cm can jump higher than 1 meter. grasshoppers and locusts have wings which supposedly disqualifies them. https://www.guinnessworldrecords.com/world-records/highest-jump-by-an-insect.
The immense mechanical power that would be required for any animal to jump so high with such a small size is unbelievably high which is why they have developed different evolutionary adaptations. not to mention that the terminal velocity of such a small creature is very low so a jump would quickly become a fall due to the air molecules slowing them down. https://www.youtube.com/watch?v=f7KSfjv4Oq0


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Why are the sympathetic and parasympathetic axons different, in terms of presynaptic and postsynaptic length?
Does the parasympathetic system have a long presynaptic efferent axon because it takes a great distance to reach target organs from the brain stem or sacral region of the spine? Does the sympathetic have a long postsynaptic efferent axon (that reaches the target organ) since the presynaptic neurons are centrally located in the thoracic and lumbar regions of the spine? What purposes do these different axon lengths between the presynaptic and postsynaptic parasympathetic and sympathetic neurons serve? I'm looking for an answer that explains their benefits.

Seems similar to this question (also not answered): https://biology.stackexchange.com/questions/42168 :)

Does anyone know the answer to this question?


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Unidentified insect seen in southern UK, near North Downs
This creature was seen in southern UK, near North Downs, just this weekend.
https://youtu.be/5VJYOrMJXaQ

Though it might resemble a woolly aphid (https://dengarden.com/gardening/Woolly-Aphids-Whats-that-Fluffy-White-Stuff-on-my-Tree). I'm more certain that it is a mealy bug instead (https://puffycarrot.com/little-fuzzy-white-bugs/). the fact that it is not on a plant is what confuses me since both these species are usually living on plants which is where they grow.
here is some images i found that look almost identical to the photo you have and give other angles to the species, you can compare it with the images in the other links:
https://www.flickr.com/photos/unique127/2539022716/
https://www.ecosia.org/images?q=white+furry+insect#id=DDEE9FF71839419EF585778C7DA8F1E1545E98D1


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Do fledglings die if they are not fed constantly?
There is a bird's nest on my balcony in the wall above the door with birds who breed. They have fledglings who already hatched. (I assume this because I sometimes hear quiet sweet chirping.) I sit on my balcony often for breakfast and sometimes for lunch almost every day. When I do this, the birds stop feeding their fledglings (because they are afraid of me or because it is some natural instinct to not reveal their nest).
A friend of mine (who installed a birdhouse on her balcony) told me that the fledglings die if they are not fed constantly. She told me that she doesn't use her balcony anymore (or at least not longer than 5-10 minutes) because of this.
So my question is: Do fledglings die if they are not fed constantly? How long can they survive without food? (like 30 minutes or so)
I would like to use my balcony because I really enjoy having my meals on it but I also don't want the fledglings to starve.

Depends on the species and their age. All birds have fat reserves that can keep them alive for a relatively long time. It's when fledglings are left for many hours or days that one should start worrying about their survival.
The following link explains more detail on how frequently birds must be fed, even if in your case I suppose you aren't the one feeding them:
https://birdwatchingbuzz.com/how-often-should-you-feed-a-baby-bird/
In my experience some species of birds might become less afraid if you leave food or water stations for them.

Thank you very much and you are right. i am not feeding them. i just interrupt the feeding process by staying on my balcony. i will look further into this topic but i guess everything will be ok as long as i dont overdo it.

Every 10 to 15 minutes.
The youtube channal: A chick called Albert
It is a good channel that is really interesting.

This is absolutely not correct.


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Gastric and intestinal gas exchange
A very long time ago, I happened across research into using an oxygenated liquid in the stomach and or intestinal  cavity.  I wondered what further results came about of that research, and am having difficulty finding anything on it.   Is anyone aware of it and it and or  can point me to articles and or research papers done?

Intestinal gas consists of ingested air and gas formed during digestion. Stomach gas consists of  15% oxygen and 7% carbon dioxide approximately; the remaining is nitrogen.
The air that we breathe contains about 21% oxygen; thus some of the swallowed oxygen is absorbed through the blood capillaries present in stomach. Carbon dioxide is synthesized by digesting food using gastric juices. Nitrogen is not absorbed.
The small intestine absorbs some amount of carbon dioxide and oxygen. And the remaining gas is passed further to the large intestine. In the large intestine,  most of the oxygen is removed and carbon dioxide is increased. New gases are produced mainly hydrogen because of bacterial fermentation. And these gases are absorbed by blood and later released via lungs.
Check out following links:
https://katesalevelbiology.wordpress.com/2017/02/14/human-gas-exchange-the-digestive-system-and-breathing/
https://www.gastrojournal.org/article/S0016-5085(19)33654-6/pdf
https://journals.physiology.org/doi/abs/10.1152/ajplegacy.1926.76.1.92
https://nyaspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1749-6632.1968.tb19024.x

Kindly let me know, if these links are useful. I can share whole research articles as some of these links need subscription.

Asking the question here inspired new terms for me to search and I belive I found information on the original article I had happened across where researchers tried to oxygenate pigs by perfusing the abdominal cavity with oxygenated perfluorocarbons.
Penn researchers use the abdomen to deliver oxygen to assist ailing lungs
Link to a research paper.
Peritoneal Perfusion With Oxygenated Perfluorocarbon Augments Systemic Oxygenation


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Is it possible for a invertebrate to evolve features like that of a vertebrate or BECOME a being similar to that of a vertebrate?
Could a invertebrate, for this lets say, a centipede/millipede, evolve into something like that of Pikaia? or something similar? Just an invertebrate turning into something similar or what would look like a vertebrate. Is that even possible in the first place? I was thinking maybe tagmosis could do some of the magic but other than that, I hit rock bottom.

Define similar.  Or consider the hummingbird and the hawk moth: https://en.wikipedia.org/wiki/Sphingidae

Your question is very vague because it covers 100 million years of evolution that happened 500 million years ago, and asks if a centipede can develop many complex features like: bones, endoskeleton, spine,red blood cells, lungs/gills, and lose all the features that define arthropods. best to read up about "earliest vertebrate fossil" and "earliest terrestrial vertebrate"

This is a very complicated question to answer. evolution of that extent might take many millions of years and nobody can say for sure whether something like that would actually happen.
If we look back in time (https://socratic.org/questions/how-did-vertebrates-evolve), organisms with exoskeletons such as ostracoderms appeared before vertebrates. So, perhaps arthropods like centipedes and millipedes could evolve into a vertebrate if it benefits the species in their particular environment.

Thank you! Mad respect


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Can the basement membrane of blood capillaries expand?
I have been doing some rudimentary research into the basement membrane and found the it contains collagen fibers which are known for their elasticity.  Does this mean that the basement membrane can expand in capillaries?

It's a good question.
Though there is hardly some evidence to answer your question.
However I will share what all I found.
So in capillary basement membrane, mostly collagen type 1 and 4 are  present.
Now collagen type 4 aids in elongation of the new capillaries-

in the ex vivo rat aortic model of angiogenesis using a type I collagen matrix, type IV collagen promoted new vessel elongation and survival in a dose-dependent manner compared with controls (no type IV collagen), which grew until day 9 and then regressed during the second and third week of culture (treatment with 3, 30, 300 g/ml of type IV collagen in 43, 57, 119% increase in microvascular length) [139]. In all then, type IV collagen seems important for stability of blood vessel formation.

The collagen in capillary basement membrane impart mechanical stability to the vessel.
Also elastin is a component of the basement membrane. Reference
Now though I couldn't find that it's the elastin of basement membrane only, but-

Comprising 50% of the dry weight of major arteries, elastin is the most prominent ECM protein in arteries [43]. In vessels, elastic lamina alternate with rings of smooth muscle forming a strong, flexible part of the arterial wall [43, 44].

Here is the article


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What is the copy number of a given gene in GRCh37?
sorry for the naive question, but how do I determine what the copy number is in GRCh37 for a gene with multiple CNVs? (e.g. DRD4).

Can you give some indications of things that you've tried or what kind of data you have access to?

Thanks for the reply! I was poking around this page: http://grch37.ensembl.org/Homo_sapiens/Gene/StructuralVariation_Gene?db=core;g=ENSG00000069696;r=11:637293-640706
but I don't know enough to understand a lot of it. I also tried looking at DRD4 within GRCh37 in the NCBI variation viewer.

A very naive approach would be to simply ask how many copies of the sequence in question are in the hg38 sequence, at some level of homology. You could do this using a tool such as BLASTN (which has a web interface that you can use to search against a human genome) or, if you have the sequences downloaded somewhere where you can work with them, using a tool such as minimap2 (which will be faster) as long as you're comfortable using command-line tools.
If you choose to do this, you will have to be comfortable setting thresholds for what counts as a copy of the gene in question.
A more involved solution would be to obtain DNA sequencing reads for the sample you're interested in and use them to quantify the copy number of the gene based on the number that map to a given sequence of interest. An older approach would be to use microarrays.
I am guessing that since you are interested in the reference genome that you are not interested in going to that kind of trouble.
Is this a homework question? If so, you should add the "homework" tag.

Thank you so much for the detailed answer. Minimap2 looks great. (This isn't a homework question, just a question I am pursuing to try and learn more.)

Ok, gotcha. Minimap2 is an excellent tool by Heng Li, who is also the author of the ubiquitous short-read mapper bwa and a million other projects. I strongly recommend using him and his blog as a starting point if you're getting started in bioinformatics etc.: https://lh3.github.io/

Ah perfect, I've been looking for something like this. I definitely will!


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educational sources for learning biochemistry
I just finished high school and am going into a biology undergraduate degree, I'm getting into biochemistry too and would like to learn more about it through online platforms or even non-fiction books to use my time effectively this summer. So far I've been using online flash cards to learn more about the jargon and would like to hear some suggestions of platforms or books to read that teach concepts strongly tied to biochemistry beyond what a basic high school curriculum would teach.

It might be prudent to find out which text books are used at your university.

There are several reference books for biochemistry, some more readable than others. I personally recommend two of them: (1) Lehninger et al. Principles of Biochemistry and (2) Voet, D., Voet, J., et al. Fundamentals of Biochemistry: Life at the molecular level. Both books contain the most important and basic features of each subject. The chapters are generally well written. I have to say that, from my own experience, I consider that Voet's book is more enjoyable, given that some of the sections of Lehninger's can be a bit tricky. Whichever book you choose, make sure you get relatively new editions. Good luck!
As a side note, even though biochemistry is one the first proper biology classes one takes in undergrad, there are some background requirements. Taking organic and inorganic chemistry courses before is important and some understanding of thermodynamics will certainly come in handy.

How are either of these books “online” platforms? What value are personal preferences without reference to the background required, your own background, the other courses the poster may be following, any teaching experience you may have and comparison with other books available. And these are introductory text books, not reference books. It is for these reasons that I regard text recommendations off-topic on a site devoted to answering problems in biology.

''books to read that teach concepts strongly tied to biochemistry beyond what a basic high school curriculum would teach.'' I assumed he was also interested in reading non-fiction books. I do agree that adding the background needed is important (as I edited the question), but I do not think the rest is needed. As a side note, what I meant by reference books is that they are very commonly used in undergraduate courses. In your view, what is a reference book then?

I'd add Stryer et al. Biochemistry as another Option. I never read Lehninger, but compared to the Voet the Stryer is a bit of an easier and more accessible introduction in my opinion. Though it's a long time that I've read those two. You can search it for free on NCBI Bookshelf, though you can't browse the book freely there.


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Are there real world examples of one way isolation between two populations?
I know that for two populations A and B, there are situations in which there is a two way exchange of individuals between the populations, and there are situations in which there is no exchange of individuals between the populations.  I have thought before of a situation involving one way isolation between two populations, in which it's easy for individuals from population A to immigrate to population B, but impossible for members of population B to immigrate to population A.
I tried searching to see if I could find any examples of one way isolation between populations, and couldn't find any examples, although I don't know if this is from not using the correct keywords to find it, not knowing where to look, or there being no known examples of it.
Are there any real world examples of the one way isolation I mentioned between populations?

pit caves come to mind.

Fishes leaving on both sides of a waterfall too high to climb up. Sunflowers living along rivers and that reproduce clonaly through cutting, where cuts gets transported by the water stream. Plants reproducing with seed flying in the air and living on a windy sea shore. Plancton living in a water stream.

@Remi.b Do you know the names of any of the specific species that would be examples of this?

Are you thinking of modern-day politics e.g. it was easy to go from one side of the iron curtain to the other, but a lot harder for the reverse?

https://www.livescience.com/nuclear-bunker-cannibal-ants.html

You might want to look for asymmetric dispersal.
Asymmetric dispersal has been found in many freshwater fishes (such as bullhead; Junker 2012), freshwater mussel (Terui et al., 2014) and in marine kelp (bull kelp; Collins et al., 2010).
That being said asymmetric dispersal does not mean that dispersal goes exclusively one way. Maybe Blondel et al. (2020) reporting asymmetric isolation caused by waterfalls in guppies can be helpful to you.
I am also thinking of polyploid and invasive lines of sunflowers that often live along rivers and reproduce clonally through cutting, where cuts gets transported by the water stream. I co-authored a paper on the evolution of these invasive sunflower lines (Bock et al., 2018) so I should know the literature well but I don't and I am not able to cite a paper that really describes the dispersal and population structure of these sunflower lines. Such patterns might be found in Mimilus as well.
Planctons follow water streams and can therefore have very asymmetric dispersal too (Pringle and Franks, 2001).
I am also thinking of plants reproducing with seed flying in the air and living on a windy sea shore or in windy wide open plane (e.g. tumbleweed). But I cannot give you a reference.

Thank You!  I liked reading about how in the case of guppies, natural selection would tend to favor traits that would make the guppies less likely to go through the waterfall in guppies living above the waterfall, which makes sense seeing as how a guppy going past the point of no return would be equivalent to dying with respect to the above waterfall population.


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Exhalation in human breath, through mouth or nose: which is most usual?
Until now I believed that breath exhalation through the mouth is common for most human beings, and this fact is implicit in several technical contexts of which I can think (sports, music, medical checks...). But recently a friend was surprised when I claimed this, and conducted a small poll around himself, giving a 100% of people inhaling and exhaling both through their noses in normal breath (then I was surprised!).
This issue is not without practical interest in these COVID-19 days, because when using a surgical mask (which filters the air going out but not the air coming in), people exhaling from their mouths and not covering their noses with the mask are still giving more or less the same protection to others, so if most people actually exhale through the mouth, this common "faulty" usage would actually not be so dangerous.
Can someone point to any scientific paper having evidence or statistics about normal mouth exhalation against normal nose exhalation?

Ok, there seems to be a possible misconception here. Breathing from the mouth, though a helpful evolutionary trait, can also have its downfalls. I didn't find many peer reviewed research papers on the reason however the internet is flooded with articles. here's a example: https://www.healthline.com/health/mouth-breathing.

@ArkLomas Thank you for your comment, but it does not really address my question. I'm talking about exhalation (the air going out), not breath intake (the air going in). Also, I need research data, online "health" or sports sites are not good enough.


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How is knowledge about farming transfered between generations in farming ants
There are some varieties of ants capable of "agriculture", e.g. dairing ants farming aphids and leaf-cutting ants farming fungus.
How is the knowledge about the techniques involved passed between generations (in the case of dairing aphids I mean e.g. milking the the aphids to get honeydew, and protecting the aphids)? In short, is it more "genetic" (so that lab-cloned ants are capable of it) or is it more part of "culture", i.e. younger ants mimicking the older ones? I'd be mostly interested in answers with references to relevant experimental research.

Knowledge and technique are probably the wrong words for what is essentially instinctual behavior.

knowledge, technique, intuition, etc. are all not well-defined terms, which is why I'd favour references to experimental research. If you have a particular definition in mind of "essentially instinctual", and there are research papers which use that definition, and which indicate that the behaviour of the farming and dairing ants is of this kind, I'd be glad to see some details. All else is an opinion.

If you're interested in opinions here's one: there exist slave-making ants which "teach" ants of other species to work "for them", and perhaps one could imagine that "farming slave-making" ants could exist, in which case farming could hardly be considered purely "instinctive". For another opinion, I consider it  more likely that instinct is involved on a higher level, imprinting the ants to e.g. "follow other workers which are successful in bringing in food etc.", whereas the particular strategies of particular species  are "learned" by means of such an instinct.

Have you searched? If so what did you find? So people don’t waste time with repeats..

I haven't searched outside of wikipedia and links there (for example to the discussion in Origin of Species about slave-making ants).


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Effect of opposing electric charges on cells
Is the affect on a cell between two negatively charged plates theoretically similar to between a positively and negatively charged plate?  In other words, would it induce charges on the inside and outside like in the other case:

But it would induce negative charges on the left and right outer sides of the membrane and positive charges on the inner sides:

Is there a context for asking this question?

Affect or effect? Sounds like the electricity has an effect. It follows the path of least resistance and most cells are generally insulative, blood and nerves probably look a bit like your illustrations.

Sorry about the title.  Just asking out of curiosity.

@Tom From the help: "You should only ask practical, answerable questions based on actual problems that you face". This seems like a toy physics problem rather than a biology one. I can ask at physics and see if they want it.

@ Bryan Krause: I see your point.  My apologies.


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What are the environmental conditions for larval Haemonchus contortus to survive?
What is known about the environmental limits for Haemonchus contortus to survive outside of a host organism in its larval stages?
I'm interested in knowing:

temperature tolerance levels
preferred humidity levels
pH tolerance
how long can it survive outside of the tolerated ranges?

Lowest temperature
2, 3, 4 and 5 week beakers containing eggs and non-infective larvae in lamb faeces didn't develop into infective larvae (L3) when exposed to fluctuating temperatures ranging from -1 to 15°C:

[...] there were no signiﬁcant differences in the number of harvested larvae
at the different time points for the faeces incubated at 15°C.
However, at 5°C and -1 to 15°C no development of eggs occurred,
although it was found that a small proportion developed into infective
larvae when incubated at 25°C for an extra week.
(1)

Highest temperature

Temperature of 40ºC negatively correlated with the survival rates of
H. contortus L3. [...]
Decreased motility was observed on day 10 after heating. [...]
Heating of L3 at
higher temperatures (45ºC and 50ºC) caused 100% lethality as early on
hour 48 and 24 of exposure
(2)

Desiccation
When it comes to dessication, there are three main things to take into account:

whether the larvae are in exsheathed or ensheathed state matters
they can survive several dessication/rehydration cycles
it is best survived below freezing temperatures

The experiments on desiccation survival showed that, after a few hours
exposure to 47% R.H., all exsheathed larvae died and all ensheathed
larvae survived. (3)

Desiccation protected the larvae against death on storage at
temperatures below freezing, but it was harmful at temperatures above
freezing. (4)

Ruminant larvae were able to survive up to 7 desiccation/rehydration
cycles, and, during anhydrobiosis, metabolic activity was decreased
and survival of the larvae was prolonged both in the laboratory and in
the field. (5)

pH

The effects of temperature on survival and development of the
free-living stages of H. contortus have been studied both by faecal
and by agar-culture methods. [...] with a pH range from 6.5 to 8.5 (6)

How long?
As usual, depends on the current environmental variables and current state of the organism and so forth. Read above sections. The article by P. T. Iliev, A. Ivanov, P. Prelezov has a few tables that can give you a good idea of these times (at least for temperature and humidity).

(1) The development and overwintering
survival of free-living larvae of
Haemonchus contortus in Sweden,
K. Troell, P. Waller and J. Höglund
(2) Effects of temperature and dessication on survival rate of Haemonchus contortus infective larval stage, P. T. Iliev, A. Ivanov, P. Prelezov
(3) Desiccation Survival of the Infective Larva of Haemonchus Contortus,
C. ELLENBY
(4) Effect of dessication on the survival of infective Haemonchus contortus larvae under laboratory conditions,
Kenneth S. Todd, Jr., Norman D. Levine and Paul A. Boatman
(5) Anhydrobiosis increases survival of trichostrongyle nematodes (abstract only),
S E Lettini, Michael Sukhdeo
(6) Trends and Perspectives in Parasitology 2 (page 84),
B. A. Newton


text:
Alternative hypothesis for learning in brain beyond the hebbian rule
I was reading on wikipedia that there are exceptions to the hebbian rule, and I was curious about the possibilities of other hypotheses of how learning occur in the brain. So I would like to know:

are there alternative (or complementary) hypotheses to the hebbian rule?

this may be a better fit for the neuroscience stack.

There is Karl Friston's free energy principle.


text:
Could there be a pathogen which does not activate an immune response?
In order for the immune system to be stimulated to produce antibodies, there must be a surface protein of the invading pathogen which binds to a receptor on B cell surface somewhat loosely. We need this first step for the initiation of the somatic hypermutation phase to produce specific antibodies.
But what if there is a pathogen which does not have such a surface protein? i.e. its surface proteins, if it has any, do not bind with sufficiently high affinity to surface proteins on existing B cells to trigger further aspects of the immune response.
One may argue that this is unlikely to be the case because:
a) naturally occurring pathogens evolve from existing ones, so the changes in the antigens will generally be minor. A new strain will have surface proteins that are similar enough to those of an existing strain for some loose affinity to present antibodies in the host.
b) I think, though am not at all sure, that pathogens need to invade cells to be dangerous.I'm not entirely sure what the nature of a pathogen which cannot invade cells would be. Perhaps not a pathogen at all? In any case, if the starting assertion is true, the dangerous pathogens have a surface receptor which binds with surface proteins on cells to enter them. What if many antibodies are based on the same proteins? (Though I have trouble believing this because the natural agonists of these cellular receptors are some biologically relevant and useful proteins, which we would not want an immune response to. For instance, a generally accepted mechanism of entry of SARS-CoV-2 into cells is by binding the ACE2 receptor, which has angiotensin II- a vasoconstrictor peptide- as an agonist.
So my questions are:
a) Could we synthesise a pathogen which has no surface proteins but which nevertheless does harm in some way? How could it do this harm?
b) Can we make a pathogen which has surface proteins such that it can enter cells or do damage that pathogens normally do, but goes undetected by the immune system?
In the above I have assumed that surface proteins (or perhaps also other surface molecular- maybe carbohydrates will do- are necessary for activating the immune response. If this is not the case, please let me know.

"I think, though am not at all sure, that pathogens need to invade cells to be dangerous."
True in the case of viruses and some bacteria.
Hiding within the cells of the host is the intracellular pathogenesis.
But other "tricks" are possible. Four examples:

biofilms
surface proteins that "catch" antibodies
fast mutation of surface epitopes, like the (in)famous HIV
using host molecules (the HIV again)

Source: Extracellular Immune Avoidance (LibreTexts)
Also interesting: How bacterial pathogens colonize their hosts and invade deeper tissues (Microbes and Infection
Volume 17, Issue 3, March 2015, Pages 173-183).


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What exactly is a DNA molecule?
Are the two strands of the double helix collectively called the DNA molecule, or is each individual strand the DNA molecule?

Been asked before. Try searching to find it. But you won’t find a satisfactory answer, because it’s not a question that concerns molecular biologists. Semantics are not where science is at in the 21st century.

Does this answer your question? Is a DNA molecule a single strand of polynucleotide or two of them linked together?

@Dirigible Kinda. There doesn't seem to be agreement between the answers posted by different users on that post, though one of the users posted a reference from a book, so I'm going with that. Thanks a ton!

@David I found the post, thanks. As you said, no satisfactory answer. Yeah, modern science isn't too concerned with the semantics of stuff, and rightly so, but sometimes there are loose definitions of some things that do confuse me sometimes while reading course material.

I have actually added an answer to that post as the accepted answer is, in my opinion, an unjustified assertion. There is, as far as I am aware, no formal definition of molecule in a molecular biological context — presumably because there is no need for one.


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Do ants know the direct (approximately shortest) path to their nest from the food morsel?
I've been studying a bit on the foraging habits of ants, and one of the things I'm not clear on is whether ants know the shortest path from the food that they find to their nest. I understand that ants can leave different types of pheromones$^{[1,2]}$, they can change their behavior based on those trails, and those trails are often volatile. What I'd like to know is how do ants find their nest once they find a food morsel. In one of the papers,$^{[3]}$ it was shown that ants change their foraging strategy based on the number of encounters they have: they follow a straighter path when the ant density in an area is low, while they follow a more tortuous path if the ant density is high.
Considering a lower ant density, an ant will travel pretty far from the nest in search for food in a path that is not always straightforward. Assuming that the pheromone trails it leaves behind do not evaporate by the time it finds the food, will the ant travel back on the same path laid down by its pheromone trail, or will it actively find a more direct path towards its nest? I might also be missing something in the sense that ants always know where their nest lies when they are foraging, and thus can find the shortest path whenever they find any food. If so, any work reflecting such research would be of great help.
References:

Dussutour, A., Nicolis, S. C., Shephard, G., Beekman, M., & Sumpter, D. J. (2009). The role of multiple pheromones in food recruitment by ants. Journal of Experimental Biology, 212(15), 2337-2348.

von Thienen, W., Metzler, D., & Witte, V. (2016). How memory and motivation modulate the responses to trail pheromones in three ant species. Behavioral ecology and sociobiology, 70(3), 393-407.

Adler, F. R., & Gordon, D. M. (1992). Information collection and spread by networks of patrolling ants. The American Naturalist, 140(3), 373-400.

Terms that may help you research are dead reckoning or path integration. From Wikipedia:

In navigation, dead reckoning is the process of calculating one's current position by using a previously determined position, or fix, by using estimations of speed and course over elapsed time. The corresponding term in biology, used to describe the processes by which animals update their estimates of position or heading, is path integration.

There are many animals and certainly some species of ants that use dead reckoning/path integration for navigation. Here are some papers about the Cataglyphis genus by one scientist and some colleagues:
Wehner, R., & Räber, F. (1979). Visual spatial memory in desert ants, Cataglyphis bicolor (Hymenoptera: Formicidae). Experientia, 35(12), 1569-1571.
Wehner, R., & Wehner, S. (1986). Path integration in desert ants. Approaching a long-standing puzzle in insect navigation. Monitore Zoologico Italiano-Italian Journal of Zoology, 20(3), 309-331.
Müller, M., & Wehner, R. (1994). The hidden spiral: systematic search and path integration in desert ants, Cataglyphis fortis. Journal of Comparative Physiology A, 175(5), 525-530.
Collett, M., Collett, T. S., Chameron, S., & Wehner, R. (2003). Do familiar landmarks reset the global path integration system of desert ants?. Journal of experimental biology, 206(5), 877-882.
The last one on the list is particularly relevant because it seems to show that the ants are not using landmarks as markers of position, because moving landmarks doesn't alter their paths.
My intuition is that the extent of path integration will depend on the environment. Species living in a fairly "flat" terrain can gain a lot from knowing the direction towards their home. In a tree canopy, however, the direction "home" doesn't matter a whole lot if your path is constrained by paths down foliage, etc.
Therefore it's unlikely to be able to make any general statement about ants as a whole group, and better to investigate individual genera/species.
However, the Cataglyphis genus from the papers above live in a desert, and their dead reckoning abilities seem to be the ones most studied (there are many many more papers than the ones I pasted here, try searching Google Scholar for "path integration" ant or "path integration" Cataglyphis).


text:
What is the role of pyrophosphatase in RNA polymerization?
In Molecular Cell Biology (8th edition) there's a fragment in chapter 5.2 that says:

The energetics of the polymerization reaction strongly favor the addition of ribonucleotides to the growing RNA chain because the high-energy bond between the α and β phosphates of rNTP monomers is replaced by the lower-energy phosphodiester bond between nucleotides. The equilibrium for the reaction is driven further toward chain elongation by pyrophosphatase, an enzyme that catalyzes cleavage of the released PPi into two molecules of inorganic phosphate.

How does the pyrophosphatase make the reaction more favorable? Does it make "harder" for triphosphates to form back again (now you have to attach phosphates one by one, not two at once)? If so, isn't one additional phosphate just as bad as two? To remove either you have to break one bond (between the first phosphate and the second), and you have a specialized enzyme to remove two of them (the RNA polymerase). Isn't forming a diphosphate (which needs to form in order to later make triphosphate) actually worse? Or maybe it somehow "reuses" energy stored in the bond between the two phosphates left?
Sorry if I didn't use the proper vocabulary, I'm new to biology.

No problem being new to biochemistry and molecular biology. You might find it helpful to understand Sethi's answer if you read this section from Berg et al. Biochemistry which explains the thermodynamic concept of Gibbs Free Energy which is often applied to biochemical reactions. There is a worked calculation on the pyrophosphatase topic in relation to a different reaction in the same book.

This question can be answered by considerations of chemical equilibrium. For any chemical reaction:
$$\ce{A + B <=> C + D}$$
It is a property of nature that removal of product ($C$ or $D$) from the reaction mixture drives the reaction in the forward direction. This is an example of le Chatelier's principle and can be explained as follows:
In a reaction mixture containing $A$, $B$, $C$ and $D$, the rate of forward reaction ($A + B \rightarrow C + D$) depends on the frequency of collision of $A$ and $B$ molecules. Similarly, the rate of backward reaction ($C + D \rightarrow A + B$) depends on the rate of collision of $C$ and $D$ molecules. The collision frequencies, in turn, increase with concentration of the relevant species. An abrupt reduction in the concentration of $C$ hinders the backward reaction while leaving the forward reaction unchanged. Thus the forward reaction begins to dominate.
The reaction catalysed by RNA polymerase is:
$$\ce{RNA + NTP <=> Longer \ RNA + PP_i}$$
By removing $\text{PP}_i$ from the reaction mixture, pyrophosphatase does exactly that and drives the reaction in favour of RNA polymerisation. Note that hydrolysis of pyrophosphate is favoured because of the negative free energy change associated with it (thanks to David for pointing that out).

And why can’t the pyrophosphatase reaction just be reversed? Seems to me that is the key point that needs to be explained.

@David The hydrolysis of pyrophosphate is favoured because of the negative free energy change associated with it. (Should I add this point to my answer?)

Yes. That is why I raised the point. The standard deltaG for the polymerization is ca –3 kcal per mol. That for the pyrophosphorylase reaction is an additional –4.6 kcal per mol. There is actually a worked example of the latter point for acetylCoA formation in Berg et al, available at NCBI Books online.

@David Done. Here is another interesting point: if the standard deltaG for pyrophosphate hydrolysis were zero, or even positive, having the pyrophosphatase enzyme would still help. This is because we are starting with PPi alone, and to reach equilibrium, at least some of it must be converted to Pi. Thus, in any case, some amount of PPi would be removed.

I think there are aspects other than the thermodynamics of the reaction. If I am not mistaken, polymerization is almost irreversible. Also, in vitro RNA/DNA synthesis can happen without pyrophosphatase. There are some old studies on PPi being a competitive inhibitor of polymerization. Perhaps you can check them out.

@WYSIWYG — I don't want to muddy the water, but I found a 1992 Annual Review in which the author argues against the orthodox view in order to make an argument for a role of the reverse reaction in RNA repair! He bases his case on measurements of PPi concentration in E. coli! I suspect this has died a death, but haven't got the facts to argue against it.

Thanks to all of you.


text:
Does DNA being circular or linear directly affect the speed of DNA replication?
Let's say we have two DNA molecules of equal length, one belonging to a prokaryote and the other to an eukaryote. It's known that replication of the eukaryotic DNA is faster in this case. One clear reason for this is that linear DNA has multiple origins of replication whereas circular DNA only has one.
Now back to the real question: Does it matter for rate of replication whether the DNA is circular or linear? Does it contribute to eukaryotic DNA replication being faster in our specific case?
One thing I found in an old revision of this Wikipedia article is as such:

One reason that many organisms have evolved to having linear chromosomes is due to the size of their genome. Linear chromosomes make it easier for transcription and replication of large genomes. If an organism had a very large genome arranged in a circular chromosome, it would have the potential problems when unwinding due to torsional strain.

What I make out from this is that the rate of replication isn't directly affected. It's more closely related to avoiding other issues that arise from eukaryotic DNA molecules being typically longer than prokaryotic ones. But in our case where we declare both DNA to be of equal length, I'm assuming circular vs linear has no bearing on the rate of DNA replication.
So am I correct on my assumptions?
Edit in response to the answer below:

It's known that replication of the eukaryotic DNA is faster in this
case (where DNA molecules are of equal length) because eukaryotes
have linear chromosomes whereas prokaryotes have circular ones

If it makes sense to form a sentence like this, presenting linearity as the cause, then it's enough to satisfy my definition of directly affected in this case. For example, it's easy to make this claim if you present the number of origins of replication as the cause. I looked at the textbook you mentioned and the quantity of origins of replication is in fact mentioned this way.
Conclusion:
I went ahead and did a bit more reading in that textbook. What
I've understood is: An eukaryotic linear chromosome has multiple
replication origins rather than a single one in order to compensate
for its much larger size. So while the shape might be a factor
(possibly, not certainly), the primary and "direct"
reason is the difference in size, not the shape.

The current Wikipedia entry has modified this to "In an organism with a very large genome, circular chromosomes could potentially cause problems relating to torsional strain.[citation needed]". The much more cautious language presumably reflects the lack of citation in support of the postulated effect of torsional strain. Naively I would imagine less torsional strain in a larger circular chromosome, but in any case, there is no evidence presented that torsional strain is actually relevant.

@David Yeah, I agree that it's definitely not a highly credible claim the way it currently stands. But still it doesn't directly matter for the real question since it was only a (somewhat baseless) idea for why circularity/linearity might not have a direct impact on the speed of replication.

I'll see if I can find anything about this when I have a moment. As you may be aware, many closed circular DNA genomes are replicated by the rolling circle method — which in itself may have different characteristics to the standard replication method.

@David Thanks. I guess if we consider the method of replication as well that might further complicate reaching an answer. It looks like this question does require generalizing and neglecting a bit to reach any answer at all.

I am not sure if I well understand what you mean by directly affected.
I will list some possibilities below (For reference you can see any genetics textbook, I use, Genetics: A conceptual approach by Pierce, but I guess any textbook would do).

Porkaryotic polymerases (usually processing circular DNA) have a higher nucleotdie per second speed than eukaryotic polymerases (processing linear DNA). Does this mean that shape directly affects speed? In this case I would say no. It's just a difference between prokaryotic and eukariotic polymerases. Some prokaryotes have linear chromosomes and their polymerase will still be faster than eukaryotic polymerases.

One prokaryotic chromosome has only one origin of replication, while one eukaryotic chromosome has several of them, so that eukaryotes parallelize even in a single chromosome. Does this mean that shape directly affects speed? In this case, I would say yes. Due to steric effects, the shape of the chromosome has to do with the ability of having several origins of replications, even if the lengths are the same. Edit: After Ved's comment, I realized that this is also not necessarily true. Not all circular chromosomes have one single origin of replication; archaea have circular chromosomes with more than one origin of replication

Linear chromosomes are easier to unwind. Does this mean that shape directly affects speed? I would say, yes for large chromosome and no for small chromosomes. Edit: After David's comment, I realized that I am not really sure that linear chromosomes are easier to unwind. A Wikipedia entry states this, but I gave a look at the paper they referenced and found no real statement about this.

Importantly, if the DNA molecules you compare are one prokaryotic and one eukaryotic and they are very short, I would bet my 5 bucks on prokaryotic (circular) being faster, because in absence of all the parallelization the eukaryotic DNA polymerases are slower than prokaryotic ones.

Could you provide a reference or detailed mechanical argument in support of your assertion that linear chromosomes are easier to unwind. This would seem to be the crux of the matter. What you say and what you would bet is not the point. The Wikipedia entry acknowledges lack of support for this sort of assertion. Please provide it if you want your answer to be considered seriously.

Actually, after your comment I realized that no, I do not have a reference. I checked tha paper referenced by Wikipedia, but actually I wasn't able to find a statement supporting my assertion (which originally I took from OP question, who was also referencing wikipedia). It is possible that I lost some important passage in the paper, but at the moment I would say it doesn't support the assertion. Thank you for pointing this out, I edited my answer accordingly.

Well in that case, could you provide a reference for steric effects affecting the quantity of replication origins? I looked at two textbooks but couldn't locate anything relevant.

While I was looking for a reference to support the steric effects affecting quantity of replication origins, I actually found out that archaea have circular chromosomes and more than one origin of replication. I edited my answer to incorporate this.

While the question may not have gotten a definite answer (might be impossible anyway), I think the findings here are indication enough to reach some conclusion at least: It's not possible to generalize and say that the shape of DNA will certainly have an effect on the rate of replication. Number of replication origins on the other hand seems to almost certainly always have a direct effect on the rate. I will mark this as the answer, thanks.

I agree that it may be impossible to generalize. But I want to point you to this paper I just found: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6056714/ . Give a look at the "separation mtDNA" section. It deals with the structural problems with the circular mtDNA, and also references some work on prokaryotes. Maybe it will not answer your question, but it may be useful for information.


text:
Pre-Mendelian genetics
In the 18th century, Joseph Gottlieb Kölreuter concluded from his plant experiments that in some hybrid generations the characteristics of grandmother generation, grandfather species and F1 generation were in ratio $1:2:1$. What does this imply? Does this mean that he observed a blending inheritance?

can you clarify the question with a quote or an example? it's not clear what the ratios refer to or how they match up with generations or what "hybrid" means in this context. (German is fine)

@MaximilianPress This is a paragraph from the Oxford's Gregor Mendel and the Roots of Genetics. Hybrids are, I think the F2 and the subsequent generation offsprings. The para tries to say that he got similar results what Mendel got but was unable to explain them. The grandmother and the grandfather I think refers to the Parental generation.

Can you provide the paragraph? Your question does not include a quote as far as I can tell. It might be easier to answer if we can actually see the text in question.


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What happens to eyeball when you push your eye muscles harder?
I have myopia and I read that the rays of light intersect before the retina.
When I can not see clearly I can push somehow my eye muscles and can see a bit clearly. The object gets clear but moves some distance ahead (getting smaller).
My question is: What is in fact happening to the eyeball? Do the eye muscles contract it and make it more round than ellipsoid thus bringing the retina forward  so the light intersects on it?
In fact I have the feeling that the eye ball gets longer (ellipsoid).

Do you mean squinting? Any sort of tension on the eyes would result in changing of the shape of the eye. A change in shape will bend light differently. The perceived effects you're describing are most likely from you changing the shape of your eyeball to take in more light.
In terms of squinting, eye strain like that won't lead to blindness or worse vision. There's more danger with UV from the sunlight (cataracts) or getting wrinkles from squinting too much in the long-run.


text:
mitochondria has more activity or the numbers of them are more?
If a cell is needing energy more than the other cells, does it mean that it has more mitochondria or the activity of them is more?

This question would seem to be related, although the accepted answer there does not provide supporting references. As part of your own attempt to answer this question, you might consult a cell biology text and look at images of cells with different oxidative metabolic activity to see whether the number of mitochondria varies.

You might also want to look into condensed and orthodox states of mitochondria. When ATP requirements are high mitochondria will change their state from orthodox to condensed. Condensed state is considered to be the active state.


text:
How do mothers handle acid from embryo bone mineralization?
This is a relatively trivial question, but, I have not seen it discussed much. It could be one factor in the "acidosis of pregnancy" (JAMA, 1929). Are the compensatory mechanisms measurable, by dietary phosphate requirements increase by 3 mmol (40% more than adult average of 7.4 mmol) or something similar?
A human fetus  acquires 30 gram of calcium during pregnancy (Kovacs, 2014). The molecular weight of calcium is 40 gram per mole, 30 gram is 30/40 = 0.75 moles. Bone mineralization releases hydrogen ions since bone mineral requires hydroxide ions (Bonucci, 1992). Calcium and hydroxide ions have a 5:1 ratio in bone mineral, bone mineralization during embryogenesis releases 0.75/5 = 0.15 moles of hydrogen ions, 150 mmol.
80% of this H+ is generated during the third trimester of gestation (Kovacs, 2014), with up to 1.5 mmol per day (300 mg calcium/day, see Kovacs, 2014) between weeks 35 and 38. When 1.5 mmol H+ is distrubuted on an average 70 kg body, with 60% water, 70 kg * 60% = 42 kg = 42 L of water, the molarity is 1.5 mmol/42 L = 0.035 mmol/L. This is equal to -log10(0.035 mmol) = pH 4.45.
References
THE ACIDOSIS OF PREGNANCY. (1929). Journal of the American Medical Association, 92(25), 2104. https://doi.org/10.1001/jama.1929.02700510034014
Kovacs, C. S. (2014). Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones. Physiological Reviews, 94(4), 1143–1218. https://doi.org/10.1152/physrev.00014.2014
Bonucci, E. (1992). V. Regulation of hydroxyapatite formation. In Calcification in Biological Systems (p. 134). Boca Raton: CRC Press.

1.5 mmol/d is nothing. By some estimates, a typical adult produces non-volatile acid at 70 mmol/d even in the non-pregnant state. (This includes H+ as a by-product of metabolism, from the diet, and due to intestinal losses of bicarbonate.) How this 70 mmol/d is handled makes for interesting reading. I believe the same processes also handle the excess H+ produced by the foetus in pregnancy.


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What causes the yellow and brown spots on our sour cherry tree?
So at the end of spring (maybe at the beginning of summer) our sour cherry tree started producing these yellowish/brownish spots on its leaves. Can you help me identify the couse of this? What can we do against it? I cannot see any bugs on it, my best guess would be some kind of a fungus, but I am way far from being an expert. Thank you in forward for the answers!
Edit: I am located in Hungary. The brown spots are not bigger than my nails, but the yellow area can cover even the whole leaves. Also, the capillaries visible on the leaves can turn red, as you can see on the pictures. Unfortunately, the exact species of the cherry is unknown to me.

how rich is the soil? is do other plants get big or do they stay small and pale white, like for a limestone soil and sandy mineral soil? brown spots in plants is an indicator of phosphate deficiency. phosophorous deficiency also produces light veins. check a deficiency leaf chart. https://www.pinterest.nz/maryinnz/phosphorus-deficiency/ it could be something else. https://www.google.com/search?q=deficiency+leaf&tbm=isch

it may also be dryness. where I live, cherries go thirsty and have messed up leaves after june, but they come back strong again the year after. they are early summer plants in hot countries and keep sugar in the tree for next spring. it can be root damage also or top soil dryness or defficiency or other causes.

also to note is that there is an inviasive species on european cherries from aisa which is a bug which lays eggs in every single cherry and causes early cherry rot. perhaps hungary freezes enough in the winter to keep their numbers down. Asiatic cherry fly (Drosophila suzukii)

The tree is most likely sick. Plant diseases take years to develop versus diseases in animals caused by either bacteria, viruses, or parasites. This is because the tree has thick cell walls that can be a huge barrier hindering viral infection. Another thing is that trees lack a circulatory system and rely on partial water pressure from the air to draw water from the roots up to the leaves.
Your tree might have a virus that is slowly killing it. Which insects are endemic to your region? We can deduce the virus if we know the main types of bugs living in your area.


text:
Is there any record of an Albino (Not leucistic) peacock
Wikipedia says there are, however gives no source to one. Does anyone know if an albino peacock was ever recorded?

There is a breed of White Peacock. I could not find any record of 'Albino' Peafowls (the gender neutral term for peacock is peafowl (females are peahens). This white variety of peafowl is similar to how there are white chicken which have been bred over many years.
Albino animals do not produce the pigment 'melanin'. Albinism can be a dangerous trait in some organisms such as birds. The lack of melanin makes albino animals very sensitive to the sun's UV rays which can cause their vision to become impaired. Therefore most birds that are adult and white are usually either a variety of bird that is naturally white or is suffering leucism which is similar to albinism but does not remove melanin from organs such as the eyes.
But not all white birds are albino and not all albino birds are white. Just because the melanin pigment is non-existent in albino birds, doesn't mean other pigments couldn't still exist. Some animals don't even need pigments to achieve a certain color and do so instead by reflecting light in interesting ways.
It must also be noted that sometimes, white varieties of birds (or birds with leucism) are interpreted as albino and mistakenly presented that way online. This goes for other animals as well.

The rate of albinoism in mammals is roughly 1/10,000 births. However, for birds this rate is around 1/1764.
Abinoism has been reported in modern-day peacocks here: https://www.treehugger.com/albino-and-half-albino-peacocks-are-simply-stunning-photos-4858413
However, I did find a 1965 paper that has documented at least 99 peacocks from 8 different species being albino: https://sora.unm.edu/sites/default/files/journals/jfo/v036n02/p0067-p0071.pdf
So based off of the tree hugger photography post, the rate of albinoism in birds, and the 1965 paper looking at albino birds in North America, I would say albino peacocks do exist and are probably occurring more often than albino mammals.

Actually, the 1965 paper is about North American birds, and the 99 cases are of albinism are in the family Phasianidae, which is described as containing "Quail, Pheasants, and Peacocks".  Since Peacocks are not North American, probably none of those 99 cases were Peafowl.


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Large Alpine Hymenopteran Seen in the White Mountains
I was hiking in the White Mountains in New Hampshire, USA, and at the peak of Mount Eisenhower saw a number of large bee-like insects. They appeared to be nesting in a rock cairn, and were strikingly large---length was about 1.5" (~40mm). Weather was clear, sunny, about 65 degrees Fahrenheit. Time of year was early July. Environment was alpine tundra, a few hundred feet above the treeline. Besides the habitat and large size, they seemed like fairly typical bees (I'm saying bees because they were almost certainly hymenopterans, but didn't have the typical "narrow waist" of wasps). The abdomen was the longest part of the body. Behavior-wise, they flew in and out of the cairn, and often rested on the ground (or on backpacks, water bottles, etc). Does anyone know what species this may have been?
(I'm sorry I don't have any photos; even if species is impossible to determine without them I'd be happy for any information on possible family or genus)

Did you notice anything about their flying? Did they seem to hover and linger? Did the sound of their "buzzing" sound "off" to you (i.e., unlike a normal bee buzz)? If yes to these, then you most likely saw a bee mimic fly called a hoverfly. [I'm not sure if hoverflies vs bees are more likely to be above tree line in NH]....If you answer "no" to my above questions, any further information you can provide (coloration, detailed behavior, number of individuals, etc.) would be helpful.

@theforestecologist I don't remember the sound, but they didn't hover at all. There seemed to be about one or two dozen individuals out and about at a time, but they didn't swarm or gather in groups. Abdomen was dark, if I remember correctly. Again, most striking feature was the size: 1.5 inches long and maybe 2/3 inch wide.

@Sol you might want to visit bugguide.net and look at the Hymenopteran families Siricidae (horntails) or Cimbicidae (Cimbicid sawflies); what you've said so far suggests to me that one or the other of those might be the answer to your question.

@ArthurJFrost thank you! Looks like they were probably some sort of cimbicid sawfly

Looks like some sort of cimbicid sawfly. Thanks @ArthurJFrost !


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Under which conditions is human energy consumption minimized?
Including but not limited to:

body state

consumed food composition
state of the digestive tract
diseases
wounds
sleep
coma, etc.; death excluded

environment state

temperature
light
pressure, etc.

Merely curious. I do not expect to find complete answers, which seems impossible, but all insight is appretiated.

Hi there, I see you're new here, please check out the biology help center (https://biology.stackexchange.com/help) to find out what types of questions are supposed to be asked in the Biology Stack Exchange and edit your question accordingly (https://biology.stackexchange.com/help/dont-ask).
You have an interesting question, just needs some adjusting for this site. Feel free to separate this question into multiple questions after reading the links provided.

come in a warm environment sounds like the most likely factor. light and pressure are negligable. people that are starving also conserve lots of energy.

@com.prehensible Thank you for the insight. I am unsure however what exactly do you mean by your first statement; could you please explain?

coma, sounds like a pretty low energy state, in a warm environment!


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Why doesn't enzyme reaction rate rise linearly with substrate concentration?
This is the graph of the Michaelis-Menten equation which describes the relationship between reaction rate and substrate concentration:

I don't understand why it is hyperbolic. Intuitively, I would think that it would be linear.
Here is my logic for a specific scenario:
Let's say enzyme $E$ converts substrate $S$ at a rate of $1 S$ per second. Now let's say we have a container with 1000 enzyme E's. And there is a tube connected to the container that pumps in $10 S$ per second.
Logically, in the one second, all 10 substrates should be catalyzed. The rate of reaction would be $10/s$. Now if we increase the pump to 500 substrates per second, you would think that all 500 substrates would be catalyzed in one second, making the rate $500/s$. Thus, a linear relationship.
The formula for rate of enzyme-substrate complex formation is also linear:
$$\frac{d[ES]}{dt} = k[E][S]$$
What am I missing here? I am looking for a mechanistic explanation (diffusion, dissociation, etc)
Edit: I've done some more thinking and I have a potential explanation. Could it be that, as the concentration of substrate goes up, the probability of a substrate interacting with an unbound enzyme goes down.
In my scenario, the first substrate has a 1000/1000 chance to find a free enzyme, the second substrate has a 999/1000 chance of finding a free enzyme, etc.

Removed the comments here. If you want to answer the question, use the answer box please.

I also use the analogy of a drive thru for my students. if you have X drive thru windows increasing the number of cars puts more car through the drive thru up to the point until all of them are full at which point adding more cars does not move cars through the drive thru any faster. The closer you get to all the drive thru's being full the less adding more cars matters.

Disclaimer
This answer is a conceptual explanation, as appears to be the request, rather than a repetition of the derivation of the Michaelis–Menten equation, which I feel inappropriate, partly because it can be found elsewhere, e.g. in Wikipedia and Berg et al.. I appreciate that, like the derivations on which it is based, some of its assumptions do not always hold, or do not hold for all enzymes, and that some with an expert knowledge of enzyme kinetics will feel that it would be better to say nothing than present a conceptual simplification. Although I welcome corrections — I am not an enzymologist — but disagree with this point of view.
Summary
The reason that increasing the substrate concentration of an enzymic reaction does not increase the reaction rate beyond a certain maximum (Vmax) is that the reaction rate is dependent on the concentration of enzyme-substrate complex, not its rate of formation. Increasing substrate concentration only affects the reaction rate in so far is it affects the proportion of enzyme molecules involved in enzyme–substrate complex, which reaches a maximum when all of the enzyme is in such complexes.
More detailed explanation
The question presents a rate constant for only one of the reactions involved in an enzyme-catalysed reaction. In fact there are four that must be considered: the forward and backward reactions for the formation of a complex, ES, between enzyme (E) and substrate (S); and the forward and backward reactions for the formation of product (P).

The Michaelis–Menten treatment considers the initial velocity of reactions, at which time little product has formed so that it is assumed that the back reaction from product can be ignored, simplifying the situation to a consideration of the rates of three reactions:

A key assumption — the steady state assumption — in Michaelis and Menten’s original derivation is that there is that there is a considerable excess of substrate over enzyme so that the substrate is in instantaneous equilibrium with the ES complex. So, in effect, at a particular concentration of substrate the concentration of ES is constant. The implication in the question that the rate of formation of this complex would determine the reaction rate is incorrect.
The rate of the reaction depends only on the ES concentration and k2, the rate constant for the formation of products, also known as kcat, which is a characteristic of any enzyme and can be thought of as representing its catalytic capability:

d[P]/dt = kcat[ES]

What the substrate concentration does affect is the position of equilibrium for the formation of ES from E and S, i.e. how much enzyme is converted into complex. However there is obviously a maximum, approached asymptotically, equivalent to the total enzyme present. This explains† the hyperbolic nature of the curve for reaction rate.
The concentration of substrate needed to reach this saturation (more easily measurable as that to achieve half maximum initial velocity) is another characteristic of the enzyme (and substrate) and can be thought of as reflecting the affinity of the enzyme for substrate (the dissociation constant). The hyperbolic nature of the rate curve is similar to that for binding of small molecules to non-catalytic proteins such as the oxygen-carrier, myoglobin, and hormone receptor proteins.
Just as not all proteins in this latter class (e.g. haemoglobin) show simple hyperbolic binding of their ligand, so not all enzymes (e.g. allosteric enzymes) show hyperbolic kinetics. But that’s another story, which has been told many times on this site.

† I have given a more extensive explanation of the hyperbolic nature of the curve in an answer to a previous question, which I must admit I had forgotten about.


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What species is this interestingly colored brown moth
This fella fluttered into a kitchen at night, maybe from the vegetation in the yard, and I got lucky to trap it in a transparent plastic bag for a while (with enough room to move, which it started doing at about the same pace it had been flying before but sometimes sitting still) so I got a couple of close-up pictures.
I think the coloring and some other features are too far off the familiar plodia interpunctella to be the same species, also a number of other features seem different in appearance and behavior. (Wings not folded straight back and much wider, doesn't like sitting still on wall for extended period of time.)
Length is about 12-13 mm (wings included and folded). It also sat down wings spread out very wide where I first found it (no picture of that posture included).
Location: Southern part of Germany, city landscape with river/lake within half a mile
What species is this and what would it live and feed on (if the adult feeds at all in this species) ?
As it was examined bottom up, I noticed a contracting and expanding movement of the abdominal segments (roughly last 2 images). What is that movement?

It could be Pyralis farinalis, the meal moth. It is a cosmopolitan moth of the family Pyralidae. Its larvae are pests of certain stored foods, namely milled plant products. I don't think it's adults feed as they do not live long after mating.
Here is a link to its Wikipedia article:Pyralis farinalis


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About how many covid-19 virus particles is required in the human body before infection and sickness follows?
Our immune systems are often able to destroy germs and virus particles.
About how many of them does it take to make a 70 year old healthy male sick ? Any ideas ?

To the best of my knowledge, we don't yet know the infectious dose of the SAR-COV-2 virus in humans. In theory, it only takes one viulent virus particle to start an infection. In practice, it's pretty hard to measure, Published estimates of infectious dose for any pathogen don't often account for differences in age or sex, per se, so it's hard to address that part of your question.
Most of the estimates of SARS-CoV-2 infectious dose I've seen are essentially experts handwaving based on previous coronavirus outbreaks. I'm not saying they're useless, but they aren't necessarily empirical. For reference, there's a perspective article here, with a section discussing infectious dose. They cite an estimate from the 2003 SARS outbreak of 280 particles to cause infection in 50% of the exposed population (ID50). They also point out that this is similar to the ID50 for other animal corona viruses and the common cold in humans.
There's no guarantee that SARS-CoV-2 will be the same, but it's likely to be in the same ballpark.
Referenced:
Imke Schröder, J Chem Health Saf. 2020 May 11 : acs.chas.0c00035. Accessed via PubMed Central, PMCID: PMC7216769

Good research article MikeyC .


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What are " temporal kinetics"?
I am new to Biology and I am reading some papers about kinase proteins. I know what kinases do in the body. However, I found it hard to understand what are "kinetics". I googled this term but it seems it is a general term and I couldn't understand it.
I came across the following sentence in a paper, and I am not able to understand it:
"many substrates of a given kinase have similar temporal kinetics"
I know what "substrates" and "kinase" means. But I don't know what "temporal kinetics" means here.
I appreciate the chance if somebody let me know the meaning of "temporal kinetics".
Thanks

The word "temporal" is unusual and is superfluous as regards kinetics. Kinases are enzymes, catalysing reactions, so in this context kinetics (Greek kinetikos: moving, putting in motion) refers to enzyme kinetics — the study of the rate of chemical reactions  in the specific case of those catalysed by enzymes. Studies involve examining the effect on the reaction rate (substrate converted in unit time) of concentration, temperature, time itself, type of substrate, regulatory molecules etc. They can be used to test models of enzyme mechanism and cellular function and in bioengineering.

I have voted to close your question as it is very basic and is readily answerable from text books, even though you seem to have been unable to find it on the web. Here is a link to a section from a biochemistry textbook that provides an introductory, if mathematical, treatment of the topic.

Temporal kinetics does not refer to the kinetics of kinase phosphorylation reactions and, since it is not standard terminology, you likely wouldn’t find its meaning in any textbook.
The authors of the paper quoted in the question use the phrase temporal kinetics to describe the phosphorylation state of a proteome-wide selection of kinase substrates (ie phosphorylation sites in proteins) over time. The general idea is that since one kinase can phosphorylate many substrates, clustering substrates based on their temporal kinetics (ie the times at which they become phosphorylated or dephosphorylated) can help identify the kinase and signaling pathway involved.
Fig 6B in the paper (shown below), for example, illustrates how 3,178 phosphorylation sites can be clustered based on the time-course of their phosphorylation and/or dephosphorylation after treatment of mouse adipocytes with insulin. As discussed in the paper, each cluster can be associated with one or more kinases based on known kinase-substrate interactions.


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Why is this Cuscuta compacta purple?
I was recently browsing the web and came across this site abut the compact dodder.

https://gobotany.nativeplanttrust.org/species/cuscuta/compacta/
The image used to identify the plant shows it as purple. This struck me as odd, as those are usually a greenish-yellow. Why is this plant purple? Is it a special sub species? Is it perhaps another type of dodder entirely, and gobotany simply messed up? I think this image might actually show the Cuscuta glomerata, but I'm not sure. Please explain this discoloration. Thanks in advance!

Is this another gold-white/blue-black dress moment? I dont see any part of the plant in the foto as purple. The ground in the background is blue. My brain interprets this as photo being taken in havily purple tinged lighting, posibly grow lights. My brain performs sort of light balance and the plant appears to me yellow/brown (fruit) and green (leafs). Only part that seems slightly purple is the leaf underside. What part of the plant do you see as purple?

the Genus Cuscuta has over 200 species varying in color from yellow, to orange, and purple (sometimes but rarely can also be green).
The organism in the photo is not likely to be a subspecies of the usual dodders you find in your area, instead it is likely to be a different species entirely (while still belonging to the same genus).
The rope dodder (Cuscuta compacta) is very possibly the species you are looking at. However, I am also convinced that Cuscuta europea is a possible candidate, particularly due to this photo of the species that I got from the European Nature Information System (EUNIS) web site:

I must admit that I do not know nor have access to photos of all the different species of the Cuscuta genus to make a truly objective analysis of your image however I hope this information as a minimum leads to some new insight on the matter.


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How do ribosomes interpret stop codons as selenocysteine and pyrrolysine?
How does the protein synthesising machinery determine that UGA and UAG in mRNA should be decoded as selenocysteine and pyrrolysine, respectively, in certain circumstances, rather than as stop codons?

Summary
Reassignment of an UGA codon as a selenocysteine codon is thought to involve the interaction of obligatory secondary structure elements called selenocysteine insertion sequences (SECIS) with the dedicated translation elongation factor that presents a unique tRNA aminoacylated with selenocysteine to the ribosome. However the location of these elements and their specificity differ between prokaryotes and eukaryotes. Less is known about the less common reassignment of UAG to pyrrolysine, but some organisms may employ similar mechanisms to those involving selenocysteine, whereas others may almost completely avoid the use of UAG as a termination codon.
Preliminary — Presentation of selenocysteine to the ribosome
Although the question specifically relates to the translation of erstwhile termination codons, it is worth mentioning how selenocysteine (Sec) is presented to the ribosome.
     In most species a specific tRNA — tRNASec — is aminoacylated with serine catalysed the standard seryl-tRNA synthetase. The Ser-tRNASec is then converted to Sec-tRNASec — in Escherichia coli, by the product of the SelA gene.
    Whereas all other charged elongator tRNA species are brought to the A-site of the ribosome by the same elongation factor (EF-Tu in prokaryotes, EF-1 in eukaryotes), there is a specific elongation factor for binding Sec-tRNASec.
Reprogramming UGA codon as a selenocysteine codon
The reprogramming of UGA as a selenocysteine codon requires a stem–loop secondary structure — the SECIS — in both prokaryotes and eukaryotes. However there are differences in how these operate. Quoting from a Nature News and Views piece written in 2007:

In bacteria there is a site-specific recoding signal embedded in mRNA that flags a nearby UGA codon as encoding selenocysteine rather than stop (Fig.b). In other organisms, ranging from worms to mammals, a recoding signal located outside the coding part of the mRNA (Fig.c) signifies that all UGA codons in its mRNA specify selenocysteine (one essential human mRNA has ten UGAs).

The mode of action  of the SECIS elements is envisaged as interaction with the Sec-tRNASec-specific elongation factor, as in this illustration from Ch 13 of Molecular Biology by Clark et al.:

A shortcoming of this cartoon, is that it fails to show that in prokaryotes the SECIS element encompasses the UGA codon. This is important as it may indicate that  termination factors are prevented access to the UGA by secondary structure, which the Sec-specific elongation factor is able to unwind. (In eukaryotes there may UGA codons may also be made inaccessible by local secondary structure.)

However sequence context effects have also been suggested.
Pyrrolysine
The situation for pyrrolysine (see, for example, Ambrogelly et al. (2007)) differs from that for selenocysteine in that it is synthesised before it is charged to a specific tRNAPyl in a reaction catalysed by a specific pyrrolysyl-tRNA synthetase. The reassignment of UAG to pyrrolysine was thought to involve a change (or almost complete change) in the genetic code of certain archaea in which it is found, with UAG not or rarely being used as a termination codon. However, according to the Nature News and Views article aleady cited, this is not the case for other organisms, in which I am unaware of the mechanism of reassignment.

In bacteria during translation what happens to the codons present downstream to the SECIS sequence? Can the ribosome easily skip over that sequence to the remaining codons?

@trinitrotoluene — The orthodoxy is yes. Once a secondary structure is unwound the ribosome keeps it apart. This was deduced early on from studies of the translation of small RNA phases, where one AUG could only be translated if other parts were displaced. Although far more sophisticated techniques are available to follow translation today, I’m not aware that they have been used for this problem. But I haven’t trawled through the recent literature. I may check it out in the next few days.

Ok, thank you so much. Just a few more follow up questions. After the SEICS element is unwound is it also translated? Do Bacteria need one SEICS element for each UGA codon?

@trinitrotoluene — If the SEICS element containing a Sec UGA is unwound, sure, it will continue to be translated until it gets to the “real” stop codon. And yes, unlike eukaryotes, bacteria appear to need a SEICS element for each UGA.

Ok, thanks for clearing my doubts.


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How can I detect which antibody is produced by the B cell?
In the primary immune response, IgM is produced (in addition to IgD ). In the secondary immune response, various types of antibodies are produced.
So how do I detect which antibody a B cell is producing at a particlular time?

The major antibody in the second exposure is IgG and in the first exposure it is IgM. IgG and IgM would be produced by Plasma Cells, which are effector B-Cells activated by Cytokines.
If you want to see which antibodies (not just antibody types) are produced by the B-Cell, I would suggest transforming a GFP gene into a Naive B cell and using a Restriction Endonuclease and DNA Ligase to insert the GFP gene to the 5'-end of the Constant (C) region of the Antibody producing gene. Then, you could see which Antibodies are produced by B-cells since the Antibodies would fluoresce.
Note: I am currently in high school so I don't have much experience with Immunology, so there might be a few things wrong about my answer. However, I tried my best to answer the question. Hope this helps!!


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If Covid antibodies disappear after 2-3 months, will a vaccine still be effective?
It looks like there have been studies in China and also in Spain that suggest antibodies don't last very long or could disappear after some time. What does this mean for the effectiveness of a potential vaccine? Could the effects wear off after a few months? Is this different from other diseases we get vaccinated for? I know we need to update the flu vaccine every year, but I thought that was due to mutations in the virus, not from antibodies breaking down. I am not a scientist, can anyone ELI5?

Humans don't constantly produce antibodies for a pathogen when the pathogen has been gone for a while. They just store the 'recipe' for making the particular antibody in memory T cells.
If the antigens that the virus contains mutate enough to not work for the antibodies an immune person has developed. Then the process starts over and the immune system will have to 'create a new recipe'.
Each new host creates a possible scenario for a coronavirus such as the current SARS-CoV-2 to mutate and develop different antigens that may cause a second wave requiring humans to develop new antibodies in our immune system and new vaccines to be distributed.
Though coronaviruses do not mutate as quickly as other viruses such as the influenza virus. It is still possible that SARS-CoV-2 having caused such a large pandemic, may develop a new strain.

As far as I have followed the papers, the genetic stability of SARS-CoV-2 seems pretty high. Can you please add some ressources to back your claim?

Thank you! This is so helpful. So vaccines help create memory T cells. But why would normal antibodies not be stored in T cells? Are they only activated when there are a certain number or strength of virus?

When a recognized virus has been detected by the immune system, the memory T-cells multiply into more memory T-cells as well as plasma B cells which are able to actually use the 'recipe' to produce antibodies that flow freely in the blood and neutralize their target antigen. For each immunity you have developed, you have specific memory T-cells that store the 'recipe' for that one antigen. eventually over a long amount of time these memory T-cells may die which is why people need to take a tetanus vaccine around every 10 years (as an example)


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How can protein allergens be passed from mother to baby via breastmilk is proteins are broken down after ingestion?
All over the Internet new mothers are urged to avoid dairy products, a slew of vegetables and even beef if their child displays symptoms of reflux.
In the case of dairy, for instance, it is said that an allergic reaction can be caused by specific proteins that exist in cow's milk.
What I don't get is this: aren't ingested proteins broken up into their constituent amino acids, which are then recombined, presumably somewhere in the milk-producing glands, to create new proteins that are then passed on to the child through the mother's milk?
If that is the case, the original, allergy-inducing proteins should be long gone by then, right? If that is indeed the case, then what is causing the allergy and is there an allergy in the first place or could the cause be something else?

What means "all over the internet"? The usual unscientific websites which claim nonsense? Or are there credible scientific reports?

Well, I try to avoid obviously pseudo-scientific sources, but even the NHS has a web page that states that cow's milk in the mother's diet can "rarely" be passed on to the child through best milk.


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Are intestinal and pancreatic lipases different?
For explaining the action pancreatic lipase, my book wrote this equation:-
$$fat\space particles + lipase\rightarrow fatty\space acid + glycerol + lipase$$
But for intestinal lipase, my book has a different equation:-
$$fat\space particles + lipase\rightarrow monoglyceride + fatty\space acid$$
So, did my book make a mistake or are intestinal and pancreatic lipases different?

Does food enter the pancreas? Where do pancreatic enzymes act?

Pancreatic lipase and intestinal lipase are almost same in their functions. In the intestine, the name of the lipase is a triacylglycerol acyl hydrolase it also called colipase dependent lipase or Pancreatic lipase,  Free fatty acids, and 2-monoacylglycerol are the primary products of lipid digestion in the jejunum. and Pancreatic Lipase also produces Free fatty acids and 2- monoacylglycerol.
so we can say that both enzymes are almost same and produce the same products.
Sources Lippincott's Illustrated Reviews Biochemistry 5th edition Chapter 15


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Is there alternation of generations in animals other than cnidarians?
Are there other animals besides cnidarians that exhibit alternation of generations (having distinct sexual and asexual life stages)? If so, what are these animals? Further, why do so few animals have this kind of life cycle? What are the evolutionary advantages of such a life cycle, and why are cnidarians emphasized in zoology?

Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Also note that you are using alternation of generations differently from any usage I have ever encountered. I encourage you to change this to avoid confusion.

According to Wikiwand the heterogamy occurs also in:

some aphids
several rotifer species
Daphnia (freshwater crustacean)