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In an ant (or bee) colony, what is the very approximate ratio of new breeders to workers?
For example, out of every 1000 eggs laid, X mature into drones and/or virgin queens.  That seems impossibly precise but it illustrates the kind of number I want well.  I'll accept answers for any species and any number of species, even one, with any amount of precision or lack thereof, because right now I can't even feel confident saying that there are more workers or more breeders, though I obviously suspect more workers.
I would also be ecstatic to have any live count just before the nuptial flight, i.e. for this colony in this study there were X workers, Y drones, and Z virgin queens just before the nuptial flight, or X workers and (Y+Z) breeders, or X% of the colony was breeders, or for this species on average X% are breeders just before the nuptial flight.
Anything.  Any one thing and I can accept it as an answer.
I can find any number of studies that talk about the sex ratio between drones and virgin queens, so I know someone is counting.  Maybe I'm not reading closely enough, but they always seem to slip away from giving all the numbers I need to figure this out for myself.

My guess is that the answer could be quite different for different species: I would recommend narrowing it down to a specific species so the question doesn't get closed as too broad.

Limiting it to a single species means that the answer can more easily be "We don't know".  I'm trying to avoid that by accepting an answer for any species because the last thing I want is "Oh, I know the answer for this other species but it's not the one you asked for so I'm going to walk away with the knowledge."
I've edited the question in an attempt to make that clearer.  If there is anything I can say to be even more clear, please let me know.

It will vary so drastically that the ratio will be exactly 1 (or 'NA' :D) for solitary species and close to 0 for species that make gigantic colony with a single queen.

I'm interested in the virgin queens that get pushed out of the hive for the nuptial flight, not the one or few laying queens in a colony.  Also, I will accept statistics for any one species, it does not have to be an average across multiple species, although I will accept that too if that is the number that's available.  I will even accept a single study that clearly publishes a number for one particular colony at some particular point in time, even if gathered incidentally while pursuing some other research goal.

So.
This answer is specific to the western honeybee, Apis mellifera, as there are massive amounts of data on them; more, possibly, than any other insect species. There has certainly been more data collected about them than any other hymenopteran.
At around the time of the nuptial flight, there may be as many as 60,000 workers in the hive, though likely number is more like 15,000 - 20,000. There will be either one (virgin) or two (one mated, one virgin) queens (the old queen will stay with the hive, if she is alive). There may be as many as 400 drones from the original colony (though usually the number is less, around 150 is typical; 10 - 50 of them will actually mate with the queen), and an equal number may join in the flight drawn from other colonies, especially in commercial beekeeping operations. Somewhere between 1000 - 6000 workers will take part in the nuptial flight with the virgin queen and the drones.
This means that in honeybees, the nuptial flight contains 1 queen:~5000 workers:~150 drones.
Data is drawn from many years working with bees and beekeepers. Opinions will vary somewhat depending on the beekeeper and the beekeeping methods. These are based, generally, on bees kept for clover and fruit pollination in the western USA.

Thank you!  I'm surprised at the high drone to virgin ratio but there you have it.


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functionality of protein based on amino acid covalently linked to something
This question is directly taken off from "challenge question" as part of my bio-engineering class.
The functionality of any individual protein covalently linked to a device is dependent on the specific amino acid through which it is chemically linked to the device.
Is this a true statement? I believe that different amino acid has different chemistry and orientation so it would affect the functionality but is it enough to say dependent on them. Also could you please provide an example if possible? I cannot think of an example. I would really appreciate your insight as well.

The if the protein is linked with a residue in the active site, for example, function would definitely be affected.

Your challenge question was meant to challenge you for a reason; your instructor wants you to reason it out. You should not rob yourself of the experience.

source: Stack Exchange

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

sort: votes


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What bug is this?
Saw this bug on a window in my house. Never saw a bug with antennae like this!
Edit: I live in NY, and saw this bug about 1 PM. Also, I found there were several more on other windows and I think I might have a problem!

Please see here: https://biology.stackexchange.com/tags/species-identification/info

I am not a good naturalist but I would say some kind of Scarabaeidae

Where is your location?

In case anyone finds it relevant: many of these bugs (10-20 it seems) were brought in from outside, nearby the house, with the firewood. Apparently these bugs are drawn to wood.

Sure looks like a Deathwatch Beetle (Ptilinus ruficornis) with pectinate antenae.

Source: https://bugguide.net/node/view/59669
This Encyclopedia of Life site also has some more information.

The antennae are also a sign of the animal's sex: both figures (Q & A) are males (the antennae of a female would be sawtoothed).

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


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why do these sounds make a dog unhappy?
Cross-posted from StackOverflow
This is an odd one. I'm not sure it's the right place to ask, but maybe there are some sound / dog experts who can chime in? (no pun intended)
We use two sounds on our website to indicate success and failure on a quiz. Those are very simple and short sounds.
Somehow one of our customers reported that her dog was whimpering and really upset with both of those sounds. He's normally fine with lots of other sounds that dogs are typically unhappy with including loud sounds, hoovers etc. She even said it happens when she uses headphones!
Other than muting, or replacing those sounds (and upsetting other dogs?), is there anything we can do to clean the sound or detect what specifically makes them upset this or other dogs?

Just a note:  I'd recommend deleting the cross-post on SO.  Of course, it will automatically get deleted in a while, but as a general rule, it's better to keep questions on a single site.  Welcome to the site!

Thanks @rotaredom. Good to be here :) I'm still not entirely sure where it fits best... I'm pretty sure it would require some cross-domain knowledge (computer/sound processing, and understanding of animal physiology).

I get a message that "questions with open bounties cannot be deleted", so I am currently unable to delete it...

I just played the sounds on loud with my three dogs, all within a ~3 feet of me (they're sheepherding breeds, so they stay close to their human.) Not a one had a reaction, though I tried several times. My youngest dog, though, a Belgian Tervuren, is very sensitive to sound, and whimpers when I play the live version of Jeff Buckley's "Hallelujah" in the car. Not the regular version, mind you, just the live version, which is much more tender (as if that's possible.) So, my guess is that your main assumption is wrong. One dog only.

P.S. I love your pun!

Thanks for willing to experiment on your three dogs, @anongoodnurse. I thought about doing it, but I don't have a dog, and wasn't so comfortable trying out something weird on strangers' dogs. That's already very useful. At least it's good to know that it's not a widespread issue... at least with the current sample of 1 out of 4, ;-)


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Help me identify species of fruit fly?
I found this fruit fly in Pune/India. It was about 1 cm in size. I explored info on several species in same region, but they were different in appearance, especially that black spot in middle of body.

No, it appears similar to fruit flies from Tephritidae family like Oriental Fruit fly @Remi.b

Indeed! I removed my comment! +1

This insect might be Bactrocera dorsalis.

It looks similar to this species based on the characterstic yellow spots, shape of the abdomen, as well as the light brownish orange stripes on the abdomen.
I had arrived at this conclusion by reverse-image searching the second picture that you have posted and observing the thorax and abdomen patterns. This image shows a very similar pattern as shown in your second picture:

The Wikipedia article has quite some stuff to say,

Bactrocera dorsalis is a species of tephritid fruit fly that is endemic to Southeast Asia, but has also been introduced to Hawaii, the Mariana Islands and Tahiti. It is one of the major pest species in the genus Bactrocera with a broad host range of cultivated and wild fruits.

Considering that you had found this insect in Pune, it makes a lot of sense to conclude that this is, in fact, the insect that you have found.

Do you know Indian flies well? Otherwise, it appears really premature to state "This insect is...". There are probably hundreds of related species in India, and the general color pattern are often very similar. I have an ok general knowledge of eg Swedish hoverflies (far from being a specialist), and based on this I would rather say that it is probably not B. dorsalis since too many small things that are often fairly stable seems not to add up. These include the posterior color of the scutellum, color of the femur towards the knee, distinctness of pattern etc. Might be a related sp. though

@fileunderwater I agree. There is black dot in middle of body which does not appear in any image of Bactrocera dorsalis.


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What are the good and bad cholesterol ?
I have question about cholesterol, as I know we can get cholesterol using vegetables and meat, so what is good and what is bad ?

Whats wrong with question ?

@xusr the comment as written makes a fine answer - it's referenced and all.

Possible duplicate of What is/are the molecular differences between HDL and LDL cholesterol?

Original Answer (posted originally as a Comment)
It is now accepted that high cholesterol causes atherosclerosis. Cholesterol a major component of the plaques that block arteries. 'Good' and 'bad' cholesterol refer to the way cholesterol is transported in the bloodstream.
'Bad' cholesterol is cholesterol in the form of low density lipoproteins or LDL, and 'good' cholesterol is in the form of high-density lipoproteins or HDL.
Or at least that is how it used to be. It is still accepted that high concentrations of LDL in blood promote atherosclerosis, that is high levels of LDL may still be considered 'bad', but drugs that specifically raise the levels of HDL have had serious adverse effects.
Check out this great article: Cholesterol and Controversy: Past, present and Future by  Jeanne Garbarino, especially the section on "Deconstructing Cholesterol: “Bad” is still bad, but is “good” still good?". It is hard to know what the current position is. And check out the work of Brown and Goldstein.
Edit
Goldstein, in his Nobel lecture, famously said (see here)

Cholesterol is a Janus-faced molecule. The very property that makes it useful in cell membranes, namely its absolute insolubility in water, also makes it lethal. For when cholesterol accumulates in the wrong place, for example within the wall of an artery, it cannot be readily mobilized, and its presence eventually leads to the development of an atherosclerotic plaque.

Cholesterol may be synthesized in the body, or obtained from the diet.  The site of biosynthesis is mainly the liver. Cholesterol and fats (triacylglycerols) are transported in the bloodstream as lipoprotein particles, which may be roughly described as a lipid core surrounded by a protein coat, and may be viewed as a mechanism for transporting insoluble fat molecules (by 'coating' them with a soluble protein exterior).
There are five main classes of lipoprotein particles (see, for example, Berg): chylomicrons, very low density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL)
Cholesterol (and fats) are transported from the liver to other tissues in the form of low-density lipoproteins (LDL).  High-density lipoproteins, on the other hand, pick up cholesterol and fats in the blood and from specialized cells and transport them to the liver. Hence the names 'bad' and 'good' cholesterol.  (In reality, of course, things are more complex than this simple scenario: for a very readable account, see Berg).
The ratio of 'bad' to 'good' cholesterol, ie the ratio of LDL to HDL may be used diagnostically, and a healthy LDL/HDL ratio is about 3.5 (see Berg), but in view of the studies cited by Garbarino a low ratio due to high concentrations of HDL (rather than low LDL) might not be so great either. In fact, if LDL is in check, there may be no benefit to raising HDL (Garbarino article).  But I suppose the physicians will always find a way to waffle (and to charge for the privilege).
It is a common misconception that plants do not contain cholesterol. (My original answer to this question attempted to promulgate this nonsense). In particular, plant membranes do contain cholesterol. However, the amount of cholesterol in plants is low compared to that found in animals (Behrman & Gopalan, 2005).  But it is certainly not zero. The nucleus of maize shoots contain significant amounts of cholesterol, for example (Kemp & Mercer, 1968).
This great reference, Cholesterol in Plants, by Behrman & Gopalan (2005) suggests that the following paragraph should be inserted into biochemistry texts.

More than 250 steroids have been described in plants.
  Of these,  perhaps  sitosterol,  which  differs  from  cholesterol by an ethyl substituent at position 24, is the most
  common.  But  plants  also  contain  cholesterol  both  free
  and esterified. Cholesterol occurs as a component of plant
  membranes  and  as  part  of  the  surface  lipids  of  leaves
  where it is sometimes the major sterol. The quantity of
  cholesterol is generally small when expressed as percent
  of  total  lipid.  While  cholesterol  averages  perhaps  50
  mg/kg total lipid in plants, it can be as high as 5g/kg
  (or more) in animals.

A great generalization is the following (Behrman & Gopalan, 2005)

Prokaryotes do not contain cholesterol

These authors also suggest that one of the reasons for the common misconception that plants do not contain cholesterol is "legalities of food labeling that allow small quantities of cholesterol in foods to be called zero".
I suppose we should not be too surprised that plants can make cholesterol. They can of course, make steroids, the Mexican yam being the original source of a precursor of a particularly important one.
A key enzyme in the biosynthesis of cholesterol is HMG-CoA reductase, which is the target for statins, and these drugs  may be used to lower serum cholesterol levels (but there may be side-effects).
One interesting thing about the biosynthesis of cholesterol is that the final cyclization step requires oxygen which has lead to much philosophical and evolutionary debate (see, for example, here).
Finally, another quote from Goldstein

Cholesterol is the most highly decorated small molecule in biology. Thirteen
  Nobel Prizes have been awarded to scientists who devoted major parts of their
  careers to cholesterol. Ever since it was first isolated from gallstones in
  1784, almost exactly 200 years ago, cholesterol has exerted a hypnotic fascination for scientists from the most diverse domains of science and medicine

You cite: "While cholesterol averages perhaps 50 mg/kg total lipid in plants, it can be as high as 5g/kg (or more) in animals." That is a factor of 100. How can this make you consider your first answer "promulgating nonsense"? Quantities do not count?

The question as stated is unclear as to what is being asked.
If the question is whether ingested cholesterol from whatever source is good or bad, then the answer is that dietary cholesterol is superfluous to human nutrition since it can be synthesized by the liver, and the latest guidelines suggest to keep intake as low as possible.

While adequate evidence is not available for a quantitative limit for dietary cholesterol in the 2015-2020 Dietary Guidelines, cholesterol is still important to consider when building a healthy eating style. In fact, the Dietary Guidelines states that people should eat as little dietary cholesterol as possible. 1

The main source of dietary cholesterol is overwhelmingly from animal sources. A meta-analysis published in August 2017 of vegetarian diets found that

Of the 8385 studies identified, 30 observational studies and 19 clinical trials met the inclusion criteria (N = 1484; mean age, 48.6 years). Consumption of vegetarian diets was associated with lower mean concentrations of total cholesterol (−29.2 and −12.5 mg/dL, P < 0.001), low-density lipoprotein cholesterol (−22.9 and −12.2 mg/dL, P < 0.001), and high-density lipoprotein cholesterol (−3.6 and −3.4 mg/dL, P < 0.001), compared with consumption of omnivorous diets in observational studies and clinical trials, respectively. Triglyceride differences were −6.5 (P = 0.092) in observational studies and 5.8 mg/dL (P = 0.090) in intervention trials. 2

concluding that plant based diets reduced total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol ( as the latter is used in reverse cholesterol transport so with less circulating cholesterol there is naturally less to transport ) but triglycerides were unaffected.
So, if you eliminate animal based foods (and therefore the main source of dietary cholesterol) then the studies suggest you are likely to improve your lipid profile which is presumably one reason for the guidelines.

https://www.choosemyplate.gov/2015-2020-dietary-guidelines-answers-your-questions
Association between plant-based diets and plasma lipids: a systematic review and meta-analysis https://academic.oup.com/nutritionreviews/article/75/9/683/4062197


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what is the active ingredient in cymbopogon citratus that repels mosquitoes?
We are doing a project about mosquito repellants using lemongrass, cymbopogon citratus. But, based on our researches online, it stated that it was all a hoax and a better alternative is its cousin cymbopogon nardus.So, is the hoax actually true??? And please tell about the active mosquito-repelling ingredient.

I think the problem isn't a hoax; it's just that people are overly excited about 'natural' as opposed to synthetic remedies.
C. citratus might be hazardous - the active ingredient is citral α-pinene.
C. nardus might be hazardous, too - the active ingredient is citronellal or citronella. [There's confusion, in the article, about whether citronella has other plant chemicals in addition to citronellal.]
They're both partially effective as insect repellents.
"It is commonly assumed that plant-based repellents are safer than DEET because they are natural. However, some natural repellents are safer than others, and it cannot be assumed that natural equates to safe."
This info all comes from a 2011 scientific article about plant-based insect repellents:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059459/
Here's a link to a table with the results, summarized below:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059459/table/T1/?report=objectonly
And a table with possible toxicities:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059459/table/T2/?report=objectonly
Citronella has found its way into many commercial preparations through its familiarity, rather than its efficacy. Citronella was originally extracted for use in perfumery,..."
C.nardus is at least somewhat effective in 3 lab studies; citronellal    is the active ingredient.
C. citratus - the active ingredient is citral α-pinene.  Again, it's at least partially effective in 3-4 studies, e.g., "74% protection against An. darlingi for 2.5h"
Here's a scientific article from 2011 about the scientific basis for the therapeutic use of Cymbopogon citratus, stapf (Lemon grass):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3217679/
But it doesn't mention 'insect repellent' among its possible uses!:
"Studies indicate that Cymbopogon citratus possesses various pharmacological activities such as anti-amoebic, antibacterial, antidiarrheal, antifilarial, antifungal and anti-inflammatory properties. Various other effects like antimalarial, antimutagenicity, antimycobacterial, antioxidants, hypoglycemic and neurobehaviorial have also been studied."


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Do we know that PrEP actually prevents infection, rather than masking it?
Pre-exposure prophylactic treatment (PrEP) for HIV is commonly said to reduce infection rates by more than 75%.
Similar treatments for already-infected patient treatments do not cure HIV, but reduce viral load to undetectable levels. If treatment of these patients is stopped, viral load will eventually rise.
Do we know that PrEP actually prevents infection, rather than masking it? Are there no cases of someone engaging in no risk behaviors, then going on PrEP and engaging in risk behaviors, then coming off it, not engaging in any further risk behaviors, and nevertheless testing positive for HIV?

"Are there no cases of someone being on PrEP, coming off it, and then testing positive for HIV?" is absolutely the wrong question to ask and is not how scientific study works, but everything else here is a good question.

Edited to improve last section

Still bad. Asking "are there no cases" implies that if you saw one case, you would conclude it's a masking effect. That's wrong, especially in light of the previous claim which is a 75% reduction: clearly there are still cases that PrEP does not prevent. Furthermore, not "engaging in any further risk behaviors" is an impossible thing to ask for in a clinical trial. You would have absolutely know way to know if there is a masking effect or if people are just lying about not engaging in further risk behaviors.


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How many possible human genotypes are there that produce distinct phenotypes?
This and this Quora question ask how many unique human genotypes are possible. The answers take the combinatorial approach of raising the 4 possible base pairs to a power which is some appreciable fraction of the 3 billion base pairs in the human genome, to get absurdly large numbers like $10^\text{many millions}$. But as many of the answers point out, this is a gigantic overestimate, because the vast majority of those gene sequences wouldn't produce anything remotely resembling a human, and even among the tiny fraction that do, there are enormous numbers of sequences that produce phenotypically identical humans (after all, most mutations don't produce any detectable effect). (When I say that two genomes "produce indistinguishable phenotypes," I am holding the environment fixed and only considering the genome's contribution to the phenotype.)
It seems to me that in order to avoid counting non-human genomes or double-counting phenotypically equivalent genomes, the better approach is use genes rather than base pairs as the combinatorial building blocks. The human genome has at most 20,000 protein-coding genes, and apparently most genes have two alleles, although some have only one and others have more than two. (I'm defining an allele as an equivalence class of phenotypically indistinguishable DNA sequences that form a single viable gene. For the purpose of this calculation, we can mentally group together the two chromosomes' versions of the same gene, and increase our allele count to include any interactions between the two chromosomes' sequences.) [Edit: according to the answer below (which I find much more trustworthy than this Quora link), this is a huge underestimate for the typical number of alleles per gene, with a better estimate being ~300. Needless to say, this dramatically changes the final answer.] This would produce a maximum of $2^{20000} \approx 10^{6020}$ possible phenotypically distinguishable genomes. While this is obviously still an astronomically high number, it's an infinitesimally tiny fraction of the estimates produced in the Quora answers.
Is my reasoning correct?

When you're looking for specific estimates in biology (such as e.g. the number of coding sequences in the human genome), I recommend starting with the website bionumbers rather than Quora or wikipedia.

Is my reasoning correct?

I can see at least five major problems in your reasoning.
Do most genes have two alleles?
The claim that most genes have two alleles is wrong. Actually, the entire top answer in the linked quora post is wrong. The person answering confounds simplified cases used to teach intro genetics class with what nature really looks like.
As about one every 100 nucleotides is a SNP (bionumbers) and given that a gene is on average about 30k sites (bionumbers), the average number of alleles is probably closer to 300 although that would be counting synonymous mutations which is a bit unfair. About 20% of substitutions are synonymous (bionumbers), which would lead to an estimate of 240 alleles per gene on average. Even if you consider that 90% of these mutations have no effect on the phenotype (which is maybe an overestimation, bionumbers), you're left with 24 alleles per gene. Of course, this is a very vague estimate but it is, I think, much better than 2.
Non-coding sequences
Also, the majority of phenotypic distinction is caused by non-coding (non - gene) sequences such as regulatory sequences. You cannot ignore them in the calculation.
According to this pie chart (not sure if we can trust this chart though), 5% of the genome is made of regulatory sequences (against 1.5% of the genome that is coding).
One genotype ≠ one phenotype
If you have in mind that one genotype = one phenotype, then it would be very wrong too. There is environmental variance, epigenetic variance and other sources of variance (e.g. developmental noise) that underly phenotypic variance (see this post to understand the sources of phenotypic variance in populations).
indels and CNV
You are only considering substitutions. There are plenty of indels and ohter CNV too.
The existence of this variation does not only complicate the question, it actually renders the question a bit undefined because if you allow the genome to take any size, then number of possibilities is necessarily infinite.
Diploidy
Your calculations assume individuals are haploids. But humans are diplontic.
Gene are not atomic
Genes are not units that cannot be split. Recombination do happen in genes and it would be wrong to take the number of variants at genes (or at any other type of sequences) as basis for your calculation
Attempt at a calculation
So, ignoring many of the problems, here is my attempt at a calculation.
There are about $1.5 \cdot 10^7$ SNPs in the human genome (bionumbers). Based on this pie chart (not sure if we can trust this chart though), I will assume that about 6.5% of them are in coding or regulatory regions and I will assume (based on that paper) that 90% of them have no fitness effect and by extension I will assume it also mean no phenotypic effect (although the actually percentage should been increased). This will result in $1.5 \cdot 10^7 \cdot 0.065 \cdot 0.1 = 97500$  SNPs of interest. It results into $2^{97500} ≈ 10^{32500}$ possible haplotypes of interest. The number of possible genotypes of interest is therefore $\left(10^{32500}\right)^2 = 10^{65000}$. I also assumed absence of epistatic interactions otherwise the number would become so fantastically closer to infinity!
Interest in the calculation
I fail to find much interest in making such calculation because it entirely depends upon the model we want to consider. There is no offense against the OP's question here (and in fact the OP shows that he understands the importance of the considered model), I just want to make sure readers understand that these calculations are based on a very arbitrary model and one cannot make any sense of the given result without understanding the model.
The calculations from the Quora post that OP linked assumes that every SNP could be polymorphic. As long as the intention behind the calculation is not clearly stated, this is a perfectly reasonable model. Here, in my attempt, I assume that the number of SNPs is fixed, but any combination of it is possible. This can or cannot be a fine assumptions. Also, the estimates of the number of SNPs are of course, estimates of the number of SNPs that are at a frequency that is not too low to be detected! So, if we were, for some reason, to consider all the SNPs (by assuming some drift-mutation equilibrium), then the result would differ quite a bit. But again, it all depends upon the specific model one wants to consider.

Thank you for the thorough answer. I completely agree that the question is ill-defined and any numerical answer is pretty much meaningless. My motivation for asking the question was simply to verify that a naive calculation based solely on the number of base pairs in the genome is even more meaningless and arbitrary, and gives enormous overestimates compared to any possible even vaguely reasonable model.

i actually would also agree with @Remi.b the number of phenotypes would include all the possible physical behaviors, appearances and other properties of a living thing.  since most phenotypes are the result of combinations of genotypes in unpredictable and nonlinear ways, with continuous (as opposed to 0/1) sorts of behaviors - the number of possible phenotypes are incalculable.

@tparker "My motivation for asking the question was simply to verify that a naive calculation based solely on the number of base pairs in the genome is even more meaningless and arbitrary" One additional thing to think about here is the actual number of people, somewhere around 10^10 or 10^11 depending on how many generations you want to consider. In that context, the distinction between 10^65000 and 10^6000 is not really all that important, either, from a sampling perspective. The distinction is going to be more important if you think about more numerous organisms with smaller genomes.


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Could the protein dystrophin be artificially synthesised?
Could the protein dystrophin be artificially synthesised and if so could patients with DMD (Duchenne Muscular Dystrophy) benefit from it?
//Now I don't have much scientific background other than a high school biology qualification
I met someone the other day the same age as me who suffers from DMD, so I did some research and curiosity led to this question.
Sorry if I used the wrong tags or/and this question isn't allowed. \

Great question.
Yes, it is almost certainly possible to artificially synthesize just about any protein. There can be difficulties with certain proteins, but these are more engineering problems rather than true limits to artificial synthesis.
The problem is getting the protein where it needs to be to be functional!
A great comparison is insulin. Insulin is an important regulatory protein that floats around in the bloodstream. That makes insulin therapy a relatively straightforward solution to a problem of not enough insulin: all you have to do is make or isolate some insulin and inject it into the bloodstream.
Dystrophin, however, is a structural protein that acts inside cells. Proteins are really big, and they can't be simply taken up by cells. There's no mechanism to get an arbitrary protein inside: any proteins that can be taken up by cells need to do so via some specialized mechanism.
If you wanted to replace a defective allele for dystrophin, then, the most feasible approach would be gene therapy: getting a patient's own cells to produce a functional copy of the protein. Efforts to entirely or partially replace dystrophin via gene therapy are a current area of research, but there are still many challenges to gene therapy approaches in general.

References
Harper, S. Q., Hauser, M. A., DelloRusso, C., Duan, D., Crawford, R. W., Phelps, S. F., ... & Chamberlain, J. S. (2002). Modular flexibility of dystrophin: implications for gene therapy of Duchenne muscular dystrophy. Nature medicine, 8(3), 253.
McGreevy, J. W., Hakim, C. H., McIntosh, M. A., & Duan, D. (2015). Animal models of Duchenne muscular dystrophy: from basic mechanisms to gene therapy. Disease models & mechanisms, 8(3), 195-213.
Pichavant, C., Aartsma-Rus, A., Clemens, P. R., Davies, K. E., Dickson, G., Takeda, S. I., ... & Tremblay, J. P. (2011). Current status of pharmaceutical and genetic therapeutic approaches to treat DMD. Molecular Therapy, 19(5), 830-840.
Verhaart, I. E., & Aartsma-Rus, A. (2012). Gene therapy for Duchenne muscular dystrophy. Current opinion in neurology, 25(5), 588-596.


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Are molecular machines encoded in the DNA?
I don't know much, if anything, about molecular biology. I watched the "inner life of the cell" on Youtube which triggered my curiosity about how these molecular machines came to be. My simple understanding is that if these molecular machines are encoded in the DNA, then they are "evolve-able" by mechanisms such as natural selection. Is that case? And if so, can we identify which part in the DNA sequence have the encoding for these molecular machine such as the Kinesin? Do molecular motor machines get synthesized by the RNA as well?

I added an answer to your 'can we identify which part' subquestion to my answer.

Yes.
The "molecular machines" you are referring to are particular proteins.
The specific one you are referring to, kinesin, is involved in movement along microtubules, part of the structure of the skeleton of a cell, but other proteins act as their own kind of machine to do their own tasks: sometimes catalyzing a biochemical reaction, or responding to a type of stimulus, or forming a shape or structure, or combinations of all of the above.
Protein-coding sections of DNA are well-studied, and there are substantial databases of known proteins. If you go to wikipedia you will see a whole list of different kinesins, if you click on one, for example, KIF1A, on the right hand side it shows you it is found on chromosome 2 in a human, starting at 240,713,764 base pairs and ending at 240,820,308 base pairs. Information for the mouse is also located there.
Proteins in DNA-based life are all synthesized by first producing an RNA transcript from the DNA, which is effectively an RNA copy of a short stretch of DNA, which is then translated into protein. Other RNA molecules are involved in this process, too, as the rRNA part of the ribosome (sort of a 'protein factory') as well as tRNA which carries the amino acid components of proteins as they are being built. Transcription and translation are central to understanding biology at the molecular and cellular level.
Not only can all proteins, from kinesin to collagen, evolve, they all have evolved through natural selection and other evolutionary mechanisms, and they continue to evolve today in all living organisms. Without evolution, no biology would exist. RNA-based biology (today, mostly some of the viruses) is also subject to evolutionary mechanisms, so that isn't something unique to DNA, but rather to heredity and biology in general.

Some molecular machines are also be build entirely of RNA, in otheres like ribosomes, the functional portions is made of RNA and the proteins are there to stabilize the RNA.

Yes, it's fair to say molecular machines are encoded in the DNA.  As you say, kinesin is a molecular machine - a motor protein that moves molecules along microtubules, which are also proteins.  Protein enzymes are one of the most common molecular machines in cells - they build and break down molecules, among other things.  Membrane channels are proteins, too, and they could be called molecular machines - I'm picturing a drawbridge that lets tall ships pass when it's open and not when it's closed, though channels are more like holes in the cell membrane than like drawbridges.
The sequence of bases [A, G, C and T] in the DNA tells the cell what protein to make. And, yes, mutations occur in the DNA sequences, which results in mutant proteins - or, variant proteins, because there are often several versions of a protein that work fine.
Wikipedia's article - https://en.wikipedia.org/wiki/Kinesin - tells about the family of kinesis proteins, which are coded for by a corresponding family of genes in DNA.
Yes - RNA is important in synthesizing molecular machines. It carries copies of the DNA codes for different proteins in our genes.  It has 3 of the same bases ['letters'] as DNA - A, G, and C, but instead of T it has U, which goes in the RNA sequence wherever T would be in DNA.  The RNA copies of the genes go to the ribosome, an amazing molecular factory that takes the information in the RNA copies of the genes and uses it to make proteins, which have amino acids instead of the 4 bases of DNA and RNA.


text:
What is the difference between GFP and rhodopsin?
GFP and Rhodopsin are both fluorescent proteins. What is the main difference between GFP and Rhodopsin in terms of how they work? I know that their excitation and emission wavelengths are different, but in terms of the biological mechanism, how are they different?

Rhodopsins are photo-signal receptors. GFP does not function as a receptor.

@RoniSaiba so do you mean to say that rhodopsins carry out a subsequent biological function upon being exposed to light, whereas GFP does not have this subsequent function?


text:
How does fungi network transfer substances between plants?
How does fungi network transfer substances between plants?
I recently read a short article about fungi network. And I am wondering  about how fungi network works (Mechanism).

Plants have fungi network. And a plant which lost it gets prone to insects.

Wikipedia link

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


text:
How exactly is casein digested?
I mean it seems first step is rennin or pepsin digestion in stomach - then what happens with remaining peptides?
I am interested in the whole process from casein to amino acids.
Is there brush border enzymes involved in the small intestine or all process is in the stomach?

Casein proteins are soluble in milk but form insoluble curds once they reach the stomach, making it hard for digestive enzymes to break them apart. Slower digestion also is associated with delayed release of the protein's amino acids into the bloodstream.

milkgenomics.org/article/dairy-protein-digestion-life-slow-lane/
These properties of milk caseins may have evolved to benefit mammalian infants, but slowed digestion offers the benefit of increased satiety to milk drinkers of all ages. Eating foods, like milk, that take the slow lane may mean eating less food overall.
Casein proteins in milk form small spheres, called micelles, with the hydrophilic (water-loving) portions of the protein on the outside of the sphere and the hydrophobic (water-fearing) portions on the inside. With hydrophilic structures on the outside, the micelles are soluble in water (or milk, which is mostly water) [1,2].
But when the micelles reach the stomach, “one of the most ingenious events in nature takes place” [2]. The digestive enzyme chymosin snips one of the bonds on the exterior protein (known as the kappa subunit), leaving only the hydrophobic subunits inside [1]. Without their protective layer, the now insoluble proteins form a curd.

It looks like various proteolytic enzymes digest the casein 'curds' in the stomach and intestine.  "Human proteolytic enzymes were obtained in the
activated state by collecting human gastric (HGJ) and
duodenal juice (HDJ)" This is the article: In vitro digestion of bovine and caprine milk by human gastric and duodenal enzymes
Dipeptidyl Peptidase IV's  (DPP IV), a type of protease, has been shown to break down the proteins in gluten and casein. https://www.livestrong.com › Diseases and Conditions

It's in our intestine: https://www.ncbi.nlm.nih.gov/pubmed/7522442

Brush Border Enzymes & casein [that one gives me your stackexchange question!]
This article: "Effect of diet on enzymes of the brush border of the small intestine and kidney of rats" says: "Diets with low starch and high casein contents resulted in higher specific activity of leucineaminopeptidase in the small intestine than diets with high starch and low casein contents."
You can find out a bit more about that enzyme by reading the abstract of the article.
'Digestion of peptides in small intestine' in Google gives this: "The brush border of the small intestine is equipped with a family of peptidases. ... They function to further the hydrolysis of lumenal peptides, converting them to free amino acids and very small peptides. These endproducts of digestion, formed on the surface of the enterocyte, are ready for absorption."

www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/absorb_aacids.html
[Hint - it's google searches all the way, with an occasional scholar.google search.  ... Maybe I should get back to my own work and let you all do the searches!]

Thanks for the answer! The problem is that after a lot of hours of reading i was convinced that i will be able to digest very aged cheeses like parmesan because they are predigested by bacteria - the casein should be degraded to free amino acids - i tried 22 month old parmesan - the result was disaster. Also i eat the cheese with ginger enzymes that should work as DPP 4 enzyme - it just did not worked. So after reading your answer it seems there are a lot of things that can go wrong with casein digestion especialy from concentrated foods like cheese.

pH was a variable in a lot of the research, but I didn't talk about that.  I'm sorry about your cheese 'research' - I think I have a slight increase in mucous with dairy products, so I don't tend to eat cheese at home.  But it's only a little problem.


text:
Exact meaning of the term "clutch"
When reading a Wikipedia article to do with chickens, I have come across the term "clutch", but I was not able to entirely figure out what this word means. I was wondering whether the term clutch can be used to refer to any set of eggs by birds, reptiles, and amphibians, or whether a clutch must consist of a set eggs all by the same bird, reptile, or amphibian. In general, if a typical clutch by a well fed chicken amounts to a dozen of eggs, that seems like a lot of eggs for a chicken to hold within its body prior to laying them, hence my question about clarification and about what number would actually fit (I have seen as high as fifteen). It is this simply the number of eggs expected to live concurrently in a typical nest where more than one chicken would breed?

A clutch usually refers to all the eggs for a single reproductive event or laying or location. It can mean either all those laid by one organisms in one event or all those laid in a population in a single time and place. Which is usually clear in context.
Even just for an individual it is a bit vague however and can refer to one laying or multiple layings if they happen close together in time.
There is also a usage difference by specialization, agricultural scientists tend to favor a boarder usage for instance.

Thank you for your answers. Could you please indicate what other areas of specialization that make use of such a term "clutch" exist besides agricultural science? Thanks.

Could you please also identify the typical and maximum number of eggs which may sit in a chicken's body? Thanks.

chickens lay around one egg a day, so there clutches are built incrementally, average clutch size is around 12 eggs. rarely does more than one fully developed egg sit in a chickens body, the key term is fully developed.

As for other usages, everything from paleontology to ethology. basically any branch of zoology could be dealing with eggs

Well, strictly speaking from an etymological viewpoint, a clutch is:

"a brood, the number of eggs incubated at any one time," in reference to chickens, 1721, a southern England dialectal variant of cletch (1690s), noun from cleck (v.), which is from Middle English clekken "to hatch, give birth to" (c. 1400), which is probably from a Scandinavian source (such as Old Norse klekja "to hatch"), perhaps of imitative origin (compare cluck (v.)). Compare batch/bake.

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


text:
Are drones from one honey bee queen all clones?
The Honey Bee queen lays eggs that develop into worker bees (female) if she fertilizes the egg.  If she does not fertilize the egg, it will develop into a drone (male).
The drone only has the queen's DNA so are all drones exact copies of each other, ie clones, or is there some other mechanism that will make each brother slightly different?

The queen is diploid; the drones are haploid. Meaning the queen has two copies of each chromosome, and the drones have only one. So for each gene, the queen has two copies and passes one of those copies on to the drone.
This means the drones are different for exactly the same reason female bee siblings, or human siblings, are different: because every parent has two copies of a gene, that are often different, and passes only one of those to their offspring.
If the queen were homozygous for every allele, i.e. the two copies of all her genes were identical, then the drones would indeed be genetically identical. But this is true as well of the children of two completely homozygous parents.
See this page on inbred laboratory strains of animals (animals which are inbred to the point they and their offspring are genetically identical to each other):
http://isogenic.info/html/inbreeding___it_s_effects.html

F1 hybrids, i.e.  the first-generation cross between two inbred strains, are isogenic but not homozygous.

In other words, if you have two parents who are genetically different, but have two identical copies for all of their chromosomes, their children will be isogenic (have exactly the same genes); they all have two copies of their genes, got one copy from their father and one from their mother, and those two copies might be different from each other (their mother and father have different alleles), but all the children got those same two copies because they're the only copies their mother and father have.


text:
Why does botulinum toxin cause only NMJ symptoms?
Botulinum toxin acts by preventing release of ACh by cleaving SNARE proteins. But if it is acting on snare proteins shouldn't all vesicle releases be effected? Why is it limited only to the acetylcholine vesicles in the motor neuron bat the end plate? Why not some other neurotransmitter at some other place like GABA in the brain?


text:
Why does DNA mutate?
I just read that pregnancy in space would be super dangerous because - among other reasons - of a higher risk of mutations due to radiation. This made me wonder: why does the DNA in organisms mutate? What are the main natural reasons? Is this due to the construction of DNA and would happen even in "perfect" conditions or is it due to something that is in the environment, like radiation?
So far I got two answers on reddit and also asked this question to a doctor and what I heard is along the lines of "this is how it is". I heard about "cells being worn out". But what makes the process non-deterministic, probabilistic? I guess I don't know enough about biochemistry to formulate the question, but I guess it's related to "given certain conditions, what determines at which point (and what kind of) a mutation occurs?"

I got something that is probably at least a partial answer: "peroxides, wrong pH, nanoparticles that can go through cell membranes".

If I am not mistaken, the vast majority of mutations happen during DNA replication.
DNA must replicate itself so that cells can replicate itself. The DNA polymerase is one very important protein that replicates DNA. The human genome (to consider this example) is 3.5 billions nucleotides long. Just to realize how long is 3.5 billions letters, let's make a book analogy.
Book analogy

In the Harry Potter series, there are about one million words (ref).
In the LOTR series, there are about one 400 thousands words (ref).
In the Chronicles of Narnia series, there are about 230 thousands words (ref)
In the King James Bible, there are about 788 thousands words (ref)

This sums to about 2.4 millions words. As, in english, there are 5.1 letters on average per word (ref), this lead to a total of about 12.3 millions letters. Imagine you have to rewrite all of these books almost 300 times (12.3 millions * 300 ≈ 3.5 billions)! How many typos would you make?
There are several cell divisions between a zygote and the ovule/spermatozoid produced by this individual but as most mutations happen during meiosis, I will just ignore mitotic mutations. The DNA polymerase makes about one typo every 100 millions nucleotides (Kong et al. 2012; Rahbari et al. 2016)! So really, the DNA polymerase is doing a pretty good job!
What is causing mutations?
Shit happens
I am hoping that form the above analogy, you may have a sense that mutations are just small mistakes. They happen because the replicating machinery is not perfect. Sometimes a molecule comes sideway, does not bind very well and another molecular passing by sticks to the DNA, etc.. Errors happen just like you would be making a lot of typos, rewriting books.
Mutagens
There are of course factors that can affect this mutation rate. Physical, chemical and biological agents increasing the mutation rate are called mutagens and they include radiation decay, ultraviolet radiation, ROS, benzene as well as some viruses and some parasitic bacteria.
Variation along the genome
Note also that the mutation vary along the genome too. Regions with high repeats (e.g. AATAATAATAATAATAATAATAAT) such as microsatellites for example tend to have a much higher mutation rate.
Variation among species and Drake's rule
Mutation rate also vary among species. There is a general tendency that the per nucleotide mutation rate negatively covary with the genome size, a phenomenon called Drake's rule (see for example Bradwell et al. 2013 or one of the early Drake's paper).

Short answer, Chemistry runs off probability, and life and DNA replication are in the end chemical reactions.
DNA is a chemical, and the bonds between different nucleotides sequences are all extremely similar, if there was not an opposing strand, mutations would be extremely common becasue any sequence is essentially equally energetically favorable,(AKA equally likely probabilistically/chemically). Having two joined strands means you cant just swap nucleotides becasue they can't bond across strands equally well, there is a heavy chemical bias for only bonding with the opposing partner. A=T C=GT. Any other bond is less energetically favorable ( AKA less likely, which is not the same thing as impossible). The dual strand nature of DNA makes errors less likely but we are still talking chemistry and no chemical process is absolutely perfect, even if you burn carbon and oxygen in perfect ratios to get CO2 you will still get CO, carbon monoxide, just do to the physical (and thus probabilistic) nature of chemical reactions. Even the strength of the bond between the two stands can work against it as f a mutation does slip in the DNA will still hold together, and if it gets replicated before an error correcting mechanism catches it it will stick around. The kicker is although a DNA is very unlikely to mutate, there is a lot of it so even the extremely unlikely still occurs, DNA also has to be split apart to be replicated, during which mutations are far less energetically unfavorable.
Cells actually have dozens of error checking mechanisms and chemical stabilizers to limit how many of these can get through or occur however again this is a physical chemical process, thus it will not be perfect. Even without these mechanisms DNA replications is still fairly reliable, but many organisms have gigantic genomes meaning even reliable as a swiss watch is still not good enough. It is simply impossible to create a perfect copying mechanism that has high turnover that operates in the real world there are just to many interactions. the fact many replications are happening at once does not help since sometimes these many disjointed strands can end up bonding together causing the error correcting mechanisms to cut out entire sections, or mix them up trying to fix it.

Mutations occur due to sudden and unpredictable changes in the structure of DNA. Radiations, particularly those of energies of ultraviolet and higher are capable of breaking the bonds that make up DNA. This fragments the DNA. While DNA has mechanisms to counter this, and reform as a complete strand, it’s not perfect and the original DNA might not be made. Oftentimes, a small error such as base pair swaps or a missing pair could occur. These changes are reflected as mutations.

As ultraviolet radiation forms thymine diamers due to free radical addition reactions, this is one of the environmentatally caused damage to DNA. There are various mutagens which do the same. Since DNA is a chemical molecule the fate of any chemical molecule is the tendency to undergo changes, even during normal conditions chemical reactions occur. Take for example the transformation caused by deamination of cytosine residues which changes it into uracil or deamination of adenine to form hypoxanthine. Another important reaction is hydrolysis of glycosyl bonds between sugar and nucleotides creating a DNA lesion more commonly called depurination. 10000 purines are estimated to be lost in 24 hrs in mammalian cells increasing concentration of acids by any random mechanism might also accelerate the depurination process. So DNA like any chemical material is subjected to changes though there are processes to check this process still it happens. Moreover during replication there are practical chances of error in spite of various check points. Depending upon the chemistry of the reaction DNA is undergoing at which point a mutation would occur might be studied, numerous biochemical process takes place simultaneously further complicates the precise location where a mutation might take place.


text:
Activity driven model threshold
So I am trying to figure out a threshold for an activity driven model. That is described in this paper: https://www.nature.com/articles/srep00469
That is I don't see how the researchers got R0 to be between 0.2 and 0.5 (page 6). If they are using gamma=-2.1 and epsilon=10^-3 and threshold is defined in equation 4, my calculations give me threshold of 2.020396043515874.
Now if the power law distribution (activity) is a random number i.e. this:
http://mathworld.wolfram.com/RandomNumber.html
this yields average activity of 0.005489691793543477 using this equation:
((1-gamma)/(2-gamma))*((1-(epsilon**(2-gamma)))/(1-(epsilon**(1-gamma))))

so then following equation 4, the threshold is 2.020396043515874, but that's not what Figure 4 (B) is showing so I'm very confused.
I would really appreciate if someone could clear this out for me.

can you fill in a few more steps of your calculation?  Where does your average activity formula come from?  I'm getting 0.59 following the mean and variance formulas from https://en.wikipedia.org/wiki/Pareto_distribution - but in any case your question will be much more useful with more details

@BenBolker Average activity formula comes from $\int_{\epsilon}^{1}af(x)da$. At each time $t$ a node will be activate with probability $a$, which is between $\epsilon = 10^{-3}$ and 1 and each active nodes will get m links. We then infect 1% of node, i.e. 1% of 10,000 and run SIR model on that.

I think you just get some calculations wrong, maybe for the second moment $<a^2>$ of the activity distribution.
All the calculations are just simple algebra and definite integrals of powers.
For a power-law distribution $F(a)\propto a^{-\gamma}$ with $a\in[\epsilon,1]$, in order to have $\int^1_\epsilon F(a)\:da=1$ i.e. the correct normalization, we have:
$$
F(a)=\frac{\gamma-1}{\epsilon^{1-\gamma}-1}a^{-\gamma}
$$
The moments of the distributions $<a^n>=\int^1_\epsilon a^nF(a)\:da$ are:
$$
<a^n>=\frac{\gamma-1}{\gamma-1-n}\frac{\epsilon^{1+n-\gamma}-1}{\epsilon^{1-\gamma}-1} \quad if \quad n\ne\gamma-1
$$
The case $n=\gamma-1$ have a logarithm and it is not relevant in our case.
For $\gamma=2.1$, $\epsilon=.001$, $n=1$ and $n=2$ we get:
$$
<a>= \frac{\gamma-1}{\gamma-2}\frac{\epsilon^{2-\gamma}-1}{\epsilon^{1-\gamma}-1}= 0.00548969179354348\\
<a^2>=\frac{\gamma-1}{\gamma-3}\frac{\epsilon^{3-\gamma}-1}{\epsilon^{1-\gamma}-1}=0.00061164650162922
$$
With these numbers I get:
$$
R_0=\frac{2<a>}{<a>+\sqrt{<a^2>}}=0.36330095782279
$$
which is between $0.2$ and $0.5$.
I'm not the best at explaining things, so let me know if there are any doubts! Goodluck!

How will the threshold change on a directed graph please?

How directed? In the sense that infection can occur only if the active vertex is infected ?

Directed in a way that an infected node will be able to infect another, but not vice versa.So if node A is infected, and it has a direction to node B, A->B, the infection can travel from A to B, but not back (if A would recover). At the moment the graph wasn't directed, which made it bidirectional really A<->B, but now I want to introduce that direction in which infection can travel, which would change the threshold

If I understood well you question, you should get R_0=2 . Can you run simulations of such a system?

I get R_0 = 2 as well, does that value change for you if you have different values of m?

(A little too long for a comment, and maybe useful)
Assuming that a is supposed to represent the degree of a node, and
using the formulas from Wikipedia for the Pareto distribution, I have

mean (which I'm assuming is <a>)  =  gamma*epsilon/(gamma-1)
and
variance (equal to <a^2>-<a>^2, or <a^2>= mean^2  + var) = epsilon^2*gamma/((gamma-1)^2*(gamma-2))

Translating into R code (rather than doing the algebra):
pmean <- function(gamma=2.8,epsilon=0.001) {
    gamma*epsilon/(gamma-1)
}
pvar <- function(gamma=2.8,epsilon=0.001) {
    epsilon^2*gamma/((gamma-1)^2*(gamma-2))
}
prms <- function(gamma=2.8,epsilon=0.001) {
    sqrt(pvar(gamma=gamma,epsilon=epsilon)+ pmean(gamma=gamma,epsilon=epsilon)^2)
}

When I use the value of gamma=2.1 in the figure caption and feed it into equation (4):
2*pmean(gamma=2.1)/(pmean(gamma=2.1)+prms(gamma=2.1))

I get 0.588 (still not right, but closer ... ??)

$a$ is the activity of a node at time $t$ if a node is active, it will connect with $m$ other nodes (in this case 2). The activity is a power law from the link I've got above.


text:
Protein bands not visible after sds page coomassie dye stain
I am working with cell wall protein of Candida albicans and cryptococcus neoformans but after protein extraction and run on SDS PAGE my bands are not visible after coomassie staining. Can anyone tell me how to concentrate the protein so that bands can be seen on coomassie stain.
I am using Ammonium Carbonate buffer for extraction of protein. Also, the bands are visible on silver staining.

There are many methods to concentrate protein depending on the protein itself, volume, resources availble, etc. Perhaps you could provide some more details.

I am not working on particular specific protein. I just have to extract cell wall proteins of both and run on SDS PAGE and compare the bands using a marker. I am using Sabouraud Dextrose Broth as growth media for both of them.

I have inoculated each in SDB and kept for 7 days on shaker incubator and followed by filteration. This collected mycelia is stored at -20C. then I suspended 1g of mycelia into 10mL Ammonium Carbonate and left overnight on rocker shaker. Filtered it and precipitated with methanol (1:8) followed by centrifugation and collecting pellet. Then dissolved this pellet in Urea+ DTT(minimal amount) and microfuged to get protein in supernatant. But the protein is not visible on Coomassie staining after SDS PAGE. If you could provide any protocol it would be helpful aswell.

It sounds like you already have a concentration step. Can you resuspend the pellet in less urea?

I already did in the most minimal amount possible. I dont think less than that would be sufficient to dissolve the pellet.

I have thought of using glass beads and ammonium carbonate buffer together. Instead of filteration what if we centrifuge the broth collect and wash the pellet. suspend pellet with water and glass beads with vortexing it for 15 min. then collect the suspension and add 1ml of it for 10ml buffer for overnight followed by methanol precipitation.....do you think this can work? as I am not sure about it....and if it does, when we add distilled water along with glass beads will the protein get diluted instead?

another alternative which I think is collecting the protein supernatant and preciptate it again by methanol..centrifuge it...but I dont know if this step gives any pellet.. so if pellet is obtained dissolve it again in urea+DTT..centrifuge to get the protein supernatant...but my query in this protocol is that will the earlier urea+DTT used to dissolve the pellet earlier interfare with methanol precipitation and affect my proteins?

The problem here is concentration. Coomassie Blue stain can only detect protein band greater than or near to 50ng, in this case, the concentration of your protein is too low for detection. If you want to stick with Coomassie stain, you can try colloidal Coomasie stain instead because it has a much lower detection limit than Coomasie blue (between 10ng to 20ng).
In addition, I think what causes such low protein concentration is the poor solubility of yeast cell wall. One way to get around this is to increase solubility is through chemical hydrolysis, for example using diluted sulphuric acid1-3. This will partially solubilize mannas-protein outer layer of the cell wall and help you to obtain soluble yeast cell wall products.
References:

Theodoro, S. D. S., Putarov, T. C., Tiemi, C., Volpe, L. M., de Oliveira, C. A. F., Glória, M. B. D. A., & Carciofi, A. C. (2019). Effects of the solubility of yeast cell wall preparations on their potential prebiotic properties in dogs. Plos one, 14(11), e0225659.
OGAWA, K., & MATSUDA, K. (1994). Characterization of Manno-oligosaccharides Containing α (1→ 2)-and α-(1→ 6)-Linkages Obtained from Saccharomyces cerevisiae Mannan by Controlled Acid Hydrolysist. Journal of Applied Glycoscience, 41(4), 433-437.
Peat, S. (1961). Polysaccharides of baker's yeast. Part IV. Mannnan. J. chem. Soc., 61, 29-34.

Welcome to Biology.SE! This looks like a good answer and you've done a nice job of providing supporting links. However, in the future please include the complete reference information since links can break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. I'm also not clear on whether your "this paper" reference is to that paper or to ref 25 of that paper. Thanks!

I've converted your reference links into citations, but please check to make sure I have not make any mistakes and [edit] to correct/improve as needed.


text:
What plants use the green spectrum?
What if the only light provided to a plant was from the green spectrum would plants adapt or starve?

Green is pretty much the last color that you'd want for a plant. Thinking logically, a plant is green because it reflects green light, and hence, plants do not absorb green light for photosynthesis.
Let's take a look at the spectral absorbance of the various pigments in plants:

You can see that all the pigments show very very poor absorption when it comes to green. Plants tend to absorb light at violet, blue, and at red colors predominantly.

To answer your second question: what would happen if the sun spectrum changed to green?
For all the "what if" questions, we cannot give a definitive answer, and all of what I say will be purely speculations. Let's see what could actually happen:
Possibility 1: Plants will evolve to develop different pigments that absorb wavelengths that correspond to green light. Since the sun itself is green, and hence the entire surroundings will be green. Plants absorb all of the light that the sun is capable of absorbing, and hence will appear to be black to the human eye.
Possibility 2: Plants will die out, due to the sudden change in the sun's spectrum, which will cause the rest of the life forms that depend on plants to die out as well.


text:
How does human life expectancy change with age?
Human life expectancy tends to be given as a single number reflecting age at death from birth.
But life expectancy should really grow the longer you live, because, for example, once you hit your fifth birthday your chances of dying before age five drop to zero, so the contribution to the average life expectancy of all the people who died before age five shouldn't apply.
To put it another way, once you hit age ninety, your life expectancy calculated then and there should be at least ninety years even though that exceeds the life expectancy in every country on the planet, simply because you've clearly already made it that far.
Does life expectancy as a function of current age have a name, and what shape does this function typically take? Perhaps more interestingly, does this function take a significantly different shape in humans than in other animals (I'd expect infant mortality to significantly affect this for example)?

Maybe a survivorship curve describes what you are looking for, https://en.wikipedia.org/wiki/Survivorship_curve.

I think you might be looking for period life tables

A period life table is based on the mortality experience of a population during a relatively short period of time. Here we present the 2014 period life table for the Social Security area population. For this table, the period life expectancy at a given age is the average remaining number of years expected prior to death for a person at that exact age, born on January 1, using the mortality rates for 2014 over the course of his or her remaining life.

I read a paper once - but have not been able to find it since - that said that every (age) milestone in our life extends our life expectancy statistically and biologically. General life expectancy averages people who die of diseases that affect us at different ages: infant, child, young adults, middle-aged adults and the elderly. When you live beyond each phase in your life, you beat the statistics and at the same time show that your biological make-up has more resilience than those who succumbed during previous phases. Something that I just read reminded me of this and prompted this internet search. It said that though the average life expectancy in America is 78, when you hit your 70th birthday, you can - on average - expect to live 14 more years.

Is this the article you are referring to? Relatively new, but it is similar to what you say.

That looks like the same information. I think I was reading something like a research report. I would guess that the article you linked was written from the paper I read.


text:
Why does white light viewed through optical chopper appear purple/blue?
I looked at a light like the one shown here through a fidget spinner (I believe I was observing near where the "blades" meet the inner portion) and noticed that it appeared purple/blue, particularly when viewed for a prolonged period (I looked at the reflection of sunlight from snow and observed this as well.).  I believe this is either an optical effect (the spectrum is convolved with the Fourier transform of the "chopping function or pulse" ) or has something to do with the eye/my perception.
So what's going on here?

What color is the spinner?

@asher, good point- if the spinner color is the compliment of the visual artifact, then it is an afterimage artifact of the retina.

@Asher I observed this through a grey one as well as a red one. I

I didn't expect this to be as easy to see as you described, but I found it right away. I'm almost certain it's an effect of the time-response of the eye. Would this question fit better on [biology.se]? We'd be happy to migrate it for you.

@rob Perhaps I was naive in thinking my perception could be easily  explained by physics.  I'm ok with migrating the question.

I totally wasn't expecting to immediately duplicate this with a fidget spinner and the fluorescent light in my office.  What a neat effect!
My technique: I hold the spinner quite close to my eye, so that it occupies nearly all of my field of view, and look through the spinning part at my ceiling light.  If the spinner is very fast or very slow, I don't see any change in the hue of the light.  However there's an intermediate rate where the back part of the fluorescent lamp takes on a patchy blue tint with colored edges. The tinted region is irregular and unpredictable in the same way as a pressure phosphene, if you're familiar with that better-documented effect, and has kind of the same "feel" to it.
Trying to photograph the effect just gives the rolling shutter problem, so that's no use.  (No color change in the photo, either.)
At the rotational speed where the color change effect is the most pronounced, I estimate the frequency at which the spinner blocks nearly all of the light to be 10-20 Hz.  (How? I let the thing hit a fingernail and listened to it tap; it sounds like thirty-second notes, four to a click, at a good presto tempo.)  I've read elsewhere that the human eye can process images at 10-15 Hz. So some sort of biological stroboscopic effect, where the eye has just enough time to begin to respond to the reduced light before the light returns, seems plausible to me.

This article (https://www.wired.com/2017/05/the-phyiscs-of-fidget-spinners/) estimates the frequency at about 20 Hz as well. However, the number of blades on the spinner will affect the pulse width (I think you were taking that into account), but at least we have an order of magnitude estimate and there may very well be a connection to the "response time" of the eye so that number could be relevant.


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What's the minimum, if any, concentration of atmospheric nitrogen needed by plants?
What's the minimum, if any, concentration of atmospheric nitrogen needed by plants?  Would plants be able to grow in an atmosphere with just carbon dioxide and oxygen?

So, where would the plants get nitrogen from?

@GrahamChiu plants do not get nitrogen from the air.

@John I never said they did.  Bacteriae and fungi fix nitrogen and then supply the plants.

@xusr with no nitrogen cycle?

https://space.stackexchange.com/q/20153

@xusr so please explain how a nitrogen cycle occurs with no atmospheric nitrogen.

@xusr  http://www.azotictechnologies.com/index.php/technology/n-fix/ and exactly where is the nitrogen for the harber process coming from?

@xusr you continue to evade the question. The Haber process uses atmospheric nitrogen which can not happen since this scenario says there is none. And the link I provided is a process of plant fixation of nitrogen using intracellular bacteriae.

Zero if you are supplying them with solid nitrates in their growth medium, plants can't use atmospheric nitrogen. Some soil bacteria can and create nitrates the plants can use but this can and often is supplied by other means.
But as Graham points out you will need another inert gas to fill in the atmosphere as high concentrations of CO2 or Oxygen are both toxic.

If there is not nitrogen, then there will need to be another gas as an excess of either Co2 or O2 will cause problems.


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Prove that the worms are unicellular
In Biology class our teacher divided the class in two groups. Our group(i'm in) has to prove that the worms are unicellular(although it is not true). The other group has to prove that we are wrong. The plan for the debate for our group is to have a list of characteristics that are equal both for worms and unicellular. I wrote that they both have organelles and like the rain worm,  unicellular parthenogenesis. But now i'm out of ideas. Give me some suggestions.

You could start by contrasting the cell type and compare the structures which are found in exact type of cell. You could then go on to talk about cell division and structures that are present to enable cell division.
You could refer to sheer size, a visible worm clearly cannot be unicellular as we are in the wrong order of magnitude- unicellular organisms being measured in microns reparler them visible to the naked eye. You could use this as your opener, to them talk about the differences you would see under the microscope.
You could talk about body plans and how they have evolved differently.


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How plausible would it be for animals to normalize the birth of monozygotic twins in their reproductive cycles?
I'm currently trying to develop the world of a sci-fi story I'm working on, and a concept I've thought of adopting with the environment and characters is a common breeding system where identical twins (or sometimes not, asymmetric twins from the same egg have also been under consideration) are a commonplace byproduct of the world's evolution.
I'd like to know the plausibility of this. My idea is for two twins to be born with natural, pheromonal connections between each another. The sexual organs of the twins would be the same, thus preventing immediate inbreeding. I'd also envisioned [most] twins consistently having lifelong reliance on one another. i.e. I also want to know how reasonable it would be to expect them to coordinate efforts in the acquisition of food and evade potential predators. As for mating, I thought if they shared the exact same DNA there would be less ingrained concern over which gets to spread its genes. Would this be accurate?
Thanks in advance for anyone that tries to answer me. I'm doing what I can to keep things in the realm of reality, so it'd be much appreciated to know whether or not the universe I'm creating has a strong enough footing in the real world.

Welcome to Biology.SE. Your question appears to be a good fit for worldbuilding.SE but is rather off-topic here on Biology.SE.

Parthenogenesis, apomixis and fragmentation exist in many animal species.

Okay, I apologise. Thank you for pointing me to a more suitable venue.

As a whole, your question is opinion-based, speculative and not really suitable for Bio-SE.  However, several of the building blocks that you describe have a reasonable biological foundation, which might be useful to know.
For instance:

There seems to be a genetic component To monozygotic twinning (see e.g. ghr.nlm.nih.gov). This means that the trait could, very hypothetically, be selected for, and a population with a higher level of monozygotic (identical) twins could develop (ignoring other possible detrimental effects). Different frequencies of MZ twins is also know from castle breeds and other species.
The level of shared genes is the driving force between kin selection. This is part of the explanation  for the reproductive system in social bees (and other eusocial insects), where (usually) a single queen reproduces and her workers (all sisters), which are 75% related to eachother due to the haplodiplod genetic makeup, all work towards the common "goal" of producing new sister queens (which will then be 75% related to all the workers).
This gives some (again, very hypothetical) basis for your idea that "...they shared the exact same DNA there would be less ingrained concern over which gets to spread its genes".
Monozygotic twins often describe an especially strong sibling bond, which lends support (again, very hypoythetically) to your idea of "...expect them to coordinate efforts in the acquisition of food and evade potential predators.". There is also some research to back this up (e.g. Fortuna et al. 2011. Twin relationships: A comparison across monozygotic twins, dizygotic twins, and nontwin siblings in early childhood), but there are also studies that indicates that monozygotic twins show similar sibling behaviors as other types of sibling pairs (see e.g. Mark et al. 2017. Using Twins to Better Understand Sibling Relationships). This is not a field I know well and there is most certainly many more relevant sources to look at.

The introduction to Mark et al (2017) contains many references on MZ twins that should be relevant to your "thought experiment", e.g.:

...Fraley and Tancredy’s (2012) later work, which suggests that twin children rely more heavily on their co-twin for safety and security than do non-twin siblings.


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In a Sanger sequencing, what would be happen if different DNA sequence binds to same primer? And how this situation avoided if problematic?
Sanger's PCR chain-termination sequencing, by its theory, is a simple method to sequence DNA from organisms. But what will happen if there are 2 allelic DNA with same primer binding site, but variations in some-other part?
My question is; 1. Is such overlap practically happens? 2. If it happens, then what problem it creates? (or does it create any problem at all); and 3. if it is problematic, then what techniques used to avoid or reduce such noise?

Yes, this can happen if you are not checking your primers against the reference sequences.
Your PCR is done from two different pieces of DNA leading to two sets of chain-terminated fluorescence marked DNA. This leads to superimposed sequences, which looks like this and where you cannot differentiate, which sequence belongs to which strain (image taken from here):

It is problematic, the solution is to design new primers (which are located slightly outside the old target sequence) which only bind to one specific sequence. You cannot purify only one product, as you cannot discriminate between the two.


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Please name this plant

What is the name of this plant? It was found in a village in Bangladesh, in the month of February.

Where was this plant found and what time of year?

From a village of  Bangladesh, in the month of February.

@FaysalAhmed Add this info (and as much else you can think of) to the actual question (use the edit button).

@FaysalAhmed Don't copy the posted answer(s) to the question. It makes the Q-A pair impossible to understand for future readers.

I believe this plant may be Rotala rotundifolia
Quoting from Wikipedia,

It is a common weed in rice paddies and wet places in India, China, Taiwan, Thailand, Laos, and Vietnam, and has been introduced to the United States.

This makes sense, as Bangladesh is located near both India and China.

The emerse form has rounded leaves, the submerse leaves are narrow lanceolate. It is very variable dependent on light and environmental conditions. Under strong light, the leaves can become almost wine red. It has pale pink flowers.

(source)


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Species-ID: What kind of bug is this?

What kind of bug is this?
Size: About the size of a pencil tip
When was it found: spring time
Where was it found: In northeastern USA, inside the bathroom of our house

Anyone trying to answer will need more information: size, location, time of year.

About the size of a pencil tip, spring time, in the northeast, inside the bathroom of our house

The northeast of what? The stereotype is that Americans typically assume it is obvious to anyone that the coordinates are relative to the USA (no offense), so I edited your post to add these info assuming you meant northeast USA. Please correct it if this is not what you meant

Yes, Northeast USA

It could be a cockroach nimph. Distinctive characteristics:The overall shape and size, the long antenae, the segmented abdomen and the visible rear cerci.


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Can varied temperature while sleeping help quality of sleep?
I read an interesting article which is about relations between body temperature and quality of sleep.
I'm interested in the phrase from the article.

Other experiments that varied the ambient temperature—decreasing it early in the night and increasing it in the morning—have shown similar benefits for improving and maintaining sleep.

So I tried to find papers and experiments but it seems my searching ability is pretty poor. I can't find it. Is there someone knows the latest knowledge or papers about this?
plus) In the article, why increasing skin temperature by 0.4 Celsius make core temperature low?


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Strange Exoskeleton Found in Maine: What is It?
There is a gall like object or exoskeleton attached to a plant stem I have found. At first I thought it was a cicada but it is not. The object cannot be identified by me. Attached are some pictures of it. Could you identify it?

It's a praying mantis egg case. It won't have "legs" until the eggs hatch. If you're lucky and watchful, you'll see a bunch of tiny praying mantises around it (if you put it back) and the shrubs around it in late spring.

It seems to me the ootheca of a mantis before larvae eclosion. You can read more about it here.

.jpg

There were no legs or anything.

https://www.google.es/search?q=mantis+ootheca. If you think that is the exuvia (outer skin) of an insect because it is a thin paperlike membrane with nothing inside, then it is not a mantis ootheca because it would need to have the egg chambers inside to be one. It can not be appreciated from the photo.

Are they easy to find?

I used to find about a dozen egg cases a year on my property in PA, Sometimes more. Yet we only had three, maybe four adults active that I could find.


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Osmotic Pressure in Capillaries
In this diagram, D is apparently the point at which "the osmotic pressure into the capillaries is the greatest", but I cannot figure out why. Any help would be much appreciated!

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Fluid movements across capillary wall is determined by 2 main factors.

Hydrostatic Pressure (Blood Pressure) - tends to push fluid out of the blood vessel
Osmotic Pressure - Tends to pull fluid back into the blood vessels mainly due to the presence of plasma proteins. (especially albumin)

Important points you should know

Hydrostatic pressure or blood pressure is the pressure exerted by blood on the capillary walls.
Osmotic pressure depends on the number of osmotically active, non diffusible particles in the solutions separated by the membrane.
The main substance responsible for the osmotic pressure between blood and tissue fluid are the plasma proteins. Especially albumin.
Plasma proteins are absent in tissue fluid.

Filtration of fluids across capillaries is described by Starling Forces. (Forces were introduced by an English physiologist Ernest Starling.)
There are four main forces

Capillary Hydrostatic Pressure (Pc) - This forces fluid out through the capillary membrane.
Interstitial Fluid Pressure (Pif) - Tends to force fluid from interstitial spaces across capillary membrane
Capillary Plasma Colloid Osmotic Pressure (∏p) - Tends to cause osmosis of fluid inward through capillary membrane.
Interstitial Fluid Colloid Osmotic Pressure (∏if) - Tends to cause osmosis of fluid outward through capillary membrane. -Negligible

According to Starling forces,
Filtration = k (Pc - Pif) - (∏p - ∏if)
Filtration = k x Net Filtration pressure
Here k is the capillary filtration coefficient which is depend on permeability of capillary wall and surface area for filtration.
Look at the following diagram

In your diagram A is the Arteriole end and D is the Venous end.
Now we can calculate Net Filtration Pressure at A and D.
At Arteriole end (A);

Outward forces are;

Capillary hydrostatic pressure (Pc) = 37 mm Hg
and
Interstitial Fluid Colloid Osmotic Pressure (∏if) = 0 mm Hg
So outwards force is 37 mm Hg.
Inward forces are;
Capillary Plasma Colloid Osmotic Pressure (∏p) = 25 mm Hg
and
Interstitial Fluid Pressure (Pif) = 1 mm Hg.
So inward force is 26 mm Hg.
Therefore net force is 37 - 26 = 11 mm Hg and it is outwards.

At Venous end (D);
 Outwards forces;
 Capillary hydrostatic pressure (Pc) = 17 mm Hg
and
Interstitial Fluid Colloid Osmotic Pressure (∏if) = 0 mm Hg
So outwards force is 17 mm Hg.
Inward forces are;
Capillary Plasma Colloid Osmotic Pressure (∏p) = 25 mm Hg
and
Interstitial Fluid Pressure (Pif) = 1 mm Hg.
So inward force is 26 mm Hg.
Therefore net force is 26 - 17 = 9 mm Hg and it is inwards.
So that's why

In this diagram, D is apparently the point at which "the osmotic pressure into the capillaries is the greatest"


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What are the differences (if any) in brain activity when hallucinating versus perceiving a real object?
I was wondering if there is difference in brain activity when someone is hallucinating an object, say a giraffe compared to when someone is genuinely observing a real giraffe?


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Which scallops change their sex from male to female?
Tonight it occurred to me to look up what scallops are like when they are alive (beyond their culinary role) and it blew my mind. This post regards one detail about which I was unable to find specific information: apparently certain species are known to start off as male and then change to female later in their lives. Which species in particular are known to do this?
I am new to this SE community so please let me know if there's anything I should refine about this (my first) post.

Welcome to Biology.SE. As you're looking for advice.... Always link to whatever you've found so far. For example, link to the document where you read about scallops gender change in life.

This type of sex determination system is called sequential hermaphroditism. Clown fish are a classical example of sequential hermaphrodites.


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Why can plants handle extra chromosomes much better than animals?
Why can plants handle being polyploid way better than animals, where it is almost always fatal?
I found a 2004 paper while searching about this topic, but I'm wondering if there have been any recent discoveries and if scientists are still actively looking for a definitive answer.


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Is a spore 'alive'?
Referencing this article: What are spores?
'A spore is typically a single cell surrounded by a thick cell wall for protection.'
So a spore is a 'cell'? This implies that a spore is a living thing; and not just a means to a living thing.
If this is the case, where does the spore get its energy? Oxygen, water, etc.?  Is there a name for the mechanism with which a spore extracts/obtains energy?
So many questions!

Welcome to Biology.SE. I'm voting to close this question as off-topic because the answer is based upon the definition of life and there is no such definition in biology. Ultimately, the definition of life is a matter of philosophy, not biology. Also, the post contains several question which make it too broad.

Welcome to BiologySE! Feel free to take a [tour] of this site. I appreciate your curiosity and eagerness to learn, but please limit yourself to one question per post. This is enforced to make sure answers are not too long. You may however ask multiple questions for different aspects though :)

Somewhat related: Why isn't a virus “alive”?

Spores generally do not need energy; the cell's metabolic activity is suspended indefinitely a technical source.

Thanks all. Wasn't looking to start trouble. 'Alive' was the wrong word to use I imagine. Basically does it require energy since it is classified in some circles as a 'cell'? mgkrebbs touched on what I was trying to get at.


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Identification of a bird on the beach of a small lake
Last December in France (lake of Divonne, Ain) I took a picture of this bird looking for some food on the beach of the lake.

It looks like a specimen of the genus Anthus (Family Motacillidae) but as these specimen are quite difficult to identify (especially winter time), I would like to have some confirmation.
By the picture I found on different Internet sites, my potentials guess are (by order of confidence):

Water pipit (Anthus spinoletta)
Meadow Pipit (Anthus pratensis)
Buff-bellied Pipit (Anthus rubescens)
Eurasian rock pipit (Anthus petrosus)

The Eurasian rock pipit could be present in the region while migrating but this is the less probable in my opinion.

Anthus spinoletta seems to be the way to go. It's feather patterns and beak shape are so identical to the one that you have posted. Considering that this was taken in December in France, it definitely matches with the  seasonal locations of Anthus spinoletta.

I agree with @Twisted Genes it's a water pipit no doubt.

if someone would post an answer, i will accept it.

Water pipit
https://en.wikipedia.org/wiki/Water_pipit
I agree with what was discussed in the comments and don't like open questions.

i understand that the quality of the answer is not high. but when you down vote please let me know why. the question is still open and needs to be answered. (in this community seems to be stricter rules than I'm used to from other stack exchange communities)


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Can boiling water without high temperatures kill bacteria?
If you use a vacuum chamber to reduce the pressure of water such that it can boil at around room temperature will it still have the same effect on reducing harmful bacteria as boiling at the usual 100C?

No, it's the temperature that kills, not the fact that some water is being evaporated quickly.

@mgkrebbs Well the water inside the bacteria would also be evaporating rapidly

Pasteurization is usually at less than 100 centigrade

of course if you evaporate then collect the water and recondence it separately it will contain far less bacteria.

No, you do need to reach high temperates to kill the bacteria.
It's not about the evaporation, or the pressure that kills bacteria, rather it is the temperature that does. Higher temperatures have drastic effects on the molecular structures that occur within the bacteria, such as the denaturing of various proteins present inside the cell. As a result, if you wish to boil water to kill it, it must be done at an elevated temperature.
Wikipedia mentions that the optimum temperature for killing microbes is around 70°C,

Boiling water is used as a method of making it potable by killing microbes that may be present. The sensitivity of different micro-organisms to heat varies, but if water is held at 70°C (158°F) for ten minutes, many organisms are killed, but some are more resistant to heat and require one minute at the boiling point of water.

Hi! Do you have a source that temperature causes destruction of the cell wall? I've never heard that and given that the phospholipid bilayer forms spontaneously, that sounds kinda strange?

TLDR: No, as its not the "boiling" itself that kills the bacteria, its the effect of temperature on proteins. But maybe?, in that you can kill bacteria by changing pressure without changing temperature.
Effect of Boiling at a Constant Temperature (No)
As other answers have suggested, the aim of boiling water to kill bacteria is to denature (i.e. change the shape) of proteins in the bacteria such that the proteins required for life stop working. The other facets of the boiling (e.g. water evaporation, turbulent bubbling, etc.) are unlikely to kill the bacteria. So if we had some bacteria in water and mimicked all the qualities of boiling except for temperature change, I doubt we'd see the bacteria die. This sounds like quite an interesting experiment to try though!
Effect of Changing Pressure (Maybe?)
There are many ways to denature a protein other than high temperatures! You suggest that we could change the pressure of the environment, which might also denature the proteins and kill the bacteria. In fact killing bacteria with high pressures (~340 MPa) is called Pascalization. As per your suggestion of lowering the pressure, there are some bacteria that can survive in a vacuum (BBC, 2010) so you might only be able to kill the bacteria by raising the pressure. On the other hand, it is known that you can denature a protein with low pressure (Wiedersich, 2008) but whether this protein denaturing would actually be fatal to the bacteria is another question. The effect of low pressures may be species dependent.
Something to Consider
Lastly, consider the phase diagram of water below (from Wikipedia). Where on the diagram can bacteria survive? Most (non-extremophile) bacteria seem to be bounded from above by around 340 MPa, and bounded on the right by around 72°C, but where else are they bounded? Furthermore what is the maximum pressure at which bacteria can survive in boiling water?


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Why doesn't patients with chronic acne's body lower sebum production itself?
Background
My cousin has had nodular acne for at least 9 years. Her sebum plugs usually causes bumps on, and inflame, the skin, before the sebum emerges or can be extracted with a comedo extractor. Occasioanlly, this happens without inflammation.
Dermatologist's Feedback
He said that topical retinoids open pores to help expel the trapped sebum, but only oral treinoin (E.g. accutane) can dwindle sebum production.
Question
We forgot to ask him why the body (on its own) doesn't slack sebum production ? We're assuming the body's ability to detect the inflammation and acne nodes, and to adjust sebum production?

Don't cross post to health

Short answer there is no feedback mechanism to tell the body it is overproducing, inflammation can have a huge number of causes, many of which could actually be worsened by decreased sebum production.
Also "overproduction" is a misleading term; it is overproduction compared to the norm for the population and may be perfectly normal for that individual. It is like asking why redheads don't start growing black hair when surrounded by surrounded by people with black hair.