text:
What species of snake in India "drinks breaths" according to local customs?
In Rajasthan in India, locals know a snake called peevna in the local language. Many of my relatives live there in villages in open deserts. They see many kinds of snakes every day.
The word peevna is basically derived from the Hindi word peena, which is a verb meaning to drink. But in the case of this snake, the drinking being referred to is the process of inhaling the warm air from the nose or mouth of a sleeping man. Hence they call it peevna.
Locals describe this snake as follows:
It is afraid of light. It just sits on the waist of any sleeping human, and then it "drinks" the warm breaths. After the breath gives the snake some comfort, it releases the venom into the mouth of the human. Finally, it hits the man with it's tail and leaves. The man dies once the sun light falls on him if he is not treated.
A similar description of this snake is mentioned on many Hindi blogs. However, I can't trust these stories.
Given all that, what snake is it and is it and is it even possible that this snake behaves like this?
EDIT:
A recent case has been mentioned here. And it is real. The villagers have reported the case. But it's in Hindi. Kindly translate that page, as it would be helpful to answer.
Now a doctor also said that it is a Karait kind of snake.
When I searched it on Google, I found this.
In common names, Peewana is also mentioned. So I guess this is the snake. But doubt is, the photo on the blog I shared is different than this. No only this, my relatives also define the look and feel of the snake like the one on blogs. So doubt remains.

Usually a snake attacks only when it is not provoked/threatened or if it wants to paralyze a prey for a meal (humans are unlikely to be thought of as meals by most snakes). In this site we ask and answer questions about biology and not bust folklores and myths. Hence your question is off-topic.

The folklore or myth could be real. Don't call it myth without proof.

*Usually a snake attacks only when it is provoked/threatened. You yourself said you cannot believe these stories. Stories without proper scientific basis are usually called myths or folklores (depending on how much they are believable). Your description of the snake does not fit any known behaviour of snakes. Moreover, most snake venoms are not lethal when taken orally. The hitting by tail and sunlight have no roles per se. You told a story with no scientific basis. You did not try to check even the most obvious facts and here you are telling me to prove that it is not a myth.

Your comment was written in such a way that you made it myth, which I don't have any problem with. The thing is I wanted it in an answer. The point of question is to know whether what I stated is TRUE or not. What I believe or think is a different thing. If you had written the comment as an answer, all things would have been cleared. Your comment was too intelligent for me to understand whether you called it myth or it is myth. Please don't comment if you can't explain for better understanding.

This Times of India article mentions the name "peevna" in relation to the "saw-scaled viper".
According to Wikipedia, the genus Echis contains 12 species that are commonly referred to as a group as "saw-scaled vipers."
Of these, one clearly is found in India: Echis_carinatus (commonly called the "saw-scaled viper", "Indian saw-scaled viper", or "little Indian viper" in English.).

This same Wikipedia article provides common names in other languages, but the given common Hindi name on Wikipedia is not "peevna" but rather "aphai (अफई)." I'm not sure what to make of this discrepancy...

I have no idea if this is in fact the snake you're referencing. BUT, if E. carinatus IS your snake in question, Wikipedia provides the following info:

 Source: Wikiedi
Habitat:

E. carinatus is found on a range of different substrates, including sand, rock, soft soil and in scrublands. Often found hiding under loose rocks. Specimens have also been found in Balochistan at altitudes of up to 1982 m.

Behavior

E. carinatus is mostly crepuscular and nocturnal, although there have been reports of activity during daylight hours.

This is likely where the "afraid of sunlight" part of your myth arose form. However, the Wikipedia article goes on to say that they have sometimes been found active during the day

Wikipedia goes on to say that they are a very aggressive species known for many snake bites, which again relates to the sinister behavior described in your story:

E. carinatus is one of the species responsible for causing the most snakebite cases due to their inconspicuous and extremely aggressive nature. Its characteristic pose, a double coil with a figure of eight, with the head poised in the center, permits it to lash out like a released spring.

Wikipedia also points out that bites are fatal ~20% of the time, which I assume would be even higher in smaller villages with limited medical response capabilities.

Finally, Wikipedia points out that they move primarily via sidewinding, which in a way could be construed as flicking its tail aggressively when it moves away. This might be where the tail-hitting comes from in your description.
As for the "drinking" of breaths?...
I haven't figured out what that would be due to. My best guess is that (unsurprisingly) this snake can't handle cold weather and is known to hibernate. Perhaps the warm breath comments are relating back to its need to warm up (after hibernation??). Who knows.
This is the best I've got for you.

https://hindi.oneindia.com/news/rajasthan/desert-snake-pivna-attack-on-a-family-in-sedwa-barmer-rajasthan/articlecontent-pf223209-524634.html
Here's a recent case observed and a doctor also said something about it. Please see this and enable english translation.

I wonder why this answer is getting upvotes. 2nd answer seems more promising and more close to description given by me.

This is a misbelief and the possible answer is the "Krait" and its subspecies.

Here is a blog post by a scientist in the Tata institute of fundamental research. The blog contains data compiled from various sources for the "Special Interest Group-Snakes newsletter, I.I.T. Bombay".
As per the blog post
"In northwestern India, kraits are supposed to suck a man's breath away as he sleeps. This is perhaps the farmer laborer's explanation for the respiratory paralysis that a severe krait-bite brings on."
The blog post--Snakes and common misbeliefs.

This research paper further explains this misbelief of people--> "Krait is responsible for most deaths in North India. It bites people sleeping on the floors, mostly at night." Mass awareness regarding snake bite induced early morning neuroparalysis can prevent many deaths in North India.

Hope it answers your question.


text:
Where does the "para" in parasitism come from
He there.
So in biology there is the concept of parabiosis, that describes a relationship where one part experiences a positive side effect and the other one has no disadvantages because of that. The "para" shows, that only a half of the organisms experiences this advantage.
Then I asked myself: Where does the "para" in parasitism come from? Is it because only one of the two sides experiences the exploitation? And if so: Is there a term for a relationship, where 2 organisms exploit each other, so basically an equivalent of parabiosis and symbiosis, but for parasitism?
~Okaghana

What exactly is the question here? The title doesn't really match the text, and the text seems to have several different questions in it, all of which are rather vague. The title question isn't biology-related, it's an etymological question.

Had a small typo in there, Now I'd say the title matches. And I would argue that although the question is about the origins of a word, it fits more in a biology forum than a ethymologic forum.

Welcome @Okaghana. For future reference, you're asking about the history or origin of the word, so on pedantic grounds it'd be better suited in an etymological forum. I disagree with the close vote for 'needs more focus', it is a clear, focused question. A little off topic surely, but it's been answered well and I think we should leave it at that.

"exploiting each other" would be a negative-negative interaction, i.e. competition.  If both members of an interaction harm each other, it would be hard to maintain symbiosis (close association). A positive-positive interaction would be mutualism (and there are lots of mutualistic symbionts)

Welcome to SE Biology. Please complete your reading of the Tour, where you will see that this site is concerned with questions about biological problems, not about the etymology of biological terms, which can usually be found in on-line English dictionaries.

The prefix para- means beside; adjacent to.
Parasite (from Etymonline):

"a hanger-on, a toady, person who lives on others,"...from Greek
  parasitos "one who lives at another's expense, person who eats at the
  table of another," especially one who frequents the tables of the
  rich and earns his welcome by flattery, from noun use of an adjective
  meaning "feeding beside," from para- "beside."

So, in the word parasitism, para- refers to the relation of a parasite to its host.

But the poster could have found the answer to this English Language question himself if he had done the research that this site requires before posting an off-topic question. Answering such questions is easy, but it attracts more rubbish to this site. The Help on answering questions makes it clear that not all questions deserve an answer.

source: Stack Exchange

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

sort: votes


text:
What does it mean to say that the sympathetic nervous system is organized for diffuse activity?
"Sympathetic activities generally serve to mobilize the energy stores of the body, to increase the blood flow through certain regions (e.g., the heart) at the expense of other areas (e.g., the abdominal viscerae), and to exhibit the outward signs of alarm and excitement.
Because the sympathetically innervated effectors generally have a wide distribution, even when the sympathetic supply to only one type of effector (e.g., the vasomotor fibers to the cutaneous blood vessels) is stimulated, the bodily response is diffuse."
1-By 'mobilize the energy stores' they mean metabolize or use up ?
2-'The bodily response is diffuse' - does that mean several parts of the body participate in the response but with no major effect individually ?

"Mobilize" in this context means to:

to release (something stored in the organism) for bodily use

Merriam-Webster
"Diffuse" means "spread out": it doesn't say anything about whether the effect is "major" or "minor" and I don't think it's useful to think in those terms. Instead you should just appreciate that there is no specific target affected by sympathetic activation, rather it is a whole body response: almost every organ system is involved.
Sympathetic nervous system activation occurs when an organism needs to be ready to act immediately (such as in a 'flight or fight' response), which includes more metabolism in the muscles and increased sensory sensitivity. It also includes compensating by reducing metabolism in the gut: even though digestion is a source of energy, it is slow rather than immediate and costs a lot of energy in the short term through the processes of digestion.

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


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Are there any "thermotroph" lifeforms?
I only found chemotroph and photoroph examples of life, but are there organisms that can use a temperature gradient to convert energy?

No, because temperature is a quantity related to the motion of molecules (or particles) in an ensemble (thus, kinetic energy) but such motion does not have a mechanism to transduce it into some form of useful energy for biological purposes. Chemical gradients are easily stored because of the highly specialized biological membranes (via specific ion channels, etc). Light (photons) can also be used via some proper transducers (photoreceptors), given that there is transduction into chemical energy (i.e. in photosynthesis). But there is no way to 'store' energy from temperature directly in biology because there is no transducer. Temperature differentials in purely physical applications exist, but there is no parallel for biology. All life forms depend heavily on chemical potential and physicochemical gradients, which is deeply rooted in the evolutionary history, you can find an interesting lecture on this topic here.


text:
Can we achieve complete photosynthesis on a petri dish? Barriers and potential
If we were to place bacteriorhodopsin and ATP synthase in an acidified solution (for H+ ions) filled with phospholipids, ADP and inorganic phosphate, hopefully the bacteriorhodopsin and ATP synthase will be embedded in the same micelle. Then when exposed to sunlight, the bacteriorhodopsin will start to operate, creating an electrochemical gradient which will power the ATP synthase, synthesising ATP.
Can we create achieve complete photosynthesis on a petri dish? What are the technological barriers against such an invention? Even if such a small working model were to exist, why can't it be scaled up?

What if we could add in the Kelvin cycle and other photosystems to create a fully functional 'chloroplast'? It seems biotech researchers have been trying this since the 1960s, however, why have scientists not been able to create a fully functioning photosynthetic organ *now*?

(see edits)

Several motivations for this:

Does away the need of sugar cane farms and provide us with the most efficient
means of harvesting sugar, literally we do not have to produce a lot
of waste when processing tons of sugar cane just to obtain a little sugar, while the rest (cellulose) mostly goes to waste.
Production of biofuels since the sugars produced is the precursor of lipids, in response to climate risks

Remark: I am not looking for a synthetic system that operates by inorganic means but a system that consists of enzymes and membranous structures, very much like that in plants.

Edit:
As per the comments listed below, here are some fixes, specifically the illuminating comment by @David. I must apologise for the inaccuracies of the original question.
https://www.jstor.org/stable/57795?seq=1
Biochemists did not strive to recreate the whole system from scratch (by making a handful, if not hundreds of protein embed on a phospholipid membrane as implied by my original question), but tried to achieve complete photosynthesis of isolated chloroplasts, which is similar enough to the question proposed if not identical.
https://www.jbc.org/content/235/3/832.full.pdf
According to the paper above, there are some techniques that use chloroplasts extracts, which contain many key components of the photosynthetic cycle, and also a better chloroplast isolation method which tries to preserves the enzymes needed. It alleges that carbon assimilation occurs, even though the end product is 3-phosphoglycerate after carboxylation.
I will further update this question after I read more, but as of the time being, these immediate fixes are done to fix some damning issues as raised.

I think you are confused about how much is involved in photosynthesis. It is an organized process, this is like asking why piling all the parts for a car in a crate does not create a working car.

@John I understand how complex it is: lot's of enzymes, the electron transport chain and more, all on a phospholipid membrane and cytoplast. However, cells do assemble these as functional units. I am not a researcher, but I'm just being optimistic.

Yes cells have to ASSEMBLE these units, which is the part that is beyond us on any usable scale. this is why we use whole organisms they assemble themselves. building even a single electron transport chain from scratch would be a many step process for a researcher taking days or weeks of time, there is no good reason to do it. Think about how rough our tools are at this scale. this is like trying to assemble a car while wearing oven mitts and only having a sledgehammer as a tool.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, questions should not be used to solicit opinions. We also expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). See also this sites criteria for "homework", which can apply to questions even if they are not assigned as homework. Thanks!

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

Your two references you cite are from 1960 and 1966 — over 50 years ago. Where you alive then? I was, and can testify that our understanding of photosynthesis has advanced considerably since then. Please spend some time with reputable text like Berg et al.. As regards biotechnology, you should try to educate yourself on what the real industrial requirements are. I would not have thought the synthesis of sucrose (which is not the end product of the dark reactions of photosynthesis) was high on the list.


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Why do scientists perform most of biological experiments done on rats prior to humans?
Why do scientists perform most of biological experiments done on rats prior to humans?

Scientist gave a third ear to this rat

Source
Here is the another source claiming Researchers wants to COVID - 19 vaccine on rats.

World's scientists admit they just don't like mice

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Also that is a mouse not a rat! ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

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

@tyresome I added second sources, still how many sources are needed for my question? Any specific number?

Some sign of researching the answer to question on your own first, please read the homework policy.

Originally for practical reasons.  Rats and mice breed prolifically and are easy to keep in captivity.  (Imagine trying to perform lab experiments on say hippotami, or tigers :-))  I would also imagine, given the large number of rat & mouse traps & poisons sold, that the fact that few people would care what was done to rats might have factored into it.
As time went on, those particular animals became the entrenched experimental animals, as techniques and equipment for maintaining them became readily available.  Indeed, you can readily buy commercial rat & mouse food: https://multipurina.ca/en/rodents/products/  Various lab strains were developed having consistent characteristics such as genetics or susceptibility to cancer.  (Not my field, so someone more knowledgeable could perhaps expand on this.)

You can do a google search. However,
The rodent lineage, which gave rise to the rat and mouse, and the primate lineage, which gave rise to humans, diverged about 80 million years ago. Humans have 23 pairs of chromosomes, while rats have 21 and mice have 20. However, the new analysis found chromosomes from all three organisms to be related to each other by about 280 large regions of genomic sequence similarity - called "syntenic blocks" - distributed in varying patterns across the organisms' chromosomes. (More at genome.gov)

Welcome to Biology.SE! It isn't clear why you think this answers the question, which probably isn't a good fit for this site anyway. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!

@tyersome well, this is what he needed


text:
Can untargeted metabolomics detect epigenomic changes such as methylation?
My main focus is transcriptomics analysis and very recently I have also started working on metabolomics. From my transcriptomic data it looks like there is a gene/protein that could potentially generate epigenetic modifications. I also have untargeted metabolomics data of equivalent experimental conditions that I plan to analyse soon hoping it will complete the picture. However, I have searched for publications linking specific metabolites with hyper/hypomethylation or chromatin structure and I have only been able to find a few references (see link below) and I got the feeling that untargeted metabolomics does not seem to be an obvious technique to observe epigenetic signatures.
https://www.ncbi.nlm.nih.gov/pubmed/30125527
What metabolites would be regulated under epigenetic circumstances?
Does anybody have any experience or know of any particular study that looks into this relationship between untargeted metabolomics and epigenetic modifications? Thank you very much for your help!

This is a fascinating question, and I spent a fair amount of time looking into it. From what I've been able to find regarding the relationship between metabolics and epigenetics, it seems that metabolites drive epigenetic changes, not the other way around.
This can be shown quite well by looking at cell differentiation and induced pluripotent stem cells. The epigenetic changes that happen in these processes happen due to the cell's environment.
However, epigenetic changes cause changes in transcription rates, so it can indirectly influence metabolics. The circadian clock uses this system (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3392647/).
Cell signaling appears to be the most significant cause of metabolic change, though. The aforementioned paper also says this:

As most metabolites are not diffusible between mitochondria and
  cytosol/nucleus, accurate determination of the cytoplasmic pool size
  is critical to understand their effects on epigenetic signaling.
  Although attempts have been made, so far the technology to reliably
  measure metabolite concentrations in different cellular compartments
  is lacking.

Which, I'm sorry to say, leads me to believe that there are very few metabolic pathways that have known effects on epigenetic factors.
That said, there are several references in that paper which may put you on a good path forward.

Thank you very much for your answer and the reference :) Indeed, it is very interesting. Maybe newer techniques such as super-resolution microscopy could help to define the metabolite concentrations in cellular compartments in the future.


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Are there any DNA viruses with junk DNA in them?
I know mimiviruses and pandoraviruses have orphan DNA - DNA that is not found in other species - but this is DNA that codes for proteins. I am not able to find out if they contain junk DNA. By junk I mean DNA that does not have ANY function at all. Sort of like the junk DNA in the human genome put there by retroviruses, DNA that just sits there, doing nothing, just going along for the ride.

The terms junk DNA and non-coding DNA mean very different things. Non-coding DNA would include the part of a promoter that binds RNA polymerase but is not transcribed and other similar and regulatory regions that bind proteins (and also strictly speaking the parts of a gene that encode the untranslated regions of a mRNA transcript). Junk DNA can be taken to mean functionless DNA, although that begs the question whether it is DNA that has a function that has not been elucidated. Could you please clarify what you mean and amend your title accordingly.

To help get an answer to the "junk" part of your question, you might be interested in a similar question I asked about parasitic code in viruses: https://biology.stackexchange.com/questions/92829/do-any-known-viruses-contain-junk-or-parasitic-genomic-information

I should have been clearer. By junk DNA I mean functionless DNA that is known to do nothing. Not promoter regions or regulatory sequences. On a related note, are there retroviruses that infect other virues - that insert their own code in the code of a bigger virus? If so, can some of this code get deactivated or mutated over time to become functionless?

Best not to use the word code for genomic DNA. First because of the confusion with the genetic code, which is a cypher; second because you’re interested in non-coding DNA. How can you envisage a virus infecting a virus? Think about the nature of viruses. And if you include transposons as junk DNA you are stretching things as they encode the ability to transpose themselves.


text:
Is this a fossil?
My neighbor found this rock and asked for help identifying it as a fossil. Can anyone confirm that it is/isn't a fossil? If it is, what it is a fossil of?
It was found near Lexington, VA, USA, on Short Mountain. It is about 12cm long, 8cm wide and 6cm tall.

City's you please edit your post and add the size of the object and roughly were in the world it was found?

@Arsak Done - I had to approximate the size as I don't have it anymore, but the estimate is probably close enough.

No
It bears no halmarks or indicators of being a fossil, and it does not look like any fossil I have ever seen . it looks like simple chemical weathering.


text:
Population Dynamics problem concerning Allee Effect
I am reading Nonlinear Dynamics and Chaos with Applications to Physics, Biology, Chemistry, and Engineering, 2nd Ed. (Strogatz 2015).  I came across a problem involving the Allee Effect which I have not been able to solve.
Problem:
I tried comparing terms with the Allee effect as stated on Wikipedia,  but it is still not clear to me how to solve this.  Can someone please help?
Since my last post, I have tried plotting several values for the parameters, and I solved for the zeros of this equation.  My guess, is that I am supposed to qualitatively analyze this plot and see that it is maximized for intermediate values of N.  I am including a picture from Mathematica of my work.  Please let me know if I am on the wrong track.

You're not interpreting that Wikipedia page correctly. That equation provides an example of the Allee effect, but is not exclusive.
The Allee effect occurs when the non-zero steady state of a system is not globally attractive, so that such populations may be stable at non-zero population levels for a long time, but are unable to recover once the population density drops below a certain threshold.
In terms of your problem, the tricky bit (conditions for global attraction) is done for you as it instructs you to find parameters so that $\frac{\dot{N}}{N}$ is maximum for intermediate (positive) $N$.
So when does $f(N) = r - a(N-b)^2$ have a maximum admitted at some positive $N$? This is a quadratic, so simple mathematics is enough.

$a>0$ is needed to ensure the parabola admits a maximum
$b>0$ is needed for the maximum is attained at positive $N$.
$r>0$ is also needed to ensure the maximum is positive. This is not clear from the information in the question, but the non-trivial steady states involve $\sqrt{\frac{r}{a}}$ and so $r > 0$ for these steady states to even exist.

So overall quite boring conditions and not a very satisfying question.

In general, a population $x$ with reproductive rate $b(x)$ and death rate $d(x)$ with dynamics $$\frac{dx}{dt} = x(b(x) - d(x))$$ displays the Allee effect if $b(0) < d(0)$. This is easy to prove with a basic grasp of ODE stability.

Thank you!  It is quite clear, now!


text:
What is this insect seen in Northern Italy?
I am from Northern Italy, close to the border with Slovenia.
I saw this thing today on the window, and was sure it was a piece of a dry rosmarine branch carried there by the wind - until it started to move.
It looks like a cocoon of some kind, on the top of it there is an opening from which a head of something like a caterpillar comes out, sometimes together with some portion of its body with two (?) tiny legs on each of its body "segments". But I imagined cocoons as something attached to a branch, not moving.. While this thing moved from one point of the window to another, always attached to the window (not using what I think are the caterpillar's legs). (I must admit I am reluctant to open the window and examine it from a closer range :) ; the photograph is taken from inside the house).
What can this insect be? (the length is around 4-5 cm)

Related: Is it possible to identify this chrysalis? and Caterpillar(?) in Leaf Cocoon identification - Missouri.

This looks like some kind of bagworm moth. Their larvae would use silk and plant debris to construct a protective case around themselves. It’s hard to tell the exact species unless you open up the case or wait for it to emerge as an adult moth.
There are species on pretty much every continent and definitely some in Northern Italy. You can check out a list of observations and photos here: https://www.inaturalist.org/taxa/61415-Psychidae

As an aside, if you are interested in this kind of stuff. I highly recommend that you also join the iNaturalist community. There are many more naturalist experts of various beaches of life there to help with identification.


text:
Is there any evidence that discards the possibility of an organism-aided evolution?
The theory of evolution of Darwin is mostly accepted nowadays, while Lamark theory has been abandoned. There are many experiments that show that experiences do not alter the genes or are passed to descendance (there could be some exceptions , see https://en.wikipedia.org/wiki/Transgenerational_epigenetic_inheritance but the inheritance is not clear)
Although genes are not modified by experiences, I was wondering if there is any evidence or argument that justifies that during the process of producing sperm, maturing ovules or the fecundation, the gene selection must be completely random. I mean, I question if there could species that chose from their own genes, those who had been more useful during their life and increasing the chance that their descendants had them since their conception.

Extraordinary claims require extraordinary evidence. If someone wants to claim there is an intelligence to evolution, they need to provide evidence in support of it, rather than asking others to provide evidence against it.

I am not making any claim. I simply ask if this issue has been previously studied or considerer and if it has been discarded for a given reason.

Note that there is a difference between GENS (a group related through male ancestors), and GENES, which is probably what you want to ask about.

I mean, I question if there could species that chose from their own gens, those who had been more useful during their life and increasing the chance that their descendants had them since their conception.

There are two kinds of argument against this - one from basic principles, and one from empirical evidence.
As far as basic principles, I think Dawkins makes very good arguments against Lamarckian evolution in his book "The Selfish Gene". Essentially he points out the example of muscles getting larger when we exercise, and notes that not only isn't this universal - plenty of structures get worn down with use, not strengthened - the fact that muscles specifically do this is itself an adaptation. And he points out there is no mechanism for this adaptation arising through Lamarkian evolution if it isn't already there. There's a basic bootstrapping problem involved that Darwinian evolution doesn't have.
When we consider your example the same issue arises. By what mechanism would an organism choose which genes to pass on? Can you? Of course the fact we don't have conscious control over the genes we pass on isn't necessarily dispositive, our bodies do plenty of things we don't have conscious control over. But not only would there need to be a mechanism by which some genes are selected to pass on and not others, you would need some way for the information about which genes to select to get back to said mechanism. Making this choice is an incredibly complex issue... The things you'd have to know about the environment, the ways genes impact the final phenotype, which phenotypes are truly optimal for the environment... We humans aren't at the point of doing this. Natural selection works out for extremely dumb reasons. You are proposing a system that does this in a smart way... We already know how evolution comes up with smart systems, that integrate information about the environment and infer general rules about how the world works and predict the best actions in consequence: it makes brains. The brains it's made so far that are best at this are ours, and "explicitly choosing which genes to pass on" isn't what we're using them for so far. That might come in future decades with genetic engineering, and when it does it will be an entirely novel form of evolution. It's incredibly implausible to suppose that other organisms have been doing this all along.
Now, could some genes or gene families happen to have some kind of positive feedback property that means they get selected more when they're useful and selected against when they're not, more than natural selection could predict? Maybe. It's not like organisms that use "meta-properties" of evolution, like tuning their mutation rates depending on the environment, don't exist (see this abstract on bacteria for example: https://pubmed.ncbi.nlm.nih.gov/16677295/). That could too. But it would apply to a few specific genes in those organisms, it wouldn't be a general evolutionary property.
As for empirical evidence, the thing is the "neutral hypothesis" can be tested, because random behavior has (paradoxically) very predictable properties. I think we can generally say that in everything we see about mutations appearing, the inferred mutation history seen in DNA patterns, in the evolutionary history of various phenotypic traits, that all those things point to mutations happening randomly with respect to usefulness. But one specific example I like very much is the Lenski experiments:
http://myxo.css.msu.edu/ecoli/
What happened is that Lenski ran a long-term experiment looking at the evolution of certain bacteria, by culturing them in a certain environment and, and this is key, freezing batches every few generations to have a replayable "record" of the state of the bacteria at various points. The most famous aspect of this experiment is how some of the bacteria evolved the ability to break down citrate, a completely novel and even definition-breaking ability for this type of bacteria. And here's the interesting aspect that's relevant to our discussion here: when they looked back at previous frozen generations ancestral to the specific bacteria that did this to figure out what happened, they found that if they cultured bacteria from before a certain point, almost none would develop the ability to break down citrate. But if they cultured bacteria from after that point, plenty would. Lenski deduced that the ability to break down citrate required several mutations, and one of those mutations was developed in the ancestor at that point. Hence, all the ancestors before that point were N mutations away from developing the ability to break down citrate, but those after it were only N-1 mutations away, and so they developed it much more readily.
Now how is this relevant? This difference between before and after the potentiating mutation would only happen if the mutations were occurring randomly, as opposed to "with the goal of developing the ability to break down citrate". If the bacteria were trying to break down citrate from generation 0, and acquired those mutations for that specific goal, then there would be no difference in which of the ancestors you looked at - they'd all be on the same path, and all equally likely to reach the goal. It wouldn't matter that the older bacteria were one extra mutation away from the adaptation than the later ones: they were planning on getting that mutation anyway. It's like, say you have a toddler and you want them to walk to a chair, but they don't control their walking very well; they're weaving all over the place, it's frankly not clear they even want to get to the chair to begin with. Where you set them down will make a big difference in whether they reach the chair or not: if you put them close to the chair, their random movements are quite likely to take them there, but the further away they are the more likely they are to just wander off wherever instead. Now say instead you have a hungry 6 year-old, and you put their favorite candy on the chair where they can see it. That kid is making a beeline for the chair, and it doesn't really matter where you set them down - if they're far away it might take them more time to get there, but not much, and they are as likely to get there in the end as if they'd been set closer.
The evolution of citrate metabolism in Lenski's bacteria behaved like the aimless toddler, not the focused 6 year-old.
ETA: Actually I kind of want to expand, add yet another element to the answer, which is: why this might not even be desirable. I see other comments have given examples of genes being transmitted non-randomly. I myself didn't exclude genes being transmitted non-randomly with respect to usefulness, but said it would be a property of specific genes in specific organisms, not a general feature of evolution, and I stand by that. I'll add that I don't expect this kind of property to be an important part of developing novel adaptations in particular, and that I expect big caveats on how smart these features are. I don't know what level of intelligence OP is considering, but I'd guess they're thinking, "wouldn't evolution work better if it chose adaptations more intelligently, like we humans would, instead of randomly?", mostly because it's what I myself would think. And that's the idea I want to challenge here.
I said earlier that natural selection works out for extremely dumb reasons. That's a weird thing to say, so let me explain: natural selection works because it's constantly testing things against reality. By definition; "natural" selection is "selection by nature". On average, things get passed on if they actually help, exactly insofar as they actually help. This is what makes evolution by natural selection so powerful, and come up with such innovative solutions that would never occur to humans: everything in reality is on the table (or at least, limited by the fitness landscape, not cognitive biases), and only things that work in reality are kept.
But that power is also a limitation. Because how is it that humans design that's different? We also test our designs against reality: we build them, check that they work, and keep them if they do. But "trial and error" is notoriously slow and inefficient. The power of our design process, the intelligence of it, is that we don't just test our designs against reality: we test them against imagined realities. We imagine how the world could be, we imagine different ways designs could interact with an abstracted mental model of how the world is. This is what allows us foresight and planning... which is something evolution by natural selection does NOT have, and which is why we can do things it can't. And I think that's the kind of intelligence people who ask "what if evolution was intelligent" are thinking of. But it's also a danger, because it means we can go full forward with an idea, and find out too late that it had awful consequences we didn't anticipate. It also bumps against the limits of our own imagination, which will never encompass the whole of reality. This is the big fear with genetic engineering, and it's why I'm not convinced that selecting genes for adaptivity would be as useful to an evolving organism as just blind natural selection would. You'd gain some things (speed, ability to cross fitness valleys) but lose others (reliability, ability to find fitness paths the foresighting system did not foresee). We might pull it off, but that gets to what I was saying earlier - we, as a species, are the smartest, best-at-planning-and-forecasting system nature has come up with yet. If we're barely, debatably at the point of being able to do this, what existing biological system could do better?

I agree with most of your comment. -however, I didn't want to ask if organisms could induce mutations, but if an specie could have to ability to determine from a given pair of genes which one had been more beneficial given its experiences, and transmit it more frequently to its descendance. I am conscious that it could reduce genetical variety and that it could be quite difficult to end up developing such a  mechanism, but there are a lot of species that have developed impressive mechanisms.

@zero-point I believe that is indeed the question I was answering...

The randomness of the assortment of genes was first shown by the experiments of Mendel in his experiments with pea plants, and demonstrated numerous times in different contexts in classical genetics.
There are specific instances where the assortment is not perfectly random. This is called meiotic drive. There are some genes that will skew the meiotic process so that a particular allele will be more likely to be transmitted to the next generation. These are the exception though.


text:
If RNA transcription is 5' end to 3' end, what is the directionality of the promoter for?
I am confused. If RNA transcription always grows from the 5' end to the 3' end, what does the direction of the promoter do for the mRNA transcribed?
From what i understand the RNA polymerase always extends the mRNA from the 5' end to the 3' end. Yet promoter sequences define the direction of transcription?
Which one is correct? Does mRNA transcription always extend from 5' to 3'? Or does the promoter dictate the direction in which the RNA polymerase extends mRNA?
Or it the truth somewhere in between?

Can you explain your thinking a bit further to focus the problem?

Think! DNA is double-stranded. What exactly do you understand in molecular terms by the statement "(the) promoter sequences define the direction of transcription"? Draw yourself a diagram.

Ok Sir, so there are 2 strands of DNA, so depending on the direction of the promoter, either one of the strands of DNA becomes the coding template (get transcribed)?
Is that correct?

I’ve just seen your comment. You need to address me as @david so I am alerted to your reply to me. (I don’t have to do the same as I am commenting on your post.) In answer to your query, that’s almost right. But it’s not only the DNA strand that is different, it’s its location or direction relative to that of the promoter.


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Does RNA of virus have poly adenylate tail before or after entry into the host cell?
I understand that RNA needs to have 5' cap and poly(A) tail to be recognised by eukaryotic ribosomes for translation.
Some viruses are RNA based(like influenza and HIV).
Does the RNA of these eukaryotic viruses come with 5' cap and poly(A) tail?
Or are the 5'cap and poly(A) tail added by host cell after entry of virus?

Just to clarify, you want to know if the RNA genomes of RNA viruses have caps and tails, not whether viral transcripts made during the course of infection have these structures?

Yes sir, that is what I would like to know

What research have you done to try to answer the question yourself? Have you consulted the Wikipedia entries on particular viruses or RNA viruses in general? If not, please do and indicate what you found in your question.

@david the presence and location of a polyadenylate tail on viral RNA can vary depending on the type of virus. In some cases, the RNA genome is already polyadenylated when it is produced within the virus particle, while in other cases it becomes polyadenylated after it enters the host cell. Is that right?

It depends on if the virus genome is dsRNA, -ssRNA  or +ssRNA (in the latter case the genome is supposed to be translated directly by the ribosomes, in the former two cases the virus usually transports its RdRp protein into the virions). Retroviruses are another case as the RNA genome is transcripted to DNA before being imported into the nucleus, though the genome is functionally mRNA as it was produced as such by the nucleus of the cell where the virion formed.


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What is this insect in Southern Colorado?
We have found this insect in a bit of a swarm on a concrete pad and on some insulation next to and around our greenhouse in which we have tomato plants.
The insect is about 2mm wide at its widest, and 4mm long at its longest.
What is it?


text:
DNA Sequencing and genotyping
Before going to the details of the question let me post a few other details-
(I posted something similar and got no useful answers-probably because I didn't explain things properly or something else)-
1. My background is not genetics.
2.I am not interested in knowing how dna sequencing or genotyping is done.
3. I am interested just in the nature of the results as in-https://en.wikipedia.org/wiki/DNA_sequencing#/media/File:Radioactive_Fluorescent_Seq.jpg
Now coming to the question- Humans have two sets of chromosome in each cell. So if I say sequencing chromosome1,what does that actually mean? Which of the two chromosome's gets sequenced?
Of genotyping-do comparison take place between two+two=four chromosome1's?
Or is my entire undertanding flawed?

You should first read up on the linked pages on the other question. If you have more questions (to incite curiosity was the point of the answer), you should ask in the comments section. If you think that your question was wrongly worded you can reword the question mentioning UPDATE. And lastly, you are touching too many topics. Until further clarification I am marking this as a duplicate to the first one which you asked.

Double question. Will be merged with http://biology.stackexchange.com/questions/50755/sequencing-two-strands-of-dna

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


text:
Acetone–butanol–ethanol fermentation

Source

Source

Source
Acetoacetyl-CoA is a C3 unit.
3-Hydroxybutyryl-CoA / Butyryl is a C4 unit.
Where does the additional C atom come from? I'm suspecting it's another Acetyl-CoA -> CoA reaction, but I don't see it in the images.

What does ABE mean? Do not use non-standard abbreviations in titles and if you must use them in your question define them. This allows indexing and improves your chance of getting an answer. And edit your image so we can see the reaction you are concerned about. Have you tried other sources for an answer?

@David fixed the title and added additional images I looked at. Maybe I'm missing something obvious.

I think you are.

Well, I’m not sure I should answer this, as your question is predicated by an incorrect supposition:

Acetoacetyl-CoA is a C3 unit.
3-Hydroxybutyryl-CoA / Butyryl is a C4 unit.

Not according to Kegg:

However, my answer is worthwhile if I explain how I found this out. One way to check this sort of thing is to go to the Kegg website and search for the compounds of interest, find the appropriate pathway (shown below) and then click to check compounds and reactions.

There is also the Metacyc website for metabolic pathways, and you can check the formulae on Wikipedia.

Kind of embarrassing that I missed that. It was so fixed in my head that it's C3 that I didn't even thought of checking that assumption. But your answer, as you already suspected, is worthwhile nonetheless. I went over to KEGG and was successfully able to navigate to the same map as you did. This will be a helpful place to start searching for answers in the future.

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


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Can anyone identify this spider?

I was hiking and saw this spider in the mouth of a cave in the Ozarks in Arkansas (USA). I believe it is some kind of wolf spider. I have never seen a spider in the wild this large, except for tarantulas in Texas (USA). The approximate size from the tip of back leg to front was 7-8 inches. It was bigger then my hand and I am 6'1" tall man. The spider did not have anything to reference size and did not want get too close, though I am sure it was harmless. I can go back to cave and take same picture holding a ruler to the rock if needed.
I believe my initial guess was off mark. I am thinking this may be a fishing spider. I only say this due to it being on a vertical surface and having banded/striped legs. I have never heard of one attaining this size before. Any info on this spider is greatly appreciated.

Harmless to humans? All spiders are venomous, just some more than others, so I suspect you were wise not to get too close to something this size.

The clues that point to a Fishing Spider (probably Dolomedes tenebrosus) are the nice stripy long legs and the very large size.  I've seen numerous big females slightly less than hand-sized, and one memorable one which was just about as big as my hand (about 7" tip-to-tip the longest way).  The abdomen looks a bit bulgey for a Dolomedes, but presumably she's nearly ready to lay eggs.

looks most like a Meta ovalis with a span of about 10 CM.

The spider in the question does not appear to be in the Araneoid superfamily at all (i.e. it is not a web-dwelling spider like Meta ovalis).


text:
What is the difference (if any) between an Intrinsically Disordered Protein and an Intrinsically Disordered Region
The wikipedia definition of an Intrinsically Disordered Protein is a protein that lacks a specific 3D structure.  An Intrinsically Disordered Region is similarly defined.  Why are they often listed separately?  Isn't an Intrinsically Disordered Protein just a protein that has at least one Intrinsically Disordered Region?
Just a couple examples:
https://doi.org/10.1002/pro.3680

In contrast to structured proteins, intrinsically disordered
proteins and regions (IDPs and IDRs)

https://doi.org/10.1146/annurev.biophys.37.032807.125924

There are a number of significant differences between the amino acid sequences of IDPs/IDRs and those of structured globular proteins and domains.

This is surely just plain English. Assuming the explanation in the Wikipedia article is that generally accepted, an IDR is a  disordered region within an IDP, which may have have ordered regions as well as disordered regions (as in the animated illustration). I don’t see your problem. A region is a part of a larger entity. If the whole protein is disordered, then all its regions are, but you can’t talk about the whole protein as a region. (I assume from your name that you are a native English speaker.)


text:
Can anyone identify this spider for me, please?
I live in Northern Indiana and I’ve seen 3 of these spiders in my house before, all different ones. When I first saw it, it scared me since it’s a pretty big spider in my opinion from what I usually have seen around here. This spider was bigger than a quarter all together. I know it’s not the best picture, but this is it on the wall a while ago. Also was a very fast spider so I couldn’t capture it too well. Are they harmless? I woke up with a bite today and then I remembered this!

The spider on your ceiling looks like a sac spider, more a Cheiracanthiid (like a yellow sac spider) than a clubionid (a leafcurling sac spider).
But the colour contrast of the dark red thorax to yellow abdomen suggests it may be broad-faced sac spider, which a is actually classified closer to a wolf spider than to the above two sac spiders. It is considered non-aggressive and non-harmful to humans.
It is hard to tell from the photo whether the cephalothorax is actually red or just dark. So you are probably the best judge from here.
Compare what you saw to:

trachelas tranquillus (broad-faced sac spiders) https://bugguide.net/node/view/26291/bgimage?from=72
cheiracanthium (yellow sac spider) https://bugguide.net/node/view/3383/bgimage?from=0

I would second Trachelas tranquillus.  Nice flat face and two-toned body (dark reddish front and whitish back).  These are commonly found in houses during the fall (when they come in to overwinter) and the spring (when they re-emerge with the return of warmer weather).  They can bite, but rarely do so without extreme provocation.  Not significantly venomous to humans.

I'm also from Northern Indiana. There's only two spider species in the area that are venomous: the Brown Recluse and the Black Widow. It's hard to tell from the picture, but I'm fairly certain that its not a Recluse, and it's definitely not a Black Widow. My best guess would be a Barn Tunnel Weaver.
For future reference: https://spiderid.com/locations/united-states/indiana/ has a list species, with pictures.
https://www.in.gov/dnr/entomolo/4542.htm for more info on Brown Recluses and Black Widows.

Hi, I'm a moderator here, but really terrible at identifying species besides ones I grow in my garden or those I catch fishing in local lakes. It seems you've provided some good resources, but we like answers here to be self-sufficient since links can break. Can you expand your answer to discuss particular features that led you to a specific ID?

the link provided has a "barn funnel weaver" but no "barn tunnel weaver". The spider in question does not resemble a funnel weaver. It looks like a sac spider. The link is also a very incomplete collection of spiders in Indiana. The link given also does contain trachelas tranquillus (albeit the picture on that site appears to be a very gravid one) but I believe that is what we are looking at here.


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

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

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

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

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

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

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

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

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

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


text:
What is this dark brown organism growing on a door frame?
A few brown spots appeared on a door frame and within 1 week it has grown to this size (~15cm). I have no idea what it is. How do I remove it completely? I worry that if I just wipe it off, it will just regrow from within the door frame. I've attached 2 pictures to assist with the identification.
Edit: I poked it with a stick and tiny white insects (~2mm) came crawling out of the structure.
My location: South India

Termites.
Photograph the insects and we will try to identify further. If the insects keep running, freeze some. This could be a big problem, so get good information soon.
Online I see this article that might help.
" An identification guide to the wood destroying termites of south India"
Journal of the Indian Academy of Wood Science
ISSN 0972-172X Volume 8 Number 2
J Indian Acad Wood Sci (2011) 8:148-151
DOI 10.1007/s13196-012-0028-9

Can termites be this small(~2mm) though? Unfortunately I can't get any more pictures because this is in my relative's house and I was just staying there for a while. I'll ask them to further look into this. Thanks :)

Ask them to trace the tunnel down to the nest, if they can.

@trinitrotoluene - if your relatives haven't got it resolved already, by the time termites are coming through the outside of wood, the internal is already overflowing with them and their tunnels. It is highly likely that they have a heavy infestation and will need an exterminator to get rid of them fully, then some serious repair work to trace, remove and replace the damaged wood.


text:
Why does ATP act as an allosteric inhibitor of glycogen synthase?
Why is ATP an allosteric inhibitor of glycogen synthase? Wouldn't high levels of ATP in the cell mean that the cell has sufficient energy, and in this case wouldn't excess glucose be stored as glycogen? However ATP acts as an inhibitor of glycogen synthase.
What is the physiological basis/biological reason for this?
Reference:
Vasudevan D.M, Sreekumari S, Kannan Vaidyanathan 2021. Textbook of Biochemistry (For medical students) 9th ed. Pg.147
Nuttall FQ, Gannon MC. Allosteric regulation of glycogen synthase in liver. A physiological dilemma. J Biol Chem. 1993 Jun 25;268(18):13286-90. PMID: 8514767.

This question was asked (with similar phraseology) and answered on SE Chemistry in 2017. https://chemistry.stackexchange.com/questions/72741/why-does-atp-inhibit-glycogen-synthase  What’s going on here?

The answer there only explains the inhibition of glycogen phosporylase in detail while the question is about glycogen synthase. Moreover it explains the chemical aspect but not the physiological aspect of this inhibition. It was even suggested that the question be moved here, but no one seems to have done it. So, I posted another question.

I doubt whether you will find a more comprehensive answer than that on SE Chemistry, where the answerer offers to respond to comments. As for physiology there is nothing about it in the original or your version of the question, or I do not understand what you mean. My own objection to the question is that it provides no documentation for or details of its premise that “ATP is an inhibitor of Glycogen Synthase”. Until I am provided with this I suspect that it is a distortion or misreading. Please edit the question to include.

By physiological basis, I mean the biological reason for the inhibitory effect. I have edited to include the references.

Thanks for that. The question really boils down to the status of the 1993 paper. I was surprised to find PubMed only lists about seven citations, the latest in 1997. This suggests to me that the conclusions of the paper are not generally accepted, for whatever reason, despite being in the Indian text book you cite.  Whether or not this is justified is another matter. I will revise the question accordingly when I have a moment, and do some research on it later.

Thanks! I couldn't find this mentioned in either harper or lippincott, so I am also a bit doubtful about the validity of this claim. I'll try doing some research on my own too!


text:
Would an enrichment of pyrimidine runs of two of more nucleotides be an early indicator of DNA to be damaged?
I am analysing two categories of protein coding genes comparing their relative characteristics. What I am observing is that one of these, in comparison to the other, is enriched in pyrimidine runs (two ore more consecutive pyrimidines). I have counted the number of these runs (I do not call them dimers because I have no data underlining a cross-link between two or more pyrimidine bases) per protein coding-gene performing then a Mann Whitney test that indicates that one of these two group of genes is enriched with respect to the other. I am hypothesising that this enrichment could be an early indicator of DNA to undergo local conformation changes. By your experience, could this hypothesis be reliable or I am totally misleading what I am observing?

I find it difficult to understand your question. You talk about comparing proteins but refer to the nucleic acid base pyrimidine. Are you talking about the DNA sequences of their genes? If so, two consecutive pyrimidines are extremely common as they occur in 24 of the 64 codons. And when you say “categories” of proteins quite what do you mean by categories? The same protein in different organisms, protein kinases v. Immunoglobulins, or what? And you suddenly mention clusters — of what? You need to be much clearer if anyone is going to help you.

I edit my question you are right

Basically, I am comparing protein coding genes with and without tandem repeats investigating why we have in some these repetitions (at amino acid level) and why not in others. You pointed an important detail about codon usage that already helped me.


text:
How does one determine what sequencing coverage/depth to use?
In the context of rare diseases, what sequencing coverage will be sufficient to detect the mutated loci (for eg. SMN1, SMN2 CNVs, gene SNPS, INDELs etc) ? How does this relate to statistics and how one is confident of the results? Most commercial sequencing services are marketed as promising 95-99% at 20-30X. My question would be, how we arrive at these values. For example, why is 99% at 20X ideal and how are values derived mathematically?

"20-30x" sounds like depth rather than coverage...

OK, looks better. So, what do you think the % and X values mean in terms of sequencing?

% means the total coverage across all bases, while X is how much each base is sequenced.

Almost there. X is depth - number of times a base was covered by a sequence. So, what might those values mean in terms of sequence reliability?

Of course, I know that the higher the depth, the more reliable the sequence. I'm asking how the value itself is determined, whether 20X, 30X... 100X etc. How is it derived mathematically/statistically? Is it by calculating the power of the assay, confidence levels, binomial probability of errors, or...?

It's literally a count of the number of aligned sequences that cover that spot in the sequence. If you have 1 sequence that covers a base it is 1X, 10 = 10X etc. See: Wikipedia on sequence coverage

My question is, so why do some labs set the metric as 99% coverage at 20X? why would a benchmark of 20X be preferable over 10X for example? I'm not asking what 20X ,30X...vs 100X means, but the thought process behind setting this as a sequencing QC metric, and how it this is determined through statistics. Hope you get my question.

I don't know for sure as it will depend on the individual lab and their purpose, but 99% is about all you can achieve reasonably without repeating sequencing ($$$) and 20X coverage is enough to have reasonable certainty on a base - it's 5% error after all, which is the usual p value of 0.05 in statistics.


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Is this also a carpenter ant?
I live in Dayton, Ohio.  I've found large-ish ants in my kitchen, and I'm wondering if they're carpenter ants.
I realize there's been a few questions about carpenter ant identification, but in my defense, this one comes with video: https://youtu.be/HGWertws0oo
Picture, with penny for reference:

See the video for better shots (mixed in with bad shots, haha).
Is this a carpenter ant, or something more benign?

It is a carpenter worker ant. They usually live in outdoors , If they build a colony inside your house,then it will be a huge trouble to you to patch the walls since, they are capable of creating larger holes and cracks in the wall .I don't know what exactly is your doubt? If you can you can elaborate your specific point.


text:
Why does our visible range not include infrared or UV radiation?
As the radiation peak of the sun is in the UV region and since at around room temperature materials emit radiation at IR, I wonder why our eyes are not capable of using these wavelengths.
I guess there is a reason why we exactly only see the region between these intensity peaks?

some quick googling showed that there are lots of easy to understand answers around (https://www.ceenta.com/news-blog/why-cant-i-see-infrared-or-ultraviolet-light), (http://scienceline.ucsb.edu/getkey.php?key=3019)

The first link isn't revealing any information, just physical basics about light. The last two answers from the second link are, in return, quite interesting. Particularly, I wonder why visible light offers the possibility to notice (sharp) boundaries..

Usually we don't ask why in biology because the explanation is always the same, it was good enough for survival. But here are a couple of explanations.
The radiation peak from the sun is in the visible range of the spectrum, between 400nm-700nm with the highest point around 550nm as can be seen here or calculated from Wien's law and the sun temperature.
That's why photosynthetic pigments use the visible spectrum and following them the rest of the ecological system.
Our retina blocks most of the UV light and water absorbs the lower part of the IR, illustrated very nicely in this article, figure 1.
It is true that materials on earth emit more radiation in the IR than in the UV-visible spectrum due to their temperature but:

most objects have the same temperature approximately
the soil emits a lot of radiation
the radiation from the sun in the IR is high compared to the radiation of earth. This is the best graph I found, emphasizing the great difference between sun & earth intensities
in the IR range there isn't a lot of variance in the wavelength intensity and therefore it is less useful.
Notice how uniform the IR reflection is from this leaf spectral signature

To summarize:

UV light is dangerous so we filter it out and not use it
IR light is uniform and not useful
Visible light is the peak of sun emission and therefore the most efficient range to use

Crystal clear answer. Thanks a lot!

The first sentence is good, the following explanations not so good.  It doesn't explain why many birds & reptiles are tetrachromats and see in the ultraviolet (and some insects in the infrared), or why most mammals - primates being the exception) are dichromats, and don't see much of the red portion of visible light.

@jamesqf the question was about our, human vision. The topics you mention are interesting but out of scope in my opinion. I'd answer them in depth in a separate question if you post it.

@Hachiloni: Human vision is not qualitatively different from that of other animals.  The fact that many other animals DO see in IR and UV ranges is sufficient to demonstrate that your answer is not correct.  Also note that photosynthesis does not use all of the visible spectrum, otherwise leaves would be black, not green.

Also re your point #2, IR light is most certainly not uniform.  For instance, it's fairly easy to take infrared photographs with a modified digital camera.  (You remove the built-in IR blocking filter, and install a visible light blocking one.)  A search for "infrared photography" will give numerous examples, e.g. https://petapixel.com/2016/10/27/introduction-digital-infrared-photography/

@jamesqf if human vision was not different from other animals we wouldn't have this discussion. Photosynthesis may use the whole spectrum in different intensities, check this (https://www.simply.science/images/content/biology/cell_biology/photosynthesis/conceptmap/Photosynthetic_pigments.html) for point #2 you might be right but: 1. check the long exposure time required, that is not usefull in a biological context. 2. I was thinking of the landscape existing when vision was developed. That's why I added the leaf spectral signature. I enjoy this but please edit my answer or post a question


text:
CCTV cameras in Microbiology (Pathology) Laboratories
Isn't it highly beneficial to have CCTV cameras installed in all Microbiology Labs in the COVID-19 times?
As the COVID vaccines are already developed, the research & development carried further in studying and analysing the COVID-19 variants by the Vaccinologists would be captured in real time on the Video monitors in as well as remotely from the Pathology labs.
This will assist the Vaccinology experts to analyse the COVID vaccine development (Including variants) in real time.
https://www.google.com/search?q=real+time+sequencing&source=lmns&bih=592&biw=360&prmd=invx&hl=en&sa=X&ved=2ahUKEwi46t2Us4LzAhWa0HMBHaKjD7cQ_AUoAHoECAAQAw
https://www.iaea.org/newscenter/news/how-is-the-covid-19-virus-detected-using-real-time-rt-pcr
https://www.illumina.com/systems/sequencing-platforms.html
https://i.sstatic.net/ToQo7.jpg
https://i.sstatic.net/cowUc.jpg
https://i.sstatic.net/65aPW.jpg
https://i.sstatic.net/380mk.jpg
https://i.sstatic.net/lvbeJ.jpg
https://youtu.be/NG44AEWHtRQ!
https://i.sstatic.net/SivW8.jpg
https://i.sstatic.net/8ehHn.jpg
https://youtu.be/8TaXtCOZV4o
https://sapac.illumina.com/products/by-type/informatics-products/basespace-sequence-hub.html
https://youtu.be/Ddavr_RASKA
https://www.fda.gov/news-events/press-announcements/fda-will-follow-science-covid-19-vaccines-young-children
https://i.sstatic.net/LewYd.jpg

No - cameras would not capture the detail of the experiments being performed, nor would many of the experiments make sense without some context for the individual labels, if the camera could see them.
All of the analysis of variants relies heavily on sequencing, which is run on a sequencer (such as these ones from Illumina). The data is then transferred directly to servers and processed there through bioinformatics pipelines. None of this could even conceivably be captured by camera.
Almost all viruses are far too small to be seen with a light microscope (for this one SARS-CoV-2 is about the same size as influenza). Bacteria are about on the limits of size that is useful for microscopy. The variants are all about the spike protein configuration and possibly some changes in morphology of the virion, all of which are way way too small to see with a microscope. Electron microscopy can be used to look at protein structure, but is too slow and imprecise to work out variant analysis - much better to do this by sequencing.

Thank you. Do you feel by modifying the sequencer machines (electronic circuit) by adding video camera can assist in this regard?

No, not at all. The data is already captured by a type of camera and is electronic, but it  wouldn't make any sense to the eye at all. These are massively parallel flowcells, capturing information in the order of millions of flashes of light per second, producing terabytes of information in a few hours. The data that comes out requires some fairly specialist software and knowledge to interpret - read the bioinformatics page on wikipedia for some small sense of the scale and challenges.

Thanks for the information provided. Customised Bioinformatics Software application/s can assist in this regard.

@PrashantAkerkar, most of the software used is already open source and such things are widely distributed, used, and discussed within the community. The datasets are generally open access too, so others can already access them and analyze to their satisfaction. I doubt that anything that you could add would improve the programs that are out there designed and programmed by CS and bioinformatics specialists.

Thanks. I feel the need of the hour is to manufacture Vaccines for the Delta variant of COVID19 as quickly as possible since three clinical pre trials will again consume time along with FDA approval. https://www.google.com/search?q=fda+approved+covid+vaccine&oq=FDA+appro&aqs=chrome.3.0i433i512j69i57j0i512j0i433i512j0i512.7604j0j7&client=ms-android-lava&sourceid=chrome-mobile&ie=UTF-8      https://www.google.com/search?q=fda+approved+covid+vaccine&oq=FDA+appro&aqs=chrome.3.0i433i512j69i57j0i512j0i433i512j0i512.7604j0j7&client=ms-android-lava&sourceid=chrome-mobile&ie=UTF-8

@PrashantAkerkar - not really, the time difference there is all taken up in recruiting people for the vaccine trials and then looking at the developing immunity. The sequencers run as fast as they can and the few hours they take are nothing compared to the weeks it takes to raise immunity. The Pfizer and Moderna vaccines are still highly effective against Delta with ~5% reduction cf wild-type.


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Why does high EDTA concentration cause swelling of platelets?
According to this textbook, high ( >2mg/ml of blood) EDTA concentration causes swelling of platelets which lead to their fragmentation.
I know that high concentration of EDTA increases plasma osmolarity which leads to cell shrinkage , as is the case in all other blood cells, but why does it have opposite effect on platelets? Why osmotic effects aren't seen in platelets?

what does 'high' mean in this context?

Edited the heading.

I followed the link- apparently >2 mg/ml EDTA has this effect.

Oh, you mean the context in that way. Ok I will add it.

That's ~5 mM. Is that really enough to have an effect on osmolarity?

But the same concentration is having osmotic effects on other cell, for instance RBCs.

Is it having an osmotic effect, or some other effect?

I think it's osmotic effect, because if were some other effect then why would it not affect when it's concentration is less?

I should warn you that I have no idea what the answer is, these are just some thoughts I had. Could it be related to the chelation?

As it's reported in an old 1968-article by J. G. White:

Chelation of membrane calcium by EDTA appears to cause marked
  irregularities in the platelet wall and massive swelling of the
  canalicular system. Swelling of internal channals is the dominant
  alteration in EDTA platelets, and this change appears ultimately to be
  related to the breakdown of platelet granules.

Many articles followed the one reported above, but it seems that the main cause of platelets swelling in presence of EDTA is the reduction of calcium levels that causes a sort of platelet activation.
This acivation could also be linked to direct EDTA action as reported in this article by Golański et al.:

The influence of EDTA on platelet membrane dynamics closely mimicked
  the alterations induced upon the interaction of fibrinogen with
  platelet GPIIb-IIIa. Thus, the EDTAK2-induced platelet activation
might result from an interference with platelet membrane protein
structure and conformation and possibly relate to an “unspecific”
  trigerring of a signal transduction pathway.

Anyway in normal conditions the laboratory platelet volume quantification using EDTA tubes seems not to be affected if executed in 1 hour since the collection (as reported in this article by Dastjerdi et al.).

I like the answer but I'm a bit hesitant on the idea that this is a sort of platelet activation (I may be wrong)...my recollection is that calcium increase is necessary for activation. Maybe a morphological change similar to activation is occurring through a separate pathway? I don't know for sure but maybe you can clarify a bit?

@Bryan Yes. You are right , platelet activation requires increase in intracellular calcium levels, which is initiated by entry of ecf Ca2+.

Why doesn't it show osmotic effects while other cells show?

@JM97 maybe EDTA has osmotic effects but there is are greater effects that hide it

@BryanKrause added a quote to better explain this "sort of platelet activation"

I think your question is relying on two completely different definitions of "high" EDTA. Really, both concentrations are "high" but one of them is "really really high."
The only references (for example, here or here) I can see that say anything about osmotic effects of EDTA is in the context of blood sample collection, and specifically when too small a volume is drawn into a larger tube, for example 0.5mL blood in a 5mL tube. In this circumstance, a ~liquid (blood) is added to solid EDTA powder sitting in the tube. This is already a high concentration of EDTA, it's enough to mop up all of the calcium around to prevent coagulation.
However, if you only fill the tube 10% full, there is 10X more EDTA powder pre volume than necessary to prevent clotting. This isn't just high, it's incredibly high. EDTA is usually as a potassium salt in this context, so that could be as much as ~100mOsm which would definitely cause osmotic effects, but that's on the order of a 10-fold higher concentration than your reference for platelets (which I can't access unfortunately). When you state in your question:

I know that high concentration of EDTA increases plasma osmolarity which leads to cell shrinkage

...this seems to be the best explanation, unless you can show another reference that demonstrates substantial cell shrinkage at lower (~2mg/ml) concentrations. I'm not saying there can't be some osmotic effect at that level, just that it would only be a couple percent of cell volume and would not be noticeable on anything but the finest assays.
Then on the other side of the equation, the effects on platelets are not to do with osmotic effects but rather due to a somewhat paradoxical activation of platelets, as in @DavideN's answer. Think of platelets as cells that are "primed" to expand when needed to stop a bleed; in some circumstances, it seems like EDTA can be a trigger for this process to occur, though not in others (again, see @DavideN's conflicting references).

References:
Goossens, W., DUPPEN, V., & Verwilghen, R. L. (1991). K2‐or K3‐EDTA: the anticoagulant of choice in routine haematology?. International Journal of Laboratory Hematology, 13(3), 291-295.

So when EDTA is >2mg/dl( not 10x the required amount but slightly higher) it's causing swelling of platelets due to chelation of membrane calcium, but is causing shrinkage of other cells. If  this shrinkage is not due to osmotic effects then what's the reason for their shrinkage?

I think in this answer you're talking only about osmotic effects, and you are not giving a different answer to the question.

Anyway looking at guidelines (e.g. CLSI), in case of incomplete filling using standard K-EDTA tubes (as many other types of tubes) is cause of sample rejection and no tests should be done on that.

@JM97 Do you have a source for EDTA~=2mg/ml (not dl) causing obvious osmotic effects in non-platelets? I think there are two answers to your question: DavideN's, which answers "why do platelets swell" - they don't really swell, they go through an unspecific triggering of platelet activation, and mine, which answers "why don't platelets show osmotic effects."

@DavideN Yes I think your answer is good for telling why platelets activate, but the original question also asks: "Why osmotic effects aren't seen in platelets?" I'll edit my answer to be a little more clear, but I think the problem is the OP's question is erroneously conflating two definitions of "high" EDTA.

@DavideN And thanks for catching the university link...I really wish publishers had more standard URLs, that's the first time that's happened that the library account got carried through to the final URL.

"Anyway looking at guidelines (e.g. CLSI), in case of incomplete filling using standard K-EDTA tubes (as many other types of tubes) is cause of sample rejection and no tests should be done on that." Yes definitely. But I can't see any support for the OP's assertion that EDTA causes (clear) osmotic shrinkage of cells in any other situation but this.

@BryanKrause No, I don't have any source for that, my textbook just states that other cells just shrink( and the reason for that shrinkage is osmotic effects, was my speculation). After reading your answer I see that some other mechanism is also involved in obvious shrinkage of those cells.


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Anatomical Angle Made by the Fingers of an Extended Palm
Does the angle made by the fingers (excluding the thumb) of an extended palm (as shown in the figure below) have a name (such as the Lovibond or Cobb angle, for instance) ?

I have already checked Modeling the Constraints of Human Hand Motion, published by the Beckman Institute for Advanced Science and Technology at the University of Illinois at Urbana-Champaign, but it failed to provide any answers. (Perhaps there aren't any ?) Any input would be deeply appreciated.

I searched through a few documents such as Biesecker et al. (2009) but could not find anything so far. I would guess there aren't any terms for that. Did you make the figure or did you find it somewhere? Where is it from? Knowing your interest for this term might eventually be helpful. [english.se] could also be a good place to ask this question.

@Remi.b: The question originated in my own mind, as an unintended byproduct of various measurements performed on my own body, in an attempt to understand the ancient and medieval measuring systems, such as those still employed by the Anglo-Saxon world today.


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Plasmid specific DNA degradation
I'm interested if there is a way to degrade the plasmid DNA inside an E.Coli cell specifically so that the method does no harm to the chromosomal DNA. First I was thinking about restriction endonucleases but I'm afraid that;

it isn't specific enough and kills the cell
or it does nothing, because the E.Coli methylates the plasmid DNA too

My second thought was the CRISPR/Cas9 system but it sounds like an overcomplication of the problem. Any simpler ideas? (For eg. specific enzymes)
EDIT: the main idea is to create more competent E.Coli cells with directed evolution. Currently this is just a thought experiment, so there is no specific plasmid sequence. In details; I would transform the plasmid into the cells, then do the selection part with an antibiotic and let them grow, then transfer the cells into a medium where there is no antibiotic and add IPTG to induce the plasmid-DNA-hydrolase enzyme, then maybe an other selection part could be performed to remove the cells which still contain the plasmid (for example with FACS if there is a GFP gene on the plasmid), then make the cells competent again with CaCl2 and do this whole process over and over again.

There are a lot of (simple) solutions, but I'm not really sure what you want to achieve. Can you clarify?

Why do you want to do this? To get rid of the plasmid and re-use the cells for something else?

@Chris Exactly, the core idea was that if such an enzyme exists then I could elevate the competitive ability of the cells by directed evolution.

Do you know the sequence of the plasmid? It would not be straightforward to get rid of the plasmid especially if it is high-copy number.

@VonBeche I tried to clarify it in the question details. What are those simple solutions?

traditional method to remove a plasmid from E. Coli is to grow the cells with Etidium bromide.
http://vlab.amrita.edu/?sub=3&brch=186&sim=1097&cnt=1

Done. But really... this is like needing to reference plasmid extraction by alkaline lysis or pouring an agarose gel.


text:
Approximately how long will it take to document all existing species?
I did some research and found that there is a new estimate of 8.7 million species, plus or minus 1.3 million and that about 1.2 million have been discovered already. About how long will it take to discover the remaining species?
I just did a bit more research and found that about 18,000 species are discovered each year. If this rate continues, then the remaining 7.5 million species would be discovered in about 416.667 years. If we subtract the 1.3 million to get 6.2 million and divide that by 18K, then we get 344.444 years. If we add 1.3 million to get 8.8 million and divide by 18K, then we get 488.889 years. So by my calculation, it would be anywhere from 344 years to 489 years (rounded). Is this about right? Or are there other factors that could come into play?

Whoever downvoted, would you mind explaining why?

I didn't downvote, but it's usually useful to include in the main post links to where you found those statistics.

I voted to close this question because many good questions generate some degree of opinion based on expert experience, but answers to this question will tend to be almost entirely based on opinions, rather than facts, references, or specific expertise.

I voted to close your question because I think that it is not a question about biology in the terms of SE Biology as laid out in the [tour]. You may wish to review the three types of question listed there.

For one thing, the species concept is already a little fuzzy when it comes to macroeukaryotes, but it gets especially fuzzy when you get into single-celled organisms (which I'm guessing these estimates ignore). So, estimating the number of species will depend on who you are looking at and where you are looking. Secondly, the number of species in an ecosystem (or in this case on a planet) is not fixed. Evolution is a dynamic process which is always occurring. Populations divide and re-converge, and new species emerge, old species go extinct. The circle of life and all that.
But more importantly, extrapolating the rate of new discoveries out at a constant rate basically assumes that all species have an equal probability of being discovered at all times. Which we know isn't the case. Even if all of the species on earth were equally abundant and equally distributed, this discovery rate would not remain constant.
Imagine a giant lotto ball machine with a seemingly infinite number of balls in it, each with a random number on it. Your job is to sample this machine and document each unique lotto ball number. Say you're sampling one ball per minute. At first, almost every new lotto ball you pick is unique. You're discovering around 60 unique numbers every hour. But after a while, you start to see some numbers repeated, and after an extended amount of time you notice that more than half the balls you sample are already accounted for. You're now discovering less than 30 new balls per hour. The more you sample and record, the lower your rate of new discoveries becomes. Eventually, you are lucky if you can find a unique discovery in any given day of sampling. But you still have no idea whether you have sampled and documented ALL of the unique numbers in the machine.
If you plot the cumulative number of unique numbers you see vs the sampling depth, you get something like a species accumulation curve or a collector's curve. These generally form an asymptotic shape, like this example below. You can use some statistics based on the general shape of these curves to estimate the total number of unique species in a system. It requires making some assumptions about your sampling methods and also about the distribution of your different species, but, in any sufficiently complex community, you end up with this sort of diminishing return rate after extensive sampling.
.
Obviously, researchers are not necessarily sampling new species at random, nor are they sampling at a fixed rate. Technology is a big factor, and research funding in general will affect the rate at which new species can be discovered. But you also have to keep in mind that undiscovered species are not distributed evenly withing or between different ecosystems, and they do not have equal probability of discovery at all times. To return to our bingo ball metaphor, every different ecosystem is like a different bingo machine. In some of them, species might occur in roughly equal ratios, but in others they might have dramatically skewed ratios. Some might outnumber others by a ratio of a million to one or more. And as we add more and more to the cumulative list, those remaining undiscovered are likely to be the more rare and hard to find species.
Given all of the potential factors that might go into determining the rate of new species discovery, it would be difficult if not impossible to estimate when our efforts would reach complete saturation, but it will almost certainly slow down as greater and greater numbers of species are discovered.


text:
Converting from RU/ML to AEU/ML
I'd like to know whether it is possible to convert from RU/ml to AEU/ml.
I work in the ELISA department in our laboratory. We need to validate some kits by comparing results between our lab and another lab. They reported their values using the AEU/ml unit whilst ours are in RU/ml.
Is it possible to convert between AEU/ml and RU/ml?
RU: Relative Unit   AEU: Arbitrary Elisa Unit. The plates are read on a Biotek microplate absorbance reader via UV-VIS detection at a wavelength of 450.
Thanks in advance!

For those that aren't familiar with the terms, can you please [edit] your post and define RU and AEU? Also, what format is the ELISA readout - colorimetric, luminescent, fluorescent, or MSD?

RU: Relative Unit   AEU: Arbitrary Elisa Unit. The plates are read on a Biotek microplate absorbance reader via UV-VIS detection at a wavelength of 450

How are these units calculated? If both labs run the same set of standards to plot a linear standard curve, you should be able to make a simple mathematical calculation to convert from one to the other.

For example, if a 1 μg/ml standard gives you 1000 RU and 5000 AEU, and a 5 μg/ml standard gives 3000 RU and 10,000 AEU, you can use curve-fitting to get the formulas for each line, then figure out a translation function. Alternatively, you can use their formula for determining AEU from the raw OD450 and back-calculate your own values.


text:
Can the metatranscriptomics replace the approach of functional metatranscriptomics/functional metagenomics?
While metatranscriptomics reveals information about the expression of genes and their functions too, Functional metatranscriptomics (https://www.nature.com/articles/ismej201167) allows the characterization of genes expressed by different eukaryotic microorganisms. My question is can we use both of those techniques? I couldn't find out if they will bring the same results or each one of them will give its own.

Hi Noor, and welcome to Biology.SE.  I'm assuming functional metatranscriptomics involves isolation of RNA, reverse transcription, and then cloning of cDNAs into a model organism?  Your question would be better received if you provided links to studies that exemplify the methods you're comparing. Perhaps this and this?

Yes, perfect example, I wonder can metatranscriptomics, just the total RNA-sequencing replace that approach?

I would consider these to be complementary approaches. They don't really provide the same information, or even the same kind of information.
A big challenge with sequence-based genomics and transcriptomics is that they rely on sequence homology for functional annotations. In other words, they only provide indirect information about gene function, which can be incorrect or, in many cases, completely absent (this is why you often see annotations like "hypothetical protein xxx" in genomics papers). So what can happen is, you may identify a great number of genes with no functional annotation, so you have no basis for determining what they are doing, or worse, they are incorrectly annotated and you publish misleading reports. This is especially challenging in complex and diverse environments like soil.
The advantage of the functional approach is that you don't have to rely on sequence homology for functional annotation, since you're characterizing the phenotype directly. The disadvantage is that you can only fined the specific functions you are looking for. To bring it back the example you linked, if you're only screening for dipeptide transporters, you would not be able identify anything that doesn't directly influence that phenotype.
So, it really depends on what information your are after in your study. If you wanted to completely replace the functional genomics approach with sequencing approaches, it would only work if your genes of interest already have reliable functional annotations and if your sequencing depth is sufficient to identify them. That said, sequences from a functional study like the one you shared could be used to inform your sequencing approach, or to mine existing metagenomic or metatranscriptomic datasets for genes with share homology. Heck, if you only have a few target genes and they have some well conserved regions, you could probably come up with an acceptable RT-PCR approach too.

Here is my understanding of the terms you present.
Metatranscriptomics refers to RNA-seq of a mixed microbial community or environmental sample. This is a general approach to characterize the gene expression of all organisms in a sample, and will rely on alignment of transcripts to existing genomes or metagenomes for which genes have been called and annotated.
Functional metatranscriptomics refers to the process of isolating RNA, reverse transcribing the RNA to make a cDNA library, and cloning that library into a model host to assess cDNA-encoded functions. This is a method that allows for identification of transcripts that encode a specific function in cases where the organism(s) that produced those transcripts are not genetically tractable. In the ISME paper you link, cDNAs were cloned into a yeast strain lacking dipeptide transporters in order to look for environmental genes that complement the knocked-out functions.

My question is can we use both of those techniques?

These are two techniques that differ in the type and scope of data produced, and their utility in application will depend on the scientific questions you want to answer.


text:
Does it make sense to say that microtubules are arranged in a ring around the cell periphery?
I am reading a journal paper and it is about how the organisation of microtubules are altered in CHO cells that overexpress microtubule-associated protein Tau.
In the paper, the authors found that overexpressing Tau in CHO cells resulted in changes in the organisation of microtubules. In the paper they state:

Non-transfected, interphase cells contained typical radiating arrays
of microtubules that often could be seen to emanate from a microtubule
organising centre when labelled with the tubulin antibody. However,
transfection of tau into these cells dramatically altered this pattern
of labelling. In cells expressing high levels of tau (as judged by
intensity of fluorescence staining), bundles of microtubules could be
discerned which often formed a ring, or spiral around the
circumference of the cell (Fig. 1A,B).

I have described what the authors have discovered in the tau-transfected cells in my own words: "In cells overexpressing Tau, microtubules were bundled and arranged in a ring structure around the cell periphery".
I have read online that the cell periphery is the part of the cell encompassing the cell cortex, the plasma membrane and any external encapsulating structures.
By saying that the microtubules were arranged in a ring around the cell periphery, I want to convey that the they are arranged in a ring around the perimeter of the cell. However, I was wondering if using the phrasing "around the cell periphery" makes sense, because I do not want people to misunderstand my sentence and think that I am saying that the microtubules are arranged in a ring outside the plasma membrane by using the word around.
Any insights are appreciated.

I read periphery as meaning outside and proximal.  So I would interpret around the cell periphery as referring to something that is closely associated with but external to a cell.

Are you asking because you are trying to avoid plagiarism? Otherwise why not use the original phrasing?