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How many fruit flies from a single banana, and what is the bottleneck?
Suppose I start breeding a fruit fly population on a single rotting overripe banana which weights 100g, in an isolated container. The fruit flies don't have access to anything else, though ventilation is provided. Bodies of dead fruit flies are immediately removed from the container.
How much of the weight of the banana will eventually be turned into fruit flies?
Which banana ingredient/ingredients would likely be a bottleneck?
(What I mean by the "bottleneck" is that perhaps there is enough sugar for 90g of fruit flies but there is only enough cobalt to make 5g of fruit flies. If indeed in an experiment  we would get only about 5g of fruit flies, then I would say that the amount of cobalt in the banana is likely a bottleneck.)

highly doubt you may even get any biomass conversion since bananas are very low in protein (essential for fruit fly growth). around 0.74g out of 100g. https://fdc.nal.usda.gov/fdc-app.html#/food-details/1105314/nutrients

@ansh tandon i'm not sure the amount of proteins in a banana is directly relevant - pls see my comment to the answer of haley weiss below

If we look directly at the energy available and nothing else, the rough estimate we can find is that animals can turn ~10% of the energy they consume into body mass. The rest of the energy they take in is lost through inefficiencies in digestion, moving around, and the energy needed just to stay alive. This is called ecological efficiency. In reality, it differs between lifeforms and can be a few times higher or lower than 10%, but it's a good enough estimate.
Going online, we find that 100 grams of banana has around 89 calories. Insects are a bit more calorie dense, and we can actually find good values for fruit flies! They are roughly 5.12 calories per gram of mass. Putting it all together, this gives us a maximum of roughly 8.9 calories stores as insect flesh, at 5.12 calories per gram, is roughly 1.7 grams. If a single D. Melanogaster weighs 1 milligram, then that gives us a maximum of 1,700 fruit flies! But that is a maximum that doesn't take into account nutrition.
A banana is mostly sugar and fiber, animals are primarily protein and fat. If we look at a banana's nutrition fact sheet and compare it to the fruit flies, we can see a huge difference between the two (I have posted links below). They have an equal amount of water, so they should be fine without anything to drink. The amount of proteins and fats in 100 grams of banana is only around 6% of what you'd find in the same amount of fruit fly mass though. That's still enough for 6 grams of fruit fly mass though, or around 6000 flies. What really brings us down is sodium. Animals need sodium for neurons and other processes, but it's a lot less necessary for plants. Bananas have almost none of it. A banana only has 0.2% of the sodium in it that a fruit fly does. This brings the maximum number of flies down to 238.
That still feels like a lot of flies to me, so there might be some other minerals and nutrients that I haven't considered here. I'm not sure, but I'm willing to guess that 238 flies is somewhere within an order of magnitude of the correct answer.
https://fdc.nal.usda.gov/fdc-app.html#/food-details/173944/nutrients
https://www.researchgate.net/figure/Nutritional-value-of-fruit-flies-of-species-Drosophila-melanogaster-and-Drosophila-hydei_tbl1_340395391

Good answer. I'd consider the degradation process in there too - the banana will rot before the flies can eat it all.

nice find with sodium, I'm not entirely sure about fats and proteins even if there was less than amount for 6000 flies - according to wikipedia fruit flies mostly eat microorganisms and sugars, so they don't seem to need to consume proteins and fats from a banana directly. (also a minor issue is if even with limited sodium, perhaps they could still procreate, albeit new flies would be "sodium deficient" but not to the extent of being completely unviable, at least for a few generations - something like this happens e.g. with cobalt in some animals)


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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.

source: Stack Exchange

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Why is exercise good?
The fact that exercise is healthy is a bit counter intuitive to me. If we have any machine, a car for example, the less we use it the longer it lasts. Then how is it that using our body to do sports, to a reasonable amount, lead to longer or healthier life?
My guess is that lack of activity might resemble starvation no matter how much food we consume. Then the body instead of repairing itself tries to save energy as much as it can. Are there any other ideas to explain why exercise is good?

Re "the less we use it the longer it lasts", this is simply not true.  Machines do degrade from not being used: lubricants harden up, corrosion takes place, &c.  See e.g. "ramp rot" in airplanes, or "barn find" in cars.  OTOH, a well-maintained machine lasts longer than a neglected one: I personally fly a plane built in 1966, and drive a 1988 truck.

This question, as formulated, doesn't have a good scientific answer.

There is a similar question and answer here: https://health.stackexchange.com/questions/16786/how-does-exercise-improve-health

You may want to look into Hormesis. However, the idea that exercise works via (mitochondrial) hormesis seems controversial.

As jamesqf points out in comment, "the less we use it the longer it lasts" isn't always true even of machines. Sometimes if a machine isn't used, the moving parts start sticking together through rust or other decay processes, which does not happen when the machine is used and the moving parts move regularly against each other.
Another example that comes immediately to mind is a hybrid car, which needs to be driven regularly or the battery runs out. Granted this doesn't affect the car's longevity (I think?), but it is another example where use maintains functionality better than disuse does.
This is even more true when we actively maintain machines, fixing them as they break, replacing parts, oiling, etc.
The key point here is that decay is inevitable. It is a law of thermodynamics, and it doesn't care whether something is in use or not. Granted, things will sometimes decay faster if they're used, but not always, and they'll always decay either way. The only way to forestall decay is active maintenance. This isn't contradictory with decay being inevitable, because you can actively maintain something only for so long (it takes work and energy).
This is relevant to biological system because that is how our body works: it is constantly self-repairing and self-maintaining, for the length of the person's life. One reason we die is that it stops doing so as efficiently as one ages. But as long as we are living, these processes mean our bodies aren't a static object: they are a dynamic system that is constantly reacting to outside and inside stimuli. And that system, including the self-repair mechanisms, are set up such that they work best within a certain range of motion and activities. It so happens that range doesn't include "no motion or activities". Likely because we evolved as an active species, so being able to function efficiently when active is useful, and some of the things that make us able to function efficiently when active can cause some harm when we aren't. For example, we store fat in order to use it when food isn't available and as fuel for effort, but if too much of it accumulates it has effects on hormones and inflammation that our bodies don't deal with well. Another example is how our muscles waste away when we don't use them; this is useful for an active species that needs the muscles it uses and shouldn't waste energy and protein on those it doesn't, but an inactive species might be better off conserving its muscles through periods of inactivity, so that they would still be capable of moving well those rare times they do need or want to.
Having said that, look at high-level athletes getting injured, getting early arthritis, etc... It is possible to exercise more than the body's self-reparation abilities can handle, and that also leads to health problems down the road.

Do you have a particular source that maintenance activity is (roughly) an inverted U-shape with respect to stress?

@qeschaton: I'm not sure I made a claim that precise; indeed I don't think I said anything more precise than that a lack of activity/exercise is not very healthy, some amount of exercise/activity is healthier, and a sufficiently-high amount of exercise/activity can be harmful. Is that what you want a source on?

I'm interested in a source for "And that system, including the self-repair mechanisms, are set up such that they work best within a certain range of motion and activities." The more quantitative the better.

I don't have a source for that, I was working from the general principle that systems that work, have certain circumstances under which they work more or less well, and the most basic distribution of those circumstances is a bell curve, and that happens to fit the overall picture here. For quantitative sources of how that applies to the human body, any quantitative source will involve a very specific subset of the question, like the relationship between some specific form of exercise with a specific health outcome. But I can look and see if I find anything.

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gene manipulation books for beginners
Are there any introductory book to explain gene manipulation in yeast for non-biologist?
I had a look at this book and now I have some ideas. I like to read another book at the same level which is more applied/practical. I find this book chapter useful too, but I find it a bit more difficult to follow. Also video lectures are appreciated.

What do you mean by gene manipulation? Do you want protocols for yeast transformation?

For example, as I understood there is a plasmid which is a circular DNA. We introduce this plasmid to yeast so that the plasmid with its marker replace the desired gene. To achieve this we need to look at the flanking side of the gene to be deleted. So the plasmid must have these flanking parts. But how do I design the plasmid in for example snapgene software and how do I construct the plasmid say with PCR or other methods? After I make the plasmid then I can follow some protocol to do the transformation.

I think the information you are looking for would be contained in a genetic engineering book. not only for yeast but all eukaryotic and prokaryotes cells. I'm afraid that there will not be a book on that topic for a non-biologist but the topic is usually covered during Bachelor/Master studies.

I think that the information you are looking for could be covered on this website:https://www.addgene.org/protocols/
Not only has addgene a protocol section, it also has an education section for understanding the concepts of genetic/molecular cloning: https://www.addgene.org/mol-bio-reference/
The material is for biologist, but should be relatively easy to understand for you are starting.
They also have a nice ebook which should cover some of the topics you asked: https://info.addgene.org/download-addgenes-ebook-plasmids-101-3rd-edition
Hope that helps!


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Should there be a distance between the terminator of a protein with the promoter of another one?
I want to do an overlap PCR to get the desired gene product I want. Can I put the promoter of the second protein just after the terminator of the first protein, or should there be some distance between them filled with random bases?!


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DNA damage theory of aging and sex
If aging is due to accumulation of damages in DNA, then shouldn't the DNA in gametes also be damaged and so the next generation should be borne old! How does gametes avoid this DNA damage accumulation?

I've answered a related question, which was wondering why older people get more cancer from accumulated DNA damage and yet their children aren't immediately susceptible to it, here:
https://medicalsciences.stackexchange.com/questions/19915/why-do-age-related-dna-transcription-errors-not-manifest-in-children-as-readily/
Quoting from my answer there:

...a parent does not pass on all their mutations in all their cells, they pass on just one, which need not have any deleterious mutations at all, even if the parent has cancer themselves in some other part of the body.

If that one cell is defective in some way, it is less likely to be involved in creation of a successful pregnancy, and may lead to miscarriage. Therefore, the probabilistic process of reproduction tends to result in offspring from selection of healthier gametes.

There are in fact mutations that accumulate in gametes, but if any of those mutations are very serious, they are unlikely to support development of an entire new organism, and they are also relatively few. The burden of age on the genome is spread over all the cells in a body, and worst in types of cells that divide the most, when errors are most likely to occur.

Yes and no. Your concept about DNA damage causing aging is good. But aging is caused by DNA damage that causes the biologic / signaling pathways to not work as well as they once did. Think of biophysics and interactions among the plethora of proteins, molecules, etc. in your cells and tissues and all of the interactions therewith where even the electronic charge + vs -  and quantity of molecules (charged or not) in a vicinity influences the effectiveness of a biological pathway etc. This is aging. Basically, if you have learned about development biology at the molecular and cellular levels, you would know that much of that is not yet developed at the gamete stage. Therefore, there's not a whole lot of aging that can be had at the gamete stage because there's frankly nothing going on just DNA damage. Granted the DNA damage can influence on a grander scale as Bryan points out above - life or death (rather non-life) or the imposition of birth defects and other serious issues - but this is not how we define aging even if they are somewhat conceptually related. In short, aging is caused by the inefficiency and impairment of otherwise optimal (at birth) biological processes that slowly decay over time (silent mutations, environmental impositions, etc. that cause biophysics-based alterations at the smallest scale that impact exponentially as magnified over multiples of molecular interactions across a grand array of biological pathways and other molecular/cellular interactions).


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Effect of increasing Extracellular Na+ Concentration on resting voltage and likelihood of an action potential of occuring
If you increase the extracellular Na+ concentration how will this effect the resting voltage and likelihood that an action potential of will occur?
Please explain using the Goldman–Hodgkin–Katz voltage equation if you have that understanding.  I can typically understand mathematical functions and relationships.
My guess is that the membrane will become more hyperpolarized and the likelihood for an action potential will go down.  I have read some explain otherwise and I would like help confirming or denying my current understanding.

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How close is the U.S. to herd immunity, assuming long-term immunity?
Assuming:

infection always results in death or immunity (unproven, but no evidence of repeat infections yet)
official COVID-19-related death counts are accurate (142k at the time of this question)

How close is the U.S. to achieving herd immunity to COVID-19?
The CDC has published estimates of infection rate, mortality rate, etc. However, I haven't yet seen anyone actually do the math of how close the U.S. is to herd immunity.

You need to infect 60-80% of the population. So: Far, far (any many deaths) away.

I’m voting to close this question because it is not about biology in the terms of SE Biology but a request for statistical information about the medical state of the population in a particular country which will be out of date next week.

You are very welcome to SE Biology, but please read the [tour] where you will find what sort of questions are suitable here. There is a list of sources of information about coronavirus in answer to one of our Meta questions, or your question may be more acceptable on SE Medical Sciences.

@David I understand your criticism, but you are applying it very inconsistently, as many other answers are tied to particular "current" timeframes and events. https://biology.stackexchange.com/questions/94024 https://biology.stackexchange.com/questions/90793

I am not applying it inconsistently, thank you. I voted to close each of those questions and downvoted them. I was responsible for the Meta post (later adopted as a Community post) aimed at deflecting such posts in a more appropriate direction. The fact that sufficient others did not support me makes no difference to whether or not my view is correct. My reading of the Tour and Help for this site gives me no reason to believe it is not.

The CDC estimates R0 to be 2.5, meaning that (2.5-1)/2.5=60% of the population must be immune to achieve herd immunity.
(That is, under 60% immune and the # of cases will increase; over 60% immune and the # of cases will decrease.)
The estimated IMF (infection mortality rate) is 0.65%.
So 60%*0.065%=0.39% of a population will die to reach herd immunity.
To date, 142k people in the U.S. have died from COVID-19, out of a population of 328M. So 142k/328M=0.043% of the population has died.
Thus, based on reported deaths, the U.S. has 11% of the required infections/immunity to produce herd immunity.

Note that this assumes that high- and low-risk individuals are exposed at the same rate. If more of these infections happen among low-risk individuals, the effective IMF is lower, yielding fewer deaths to produce herd immunity. And the inverse is also true.

I am curious why you are using the SE Q&A format to post your calculations on SE Biology.  Would I be allowed to tell Stack Overflow about the current stock market price of computer chip companies or the percentage of European networks that depend on Huwai?

Paul, perhaps you should generalize your question, e.g. to be about how one can find out how close a country is to reaching herd immunity.  Then your answer can be modified a bit to explain how to calculate and use current U.S. numbers (showing how they were found) as an example.

@mgkrebbs I feared that would be too broad. FWIW, StackOverflow would be an odd choice for your computing cost question, as SO is  focused on software, but people can and do ask such questions on ServerFault.


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is there a limit to how much humans can taste?
kind of a weird question, sorry, but i was wondering--is there a threshold at which our taste buds become overwhelmed? if i, say, put some supersweet compound in my mouth, would there be a point at which adding more compound would not increase the level of sweetness i perceive? i'm sure that if i experienced too much sourness or spiciness, my tongue would probably go numb, but what about sweetness and bitterness? and what is that amount? does it vary from person to person, or are people's opinions on different sorts of food just preferences, and the threshold at which they become unable to process more of a specific taste the same for everyone?
thank you. i hope this makes sense.

Have you done any research by yourself?

no, i felt like i couldn't word my question such that a search engine would understand.

Yes, there is a threshold of taste.
According to this article

The taste system encodes information about the quantity as well as the identity of stimuli. In general, the higher the stimulus concentration, the greater the perceived intensity of taste. Threshold concentrations for most ingested tastants are quite high, however. For example, the threshold concentration for citric acid is about 2 mM; for salt (NaCl), 10 mM; and for sucrose, 20 mM. Since the body requires substantial concentrations of salts and carbohydrates, taste cells may respond only to relatively high concentrations of these essential substances to promote an adequate intake. Clearly, it is advantageous for the taste system to detect potentially dangerous substances (e.g., bitter-tasting plant compounds) at much lower concentrations. Thus, the threshold concentration for quinine is 0.008 mM, and for strychnine 0.0001 mM. As in olfaction, gustatory sensitivity declines with age. Adults tend to add more salt and spices to food than children. The decreased sensitivity to salt can be problematic for older people with electrolyte and/or fluid balance problems.

Interestingly,

In fact, all of these tastes can be detected over the full surface the tongue. However, different regions of the tongue do have different thresholds. Because the tip of the tongue is most responsive to sweet-tasting compounds, and because these compounds produce pleasurable sensations, information from this region activates feeding behaviors such as mouth movements, salivary secretion, insulin release, and swallowing. In contrast, responses to bitter compounds are indeed greatest on the back of the tongue. Activation of this region by bitter-tasting substances elicits protrusion of the tongue and other protective reactions that prevent ingestion

And in most of the individuals, this threshold is same for both right and lefts parts of the tongue.
Reference
Now as stated by the first article, taste threshold depends on the age of the individual.
More interestingly, it also depends on the individual's state of mind, i.e. whether depressed or anxious.

Circumstances in which serotonin (5-HT) and noradrenaline (NA) are altered, such as in anxiety or depression, are associated with taste disturbances, indicating the importance of these transmitters in the determination of taste thresholds in health and disease.

Measurement of taste function in healthy humans before and after a 5-HT reuptake inhibitor, NA reuptake inhibitor, or placebo showed that enhancing 5-HT significantly reduced the sucrose taste threshold by 27% and the quinine taste threshold by 53%. In contrast, enhancing NA significantly reduced bitter taste threshold by 39% and sour threshold by 22%.
Reference

Hence threshold value varies from substance to substance as well as from individual to individual.
Here is a good article giving threshold values of different chemicals in various food items.
Hope all your questions are solved :)

thank you so much!!!!

@mye Welcome to Biology SE. You should always give an upvote atleast or accept the answer, if you are satisfied with the answer; so that it will encourage other users to answer your questions


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Is this a bed bug skin?
I found this bug skin on my friend’s couch. Is it a bed bug? Could it be any other bug?

Here is a photo.


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Genotypes without Recombination
When given that the parent generation's genotypes are linked traits, how do you determine the genotypes of the F1 generation when no recombination has occurred.  For example, given the parents BbNn and bbnn what would be the expected genotypes of the F1 generation to be?
My current understanding is to follow Meiosis and separate the homologous pairs into Bb Nn and bb nn. Then, because no crossover is occurring, my guess would be that the daughter genotypes are BbNn and bbnn.  However, in reality, the answer should be Bbnn and bbNn.  Am I doing something wrong?  How would I draw the related chromosomes?

My current understanding is to follow Meiosis and separate the
homologous pairs into Bb Nn and bb nn.

No.  If the alleles are linked, then you either have one chromosome with BN, and the other with bn, or you have one chromosome with Bn, and the other with bN.  From this information alone, you can't know which.  Your answer assumes the first situation is how the alleles are linked, the given answer assumes the second.

So.  Just to make sure I'm following, the link could either be BN and bn or Bn and bN but it is impossible to know which.  Thus, either answer would be correct?  If not, how you would you know which way the linking is taking place?
Note:  I am studying from the following practice set if you would like to see the original question text:  https://ocw.mit.edu/courses/biology/7-01sc-fundamentals-of-biology-fall-2011/genetics/linkage-and-recombination-genetic-maps/MIT7_01SCF11_3.2sol1.pdf

It's impossible to know which given only what you posted.  If there's more information, that would change things.

@hhghh You can often figure out the gametic phase of BbNn parent from genotypes of its parents. Sure enough, this information is included in the link you provided. By omitting it in your question you have rendered your question unanswerable.

Ah.  Okay.  Could you elaborate more on how you would do that?  I'm not 100% sure I understand.  Sorry.  So the parents of BbNn are BBnn and bbNN.  From this, how would you determine how linking is taking place?


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Why don't the cell organelles settle down in the cell under the influence of gravity?
In cuboidal or columnar cells or cells of any other shape the nucleus and the other organelles and inclusions remain suspended in the cytoplasm. Why doesn't gravity affect them ?
Could this be because all organelles are of colloidal size ?
Or is it the result of being held in position microfilaments and other cytoskeletal structures that facilitate cytoplasmic streaming ?

It's the cytoskeleton - cells are surprisingly full of it.

okay thanks....got it


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What is Lysoferrin?
I was going though my Guyton and Hall Medical Physiology when I came across the name of an antibacterial lysosomal enzyme - Lysoferrin. It said that Lysoferrin "binds to iron and other metals that are essential for bacterial growth." I looked across the web to find some context about it but found every site quoting the exact same Guyton lines. Some more information about this enzyme would be a real help.

Have you looked to see if your text provides any primary references to their claim? I'm wondering if this is just an outdated term for something else. From the description, It sounds a bit like Lipocalin-2. Lactoferrin and Ferritin are also iron-binding proteins that can be unregulated during infections, but they both serve other functions in maintaining iron homeostasis.

A Japanese patent filed by Raymond Jay Bergeron, Jr JP2000514089A notes lysoferrin as the siderophore
N1, N4-bis (1-oxo-3-hydroxy-3,4-dicarboxybutyl) diaminobutamate. The US counterpart of this patent, jointly filed as US application No. US08/783,306 and later issued as US 5,739,395 covers rhizoferrin in its embodiments. So it seems that the term lysoferrin is just another name for rhizoferrin, perhaps a translation aftefact?
Rhizoferrin Drechsel, H. et al.  (1991) Biol. Metals 4:238–243 has the following structure .
Edit: Just to be clear, lysoferrin is not an enzyme, but the siderophore pictured above.
Here’s from Wikipedia:

Siderophores are small, high-affinity iron-chelating compounds that are secreted by microorganisms such as bacteria and fungi and serve primarily to transport iron across cell membranes, although a widening range of siderophore functions is now being appreciated. Siderophores are among the strongest soluble Fe3+ binding agents known.


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Data treatment for long-term mark-recapture study
I am looking to calculate population estimates for two species at a site where mark-recapture work has been conducted since 2010. Due to the long-term nature of the study, I an open population model will need to be used to account for mortality, recruitment, etc. over the years. Hundreds of individuals have been captured and the recapture rate for both species is >10%.
However, capture work was not conducted at the same time(s) every year, and effort during those visits also varied. For example, in early years the site was visited multiple times during the spring and autumn, there are two years where the site was not visited at all, and in later years the site was only visited one to three times at different times of year. I'm looking for advice on how I should divide this data into discrete survey events (ex. by visit, by month, by season, by year) for as accurate a population estimate as possible and how best to take into account the varying effort each year depending on how survey events are distinguished.

Jolly-Seber models can estimate return rates and survival rates that vary between survey intervals, which would accommodate the different seasons, intervals, and effort of the surveys. I think this would let you simply divide the data by visit?


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Why does only 97% Oxygen transport occur as oxyhemoglobin?
I learnt that 97% oxygen is transported as oxyhemoglobin where as 3% is transported in the dissolved state through plasma. Moreover I've also seen that in the Oxygen Haemoglobin dissociation curve, saturation occurs at 97% instead of 100%, I can't relate why this happens.
Also what would happen if 100% saturation occurs?

so you are asking why a biological system is not perfect?

97% is transported as oxyhemoglobin and only 3% in dissolved state because oxygen has low solubility in plasma which cannot meet the body requirements so haemoglobin is the pigment which helps to make the transport easier.
If we see oxygen haemoglobin dissociation curve it gives us idea that what is the percentage saturation of the haemoglobin at particular partial pressure of oxygen. The near-complete saturation would be essential for an efficient oxygen transport to tissues and organs. 100% saturation of haemoglobin will occur only when the partial pressure of oxygen is very high which is not possible under normal conditions.


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Do we already have the necessary code for antibodies against various diseases?
Whenever we get exposed to a particular antigen, we form antibodies against it. Doesn't this suggest that we already have the genetic code to code an antibody against that particular antigen? If not so how are we able to form a new antibody as soon as we are exposed to an antigen?

Famously "The immune system is very complicated ...". You may want to consult a good popular book on the immune system like An Elegant Defense.
There is a portion of the region of the genome responsible for the building antibodies called the V(D)J recombination region. V(D)J stands for "variable–diversity–joining". At a certain stage in the division and development of some white blood cells, these segments of DNA rearrange themselves in a more or less random fashion. Antibodies share most of their structure with other antibodies, but this variable region is the bit of DNA that codes for the part of the antibody that binds to antigens. So you end up with  white blood cells that can generate different antibodies that will bind to different antigens.
There are many different types of "white blood cells", all playing different roles in the immune response. But very roughly, if a white blood cell doesn't happen to encounter a protein that matches its antibody, it will eventually die, and that particular version of the antibody will be forgotten. If it does encounter the matching protein it will trigger a complex feedback loop, which will result in the white blood cell with the "right" antibody" reproducing at a massive scale, pouring out antibodies and attacking the pathogen that had the foreign protein. After the pathogen is killed off, some of the white blood cells specific to it will hang around, and be ready to go if you encounter that pathogen again.
Note that we do not form new antibodies as soon as we are exposed to an antigen. It's a matter of chance how long it takes for the correct antibody to be formed, and how long it takes for it to encounter its antigen. This means there may be a period when the pathogen is rapidly growing within you, but you have no or limited immune response to it. If the pathogen causes disease, you may die before your immune system is able to catch up, or because the immune response is so large that it starts damaging your body itself.
This is why vaccines are so valuable. They expose your body to the antigens associated with a pathogen, but there is no danger of the pathogen replicating and killing you. This gives you the time you need to develop a healthy immune response to that pathogen

In contrast to Charles’ technical answer, here is a simplified version.
Yes, our bodies already have the code on how most of the antibody should be shaped; that is apart from the most crucial part which recognises the pathogen (let's call it the recognition part, RP). The original 'template' for RP is pretty much the same in all cells that go on to produce antibodies in our body, but each of these cells warps the 'template' in an individual way, leading to a large number of randomly reshuffled versions.
The body first has to notice the antigen and move it to the lymph nodes, where cells can then test various RP shapes until they find one that works!

Why the downvotes?

Perhaps because there is no code, in the recognized sense of the word, and talking about the body “knowing” is the worst kin of anthropomorphism.

Because instead of stating it more simply, you've dumbed it down to a terrible answer?

Sorry, if any of you could come up with a good edit, I will happily accept it

@Harrychink You should look at other answers and try to model what they do - add references and links for people to find out more. You should also use proper terms. Charles' answer isn't highly technical at all; the most complex bit is the V(D)J part and even that has a link to explain it. I would expect a late high-school student (say last 3 years of high school) to be able to understand the content in there without difficulty.


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What predators are in Afrotheria or coexisted with them while Africa was an island?
I have read (mostly from wikipedia) that while Africa was separated by water from the rest of the world the Afrotheria underwent convergent evolution to produce species similar (or at least equivalent) to many species outside Africa.  However I didn't see any mention of large predators.
Are there are any large predators in this group, or alternatively what were the large predators that they co-existed with before the arrival of Laurasians?

Apologies if the tags I selected are a bit random.  Please edit if there are better ones.

Did you look at the Evolution of Mammals linked from the Afrotheria page? It has a pretty clear tree that might help you understand. Look at the clades with the animal groups and recognize that Afrotheria weren't the only animals on the continent at the time.

I think the question implies that I know that.  I'd still appreciate some examples.

Ah, I should learn to read more, my apologies... I thought you were thinking that they were the only mammals on the continent. It might be helpful for you to expand on what you know about this - i.e. what other mammals you know were there and time timings of the breakups of Gondwana and the various sub-continents from that.

Thats an interesting question! Recently, I stumbled over a group called "Ptolemaiida", which recently have been placed to the Afrotheria. They are wolf-sized carnivorous mammals. However, one should mention that they are quite poorly understood in general (in fact, it is even not completely clear whether they were really carnivorous). Besides this, I am not aware of "large" predators within the Afrotheria. (Of course, striclty speaking, many afrotherians are carnivorous, since the group includes many insectivorous animals, but I assume you referring to big predators).

Besides this, there were also many "Creodonta" in africa, which during the Oligocene were the dominant predators of the continent. The Creodonta are related to the Carnivora (so they are Laurasiatheria), but not their ancestors. Furthermore, they are probably polyphyletic, i.e. consisting of different not closely related groups.

@G.Blaickner, thanks!  If you want to make that into an answer I'll accept it.

@TomV Your welcome! I added an answer.

As suggested by the OP, I transform my comment(s) into an answer (plus some extensions and sources):
Let me first recall the timing of Africa as an isolated continent: The supercontinent Pangaea began to split into two parts during the Late Triassic period (around 230 million years ago), namely into

Laurasia in the Northern Hemisphere (North America, green land, and
the majority of modern Eurasia)
Gondwana in the Southern Hemisphere (South America, Africa,
Antarctica, Australia, New Guinea, India, Arabia, and Madagascar)

By the Early Jurassic (about 180 million years ago), Gondwana started to break apart. Following the mid-Cretaceous (Albian–Aptian) separation from South America approximately 100 million years ago, the African continent remained isolated until the early Miocene (about 20 millionen years ago), when Afro-Arabia collided with Eurasia.
As you probably know, Afrotheria, one of the three major groups of placental mammals (alongside Boreoeutheria and Xenarthra), is thought to have diverged from other mammalian lineages around 100 million years ago. Today, most afrotherians are found in Africa, suggesting an African origin for this clade. However, it's important to note that the earliest known afrotherian fossil, Ocepeia, dates to only about 60 million years ago, so there is a significant gap between molecular clock estimates and the fossil record (but the same is also true for the other groups, like for the Xenarthra for instance).
The Afrotherian group primarily includes large herbivores, such as Proboscidea (elephants, mammoths, and their relatives) and the extinct Embrithopoda, as well as smaller insectivores, like Afrosoricida. The only known predatory afrotherian group are the extinct Ptolemaiida, which were wolf-sized animals that lived in northern and eastern Africa during the Paleogene period (late Eocene to Miocene). However, not much is known about these animals. (in fact, they have only recently been placed to the Afrotheria)
However, while Africa was an isolated continent for more than 70 millionen years, as noted in this very nice article,

The isolation of Africa was broken intermittently by discontinuous filter routes that linked it to some other Gondwanan continents (Madagascar, South America, and perhaps India), but mainly to Laurasia. Interchanges with Gondwana were rare and mainly “out-of-Africa” dispersals, whereas interchanges with Laurasia were numerous and bidirectional, although mainly from Laurasia to Africa.

So, you see, that there have been some interchanges between Africa and other continents, also before the connection between Eurasia. In particular, during the Pleistocene, the Laurasiatherian group Creodonta where the dominant carnivorous placentals during the Palaeogene period, in the near
absence of carnivorans (see also this article). Creodonts, once thought to be the direct ancestors of modern carnivores, were among the first mammals to adopt a predatory lifestyle after the age of dinosaurs. They are now considered to be a polyphyletic assemblage consisting of two groups

Oxyaenidae: bear- or cat-like animals with short limbs and
robust bodies, adapted for climbing and ambushing prey, mostly found in North America and Asia.
Hyaenodontidae: More widely dispersed animals with longer,
lighter bodies, similar to modern wolves or hyenas. They appeared
earlier in Africa and Eurasia.

Last but not least, let me note that besides mammals, there also have been other predatory animals in former times. For instance, there are records of Phorusrhacidae ("terror birds") in Africa, see for instance this article.


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Is saying, "Xylem and phloem are located in the vascular bundle (of root)" wrong?
So basically, this was a question in 2022's NEET paper
Read the following statements about the vascular bundles:
A. In roots, xylem and phloem in a vascular bundle are arranged in an alternate manner along the different radii
B. Conjoint closed vascular bundles do not possess cambium
C. In open vascular bundles, cambium is present in between xylem and phloem
D. The vascular bundles of dicotyledonous stem possess endarch protoxylem
E. In monocotyledonous root, usually there are more than six xylem bundles present
Choose the correct answer from the options given below.
a. A, C, D and E only
b. A, B and D only
c. B, C, D and E only
d. A, B, C and D only
As per the exam conducting body, the correct answer is option 'c', because statement 'A' is wrong. They claim that "Xylem and phloem are located within the vascular bundle" is a more correct statement and not "Xylem and phloem are located in the vascular bundle"

But is it not appropriate to use 'in' in the place of 'within', at least in this context?

I’m voting to close this question because because the function of this site is not to express opinions on the use of prepositions in MCQs.


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Interphase is the process in which DNA is duplicated/replicated and is the longest phase
A test question that I completed as True just wanted to know if I'm right or not:
The Question goes as follows:
Please write True or False for the following question; if False, correct the Bolded portion!
Interphase is the process in which DNA is duplicated/replicated and is the longest phase.
Context: The test was to do with animal and human cells and mitosis
I would really appreciate a simple answer, as some google posts say Yes and some say no, so I kind of am confused.

It would be true, Because interphase takes about 90% of cell division and comes before Mitosis, and interphase contains three subphases, which are the following
G1 - the Cell PREPS to preform DNA Replication;
S - DNA Replication occurs;
G2 - cell makes protein and organelles in prep for Mitosis.
Cells that do not longer divide go in a quiescent, G0 phase.


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Availability of information on genes in Gnomad VCF data
Im new to gnomad and genetics in general and i was wondering does the gnomad genome data that is downlaoded in the vcf format on variants contains information of what is the nearest gene and is the genomic location available also: exome/intron..... , if yes then what are the columns that contain this data? is it the INFO column?
thank you:)

Can you paste a snippet of the first few lines of a gnomad file here for us to look at? Generally speaking VCFs can be annotated with genes according to your favorite annotation, here is one of many tools. Alternately, bioinformatics SE might be a better place to get an informative answer.

@MaximilianPress hi it is the regular VCF file for variants that gnomad has on the download page

can you reproduce or link it here so that we don't have to go remember the exact url for that file?

(I'd suggest going and looking at the file header or the first few lines of variants, which directly answer your question)

@MaximilianPress the first lines of the variants are chrom position ref/alternate allele i was wondering if the information is in the INFO column?

Given that the cross-posted question got answered, I am going to see if I can mark this as a duplicate.


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Does the most known image of Long-finned pilot whale depict one with the melon inflated or not inflated?
The most common image of the Long-finned pilot whale shows a bulbous head. Some may think this is merely an inflated melon:

https://upload.wikimedia.org/wikipedia/commons/thumb/7/76/Pilot_whale_spyhop.jpg/330px-Pilot_whale_spyhop.jpg
...but images of an inflated melon in Long-finned pilot whales show what seems a lateral position:

https://s3-eu-west-1.amazonaws.com/wwhandbook/sidebar-images/_sidebarPromo/PIFSC_20170901_S104_G-0384_PAO.jpg
...so does anyone knowledgeable in LFPWs know if it's an inflated melon or a big brain in top picture?
After all, they have the highest neocortical count:
https://www.frontiersin.org/articles/10.3389/fnana.2014.00132/full


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Why do you have to submerge your gel in buffer before adding DNA
When you run a gel electrophoresis, you add your gel and then submerge it in TAE or TBE buffer before you pipette your ladder, DNA, loading dye, etc. Why must the gel be submerged in buffer before you add anything? If anything, doesn't this make it harder to pipette into the well due to the diffraction of the buffer?

This has a very simple reason: Adding the buffer later poses the risk to wash out your sample from the well as well as mixing samples.
There is another reason: It makes loading easier. The sample is mixed with loading dye which contains glycerol. This mixture is denser than the buffer and makes the sample sink to the bottom of the well. So you only need to get your pipette tip into the well (and not all the way down the bottom to deposit a very small drop of sample) and then you can release the sample from the tip. It will sink down due to gravity to the bottom of the well.


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Does decellularization with sodium lauryl sulfate break down enzymes?
I am currently looking into decellularization with sodium lauryl sulfate since it is effective and cheap. My goal is to break down the cells of a plant leaf and release the chloroplasts to be viewed under a microscope(I realize you can do this without decellularization but I'm still curious). My question is, will sodium lauryl sulfate break down the cell membrane and cause no further damage to the organelles or enzymes? If not, what chemicals can break the cell membrane without causing any more damage to the organelles or enzymes?

Welcome to the site. Please take a [tour] and visit the [help] for more information about this Stack and what we do here. In addition please note the homework policy, which generally asks that the person asking the question demonstrates what they know about their question. So... what do you know about SDS/SLS and its chemistry?


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Why do the host cells containing iC3b fragment not undergo phagocytosis?
As far as I understand, in complement system C3b gets deposited on pathogen surface but it can also be deposited on host cells. Host cells have some negative regulatory system such as membrane cofactor of proteolysis MCP, decay associating factor DAF etc which either removes C3b or cleave it using factor I to iC3b which can not form a C3 convertase or C5 convertase so no production of membrane attack complex on host cells.
However, phagocytes contain complement receptors CR2, CR3 etc that specifically recognise iC3b and engulfs the cells bearing it. While it is very useful for pathogens bearing iC3b (In those cases where pathogens contain sialic acid residue which attracts factor I and prevents forming MAC on those pathogens) wouldn't it be very dangerous for host cells?
So if there is receptors against iC3b on phagocytes then what is the point of host cells converting C3b into iC3b, they get killed one way or another anyway

There's a relatively new concept of self-associated molecular patterns (SAMPs), which much like DAMPs and PAMPs, help immune cells make a decision in a slurry of signals. There's at least a fair article on SAMPs here, and to go even further, the suggestion that tumor-associated SAMPs can dampen immune clearance of cancer cells.
In my head a few things are going on:
(1) The opsonins are potentially binding to everything. Of course, there are surfaces like ECM that don't have any receptors or patterns that you don't want getting damaged, and there's at least some evidence that complement clearance by factors I and H (paywall) may contribute to ablating that effect.
(2) The actual targets for the immune system are expressing patterns that specialized pattern recognition receptors on your phagocytes and so forth can recognize.
(3) Self cells are expressing receptors and patterns that tell the very same cells there's no threat, either through direct inhibition or degradation of kill signals.
Remember that when self cells are damaged, the expression of DAMPs help macrophages and the like come clear them away, so there's obviously a way for self cells to control that effect.


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Text Book Recommendation: Cell & Molecular Biology + Organic Chemistry
I am studying undergraduate biology course and I have cell biology and molecular biology in my next semester. Our college recommends three books : Cooper, Lodish & Bruce Alberts. It would be really helpful if you give me your opinion on which of these (or your own recommended book) would be the best to learn these subjects properly. The only thing I need is the book to be easy to understand because it will most probably be totally self taught because our instructors are not always helpful in explaining stuff properly.
We also have an organic chemistry class and the recommended books are Solomon's&Fryhle & LG Wade. It would be helpful if you help me choose between these as well, my requirement stays the same. Book should be easy for self learning.
If you know about online video lectures about organic chemistry and molecular biology do let me know. MIT OCW doesnt really have good bio videos. I cant seem to find video lectures anywhere for gre preparation. Thank you

Cell & Molecular Biology belongs to Biology Stack exchange and Organic Chemistry to Chemsitry SE. Also your question needs a  bit more details, you have only covered the last criterion,level of study.

Along with Molecular Biology of the Gene, Alberts' Molecular Biology of the Cell is one of my favourite text books.

@Sanjukta Ghosh I do know that these two belong to different SE but I wanted opinions from biologists not from chemists because my o.chem course is not advanced one, also it would be helpful if you mention what details you are looking for in my question. I just want an easy to learn textbook and can't try them all because 1) These books are expensive 2) I wont have much time to experiment with different books. I need to pick one and stick to it

Basic books of any subject (here Organic Chemistry) would be the same from both Biologists' and Chemists' perspectives as they teach the basics which stand on the ABCDs of that subject which has nothing to do with the domain knowledge of other discipline(here biology),  so I woud suggest you asking them because it is off-topic in Biology. Besides from my experience no single book covers all the topics well (in any discipline) and multiple sources (books and often papers) are required to learn something clearly.

Your post is missing what topics you want it to cover, you have to be more specific (see the scond point in the prev. link). Your post may get closed due to two reasons-off-topic and too broad if the issues are not resolved.

Sorry but I'll have to disagree with what you said about basic books. This semester we had physical chemistry and I asked for book recommendation in chemistry se. They told me I should go for Atkins but it was a waste of money. Not because it is a bad book, I am sure it is a great one due to its strong reviews but for a bio student like me it was very difficult to deal with, thats why I did not want to repeat the same mistake once again. Ignoring chemistry if you can help me with molecular biology book like  canadianer and AlexDeLarge did it would be helpful. Thank you

Given your requirements I would go for the Alberts for molecular cell biology.
For organic chemistry, in my opinion, there is no better book then the Clayden. It is targeted at OC students but I - as a biologist - learned a lot from it and still sometimes love to browse through it even though my work is far away from organic chemistry.
In general, I would advise you to go to your local library and take a look at the different choices before getting one. Take your time to get a feel for the writing and teaching styles and pick the one you find most access to (and maybe give feedback as a comment/an own answer to your post which book you took and why, for future reference).

I got myself a copy of Bruce Alberts, lets see how it goes!

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
What lysis buffer recipe is good for just breaking the cell membrane?
I am interested in the decellularization of plant leaves(more specifically maple) and thus need a lysis buffer. I want the buffer to only break the cell wall and cell membrane and I want to observe the proteins in the cytoplasm so the buffer can't be too strong as to deactivate the proteins/enzymes in the cytoplasm(I don't care about the nucleus). I looked at RIPA, SDS, and NP-40 but they are all too strong and can damage the proteins. Is it possible to only use salt in a buffer solution without any detergent and if not, could you please recommend me a lysis buffer solution? For more clarity, I am mostly interested in looking at hexokinase. Thank you for your time.

Look for lysis buffer kits labeled for creating nuclear extracts. There are generally two buffers: one to lyse the cell membrane, after which the lysate is spun down and washed, then a second buffer to lyse the nuclear membrane. I don't have time at the moment, but I'll try to find a reference for you later.

I just realized that you're talking about plant samples, where you also need to lyse the cell wall. Have you considered mechanical lysis, either with a mortar and pestle or sonication?

If I were you I would look into dounce homogenizers, along with the use of a cellulase to break down the cell wall.

Thank you for your answer, I have considered mechanical lysis but I am working with small samples so it isn't as efficient as chemical lysis. Mechanical lysis can also create localized heating which can denature some proteins so if possible I would use chemical lysis over mechanical. Using a cellulose is a good idea but I still need to break the cell membrane with chemical lysis

Also, can alcohol also break the cell wall like cellulase?

Centrifuge. Use a diluted salt solution and centrifuge the sample to separate the cell wall.


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Sourcing sulfur-oxidizing bacteria
For a research project, I need a species of sulfur-oxidizing bacteria but I cannot find a biological company that sells anything like that. I know ATCC sells some species of sulfur-oxidizing bacteria but those are usually too filtered out than I need thus costing more than $400. Can you provide me with any biological company that sells bacterial species under sulfur-oxidizing bacteria? I know I'm not making it very specific but at this point, I'm good with anything you can find. I would prefer green or purple sulfur bacteria, but anything that can use hydrogen sulfide is good for me.

There are numerous collections around the world that supply bacterial species. You've already found the American Type Culture Collection (ATCC). If you are in academia or even sometimes in industry, you can contact authors of papers who have an organism you want, and they will supply a starter culture to you, usually free (for the organism itself), but you will always have to pay shipping (whether from a supplier or a researcher), which will often run into the hundreds of dollars, depending on shipping type. Many species will only be able to be shipped under certain conditions, such as frozen on dry-ice (about -89 C), or frozen as freeze-dried. These types of shipping cost $$$.
In addition to the shipping there will be some legal things to sort out. Typically this is a Material Transfer Agreement, which is a legally binding document between your organization and the supplier and/or the people the supplier got it from. These often limit what you can do with the organism in question - usually limiting you to research applications only. If you are intending to commercialize you will need to get a commercial agreement signed up! Not doing so opens you and your organization to legal liabilities that will cost a huge amount of money to litigate and usually result in substantial fines.
In Europe there is the Belgian Coordinated Collection of Microorganisms, which has a price list here. There is also the Leibniz-Institut DSMZ-Deutsche Sammlung von Mikroorganismen und Zellkulturen GmbH (known as the DSMZ) in Germany and the Culture Collection University of Gothenburg (CCUG) in Sweden. The UK has the NCTC (National Collection of Type Cultures) too.
Japan has the  Japan Collection of Microorganisms at the RIKEN organization. China has the Chinese General Microbiological Culture Collection Centre
India has the NCCCC (National College Culture Collection Centre) in Pune.
In addition there are lots of smaller ones around the world. There is also the Global Catalogue of Microorganisms, which lists 152 current affiliates from all around the world, including those listed above.


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Can Iron(III) accept electrons from NADH without the other enzymes?
During the electron transfer chain in cellular respiration, the NADH turns into NAD+ while donating an electron. Those electrons pass through many enzymes and chemical reactions. One such chemical reaction is when it passes through iron II or iron III. Is it possible for NADH to react with iron II or III without any other reactions with enzymes and chemicals? I am asking this because I am interested to know if the reaction between NADH and iron can give oxidize NADH and reduce iron.

Please clarify. 1. When you refer to iron II and iron III, please indicate whether you are talking about free iron or iron in cytochromes etc. 2. Are you talking about what actually happens in the electron transport chain (ETC) in cells or what would happen if iron were mixed with NADH in a test tube? 3. Or are you asking why the many redox pairs are need in the ETC? Your language ("turns into", "chemicals and enzymes") suggests you might benefit from reading about the ETC and redox couples in a biochemical text (best) or on line. Are you aware that oxygen is the ultimate electron acceptor?

Thank you for your response and for clarification: 1. I am referring to free iron atoms and 2. I am asking what would happen if iron were mixed with NADH in test tubes. I realize oxygen is the ultimate acceptor but my main question is: if iron(II) or iron(II) and NADH were mixed, could NADH transfer electrons to iron? and lastly, could NADH donate electrons to regular iron?

Preamble
Although the question relates to a non-biological test-tube reaction, I feel it worth posting an answer because the principle involved is relevant to biological redox reactions.
Qualified Answer
For a chemical reaction to proceed requires two things:

That ΔG, the overall change in Gibbs Free Energy, is negative.
That the activation energy for the reaction can be overcome.

As regards 1: For reactions consisting of two redox half reactions, one needs to first calculate the reduction potential and then, from this, ΔG. (A positive ΔE gives a negative ΔG.) A table of standard reduction potentials taken from this on-line source is shown below.

Without actually doing the calculation (I’ll add it later as an appendix, if requested) it can be seen that ferric iron is almost as good an oxidizing agent as molecular oxygen, and thus has the potential to oxidize NADH.
As regards 2: I know nothing about the activation energy for the reaction of ferric iron with NADH in a test tube, so cannot say whether it would occur spontaneously.
Fe(II) as oxidant
Whether or not a reaction is energetically feasible in which ferrous iron (Fe(II)) oxidizes NADH depends on the redox potential of the half reaction for the reduction of ferrous iron. I cannot find anything for Fe(II)/Fe(I), so perhaps only Fe(II)/Fe(0) is possible, values for which can be found on this Wikipedia page. I leave it as an exercise for the reader to do the calculation.

Thank you for your answer, this was very helpful!


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Metabolism of Purple non-Sulfur bacteria
I am a high school student who is currently experimenting with hydrogen sulfide absorption using bacteria. I know species of purple sulfur bacteria or green sulfur bacteria are able to oxidize hydrogen sulfide but the only species that is available to me is Rhodospirillum rubrum which is a purple non-sulfur bacteria.
I know under anaerobic conditions, r. rubrum receives energy by oxidizing hydrogen with carbon monoxide or uses sulfide as an electron donor in photosynthesis(source).
Is it possible for r. rubrum to use hydrogen sulfide as an electron donor similar to purple sulfur bacteria? They both use the photosynthetic pigments Bacteriochlorophylls so does this mean both r. rubrum and PSB can use hydrogen sulfide as an electron donor and thus oxidize it?


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How do I grow 5 liters of purple non-sulfur bacteria?
I am running experiments for a project that requires large amounts of purple non-sulfur, Cyanobacteria and nitrogen fixing bacteria. I plan on growing all the species in separate tanks. The species' I am using are rhodospirillum rubrum, anabaena, nitrosomonas, and nitrobacter. All the bacteria will be grown in separate tanks except for the nitrosomonas and nitrobacter which will be grown in the same tank. I need roughly 5 liters for each of these species.
In previous experiments where I only needed a few ml of bacteria, I used Alga-Gro® Seawater Medium which is technically used for algae growth. I doubt this will be viable for growing the bacteria up to 5 liters. Additionally, I am worried about contamination since I need relatively pure populations for my experiments. I am not sure if I can use the same growing techniques for each species and I don't how if growing this large a population can be done by just adding an agar solution.
I am new to growing bacteria in these quantities so any advice would be greatly appreciated.

This really sounds like something that your supervisor should be your first port of call. You could also look in the literature to see what others have done.


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Please explain what a gene isoform is in lay terms?
I am a physicist by training, however I am now doing computational biology research. I know what genes, DNA, proteins, enzymes, introns and exons are.  I sort of understand how DNA is used to create RNA, which is used by ribosomes to manufacture proteins.  That is the extent of my biology and genetics knowledge.
So, could someone explain what a gene isoform is in lay terms?  There is a related question here and wikipedia has an explanation.  However, there is a significant jargon barrier for me.

Gene isoforms are all the different RNAs that can be synthesised from a single gene. You may be referring to splice variants, which are systems of getting different mRNAs from the same sequence using different combinations of introns and exons.

(source: riken.jp)
Translating your wikipedia article:
Gene isoforms are the different RNA products obtainable from a gene that can vary on the place where the translation starts (protein synthesis), that have different sequences in the coding region (thus giving different proteins, sometimes with different functions) or by having different untranslated regions, UTR (the overhangs of the sequence that are not translated in the mRNA). This last difference, the UTR, normally gives rise to different stability within the cell as UTR secondary structures usually control the speed of degradation of an RNA.
Hope it helps


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Y285 Yeast Strain: Where to obtain from?
Often I see yeast strains mentioned like Y285 or Y301 etc. in papers. Is this some sort of universal notation? (Link to poster: https://ddd.uab.cat/pub/tfg/2014/119349/TFG_narcisferrerledo.pdf)
How does one go about locating such a strain to try in an experiment; are there repositories where you can get a strain from?
e.g. I tried searching the strains databases at Yeastgenome.org & DBVPG but these names ("Y285") don't produce any hits. Is there another canonical name I should be using to search them by?
http://wiki.yeastgenome.org/index.php/Strains
http://www.dbvpg.unipg.it/index.php/en/database
I even tried searching in the "National Collection of Yeast Cultures" but no luck. Any tips?
https://catalogue.ncyc.co.uk/catalogsearch/result/?q=Y285
Edit:
Found this related thread on SE-Biology that gives links to other useful Repositories.
Sources for common laboratory Saccharomyces strains?
Am I just searching with the wrong name? Is it common to refer to Y285 by some other name?

Y285 or Y301 sound like specific mutants (at tyrosine 285/301 of a particular protein) but we can't really be sure without the paper you're referencing [and I'm not very familiar with yeast strain nomenclature]. Could you provide a paper link?

@Luigi Thanks. I've added the link to the source in the post: https://ddd.uab.cat/pub/tfg/2014/119349/TFG_narcisferrerledo.pdf


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When did the mammalian outer ear evolve?
All Eutheria and Metatheria have outer ears, and as far as I found out, monotremes once also had them, so they seem to be universal for mammals. Did other synapsids have them, too?
I know that soft tissue doesn't fossilize well, but isn't there any other way to find out, like muscle attachment? Has it something to do with mammalian ear bones?

Yes, it is believed to be linked to the mammalian inner ear bones. Since they act as amplifiers, the faint sounds gathered by the outer ear have a greater benefit. But really early mammals show many adaptations that they were relying very little on sight and a great deal on hearing. External ears just might not be beneficial enough unless you are really relying on hearing. The only other vertebrates that rely that much on hearing, the owls, also have external structures to help gather sound.
The fact that both developed at the same stage is circumstantial evidence that they may be linked as well.


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Mesoderm vs Mesenchyme- what's the difference?
My embryology textbook states that mesoderm can exist as Mesenchyme or Epithelium. I'm not sure what 'epithelium' means. Here is a quote for context:

Somatic, splanchnic, and somite mesoderm can be temporarily an epithelium.
  The temporary epithelium transforms to a secondary mesenchyme

What does this quote mean?

Mesenchyme is the meshwork of embryonic connective tissue in the mesoderm; from it are formed the connective tissues of the body as well as blood vessels and lymph vessels.
So it's a part of mesoderm

Welcome to BiologySE...thanks for taking a stab at this answer. We always appreciate some references/links for answers so other users can read more about your answer. It will definitely help the strength of your answer as well.


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Is the CNS vascularized?
I was under the impression that the CNS is never penetrated by blood vessels, which explains why one never sees them in histological samples.
However a google search reveals I am wrong. So can someone please tell me what the purpose of Cerebrospinal fluid is?
B) Why one does not find blood vessels in histological slides?


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Why Hfr cells are called high frequency recombination cells?
I understand that Hfr cells are formed when fragment of bacterial plasmid integrates itself in another bacteria's (host) genome through homologous recombination but my question is why do we call these cells as "high frequency recombination cells". Where is the term high frequency coming from?


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What is GST RhoA fusion protein?
Would you please explain to me what GST RhoA fusion protein means and how it differs from RhoA protein? I am a kind of doing an experiment using this protein.

GST is glutathione-S-transferase, an enzyme that binds reasonably tightly to glutathione. It is often used as a tag to purify proteins of interest. In your case, GST has been fused to RhoA most likely so that you have some means to purify it by applying it to a glutathione conjugated column. See here for more information.


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Why haven't we cured the common cold yet?
Researchers think they’re close to a cure for the common cold, but they first need to solve a complex problem that’s perplexed scientists for decades. Polio, smallpox, hepatitis A and B are all serious viruses humanity learned to subdue with effective solutions. Even the flu, which can shift and mutate each year, has a vaccine. And yet, there’s no remedy for the lowly cold.

It's a naming fallacy.

Which common cold? Them buggers mutate so fast we can't even name them properly.

We have cured it, but by common language usage instead of medicine.  Nobody I know has gotten a cold for 20 years.  They still get the sort of infection we used to call a cold, but now everybody calls it the flu.

Masks help. I have been cold-free since the start of 2020, while I suffered at least one cold per late autumn, winter or early spring before that, all my life.

There's also a cost/benefit issue. It's easier to spend billions on research for a disease which can cause deaths (especially if a lot of them), a lot more difficult for diseases which just cause you relatively mild symptoms.

There is one simple reason: Contrary to the viruses you named in your question, which are all caused by one virus (or from the same family), there is nothing like "the" cold virus. This makes it a manageable task to find a vaccine for the former, although it doesn't mean it is simple.
A cold is viral infection of the upper respiratory tract which are caused by a wide variety of different viruses. The term "cold" is an umbrella term for a wide variety of symptoms following such an infection including coughing, sore throat, runny nose, sneezing, headache, and fever. See reference 1.
The paper in reference 2 lists about 200 serological different viruses, with Rhinoviruses being the most common. Other viruses occuring include adenoviruses, human coronaviruses, human respiratory syncytial viruses, other enteroviruses, human parainfluenza viruses, and human metapneumovirus.
Although there are seven human corona viruses (see here), only four of them are associated with the cold:
229E (alpha coronavirus)
NL63 (alpha coronavirus)
OC43 (beta coronavirus)
HKU1 (beta coronavirus)

The other three can cause a considerably more severe disease and are not seen as causing a cold:
MERS-CoV (the beta coronavirus that causes Middle East Respiratory Syndrome, or MERS)
SARS-CoV (the beta coronavirus that causes severe acute respiratory syndrome, or SARS)
SARS-CoV-2 (the novel coronavirus that causes coronavirus disease 2019, or COVID-19)

See reference 4 for a more detailed look on them.
This list should make pretty clear why there will be nothing like a general cold immunization, since the number of viruses is too big. Additionally, all these viruses can change over time due to mutations which would need permanent adjustments to such a vaccine. This is already a big deal for influenza, but there are only limited viruses around there.

Understanding the symptoms of the common cold and influenza
Understanding the symptoms of the common cold and influenza
Epidemiology of Viral Respiratory Tract Infections
The human coronaviruses (HCoVs) and the molecular mechanisms of
SARS-CoV-2 infection

Thanks for this instructive write-up. I was vaguely aware of several viruses being responsible, but you put it together very nicely, and with references, and put it in context with SARS_CoV-2: Good job.


text:
Why do apes still exist?
If we are evolved from apes, why don't all ape evolve and become human.
Or

Why the today's ape stop evolving to become a human?

Because their environmental niches suit being apes.  Evolution does not have a goal.

Okay. But why is my question downvoted?

@jamesqf Why don't all apes evolve then?

Why do you think apes don't evolve?  Like any and all other creatures, they continuously evolve to become better suited to their environment, which is why there are about 20 species of living apes, each suited to their particular environments.  And I downvoted your question because I think it is pure creationist claptrap.  If it's not, the answer is pretty obvious: why do we have different species of cats, bears, equines, or any other group?

I am not going to bother putting any references for this answer as all the information is a google search away.
Humans did not evolve from apes. Extant humans and apes developed from a common ancestor. One lineage from this common ancestor evolved and became apes. Another lineage went on to become humans.
Some study material here and here.

Unless one can describe a "common ancestor", this phylogenetic knee jerk response begs the question. Humans evolved from animals not distinguishable taxonomically from apes. Phylogeneticists invoke the common ancestor explanation because their analysis is actually a form of cluster analysis, where groups of traits split dichotomously into smaller groups of traits. This is not a model of evolution.

OK, so what is a model of evolution?

Can you provide a link to explanations of alternate and feasible hypothesis?


text:
Is the basic reproduction number unique?
Given any epidemic model of an infectious disease, there are various ways of computing a basic reproduction number($R_0$) such as;  the next-generation method, survival function, largest eigenvalue of the Jacobian matrix and so on.
My question is,

Do we get the same $R_0$ for the same model but using different methods of computing $R_0$?

If we don't(if $R_0$  is unique) what is the explanation?
Are we allowed to use "this" different $R_0$ in writing a paper?

Generally, as with all statistical model fitting, you need to separate between the actual (unknown) value of R0 and the estimate of R0, based on model fitting from empirical data. If you consider this, different estimates of R0 are rather unproblematic (and expected). However, large deviations between estimates using different methods is worth digging into, since it could indicate problems with some of the data.

It should be noted that many of the methods you talk about aren't necessarily for getting a number but rather a formula for $R_0$, all of which should be equivalent.
However, when those methods step into the realm of getting a number by fitting parameters, they may give different results as they handle certain aspects of the data differently.
You are certainly "allowed" to use any formulation of $R_0$ you want - just document what you did.


text:
How a nerve impulse reaches the correct destination?
Say your brain wants to retract your right hand.
If there is some information coding playing a major role here, then what is the mechanism to find the correct path to reach the correct muscle?
Or is it every part has a single nerve connecting to the brain?
Any difference when it comes to withdrawal reflex comparing to brain initiating action? i.e. how the reflex round trip reaching the correct muscle?

This is a fairly basic question. Have you tried google? Do you know the difference between neurons and nerves?

Yes, tried but no avail. "how nerve impulse finds the correct path" is what I tried. But I only found results about how a nerve impulse travels, but not the mechanism on how it can select the correct path to reach the correct destination.

Here's a recent video I made in response to a similar question. It's called "Spinal cord is (not) a bus". https://www.youtube.com/watch?v=e5TRfya3FPk ---------- >! Basically, spinal cord is pretty much a labeled line!

OK, I think I can answer at the right level now.
Firstly, a nerve is a bundle of neurons, each neuron is like a fibre. So the sciatic nerve in the leg will carry fibres from the spinal cord to the muscles in the leg, like a data cable might connect many computers in an office to a server on another level.
Each neuron will form connections with a specific area on a specific muscle, at a specialised synapse called the "neuromuscular junction". When a signal travels down that particular neuron, it will release neurotransmitters that activate that particular muscle region. So by sending signals to the right neurons, the muscle to be activated and how much to activate it can be selected by the CNS.
A nerve impulse is a slightly misleading term as it refers to the collective activity of signals within the many neurons of the nerve, so an individual neuron won't register on an impulse. The signals in neurons are called "action potentials".
There is some information coding in the frequency of action potentials within neurons, but it is used to control the response of the muscle, rather than locate the correct muscle.
Wikipedia is pretty good on the subject if you know where to look:
neuron
withdrawal reflex
sciatic nerve

Right ok. The question is still there: "How to select the right neuron so that the correct destination can be reached"? Using computer terms, we have router to send signal to the correct computer and the router can look at the signal header to know which ip to send.

The motor cortex in the brain is divided into regions associated with each part of the body: https://www.memrise.com/mem/3977517/primary-motor-cortex/ so activity in the part associated with the hand will lead to movement of the hand. i.e. if you stick an electrode into someones motor cortex you can trigger twitches in certain muscle groups. It involves a massive amount of processing, and learning to generate smooth, controlled movements.

Thanks. You mean the only selection point is at the brain? And the rest is just signal propagation to the nerve end point? Isn't there some intermediate relay nodes like from the brain to the spinal cord? Or these relay nodes are also 1-to-1 mapping to the brain cortex?

Sort of, there is a relay in the spinal cord, where upper motor neurons pass signals to lower motor neurons, but yes I believe it's one to one. There is also input from other brain areas, such as the cerebellum and brainstem that helps fine-tune movements, but I can't remember much about it. Also sensory neurons (usually pain) can directly activate motor neurons in the spinal cord, e.g. during the withdrawal reflex, so no brain input whatsoever.


text:
Is it true to say neurons like to be stimulated?
I believe I have heard people saying "Neurons like to be stimulated". Although I know stimulating the brain promotes more neurons and connections growth, but does stimulating a neuron benefit the neuron itself? Or on the contrary, if a neuron is not stimulated long enough, does that cause any harm to itself? And then if that is true, can I say that limiting oneself to a narrow spectrum of stimuli is not good in general, considering there are other parts of the neural network not stimulated enough equally?

There's some anthropomorphism here, which might be unhelpful to your question, and then there is a huge generalization, which technically does not follow the first question. What's good for the goose here (the neuron) isn't necessarily good for the gander (the brain), as they are not equal.

I think it's necessary to clarify what someone means when they say this before evaluating whether it is true or not. Too many possible meanings to evaluate otherwise.


text:
In theory, would it be possible to create an injection of Vitamins, Minerals, sugars etc so that eating was no longer necessary?
I am wondering, out of pure curiosity, whether with current medical & biological science, (or indeed with accepted probable future developments in those areas), in theory, would it be possible to create an injection of vitamins, minerals, sugars etc so that eating was no longer necessary, and in fact, an average life with average energy usage could be continued?
I am not a biological professional nor academic, so apologies if this is on the wrong Stack Exchange site, however I thought this was closest to the mark. If there is somewhere more appropriate please direct me, and I shall delete the question and post it there.
Also, if no, would there be certain parts that you couldn't replicate in an injection or something of the like?
NB: This doesn't have to be an injection, any simple method of ingesting or attaining everything the body needs. This could be a pill, or anything. I simply used an injection as an example.
Thank-you very much.
Edit:
Having found this question,
Has there ever been an attempt to create nutritionally tailored food for adult human consumption?
I would like clarify. This has given me a lot of information, however, I am looking for any method APART from food. Thanks.

The quantity of nutrients the body requires takes much more physical space than can be included in a simple pill or injection (used only a few times a day).  But nutrition can be provided by IV (intravenous administration), and it is used today for some medical conditions.  When the IV completely substitutes for normal digestion, it is called total parenteral nutrition (or TPN).  The procedure is simple and reliable enough that it can sometimes be used outside of a hospital setting and be self-administered by users at home.

I'd like to point out that TPN isn't considered simple in hospitals and requires a huge amount of extra patient monitoring and observation in addition to causing a number of additional complications - meaning that its usage is always a last resort.

@mgkrebbs Brilliant. Thanks, very useful. The highlighting of specific terms for future research was the largest benefit of this answer. Thanks again.


text:
Why do we feel asleep at night?
Why do we feel asleep at night mostly?
 I tried not to sleep but I could not resist my sleep at night.

You may be interested in this Q&A about the evolution of sleep. Currently your question could be a book title. It's a tad broad.

Do you mean "feel sleepy" or "fall asleep"?  Some of it is simply habit: I tend not to feel sleepy until midnight or so, but when I've shifted my sleep pattern towards early rising (which requires a concerted effort :-)), I would start to feel sleepy earlier in the evening.


text:
Insect identification Colorado
We found this bug in our house today. So far have not been able to identify it after past hour online. Its pincers look way larger than most normal beetles I can find. Can someone help us finger out more about this critter? Thank you

Perhaps the closest I can find is a stag beetle? Although we are in the city and not heavily forested

It looks a lot like dorcus curvidens, but according to the wikipedia page, it's found in Japan. But I would lean heavily towards a dorcus species.

That is a cottonwood stage beetle. Lucanidae, Lucanus mazama https://bugguide.net/node/view/666700/bgimage


text:
Does the change in eye color (melanin concentration) affect the iris pattern?
In cases of acquired heterochromia, is there a quantifiable change in the iris pattern; the clefts , furrows, etc.
If yes, what changes are observed?
And if no, are there any diseases or acquired conditions that cause a change in iris patterns?


text:
Do any plants grow leaves beneath the ground?
We have a pretty common California weed in our yard. When we dig in the ground, we often find small ones there, with green leaves!  It's as if they form green leaves before they come to the surface. While that seems counterintuitive, there's no purpose in having green beneath the soil, it doesn't seem impossible.
We had our yard redone 6 months ago. It's possible that some mature plants were buried- but would they stay green for six months?  Or perhaps they expect to be close to the surface, so after creating a couple inches of roots, they form green leaves, even though they're buried deep enough that they're not at the surface yet.
Is this a known phenomenon?  How common is it for plants to be able to make green leaves before coming to the surface?
Thanks much...

Could it be the case that those plants have been brought underground by ants recently? Do you dig up any ant nests with the leaves?

It is a known phenomenon. A good example of the same can be observed in Philcoxia minensis.
This plant is predominantly found in sandy areas of Brazil and its underground leaves photosynthesize using sunlight energy through the relatively opaque sand particles.
These leaves also play the function of trapping and digesting nematodes underground supplementing nitrogen in the leached soils. This article [with pdf] explains this mechanism in detail.


text:
Why is the 5′ end of DNA a monophosphate?
According to my textbook:

While the 5′ end of a DNA strand is typically a monophosphate, the 5′
end of an RNA molecule is typically a triphosphate.

Source: Biology: How Life Works, 3rd Edition
How do we know the 5′ end of DNA a monophosphate? I understand that...

DNA and RNA synthesis cleaves nucleoside triphosphates into nucleoside monophosphates to form the sugar-phosphate backbone.
Necessarily, the first nucleotide will have three phosphates intact.

What I don't understand is why DNA doesn't have a triphosphate on the 5′ end like RNA. How does that happen?

Related but the answer states the opposite is true and has not been accepted by the asker: https://biology.stackexchange.com/questions/81656/how-many-phosphates-are-in-the-5-end-of-a-dna-strand

My comment serves to show that I did my work by searching for an answer in a few places.
I didn't understand the linked answer, it was too specific of a response to a general question. Secondly, there was too little activity in the linked question so I couldn't trust its accuracy. Lastly, the answer contradicted the textbook, so I thought it was appropriate to ask a new question.

@David ...He is the original poster and I find your comment quite rude..

@Andrew — The original poster of the post the poster of this post referenced. I was explaining why if that post was a duplicate of this it made no difference whether an answer had been accepted or not. Indeed it makes no difference whether it has been answered or not. If you or someone managed to persuade a mod that was rude I can only shake my head in disbelief

The deleted comment: "Whether or not the poster has accepted an answer here is irrelevant. He didn’t know in the first place so he has no authority. It works better on the original computing site Stack Overflow, where the problem is generally practical, and one accepts the solution that works. The answer to the other question actually shows a table of different genomes, so is based on experimental evidence. Have you read it? Do you understand it. Perhaps like the original poster you didn’t realize the true complexity that your probably deficient text ignored. – David 2 hours ago"

This problem wouldn't arise in bacterial chromosomes, plasmids and other circular DNA molecules, for a circle has no ends. :P As far as eukaryotic chromosomes are concerned, they have telomeres. I think reading about telomeres and the associated replication machinery from http://www.hammiverse.com/lectures/16/4.html should answer your question.

I only saw your post by chance. To draw someone's attention to a post other than the poster of a question or answer you need to preface their handle by @ . The question of reviving duplicates — answered or unanswered, accepted or unaccepted belongs on Meta. As I guessed, you didn't understand the linked answer because — from the nature of your text you are study biology, rather than molecular biology — and you would be unlikely to know about the detailed chemistry of the initiation of RNA and DNA synthesis. To say so is hardly rude.

...However the important thing for you is to help you understand your book, and for anyone who wishes to help you they need to know the context of what appears a strange statement in a book published recently. So can you perhaps give an indication of the title of the section this appears in and what follows this statement. The reason one finds this strange is that "a typical DNA strand" is unclear. I would take it to mean the ends of a chromosome — as does the linked reference. Likewise the end of an RNA molecule depends on whether it is mature and what type of RNA it is. Can you clarify?

The quoted text is from chapter 3 (nucleic acids & transcription) section 2 (DNA structure) a sentence or two after describing the nucleotides used in RNA, but before any description of transcription. It doesn't assume eukaryote/prokaryote either. I think typical may mean lacking edge cases, but I recognize biology is full of them. I interpret the text as meaning if you follow such a typical strand to its 5' end you will encounter a monophosphate and then no more nucleotides. My confusion is why this isn't a triphosphate.


text:
Why is cannibalism not an evolutionary stable situation?
In the 'the selfish gene' Dawkins writes (page 109):
"The reason lions do not hunt lions is that it would not be an ESS (evolutionary stable situation) for them to do so. A cannibal strategy would be unstable for the same reason as the hawk strategy in the earlier example."
To quickly summarise this: we consider an interaction between two animals where one possibly stands something to gain. Dawkins then defines 'hawk' behaviour as attacking behaviour, whilst 'dove' is described as peaceful and retreating behaviour. He then argues that a population of purely hawk or purely dove is unstable, since in either of the situations the other kind of behaviour is more favourable. As it turns out, the stable situation is 7:5 for hawk:dove.
Turning to cannibalism, we can regard the hawk behaviour as 'engaging in cannibalism' and dove to be the refraining party. Why, then, don't we see similar behaviour when considering cannibalism, i.e. why don't we see a reasonably large amount of lions engaging in cannibalism whilst the others refrain from it? If I am not mistaken we see in fact the situation more closely described by completely dove?
Any insights are appreciated!

Cannibalism is incredibly common in nature. There are more species that eat their own kind than do not. Chimps eat other chimps. Lions eat other lions. Wolves eat other wolves. Prairie dogs go into the burrows of other prairie dogs and eat their babies to get the protein-rich meals needed to produce milk for their own litter. The only animals that don't regularly engage in cannibalism are some birds, and that is more because they physically cannot fit other members of their species down their throat than any moral qualms.
However, cannibalism is typically a bad evolutionary strategy, long term. For several reasons...

in a dioecious species (i.e., one with two sexes), cannibalism means a 50% chance of eating a potential mate and losing the opportunity to pass on your genes
diseases are more likely to transfer between species the more closely related they are. If you are a cannibal you are eating a species with a 99% similarity to you and are more likely to get diseases or parasites. Like kuru/mad cow/chronic wasting disease.
it precludes social behavior and all its benefits. Why engage in mutually profitable behavior when you can just eat those around you? This is thought to be one reason why pack-hunting is rare in some groups of vertebrates like monitor lizards.
on a broad-scale evolutionary perspective, cannibalism means removing members of your own population from the gene pool. It may be good for the individual but it's bad for the species as whole
cannibalism means you are feeding on an animal that is potentially your own size. That's a bad strategy in general. Most cannibalism in nature tends to be adults eating infants or adults scavenging carrion of their own species. By contrast predators are normally larger than their prey, with a few exceptions like pack-hunting wolves and lions.

Perhaps one also needs to distinguish occasional cannibalism and a situation where cannibalism is the main source of food. In this latter case the birth rate is always behind the rate of the population decrease due to the cannibalism. It is obvious for lions, but I think the argument could be made general for all species, based on energy considerations.

Further WRT point #5, if you are to be a successful carnivore, you really don't want to be hunting prey that can fight back, since that sort of prey can either kill you (making you an unsuccessful carnivore :-)), or injure you badly enough that you can no longer hunt, with much the same result.  So you would expect intra-species cannibalism to only involve eating weak members of the species - young, or moribund adults.


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

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

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

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

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

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

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