text:
How are constitutive enzymes regulated?
I found that inducible enzymes can be regulated by many ways, but
I cannot find how constitutive enzymes are regulated...

A constitutive or "housekeeping" enzyme is usually defined as an enzyme whose expression level (amount of protein) is always constant, independent of any environmental factors. Hence, regulation of constitutive enzymes must be post-translational, for example allosteric regulation of the enzymatic activity by substrates or products.
Note that constitutive enzymes is mostly a theoretical concept. There are probably no enzymes whose expression is completely unaffected by any environmental factor.

why do you say constitutive enzymes is mostly a theoretical concept?

Because I have yet to see an enzyme whose expression is not regulated at the transcriptional/translational level in some experimental condition. An enzyme's protein level might be constant in some particular experiment, but who's to say what will happen in another setting. It's the same problem as with "housekeeping genes" in RT-PCR.


text:
Relation b/w venation and transpiration
What purpose does reticulate venation in dorsiventral leaf or parallel venation in isobilateral leaf serve?
Does it have any relation with unequal transpiration in dorsiventral leaf or equal transpiration in isobilateral leaf?

source: Stack Exchange

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

sort: votes


text:
What are sources for learning bioinformatics for self-learning?
What are the sources for learning bioinformatics(books, websites/MOOCs)? Does it require prior knowledge of programming language because I am a complete noob when it comes to programming language.

If you want a simple place to start, try Rosalind http://rosalind.info/problems/locations/

Coursera has good introductory R and Python courses. They also have good intro courses for genomic data science. Edx also offers some interesting stuff for biological data science. You can find more but those are the courses I personally looked at and had a little fun with.

I agree with @CMosychuk - coursera is a great place to start learning for this field.

If you're looking for a book, Vince Buffalo's book "Bioinformatics Data Skills" gives a nice overview.  The first chapter is titled: 'How to Learn Bioinformatics'.  There are several chapters on familiarizing yourself with unix and one rapid introduction to R.  When I read the book I thought to myself, I wish I had this when I first started!

I recommend starting with a programming language that you are likely to use soon. And nothing in biology is more crucial than statistical analysis for which R is the golden standard. Datacamp.com has wonderful and coherent online site for learning R and applying it to statistics. I'd suggest to start with the free "Introduction to R" & "Intro to Statistics with R: Introduction" courses. They only take several hours and get you going. Then it is 9$/month (for students) for the other courses, but it's well worth and you can complete most of the courses in just  a few months anyways!

Learning a language such as python or perl is almost necessary.
You might have a look at coursera.
There are quite some bioinformatics-oriented courses:
https://www.coursera.org/courses?query=bioinformatics&languages=en
University of California San Diego has a series of bioinformatics courses, with one that seems made for beginners in programming:
https://www.coursera.org/course/algobioprogramming
I haven't had a detailed look at this one, but I liked their more advanced courses.
In coursera, the courses are often organized in so-called "specializations" which give you a certificate, but are not free. However, you can normally enroll to individual courses without paying.
I would also advise learning how to use a UNIX-like command-line environment, and tools such as sed, awk, grep.
The following sites might be good for this:
http://www.grymoire.com/Unix/
http://software-carpentry.org/lessons/
The scope of the latter is broader, and the things they teach could be valuable if you want to do scientific programming in general.

From what you say I would definitely not start by learning a programming or scripting language which may only be applicable to certain types of problems.
I would start by reading an introductory book on bioinformatics with a wide general scope. Then you can see what area or areas interest you and find out what tools (programming or otherwise) you need to become familiar with to solve problems in that area. (Because to really learn bioinformatics you have to solve problems.)
There are no doubt several suitable books. The one I am familiar with as it was used in my University is "Introduction to Bioinformatics" by Arthur Lesk (Oxford) 4th ed (2013). However it doesn't cover RNAseq, so unless there is a new edition in the pipeline you may be better with something more recent.

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


text:
What is DNA-cellulose chromatography?
I am going through a paper where they have done DNA-cellulose chromatography to study the interaction between protein and DNA. They are adding the protein to the column and eluting with high salt concentration.

DNA-cellulose chromatography is used to purify proteins that bind DNA (Potuzak and Dean 1978, Abdullah et al., 1985).
The idea behind it is quite simple: you attach DNA to a cellulose matrix and keep conditions so that the DNA does not dissociate from the cellulose. This stationary phase is then used as a bait for DNA-binding proteins from the mobile phase. The purified DNA-binding proteins can subsequently be dissociated from the column with high salt concentrations.
The method was (as far as I know) first described by Litnam (1968) who used it to extract a DNA polymerase from Micrococcus luteus.


text:
What is autophagy?
Recently Japanese scientist won Nobel Prize in Medicine for "Autophagy".
Can someone explain what autophagy is?
https://www.google.com/amp/s/www.livescience.com/amp/56349-japanese-scientist-wins-nobel-prize-in-medicine.html

I'm voting to close this question as off-topic because questions about diet and nutrition are off topic unless directly related to medical care.

@CareyGregory I've edited the question. Is it valid for the site now?

You fixed the nutrition problem but asking how this will benefit people is purely speculative, and therefore opinion. So I edited your question down to the root question you're asking and reopened it. People can add their thoughts on what it might lead to in their answers, but get the basic question answered first.

Welcome, @Saksham, I've closed your question as a duplicate because I think a Q&A here already answers your question. This isn't any sort of punishment, it's just the way SE is meant to streamline questions. If you have further questions that are not answered in the marked duplicate you can ask a new one. Thanks!

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


text:
Anyone know what emerged from these cocoons?
Found a little universe in the back of a ceramic decoration I put up outside in summer...the concave back was full of grainy soil and several exited cucoons...anyone know what critter this is/was?!

Could you please add the size of these cocoons and your geographical location?

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


text:
How to find idea for essay
I'm studying microbiology in Iran
The university that I'm studying in doesn't provide that much help in research areas and we don't get to research or write essays that much ,while I'm trying to write an ISI essay and communicate with universities abroad in order to get admission for my masters degree and be able to study abroad
But the problem is , I don't know how to start and find ideas for writing papers and research
Like, what is the first step you take as a scientist when you want to start research?

This question would be better suited to the academia stack exchange.

You might want to start by browsing the research papers (think of them as "essays") at https://www.plos.org/ to find the areas you are most interested in.  They have thousands of peer-reviewed articles which you can read for ideas for your essay and research ideas.   You might then consider contacting the authors of those papers to inquire about education or work at their institutions.


text:
Skin (histology)

Our instructor share this image with us. She didn't specify much. She only said it was a skin sample.
Could you tell me what is the thing that was pointed at with the blue arrow?
I believe that I found a similar image in Ross' Histology (e6) Plate 44.
Thank you

Could you please edit your question and add, what you think this is? And what are the pros and cons of your solution?

It is difficult to say based on the limited informations about the sample, but I could assume that this is a Masson's Trichrome staining. Briefly: blue/green - collagen, red/pink - cytoplasm, dark pink/brown - nucleus.
Presence of the adipose tissue (white area on the right) and a lot of collagen (green) suggest that the sample highly likely comes from dermis. The large structure pointed by the arrow looks like an eccrine sweat gland. Here, you can see it in classical haematoxylin and eosin staining:

Alternatively, see: http://medcell.med.yale.edu/histology/skin_lab/eccrine_sweat_glands.php


text:
Why in the Electron Transport Chain does PS2 go before PS1?
Why in ETC does PS2 go before PS1?

It's just because PS2 was discovered before PS1.

If your question is related to numbering, the photosystems were named in the order of their discoveries not participation.
In cyclic ETS PS-II doesn't participate at all.
PS-I would have gone first if PS-II was named PS-I.


text:
The wood wide web strengthening/expanding the heartwood of damaged pines
My grandfather told me about a practice: girdling/ring-barking (not sure which was employed) of pine trees in order to make the wood stronger. Now, he didn't give too many details, so I had to do some research. He said the resultant, strengthened wood is called adel, adl or al, which is Norwegian.
When I searched for it, I found that these terms mean the same as heartwood, but in the context of pines. I believe that this process he explained in essence just strengthen and/or expands the heartwood of the pine. Such pine wood, that contains higher amounts of heartwood, is called ore-pine, and this Wikipedia article states that this was achieved through the removal of branches, as opposed to girdling/ring-barking, which is what my grandfather said.
Now, whether the mechanism of expansion/strengthening of the heartwood is via branching or girdling/ring-barking is one question. However, the question I am most interested in, is the mechanism of how this process happens. I know it has something to do with the increase of resinous substances in the wood, but what I'm wondering about is if this strengthening is happening via the "wood wide web". When my grandfather started talking about this, I said that it probably happened via the wood wide web. The damaged tree sends out information of its damaged state, and the other trees in its vicinity divert more resources to it, leading to the strengthening and/or expansion of its heartwood. My grandfather however, said this process did not involve the wood wide web, and that this process happened completely locally at the tree.
Which is correct (if either)?

This is a guess based on my knowledge of tree physiology. Sapwood is formed by the cambium of the tree. Perhaps when you cut off sap from the cambium by girdling, the tree cannot grow sapwood as quickly and diverts resources to the heartwood. Evidence on the role of the wood wide bed (common mycorrhizal network / CMN) in supporting stressed plants is mixed, and sometimes results in the fungi taking extra resources from the dying roots.


text:
Why do antibody tests target different antibodies?
I've noticed in various COVID-19 lateral flow assays, they seem to target different antibodies (S1, S2, NP). What are the benefits or downsides of choosing different antibodies? I know that some have a higher chance of cross-reactivity, but why wouldn't all tests just use the ones with the lowest cross-reactivity?

I think you're confused by polyclonal tests https://www.nature.com/articles/d41587-020-00010-2

I've used multiple assays. Some only respond positive to N Mab others respond positive to S1 Mab.


text:
Selection of recombinant host by color selection method
In recombinant DNA tech,
To select a recombinant host from non-recombinants, we have different types of techniques available.
The one I'm talking about is the color selection method with the use of 2 markers(one antibiotic resistant gene for eg. Ampicillin, and the other Z-gene).
We use Z-gene as the reporter gene.
We use vectorless E. Coli as the host cell here.
Now, when we add add Ampicillin to the petri dish containing all of the variants (transformants and non-transformants), - the non-transformants will die.
The transformants survive.
Now, we add X- gal to the replica of this petri dish, and we see some of the colonies turning blue due to the action of the enzyme β- galactosidase, which in turn is produced by the intact Z-gene in the plasmid.  That means our blue colonies are the non-recombinant ones.
My question is-
The medium taken in the petri dish should contain glucose too , shouldn't it? Otherwise the recombinants would too give the colour reaction (X-gal is a homolog of lactose) due to the Z-gene present in their chromosomal DNA (operon concept).
The question maybe silly since it's kind of obvious we have to supply basic necessities for the growth of bacteria(which obioviously is glucose).
Just wanted to confirm in case we don't have glucose available ! =p

The Z gene you are talking about should be lacZ that encodes the $\beta-$galactosidase, which is made from $\alpha$ and $\omega$ peptides. Neither peptide is functional by itself.
$\beta-$galactosidase will cleave the glycosidic bond in X-gal and form galactose and 5-bromo-4-chloro-3-hydroxyindole. The latter product then dimerizes and oxidizes to 5,5'-dibromo-4,4'-dichloro-indigo, an intense blue product that is easy to identify and quantify.
Next, you should check out the genotype of your bacterial strain because they typically have only the $\omega$-peptide encoded in its genome. Thus, the enzymatic activity of the $\beta-$galactosidase is only recovered when the $\alpha$-peptide is in the environment, and the process is called $\alpha$-complementation.
Two commonly used strains for cloning and expression in E. coli are Dh5$\alpha$ and TOP10.
The genotype for Dh5a is like this:

F– Φ80lacZΔM15 Δ(lacZYA-argF) U169 recA1 endA1 hsdR17 (rK–, mK+) phoA
  supE44 λ– thi-1 gyrA96 relA1

Here, lacZΔM15 indicates that the M15 segment is lost from lacZ, and the mutant protein will only have the $\omega$-peptide.
The genotype for TOP10 is like this:

F– mcrA Δ(mrr-hsdRMS-mcrBC) Φ80lacZΔM15 ΔlacX74 recA1 araD139 Δ(ara leu) 7697 galU galK rpsL (StrR) endA1 nupG

Again, you will notice lacZΔM15, which is still a non-functional peptide segment after all.
Finally, to your question. Even if the there is no glucose as primary energy source in the medium and only X-gal is present, the operon of your host bacteria(I suppose it's E. coli) cannot produce the functional $\beta-$galactosidase on its own. Moreover, the recombinants, with the vector sequence encoding the $\alpha$-peptide disrupted, will not exhibit $\alpha$-complementation. No color reaction then! :D
Reference:
1.Genotypes of Invitrogen™ competent cells - TOP10, retrieved from: https://www.thermofisher.com/cn/zh/home/life-science/cloning/competent-cells-for-transformation/chemically-competent/top10f-genotypes.html.
2.Genotypes of Invitrogen™ competent cells - DH5a, retrieved from: https://www.thermofisher.com/us/en/home/life-science/cloning/competent-cells-for-transformation/chemically-competent/dh5alpha-genotypes.html.
3. Langley, K. E.; Villarejo, M. R.; Fowler, A. V.; Zamenhof, P. J.; Zabin, I. (1975). "Molecular basis of beta-galactosidase alpha-complementation". Proceedings of the National Academy of Sciences of the United States of America. 72 (4): 1254–1257. doi:10.1073/pnas.72.4.1254. PMC 432510 Freely accessible. PMID 1093175.
4.

So basically, we use different kind of bacterial strains here {the ones those have either of the 2 genes(the peptide coding ones) present in the chromosomal DNA, not both of them simultaneously}? Are they mutated versions (made in lab) of normal E.coli or were they present naturally?

In your case I believe they are mutated since you are doing recombinant DNA experiments. Wild type E. coli carry functional LacZ, while lab strains are deliberately mutated so we can apply the blue-white test at ease. But if you are still not so sure, I suggest you to check the precise genotype of the strains online, if you can get them.

I'll take your words for this. I'm not actually experimenting nor do I have the qualifications or the facilities to perform this experiment. Plus, i don't know how to check the genotypes of strains online. Anyways, thanks for clearing that up! =)

@anamikaSingh For commercial strains, you just look them up on its provider's website. Usually you will find details. Hope this can help you!

Yes! I looked it up. It was really helpful.  Thanks!  =)

@anamikaSingh No problem. :)


text:
What does it mean by “end effects can be ignored”
I have been reading a book ( Statistics for Biology and Health) and i encountered many of following bold text.

Consider a long DNA sequence of length N, where N is assumed to be
so large that end effects can be ignored in our calculations.

In Shotgun sequencing also the saw similar thing :

The fragments are assumed to be taken at random from the original
full-length sequence, so that if end effects are ignored, the left-hand ends
of the fragments are independently distributed with a common uniform
distribution over [0,G].

What does " end effects can be ignored " means?

They are considering a model of a DNA sequence of quasi infinite size. They consider a case where the DNA sequence is so long that the fact that it has ends will only negligibly affect the conclusions of their model. This is likely the same as considering the DNA is circular.
To give you a similar logic, imagine a species where individuals live in different populations. All population can be placed on a one dimensional axis. The migration rate from one population to the neighbouring population is 0.1 (this is called a "stepping stone model" btw). Hence, the probability of not migrating is 0.8 (1 - 0.1 - 0.1). I can draw conclusions from such a model but it would be important to specify that I neglected the end effects and hence, I assumed there are a lot of populations (or that the population form a loop). Why did I neglect the end effects. The last population on each side cannot have a migration rate of 0.1 toward a population that does not exist. Hence, their migration rate must differ from the other populations. This is commonly called edge effects (rather than "end effects")

Out of curiosity, do people actually call these end effects in the context of DNA when this comes up? The more common term for these issues in a broader mathematical context in English is usually "edge effects."

@BryanKrause I agree the term edge effect sounds more common, esp. in its use in population biology (info added in post). I am not sure I had ever heard "end effects" before but the term makes the meaning quite intuitive.

Thanks - I suspect the author (or translator) of the text the OP refers to made a bit of a mistake here. I think if they had called them edge effects it would have been more easily investigated by the OP. That said, anyone familiar with the field would probably quickly infer that they meant 'edge effect' when writing 'end effect.'

Perhaps end-effects is strictly correct when considering a one-dimensional object, such as a DNA-sequence. If you were considering a two-dimensional object, as you might in ecology when looking at a particular geographical area, then the area would truly have an edge, whereas a DNA molecule could be said to only have 'ends', not edges.


text:
Brownian motion : Understanding the output of mvBM function.?
To fit the brownian motion for independent evolution of traits i used below code:
rownames(carni)<-gsub("_",".",rownames(carni))  #Renaming to match the tip of tree
#Independent Evolution
brown_indepen <- mvBM(carni_tree,carni,param=list(constraint="diagonal"))

mvBM is the function from mvMORPH package. It seems by giving constraint="diagonal" would fit the model for traits to be evolved independently. I would like to know the idea behind it. Also, i got the below output after running the code. I would also like to know what below output means.
LogLikelihood:   -589.2373
AIC:     1186.475
AICc:    1186.771
4 parameters

Estimated rate matrix
______________________
      size    range
size  73.70335  0.00000
range  0.00000 13.54524

Estimated root state
______________________
       size    range
theta: 38.43947 13.78439

Size and range were the two traits.

This seems appropriate for the biology forum, but consider posting/migrating to statistics or bioinformatics--they may be more familiar with mvMORPH


text:
Can Tajima's D and other population genetic tools be used to copare Arabidopsis ecotypes?
I am currently investigating 2 genes in Arabidopsis taliana that are a product of a recent duplication even (observable from synteny and phylogenetic analysis). In addition to the molecular and biochemical functions of these genes, I was wondering how evolution is acting on them at the population level. There the genome sequence of 1300 ecotypes of Arabidopsis from all around the globe available. So, I was wondering if I could use all these sequences to quantify nucleotide diversity and/or Tajima´s D? However, I am not sure if this is conceptually right, since I am not using an actual population, but I am just aligning 1300 sequences as "global population". what do you think?  is this a good approach to see the level of variation for each gene "globally"? is this "global" view scientifically and statistically relevant?
Regards


text:
Is it possible for a fire to start inside of a live human body?
Over the years, I've read about spontaneous combustion in the news, but now I am wondering if it's possible.

I'm voting to close this question as off-topic. We welcome new users to SE Biology but expect them to read about the site first. The tour explains that this is a "site for biology researchers, academics, and students".  This implies a certain standard that unfortunately this question does not reach.

Like any community, this one has rules. If you join you are expected to read the rules and abide by them. The community is self-regulating, and requires the votes of five members of sufficient experience before a question is closed. It is generally thought helpful to explain why one has voted in a particular way. I am afraid that it is your response rather than the explanation of my vote that is rude.

@WillyA - Do not call people a troll who are trying to guide you through the site's conventions. David's investing time and effort in your question. I concur that the question is underresearched. If you could provide a web-link and explain why you doubt the process of spontaneous combustion that would be helpful.

Willy, please stop flagging every comment that you don't like. Secondly, FYI, the diamond behind a name means they're a mod - flagging comments from such a user doesn't make too much sense, as they are the ones handling flags :)

@AliceD please note that this user may be an attempt to get around a 10 year suspension by this user.  The user has asked and had closed and deleted the same question that he was repeatedly posting as willy150. He is also engaging in the same behavior of posting questions on multiple stacks (see the aspiration pneumonia question).

@AliceD see this meta discussion.  The repeat aquagenic urticaria question link is here

@DeNovo thanks heaps for your vigilance. However, I am unsure at this stage whether it is actually the same user.

@AliceD yep, could be another Willy who is also interested in aquagenic urticaria :) But yes, I suppose you'd need more than a similar user name and similar behavior to take any action. I just wanted to alert people that this may be an attempt to get around an account suspension

@DeNovo - I checked it out and I can't find any evidence, unfortunately, because I understand your hunch.

Short answer: No, there is no evidence that this is possible. Reported cases can usually be explained by an external source of ignition (https://en.wikipedia.org/wiki/Spontaneous_human_combustion)
Edit: ok, let's add some more information..
The human body consists mainly of water and is therefore hard to burn. It nevertheless contains burnable material such as fat. Not to forget the easily ignitable hair and of course clothing.
If a body (or its surrounding textiles) is burning long enough, its body fat can liquefy and keep burning even on lower temperatures. This is called the candle effect. Like with a candle, the fire does not easily travel horizontally and can keep the surrounding furniture intact. In many cases, arms and legs remain mostly intact, which is probably due to temperature gradients in the limbs and a lower mass of burnable material.
It is though that in most cases the victims were already dead or unconscious due to e.g. drug intake before their body started burning. Often they were smokers or found in a room with an open fire place, which are possible sources of ignition.
Since victims often were alcoholic, one theory was brought forward that the flammable alcohol was causing an ignition within the body. But to bring the alcohol content of a body to a flammable amount, you would die of intoxication long before that..
This study posted by user1136 also mentions the points made above: https://www.jflmjournal.org/article/S1353-1131(00)90353-5/abstract
Yes, a body can burn. But there is no evidence that it can ignite spontaneously without an external source. There might be a few cases where no source was found, but that doesn't mean it wasn't there (a cigarette fallen onto the clothes would be burned). The media likes to push sensational news on "mystery cases", but that doesn't mean that humans just spontaneously turn into walking torches for no reason.

+1 for your reference - I've cleaned up the chit chat


text:
How is the right amount of nucleotides synthesised during homologous recombination?
I'm reading about homologous recombination in the context of double-strand break repair. It seems like the trick is that around the break, homologous recombination uses a template duplex to generate some overlap between the broken parts so that the strands can just be complementarily repaired. However, when reading from the template, unbroken duplex, it seems like it's quite important exactly how many nucleotides are generated to form the overlap between the two broken strands. Too little, and no overlap is formed as the broken strands still form two disjoint sequences. Too much, and the broken pieces no longer fit together, there are parts doubled. It's like a puzzle where some pieces describe overlapping regions.
How does the polymerase know to add exactly the right amount of nucleotides?

Recombination is not my thing, but I’m sure it would help if you could provide a reference to the text you are reading — or an online source with a similar diagram to clarify your problem.


text:
Is there any universally accepted definition for pain?
There are many terms in the literature of any domain of knowledge that does not have a standard or universally accepted definition. There can be several definitions from several organizations or textbooks. As a CS student, I am aware that there is no single definition for 'Artificial Intelligence.
I believe the same for the word 'pain' in biology. When I read about the opinions and research papers about 'pain in plants', I realized that some experts do believe that plants experience pain and others argue don't as they don't have any central nervous system. As a layman, I feel that pain can be subjective and pain for animals may not be apt to interpret pain experienced by plants.
Is there any universally accepted definition for pain in biology that encompass all living organisms?

“Pain in plants”? I remember someone in my university Philosophy Department who agonized about this. He left his wife and went to Australia. I’d check whether there is a more appropriate SE site for your question. There are medical yardsticks (I seem to remember childbirth scores high) but universally accepted biological definitions… I think not.

@David oh. I got the answer from you. If the question is not apt for this site. Please tell me. It is okay for me to remove it if needed.


text:
why can a queen wasp sting many times but a worker bee can only sting once?
wasp queen and workers can each sting you several times but a bee can only sting you once. As all of the stings have barbs on them, how can this happen?

Your question is unclear. You seem to have partially answered your question (bee stingers have barbs while wasp stingers don't) . What do you mean by "how can this happen"?

It's not true that all stingers have barbs. Wasps, and many other species, don't have barbed stingers, and therefore they can afford to sting you repeatedly without being killed. Worker bees, on the contrary, have a barbed stinger that gets stuck in your skin.
Although wasps have a more powerful venom than bees, with bees usually the venom sack remains attached to the stinger and will keep pumping venom even after the bee itself has run away and died, causing the sting to be more painful. However, because bees died after stinging, they are less likely to sting you compared to wasps, hornets, yellow jackets and bumblebees.


text:
After how many hours water drunk is expelled from the body?
If one drinks a liter of water at 7 am when (in what span) will that water be eliminated through uresis?
Is that process influenced by any factors such as empty stomach, sleep or other?

The time from drinking to urination depends mainly on your hydration status and the presence of food in the stomach.
Scenario: You have drunk enough fluid in the previous days, so you are normally hydrated. In the morning, you get up from the bed, urinate, drink 1 liter of water in 5 minutes and eat nothing.
Some water can come through the stomach and can be absorbed in the small intestine in about 5 minutes; the entire liter may need more than 2 hours (sweatscience.com).
When some water is absorbed into the blood it can immediately trigger diuresis - the excretion of the urine through the kidneys into the bladder. It may take about 3 hours for the entire amount of water drunk to be excreted. So, the approximate time span (from start to end of water excretion) could be 5 - 180 minutes. But not likely the entire liter of water will be excreted, because, in the morning, you are in a slightly negative water balance, so some water will stay in your body.
If you are dehydrated before starting drinking, much less urine will be excreted in the first few hours.
If you drink after eating, the food in the stomach can delay water absorption and excretion by more than an hour. This also happens when you drink nutritional fluids, such as milk or juice.
This is from my experience and understanding basic physiology. I'll try to find some references.

Thanks for your exhaustive reply, I regret I cannot upvote your or any answer, but I'm sure others will see to it.Can you clarify one thing for me, since what you say clashes with my experience: waking up at about 7:30 am I drink in the excess of half a liter water and at breakfast I have some 30 cl of milk, then at dinner at supper little more water, yet 80% of diuresis takes place during the night between 10 p.m and 7:30 am. I thought it took at least 15 hours to excrete all the water !!

If I take literally what you said about 80% diuresis happening at night, does this mean you urinate 4 times at night and once during a day? The most common reason for frequent urinating at night in healthy people is drinking in the evening. Another reason is that when you lie down, some fluid shifts from your legs toward the heart and the heart detects this as an increase of blood volume, which triggers diuresis. Also, diuresis does not occur only due to drinking but because the kidneys constantly remove waste from your blood in the form of urine.

It is a hypothetical question which is not a true scenario I would try to explain the process of water absorption and excetrtion.
when a person consumes water it is absorbed into blood stream (liquid as well as in the form of water in food consumed). The amount of water absorbed in the stomach and how quickly water is absorbed depends, in part, on how much has been eaten. If someone is drinking water on an empty stomach, they are more likely to experience a faster rate of water absorption – as quick as 5 minutes after taking a drink. Whereas, if a person has eaten a lot of food before they drink water, the speed of absorption will slow down accordingly and absorption could take up to a few hours.
Approximately only 20% directly makes to the bladder remaining water would be utilized for performing vital function of the body.
Once the human body uses up all the water it needs to function efficiently, it begins the process of removing excess water.The water is not only excreted solely through uresis (urine is only 95% water), the other routes for water excretion is sweat, fecal route and saliva.Small droplets of water also exit the body via the breath.
As water is not excreted thought sole route is not possible to calculate the exact time taken for removal from the body.


text:
Can blood that has had an anticoagulant added to it be boiled without coagulating?
If I understood the information I've found elsewhere correctly, you can't boil untreated blood without it coagulating, right? But what if you added an anticoagulant to it? Would it be possible to boil that blood or would it coagulate in spite of it? Thank you in advance!

Coagulation, or clotting, is a proteolytic cascade that generates an insoluble fibrin based protein net, or mesh.
Anticoagulants are things like EDTA (?) that chelate divalent cations required for the clotting cascade.
Boiling blood will denature most, if not all, of the soluble serum proteins, forming an insoluble precipitate.  This is structurally different from a blood clot.
Think about what happens to the white part of a chicken egg when you boil (or heat) it.  That is protein denaturation.


text:
Is callus totipotent or pluripotent?
Is callus (in the context of plant tissue culture) totipotent or pluripotent? As I understand, the difference between totipotency and pluripotency is an ability to differentiate into extraembryonic cells. So, I stuck on the question: what is extraembryonic plant cells and could callus cells differentiate into it?


text:
Why some plants can be propagated from a leaf cutting but some can not?
I understand the process of leaf-cutting propagation as following:
1) with the help of auxin from the leaf, callus is forming on the wound and then roots are forming from callus,
2) with the help of cytokinin from roots, shoots are forming.
Is it wrong or too simplified or do I miss something? Why some plants can do this and some can not?

Can we ever really know the plant cannot do this? All we can know is that combinations of conditions that have been tested did not work for that particular species/genotype.

You have a point. It seems like theoretically any plant can be propagated by leaf cutting in some specific conditions within some time. In this case are there any clearly identifiable characteristics of particular species/genotype that affect this ability, ceteris paribus? Or is it rather complex thing?

What I have seen people to do is mostly trying protocols that work for related species and trying large matrix of conditions on large set of genotypes etc. Once the protocol is established people seem to move on to using it instead of researching deeper reasons. If you find any overarching theoretical work on this matter I would be very much interested.

A major factor would be how fast a leaf dries out, A leaf that dries out quickly will not be able to keep photosynthesizing long enough to grow roots to collect more water.

The plant has to be able to develop meristems from the leaves, and plant stem cells for the roots?

@John it is necessary but not sufficient condition, isn't it? There is at least a problem of "blind" cutting: the cutting roots but does not produce any shoots to develop new full-fledged plant.

I have mostly experience with plant tissue culture on agarous media where drying of leaf is not problem. Still, some plants respond and some don't. Species I work with has been considered recalcitrant to in vitro for decades but then a different cytokinin molecule was tried and shoots started to form.


text:
What is the average human body density?
Looking for values of the average human body density on the Internet, one often finds the values of 0.98 for male, 0.87 for female. Other values are 0.985 for male and female. However, I can find no scientific reference confirming these values.
Instead, I found multiple articles giving numbers closer to 1.05 for male and 1.03 for female (Durnin and Womersley, 1974). The difference probably comes from the air comprised within the lungs, but I do not know how much it can change the density and how full our lungs are in average. Would anyone have a reliable reference on this matter?
Ultimately, I would like to understand the effect of breathing on the floating in water and compare this effect for male and female. I would like to see if it can account for women tending to float, even after deep expiration. It upsets a friend in her diving lessons. :)


text:
What is this plant ...?
I would like to know what is this plant ? Does anybody have an idea ? Somebody offered it to me but there is no explanation about how to care about it...
Some purple flowers appeared, during 2-3 days. And now it seems it lacks something, but I don't really know what to do :(

Any idea ?
Thank you very much !

What other information can you add about the plant? But also see this meta post.

As we can see on the picture, there are green small and thin leaves, and a big pink part in the middle. When I give water to the plant, this pink part seems to "drink" and fill up with water, as when we touch it, it is wet, like a sponge...
A few days after I got the plant, purple flowers appeared (as on the picture), and wilted 2-3 days after.
Now, the pink part is fading, and turning grey/green...
I have no idea about where this plant is from. But it seems that it is an indoor plant.

That is a beautiful Pink Quill, or Tillandsia cyanea. I have included two websites below about this plant, both of which include care tips.

http://home-and-gardening.info/2009/09/18/a-guide-on-growing-tillandsia/
http://houseplants.about.com/od/bromeliads/a/Bromeliads.htm

My pleasure! Enjoy!


text:
Mean and standard deviation of human bone density?
Are the human bones about equal in density? Or is there any published data on the mean + s.d. density for a given bone available?

Interesting question that I'd not considered before.
Bone density is commonly measured by assessing the bone mineral density (BMD) using dual-energy x-ray absorptiometry (DMA), literally the g/cm2 of minerals in the bone.
Having had a search I can only find values for a small number of bones commonly measured when testing for osteoporosis (characterised by reduced BMD). Unsurprisingly the age and sex of the individual has a large effect on BMD; after puberty males have higher BMD (1) and during ageing this then declines, sometimes dramatically (2).
These values are from a Vietnamese study (3) show that the hip and the spine are different.
Men [ mean (SD) ]

Femoral neck: 0.85 (0.13)
Total hip: 1.00 (0.13)
Lumbar spine: 1.05 (0.12)

Women  [ mean (SD) ]

Femoral neck: 0.80 (0.11)
Total hip: 0.95 (0.12)
Lumbar spine: 0.96 (0.11)

There must be other reference values for other bones in different populations but I don't have time to look them up now! Good luck in your own research.
I found this website by the US National Institute of Health and this PDF by the World Health Organisation immeasurably enlightening.

Bonjour JP, Rizzoli R. Bone acquisition in adolescence. In: Marcus R, Feldman D, Kelsey J, eds. Osteoporosis. San Diego, CA, Academic Press, 1996:465–476
Cummings SR, Kelsey JL, Nevitt MC, O’Dowd KJ (1985) Epidemiology of osteoporosis and osteoporotic fractures. Epidemiol Rev 7:178–208
Ho-Pham, et al. (2011) Reference Ranges for Bone Mineral Density and Prevalence of Osteoporosis in Vietnamese Men and Women. BMC Musculoskeletal Disorders, 12:182  doi:10.1186/1471-2474-12-182


text:
From DNA data, is it easier to conclude that chimpanzees are our close relative, than it is to do a paternity testing?
Well, today I was contemplating on how to explain evolution, approaching with the dialectic method. When it came to why chimpanzees and us being so close in the tree of evolution isn't outright absurd, I formulated a witticism, "Well, today a glance at humans' and chimpanzees' DNA would confirm how much close we are. Compared to that, if you were to do a DNA paternity testing, you would have to do a bit more grunt work in that you would have to look for more nitty-gritty details that separate (and make similar) one human from another. So, ours and chimpanzees' closeness would actually be easier to conclude than to tell your parents apart from non-parents."
Well, was I correct? That this would be easier than that?

Hi Tony and welcome to Bio.SE! If I understand your question, you are asking "is a paternity test easier than a chimpanzee-human comparison"? This is true, but not for the reasons you suggest. Paternity testing uses minisatellite comparisons. This involves looking at specific regions of repeating regions where the number of repeats varies between individuals. Those tests are cheap. Comparing species, on the other hand, requires WGS (whole genome sequencing) which requires much more work and gear. These can cost more than 10 times as much as a DNA fingerprint test, depending on the species.

Please re-read the Tour for this site to find out why this question is a bad fit. It is not about a biological problem, but asking for subjective opinions about the comparative difficulty of two procedures. As far as subjective opinions go, I doubt that your students will find your “witticism” either witty or helpful.

@James's comment is an answer.

@David, I don't agree that this is a subjective question.  It's a question whose answer could be complicated, but the answer concerns how genetic data has to be processed and tested statistically for different purposes.  Both paternity testing and genetic comparisons of species have methods that have been discussed in numerous publications.  That is not to say that there is an easy, simple, or single answer--the relevant methods change over time--but that should not be the criterion for questions.  Other SE sites don't require that.

@Mars The question hits on a few topics and biological concepts all at once. My comment only addresses which experiment is easier to do today. A complete answer would have to be a bit more comprehensive.

The answer is complicated. In the early days of molecular phylogenetics, it was extremely difficult to demonstrate whether chimps or gorillas are our closest relatives. This is because the common ancestor of chimps and humans lived between 5 and 8 million years ago, and the common ancestor of gorillas and humans (and chimps) lived around the same time, just a little older. This means that there was a rapid split of three lineages, and it was difficult to disentangle them. As molecular phylogenetics advanced, we could generate larger datasets, and it because clear that chimps and humans were sister taxa. The smoking gun that demonstrated that chimps and gorillas were not one another's closest relatives was found when sequencing across the chromosome region in humans that corresponds to where two of our ape ancestors chromosomes merged. Orangutans, Chimps and Gorillas have 24 pairs of chromosomes, humans have 23. Sequencing across this region shows the exact splice site, which can be associated with the same regions on two chimp or gorilla chromosomes.
To answer your specific question, if you sequence any two genes between chimps and humans, you will find that the sequences are almost identical, with perhaps 1 in 100 nucleotides being different. If you sequenced a human and a gibbon for the same gene, you would find more differences. But finding that the sequences are similar is not the same as finding relationship, which requires sequencing multiple genes from multiple animals. For example, some genes between humans and rabbits would be extremely similar. So inference of relationships takes a lot of data from a lot of different animals. As for paternity testing, these practical tests are based on a different technology, targeting many DNA repeat regions or single nucleotide polymorphisms at specific sites that vary among human populations. But since the test is prescribed, and established, they are cheap, quick, and easy.


text:
Will renal blood flow decrease in response to dehydration?
If dehydrated, does the correction of ECF osmolarity happen slowly enough for ECF (and therefore plasma) volume to be temporarily depleted and therefore reduce renal blood flow?
If dehydration is taken to mean ECF hyperosmolarity, would fluid not just move out of cells to restore normal osmolarity, without affecting ECF volume or renal blood flow?

Please spell out any abbreviations that are not widely used. Specifically, what does ECF mean?

Apologies: extracellular fluid.


text:
What happens to glucose taken up by the liver in type 1 diabetes?
Type 1 diabetes is caused by insufficient insulin production.
Unlike in muscle and adipose tissue (GLUT4), glucose uptake by the liver is by GLUT2 and thus insulin-independent. Consequently, under very high blood glucose concentrations, glucose will move by facilitated diffusion into the liver.
However, insulin is not available to stimulate glycogenesis, or lipogenesis; glucagon will be secreted due to high blood glucose concentration, doing the opposite. What happens to this glucose? Does it simply diffuse back out (GLUT2 is bidirectional)? Presumably glucokinase produces glucose-6-phosphate, but the highly controlled points of glycolysis (e.g. PFK-1) will lack stimulation due to loss of insulin. Does a lack of glucagon (due to glucose still reaching pancreatic islet cells, also via GLUT2) have a positive effect?

It would seem to me that as GLUT2 is not insulin-dependent, the net transport of glucose by it depends only on the difference between intracellular and blood glucose concentrations. I assume the liver has a high intracellular glucose concentration in diabetes because it is performing gluconeogenesis. Your question would then boil down to why is it doing this latter as the "starvation hormone", glucagon, is not secreted from the pancreas in diabetes (something I did not know, but checks out). Would this interpretation be correct?

That's true, presumably the net flow of glucose in type 1 diabetes in the liver is still outwards, due to excessive gluconeogenesis.
I read that glucagon is still secreted by the alpha cells of the pancreas in type 1 diabetes (though the alpha cell mechanism is generally unclear; this might be due to paracrine signalling between beta and alpha cells; or some influence of the brain). In which case this would stimulate gluconeogenesis. Perhaps the lack of inhibition of gluconeogenesis (no insulin) is enough to tip regulation towards it rather than glycolysis (via F-1,6-BPase stimulation?).

Seems reasonable. I should know the details of the regulatory control of the key points in the pathways, but only taught metabolism from the standpoint of feeding and fasting. If I had time (I'm away for a long weekend) I'd check it out in detail, but it appers that others may be saving me the task.

1) Hepatic glucose intake may not be much greater in hyerglycemia than in normoglycemia:
Regulation of Hepatic Glucose Uptake and Storage In Vivo (Advances in Nutrition, 2012):

...neither hyperinsulinemia nor hyperglycemia can independently induce
  much net hepatic glucose uptake.

2) Glucose can be used for de novo lipogenesis in the liver despite the lack of insulin:
De Novo Lipogenesis and Cholesterol Synthesis in Humans with Long-Standing Type 1 Diabetes Are Comparable to Non-Diabetic Individuals (PLoS One, 2013):

Fasting total hepatic lipogenesis (3.91±0.90% vs. 5.30±1.22%;
  P = 0.41) was not significantly different between diabetic and control
  groups...


text:
Why does the liver produce ketone bodies instead of exporting acetyl-CoA from beta-oxidation for use elsewhere?
Under conditions of low oxaloacetate in the liver, acetyl-CoA that cannot be oxidised in the TCA cycle is converted to ketone bodies, which can then be exported for use as fuel in non-gluconeogenetic tissues (e.g. heart, brain).
To avoid this pathway, and the additional enzymes it requires, as well as the enzymes in the receptive tissues which are needed to reverse the pathway and re-produce acetyl-CoA, why does the liver not just export acetyl-CoA directly?
One consideration is an inability to transport acetyl-CoA across membranes, but fatty acyl-CoAs deal with this using a carnitine shuttle across the mitochondrial membrane. Would developing a transport system not, evolutionarily, be a more efficient solution?

Think. What are the conditions you describe as “low oxaloacetate”? What is the source of the acetylCoA and why is it being produced (rather than stored as fat, for example)? What are the needs of the organism in these circumstances? In other circumstances where acetylCoA might be useful to other tissues, how is the molecule from which it arises exported from the liver? Look at the big picture.

"Low oxaloacetate" will presumably occur mainly when it is being taken out of the TCA cycle, for gluconeogenesis (i.e. in the fasted state). The excess acetyl-CoA in this instance is being produced from beta-oxidation of fatty acids, since lipogenesis is inhibited (high glucagon, low insulin in this state). The organism needs to produce glucose, but also maintain a supply of ATP.
Acetyl-CoA can also derive from pyruvate (via pyruvate dehydrogenase). Do you refer to the Cori Cycle, where lactate is returned to the liver, oxidised to pyruvate, and then converted to glucose?

— Ok. You’ve thought about it, but don’t see what I’m driving at. I’ll try to answer your question later today (in a different time zone).

This is simplified version of a complex situation, but in summary:

A key role of liver is to control the distribution of metabolic fuel
for the other tissues (it always has enough for its own
requirements).
The way it behaves differs in the fed and fasted states (because of control by hormones and the concentration of metabolites).
In the fed state (after storing some sugars as glycogen) the liver will synthesize triglycerides and export them as lipoproteins to the adipose tissue, which will take them up and store them. (Other tissues in the fed state will be able to obtain glucose or fatty acids from the blood.)
In fasting and starvation the triglycerides in the adipose tissue will be broken down to fatty acids and glycerol, much of which will be used by tissues such as muscle.
The priority of the liver in starvation is to provide fuel for the
brain and nervous tissues in the form of glucose, by gluconeogenesis. The substrates for net gluconeogenesis under these conditions include glycerol and some amino acids derived from breakdown of protein.
Other amino acids, produced in protein breakdown lead to acetyl CoA,
which cannot serve as a precursor for gluconeogenesis. However it can
be converted to ketone bodies (acetoacetate and β-hydroxybutyrate)
that the brain can use to replace some of its glucose requirement.

With this in mind, it can be seen that the reason for producing ketone bodies is not to generate a molecule that can cross the cell membrane into the blood, but to generate a molecule with special properties, lacking in fatty acids or acetyl CoA, that allows its use by the brain in life-threatening circumstances.
Of less importance, but worth mentioning, is the fact that citrate is used as an export form of acetyl CoA (when there is sufficient oxaloacetate available), a surrogate role it plays in any case in the transfer of acetyl CoA across the mitochondrial membrane for fatty acid synthesis. So it is not necessary to export acetyl CoA, and perhaps preferable to it keep intracellular.
A more detailed account of this is available at NCBI bookshelf online in Berg et al. sections 30.2 and 30.3


text:
How are newly synthesised proteins targeted to the plasma membrane?
There does not seem to be a definitive answer to how proteins destined to be intrinsic plasma membrane proteins are directed there. Presumably, assuming starting at a cytosolic ribosome, the pathway is via the SRP/Sec61 translocon system into the ER co-translationally, followed by COPII vesicular transport to the Golgi for modifications.
From here, is the system that of COPI transport back to the ER? I think I read that if sitting in the ER membrane, proteins can 'slide' into the PM via some vague endomembrane system juggling. Or, packaging into vesicles which can then fuse with the PM?


text:
What is the consensus, if it exists, on the (absence of) biological effects of artificial sweeteners?
I tried to Google (and PubMed) the question, but it seems to be fairly polarized debate and there does not seem to be a consensus as to whether sweeteners like asparatme, acesulfame etc. have meaningful biological effects.
Some studies point to molecular effect with little to no explanations about their relevance for health, and since statistical significance and size effects are quite different things, question remains unanswered.

If the scientific research papers can't provide a clear answer to this, then likely there is no consensus effect known. Whether this is interpreted that as 'no actual effect whatsoever' or 'we have't looked deep enough' is up to you I guess.

I remember checking out a lot of papers on the subject at some point and most of them report a slightly impaired glucose intake insuline response as the only side effect of chronic artificial sweeteners consumption. Also another conclusion was soda with these sweeteners does help weight loss but not as much as not drinking any kind of soda at all. I can try to search for the papers later again


text:
Design rules for DNA linkers
I want to use double stranded DNA linkers to physically bind two "things" together, by grafting ssDNA on each one of them and using DNA hybridization as the locking mechanism.
I do not expect the nature of the two things to be important for this question, but if it is, let's say I want to link a solid surface and a protein.
Let's say that my only constraint is that I want this crosslinking to be stable at 37°C.
There is a gazillion ways I could design the sequences, and pretty much anything above 20bp without massive self complementarities should work, in theory. But I don't like to pick bases randomly. So my question is this: is there anything I can look for, except for the two constraints above, to design a good linker sequence?
For example, if the melting temperature is 50°C vs. 65°C, I would expect the structure to be stable (infinitesimal dissociation constants in both cases). Would there be any reason to choose one over the other, except for maybe oligo synthesis price? For a given melting temerature, is there any difference between a long AT rich sequence and a short GC rich sequence?

You might want to pick something that has little or no homology with anything that exists in any organism in the databases, just in case.
Gut feeling says to go for balanced oligos in the middle between AT-rich and GC-rich, and not have repeats or homopolymers.  If you go for AT-rich, then your complementary will be GC-rich, and vice versa. I'm pretty sure there would then be a differential in the mechanical properties of the two oligos - maybe this would be something useful to have for other reasons though?
It seems like most of the design principles might be constraints (do nots) rather then goals (dos), so you could do worse than have a generator churn out random sequences, and score each one against the various constraints.  Random seems OK, if you are then checking each randomly chosen pair against some strong rules.  Then pick ten or so pairs that all score well, get them synthesised and see whether any work...


text:
Infecting yeast with viruses
Is there any virus, either natural or engineered, known to infect yeast through mechanisms similar to phages/human viruses, that is, by horizontal contamination mediated by extracellular viral particles?
I have found examples of eukaryotic viruses replicating in yeast (Zhao, Microb Cell, 2017 - link) but it seems that natural yeast viruses only transmit through mating or vertical transmission, without extracellular steps (Luque, Viruses, 2018 - link).
Has anybody ever reported, say, non-specific mechanisms like VSV-G mediated fusion, to fuse virions with yeasts?


text:
Beyond anabolism, what are factors that restrict growth rate?
Beyond obvious constraints in the case of nutrient limitation, what can explain the relatively slow growth rate of cells in rich media?
Lab strains of E. coli grow really, really fast. The cell cycle in rich media is even faster that the genomic replication (!). But for many other organisms, that is not true. Is there anything else, beyond the lack of food / environmental signals that can act as intrinsinc barriers to the growth rate of cells, assuming that parameters like pH, temperature and oxygenation are properly chosen?
For example some cells have genomes about the same size as S. cerevisiae but divide much, much slower, why is that? Is it necessarily a sign that something in their growth medium is lacking? Maybe checkpoint kinetics (if so, can the issue be fixed by mutating cyclins, for example)?


text:
Defining cell state and type without calculating distances in expression space
Usually, cell types are found by clustering cells in expression space (or some lower dim. projection of it), and calculating differentially expressed (DE) genes. These DE genes are then used to annotate the cluster to a particular type. Cell states are then thought of as a 'fine-grained' view on this cluster, making some reference to a biological process.
However, this means that a particular cell state can never be present across cell types, whereas we do think of them like this. For example, "being at a certain point along the cell cycle" can be thought of as a state, or "being under stress", and cells of different types can be in these states simultaneously. Is there some principled way to extract such states from single cell gene-expression data? It should be able to annotate different, far removed regions in expression space as being in the same state, so probably cannot be based on distances in expression space.

It kind of sounds to me like you're thinking only like a computer scientist and not like a biologist. If you want to know where a cell is in the fell cycle, consider looking at cell-cycle related genes. If you want to look at stress, look for expression of stress-associated genes.

That is true, I am approaching this as more of a computational problem. That said, I think there would be added value in being able to detect novel states, not just ones for which you know a set of marker genes. For example, there might be a state defined by three genes (A, B, C) being expressed together. It could be the case that these three are only expressed together in distinct but disjoint locations in expression space. I was wondering if there are known methods/algorithms for detecting such states.

I would expect that the kind of correlation structure that you describe would be amenable to multivariate analysis. As a very simple-minded approach, you would expect that PCA would find a projection in which (A, B, C) are all strongly loaded and other genes are at the noise level if their signal is strong enough and your data are properly normalized (how to normalize is a separate question), even in the presence of other large expression signals like cell cycle etc. Can you add more specifics about what exactly you have tried?

My suggestion is that you rethink the premise of your question. Projections and distance comparisons can be used to define cell states that apply to multiple cell types.
Here is an example. A and B are two cell types. S and T are two cell states. x and y are two genes used to define these states. The plot below shows expression of gene x on the x-axis and gene y on the y-axis. The vertical line separates cell types. The horizontal line separates cell states.
                gene y
                ^
                |
    state: S    |    state: S
    type:  A    |    type : B
                |
<==============================> gene x
                |
    state: T    |    state: T
    type:  A    |    type : B
                |

Thanks! This is a very useful diagram, and indeed how I had been thinking about it. I've accepted your answer as I think it illustrates the point nicely.


text:
Are the chemical constituents of human bodily fluids similar to sea water?
I have heard a comparison of human bodily fluids to sea water from various sources in the past. The most notable was a teacher who claimed, if I remember correctly, embryonic fluid is comparable in chemical content to sea water. I am wondering if this claim has any scientific basis. If not, is there another bodily fluid known for this characteristic? I tried doing some google searches and did not find any supporting evidence. If this is a myth, has anyone else heard such a claim and how it may have begun?

I also remember the teacher adding a disclaimer that it was not just any sample of sea water, rather an average or maybe seawater in the open ocean. She implied this comparison did not necessarily apply to various "sea water" bodies like bays or coastal areas.

Let's just consider mineral salts, since obviously sea water does not contain animal proteins or cells, and (fortunately) our bodies don't contain phages, micro-algae etc.
Sea water is very salty; on average about 0.5mol/L of NaCl (the main salt dissolved in sea water).
On the other hand, human biological fluids like plasma and the intracellular space are at least 2-3 times more dilute.
Unless some other human bodily fluids are exceptionally salty, it seems that there is a pretty big difference and it is not very accurate to say that bodily fluids and sea water have close chemical compositions.
There are not many fluids that are very close from bodily fluids in term of composition. Popular culture tells the tale of emergency transfusions of coconut water during WWII, but that's not supported by medical literature; even though more recently, in exceptional emergency cases, it has been reported to be possible as a short term solution because of the similarity of osmolarity between plasma and coconut water.

I'd guess the teacher was just making the broad comparison that bodily fluids and seawater can both contain $\ce{Na+, K+, Cl-}$ even if they're not at the same concentrations or the only constituents of those fluids.

Yes, I was meaning chemicals, ie minerals, or just elements, and not to include specifically other biological organisms. @Jam what you are saying sounds similar to what the teacher said. I think she did refer to those elements specifically.


text:
Does the male and female always split evenly the genetic material given to their offspring?
Are there animals known to have a different percentage of splitting of genetic material, like the male give 75% and the female just 25%. I know that drone bees have only genetic material from their mothers, I would like to know if there are also instances in larger animals (mammals and reptiles).
If the answer is no, then do we know why it is always evenly split.


text:
Why are market squid attracted to fishing lights but also avoid naturally lit surface waters during daytime/full moons?
Squid fishermen use really bright lights (which can be seen from space!) to attract squid to the surface at night, but a lot of squid also naturally avoid surface waters that are lit during the day (by the sun) and at night (by full moon). As far as squid are concerned, what is the difference between the bright artificial lights and diffuse light that naturally occurs?

Great question...I don't know the answer but I look forward to hearing from someone who does!

Despite many sources stating that the lights attract the squids, the explanation given here is much more logical. Squids feed of small fish, crabs and shrimp, which in turn feed on plankton. Zooplankton is known to migrate vertically during the day (up at night, down during the day), which has also been reported for squids, probably following their prey.
The reason for this migration is that zooplankton feeds on phytoplankton, which can be found at the sea surface, where it gets most of the sunlight. During the day the zooplankton stays in deeper waters, because at the surface its easier to be spotted by predators. It's safer to move up during the night to feed. Other predators feeding on zooplankton follow, including the squids.
The vertical migration might be coordinated by an internal clock rather than light. It would therefore not be inhibited by the bright fishing lights. The squids don't seem to respond to the light, but rather to their prey.
Therefore, rather than attracting the squids directly, the fishing lights will attract phytoplankton, which attracts zooplankton and small fishes, which attract squids.


text:
In oscillometric blood pressure measurement, why do we assume that highest oscillations correspond with mean arterial pressure?
As far as I've seen, the point on the oscillometric curve where there are greatest oscillations represents the mean arterial pressure (MAP).
My question is - why? What is the logic behind this assumption? Or is it just an empirically observed coincidence?


text:
How does chest wall compliance affect functional residual capacity (FRC)?
The functional residual capacity is made up of expiratory reserve volume (ERV) plus the residual volume (RV) - i.e. the volume of air remaining in the lungs after passive expiration.
Compliance of the lungs is said to affect FRC. For example, if compliance of the lung increases (e.g. in emphysema), there is less elastic recoil and less air is passively expired, resulting in increased FRC. Could one explain this as increased compliance (where compliance = ∆V/∆P) meaning that the same intrapleural pressure at end of passive expiration results in a greater lung volume (FRC) at that time? This seems to explain instantaneous volumes rather than the actual expiration of less air.
How does this translate to compliance of the chest wall? As recoil of the chest wall tends to be outwards, would reduced compliance mean that there is greater tendency to recoil outwards, making intrapleural pressure more negative and reducing expiration of air, leaving greater FRC?

How is recoil of the chest outwards?  Doesn't the chest tend to recoil inwards?  Expiration is passive due to recoil of the chest inwards.

Recoil of the lungs (alveoli) is inwards, but chest outwards, I thought? As this is what sets up an equilibrium that allows the intrapleural pressure to be negative relative to atmosphere?

As far as lung is concerned both inspiration and expiration are passive. Lung just responds to intrathoracic pressure by accommodating more air during inspiration and expelling air during expiration. The active processes in the lung as far as air flow is concerned are limited to the bronchial tree smooth muscles which can increase or decrease the resistance to air flow. The compliance of the lung parenchyma is a function of its anatomical composition.
During inspiration the thoracic volume is actively increased by:

Outward expansion of ribs by the intercostal muscles
Downward expansion of diaphragm

This increase in thoracic volume is refected in all intra thoracic organs:

Venous return increases due to the negative pull
Negative pleural pressure causes air to be pulled into the lungs

Normal expiration on the other hand is passive due to relaxation of the above mentioned muscles. Relaxation will cause a decrease in the thoracic volume which will push the excess air and blood out.
An increase in the compliance of the thoracic cavity would mean weakening of the fascia and bones of the thoracic cage. In other words, the structures that the muscles attach to will become weak. This will cause muscle action to cause excessive expansion of the thoracic cage during inspiration and during expiration due to weaker pull by the attached structures, even residual tone of the muscle may cause distortion of anatomy preventing adequate reduction in the thoracic volume causing increased residual volume. Thusb reducing the volume of the air expired.


text:
At small axon diameters (<1 µm), why does myelination not increase neuronal conduction velocity?
As per the diagram below (and other graphs available online), why do unmyelinated fibres have a higher conduction velocity than myelinated fibres when the axon diameter is less than around 1 µm?

Graphs like these are based on a complete cross-sectional area. Myelination adds thickness, so if you want to add myelin outside and keep the same diameter, you have to have a smaller lumen inside the axon.
As you can see in the "unmyelinated" plot versus diameter, smaller fibers have lower conduction velocity. Since the benefits of cross-sectional area are most important at small diameters (because the velocity changes with the squart root of diameter), for small diameter axons you end up losing more from losing internal area than you gain from adding external insulation.
If you keep the internal diameter the same and just add myelin, you will always increase the conduction velocity, but the total diameter including the myelin won't be the same anymore.

This explains it perfectly. So going from unmyelinated to myelinated is always beneficial in terms of conduction velocity, but it may not be in terms of space-saving. Thank you!

@pincushion44 Exactly, and space is at a premium in nervous systems!

That's observed due to passive conduction. With more area of cross section resistance is decreased (ohm's law). Myelin has just function of insulation the graph showing conduction in neuron fibre varying with thickness of neuron (hereby also thickness of myelin sheath).
Conduction is ruled by multiple factors not only just thickness of insulation. check this out https://www.ncbi.nlm.nih.gov/books/NBK10921/
When the area is so less than certain level the resistance is really high and insulation provided by myelin sheath works against conduction rather than supporting it. Conduction happens superficially instead in the bulk.
Where as in non myelinated fibre the insulation of myelin is not barrier.
Straight line tells me that my reason is legible probably since current is proportional to (1/R and hence) A

Sorry, I am slightly confused as to why insulation from myelin works against conduction when the area is low (and so longitudinal resistance is high)?

will try to make answer better after studying more about it

try that citation if it helps tell me.

It might also be possible that at smaller diameter cohesive forces of myelin sheath material close the node of ranvier and reduce it in significant amount


text:
Do species ever move into new territory and then die out because of the local diseases?
We usually hear that an invasive species has brought with it a disease which it itself shrugs off easily, but which then decimates the local population which has never encountered it before. It's a very common story. But it doesn't make sense to me. Surely it should be far more common for the reverse to happen? Surely a newly arriving species has to face not just one or two new things in the new environment, from one or two new individuals, but an entire environment coming at it from every direction with hundreds of viruses, bacteria and competitors it has never come across before. So how come the story is always that the invading species kills off the locals, when you would expect the invading species to have hundreds of totally new threats and strange foods to handle, would be unable to cope, and would die out?

So how come the story is always that the invading species kills off
  the locals, when you would expect the invading species to have
  hundreds of totally new threats and strange foods to handle, would be
  unable to cope, and would die out?

There is a problem of observation bias for these two scenarios.  In the first scenario a few members of an invasive species enter a new range, transmit a novel disease to the pre-existing species, which suffers a massive (easily observable) die off. In the second scenario, a few members of an invasive species enter a new range, catch a local disease, and die in short order (unobserved and unnoticed).
In other words, a few individual deaths from any cause will generally go unnoticed. Thousands or millions of deaths of deaths from a novel disease are more likely to attract attention.

That's a good answer, thanks.

Charles is correct.  You might want to look up 'failure to thrive', and 'introduction failed' when humans tried to introduce new species (the existing environment ate them up), and it didn't work out.
We tend to record successes, and bury failures.


text:
How is Saccharomyces cerevisiae grown on acetate and ammonium able to produce TCA intermediates?
I am working with a metabolic model of Saccharomyces cerevisiae and I am studying its growth on acetate and ammonia. I am performing Flux Balance Analysis to compute the growth rate and then I am exploring the flux distribution over all metabolic reactions.
The flux distribution shows that acetate is uptaken and transported to the mitochondria, where it produces Ac-CoA, which enters the TCA cycle. But also some acetate remains in the cytosol and produces Ac-CoA, which is used to synthesize fatty acids and to enter the glyoxylate cycle.
My question is the following: if acetate is the only carbon source supplied and ammonia is the nitrogen source, how can initially Ac-CoA enter the TCA or the glyoxylate cycles? In both cases oxalacetate is needed, which cannot be produced directly from Ac-CoA from other alternative pathways.
My only guess is that TCA cycle intermediates are being produced somehow and keep the cycle running, but as the nitrogen source is not even an aminoacid, I do not understand where this whole thing starts.
Thank you very much for your help!


text:
Does the renal vein have a greater glucose concentration than the renal artery?
My IGCSE markscheme says that the renal vein has a lower concentration of glucose? I would expect the renal artery to have lower glucose concentration as water is lost from the kidneys. Why is it so?

What is an "GCSE markscheme"? Can you add a quote of a few sentences to show the context?

The kidneys use glucose from the blood as a nutrient, so, this is the reasoning behind your source saying there is less glucose in the renal veins than in the arteries.
If the renal vein contains both less of water and glucose than the renal artery, the concentration of glucose in the renal vein still be lower. This agrees with Bioninja.com.au:

Blood in the renal vein (i.e. after the kidney) will have:

Less urea (large amounts of urea is removed via the nephrons to form urine)
Less water and solutes / ions (amount removed will depend on the hydration status of the individual)
Less glucose and oxygen (not eliminated, but used by the kidney to generate energy and fuel metabolic reactions)
More carbon dioxide (produced by the kidneys as a by-product of metabolic reactions)

On the other hand, an article in Scielo.br says:

Unlike the proximal nephron, cells in the distal nephron are fully
  capable of glucose utilization. In physiologic conditions, the amount
  of glucose utilized in the distal segments of the nephron equals that
  derived from the renal gluconeogenesis in proximal tubules. This is
  confirmed by the common finding that the arterial-renal vein blood
  glucose concentration difference in the post-absorptive state is near
  zero.

In conclusion, your source can still be right.


text:
Spermatozoa and sperms
Does  spermatozoa and sperm have different meaning?If they are same why do wikipedia have 2webpages ? But most websites mention them as the same thing.I am confused .Thank you in advance

In broad way we call it sperm but the motile sperm is precisely called spermatozoon and plural form of spermatozoon is spermatozoa. A non motile male gamete is sperm but not spermatozoon but there is a term for that too its spermatium.

Not just in humans most animals have sperm, in fact non-motile sperm cells would be the basal condition.


text:
Can I change the genetics of a group of plants naturally?
I have been thinking about introducing all sorts of types to certain environments where the plants will have to adjust to survive.
For example having a dark area with one light source right next to the plants so they all want to grow towards the light.. however this could be made more difficult by either introducing slight angle adjustments or artificial wind (custom controlled fans).
Would it be possible to start slowly introducing such challenges to change the plants? for example strengthen their stems to be able to fight the gravity or wind?

Of course, you can place a population of anything (incl. a population of plants) into a specific environment and you could expect this population to slowly adapt to it.
Most plants don't have a particularly fast generation time and therefore, the evolutionary experiment might take longer than your lifetime. The experiment would be much faster if you choose some unicellular algae such as Chlamydomonas reinhardtii for example.

Related: https://biology.stackexchange.com/a/59670/27148

Can I change the genetics of a group of plants naturally?

Of course.  Start with a mix of plants with a mix of traits.  Kill off all plants which lack the traits you want.  You now have a group with different genetics than you started with.

For example having a dark area with one light source right next to the
  plants so they all want to grow towards the light

Plants already have the genetics to grow towards the direction of light.  Making them all grow sideways would not be a genetic change.

Would it be possible to start slowly introducing such challenges to
  change the plants? for example strengthen their stems to be able to
  fight the gravity or wind?

Do you understand that you cannot change the genetics of individual organisms?
But sure, kill all the plants that don't have the trait you want.  Let the survivors breed.  The offspring will be genetically different, due either to recombination or mutation.  Keep culling the ones you don't want, and the population will have different genetics than the original population.

I meant to slowly introduce these over multiple generations.


text:
Why did this Rabbit behave like this?
https://youtu.be/B3_S3Uj18G8
In this video, inappropriately titled autistic rabbit, we see the rabbit first lying motionless before suddenly starting to spin around and jumping around.
What caused it to behave this way? Is it suffering from a disease?
I'm sorry if this is off topic. Please direct me to the appropriate site if it is.

Your question may be on-topic but since the video is not a part of a carefully designed scientific study it is almost impossible to conclusively say anything about the rabbit's behavior.

@WYSIWYG Your point is correct. Any conclusions would ultimately be impossible to conclusively verify. I was hoping that someone could lead me into the right direction so I could do the further research myself.

Doesn't look like voluntary movements. Probably some brain damage. Could be caused by lots of things...

Almost certainly diseased or injured.  The initial lunge seemed to be towards the person, and then there were frenzied but partially paralyzed movements. To my untutored eye this suggests it might be rabies, which can affect most any mammal, though seldom noted as occurring in rabbits.  (see Rabies in Animals)


text:
Is there random assortment in metaphase II?
First, a little notation. Call a the first chromosome from my mother and A its homologous partner from my father. b and B would be the second pair, c and C the third, and so on, down to w and W (the 23rd).
The tetrads in interphase would be expressed as aa AA...ww WW (so, for example, AA are sister chromatids). Finally, use the notation a' and A' to express that those two chromatids have crossed over via recombination.
Ok: I understand that in Metaphase I, there's a random assortment of chromosomes at the equator, so that we might end up with a division like so:
aA'    Aa'
bB'    b'B
CC'    c'C
...
wW'    Ww'

Which pair ends up on the right or left is random, and there are therefore $2^{23}$  possible arrangements.
My question is whether an analogous shuffle happens during metaphase II? I visualize metaphase II as taking one of the columns above and turning it on its side, so that for instance taking the right column you have:
a' B  C  ... w'
A  b' c'     W

These "rows" are then split to become 2 of the 4 gametes.
The question is whether at this stage, before this final split, there is an analogous shuffling possible whereby, say, the A and a' could switch sides?
My intuition is yes, of course, but in all the accounts of meiosis I can find online, the "random assortment" and shuffling is all described as happening in metaphase I.
(I think whether the shuffling between this particular A and a' happens in metaphase I or metaphase II is inconsequential in terms of which one ends up in which daughter cell... but I'd still like to have a sense for what's literally physically happening.)

Metaphase I
Your understanding of the metaphase I is not entirely correct. In normal (human) metaphase I homologous chromosomes separate. Therefore, sister chromatides go together. More precisely sister chromatides are kept together at centromere. You have only two possibilities for each chromosome:
<-AA   aa->

or
<-aa   AA->

If we multiply the two possibilities for all 23 chromosome pairs it leads to correct number  223 of possibilities.
There can be one or more crossovers between two or more chromatides but the fate of crossovered chromosome arms is determined by the fate of centromere they get connected to.
Your diagram of random assortment, if I understand it correctly, allows for more than 2 possibilities for chromosome pair:
<-Aa   Aa->
<-aa   AA->
<-AA   aa->
...

And it would lead to incorrect number of possibilities (more than 2)23
Metaphase II
In metaphase II sister chromatides separate as they would in mitose. Yes, there is random asortment of which chromatide goes left and which goes right. With your notation it could look like this:
<- A   A'->
<- b   b'->
<- C'  C ->
<- D   D'->
...
<- w'  w ->

However, as I said earlier, some chromosomes can crossover more than once, so you can have thinks like:
<- g''   g'->

or
<- F'''   F ->

or
<- h'    h'->

Inverse meiosis
For every rule in biology there is an exception. Some species have inverse meiosis. This means they do it in reverse order. In metaphase I they separate chromatides and in metaphase II they separate homologous chromosomes.


text:
Why does the seed of the coconut tree have a liquid in it?
What is the purpose of water in the coconut seed?  The reason I ask this is that I was reading about coconut water and all the benefits it has for us Humans.  But why does the tree put a liquid in the seed?  I read a lot more and learned that the liquid becomes a solid and is called endosperm, which is food for the coconut tree.  I'm still not happy with that answer because all seeds are food for the plant they become.  They are also a lot more.
I have come up with a very good explanation for the existence of coconut water and I want see if anyone else has any ideas.  Remember, I am not trying to find out why there is food in the shell.  That's obvious.

Hi! "I have come up with a very good explanation" -- you should post it here, members will be able to tell you what biology prevents your explanation or supports it

I think it's because the coconut is hollow and designed to travel on the sea for more than 100 days and 3000km. At sea, the sunshine and the salt has a strong drying effect on the coconut, so fresh water helps it resist sun and the osmotic force of the seawater.

I like your thinking.  I agree with your points on the design allowing the coconut to survive for 100 day and 3000 km.  But if you think about it, all the nutrition, including the liquid is inside the endocarp. Protected from those environmental dangers.  The Exocarp is very thick and robust and the endocarp is made of a hard woody material, which is why I am not convinced that your answer is correct.  Thank you for your comment.  I really appreciate it.

I will give my explanation after I feel that enough time has been given to this community of thinkers.  I really respect other people's points of view and am sincerely interested in seeing if anyone else can come up with my solution.

Since we talk about travelling on sea, maybe it is simply a reserve of freshwater for when the tree will start to grow if rain is absent in the first days. As you said most seeds have a reserve of food for the newborn plant, this one just has a reserve of freshwater as well in case the coconut ends up on an island surrounded by saltwater. It might also matter the way water affects how the cononut rolls, moves or falls from the tree. or maybe it helps the coconut resist impacts ?

I like your ideas about helping it roll and move once it falls from the tree.

It is a transitory state.
During coconut development the "milk" actually starts as a spongy solid a multinucleate endosperm. As the coconut develops it absorbs this tissue. Because of a coconuts hard structure this leaves a cavity since the coconut cannot change shape as the tissue density changes, some fluids including oils are left behind as hte tissue is broken down and reabsorbed. But this fluid will be reabsorbed as the the developing cotyledon fills in the cavity. The fluid is a by product of the cavity but the the cavity is needed due to the unusual development of the coconut.
As a side note most comercial coconut milk is actually squeezed out of the solid endosperm.

That is the milk part, not the water part.

@Coconut They are the same part, commercial coconut milk is made in a different way, but then commercial cheese is one step away for plastic that does not mean much.

Here are two things that I have not see anywhere else in my research on the subject.
First, I will explain why coconut trees at the edge of the beach seem to "reach" toward the sea, but usually go straight up when planted away from the beach.  Then I will get to why the coconut tree puts a liquid in its seed.
The main purpose of many seeds is to to take themselves away from the parent to start a new life somewhere else (hopefully better).  Just like us humans the coconut tree wants it's offspring to migrate.  It uses the sea as the medium on which it travels.   The coconut is too heavy to move toward the sea using wind or animals. It's also too tough for most animals to be able to get the nutrition locked inside it.  So the tree, which in nature would most likely find itself on a beach, contorts itself so that it's "head" is above the sea and then it drops is seed in the ocean to travel and find a new place to grow and propagate.  That would be my reasoning for explaining the commonly seen phenomenon of coconut trees leaning over the ocean.
So now that the coconut has started it's travels into the unknown, it needs to find a place to grow.  The seed bobs up and down on the ocean until it lands somewhere.  It could land on the same island or travel thousands of kilometers and land on another island or coral atoll or a sandbar.  This is where the liquid comes in to play.  The liquid which has been moving inside the coconut suddenly stops.  After a certain amount of time the next step in it's growth is triggered because of the still liquid.  Also, the cavity in the coconut keeps it from drowning.
That's it.  The "water" is a "level" that tells the coconut when to "drop a root and send a shoot"
Let me know what you think.

I've edited your post to remove the bit at the top about being back and ready to talk about this. Thank you for contributing. We can see that you're back and have something to share because you posted!

It looks like this post is mostly from your introspection about possible reasons. This is a great method for developing hypotheses, and can sometimes be a great place to start when a lot is known generally but not specifically, but in this case I suspect this is already better studied. Can you provide some references that support your conclusions?

you are right to say that the post is based on introspection.  I wanted to post this hypothesis on this medium because there are a lot of scientists that have knowledge pertaining to this subject.  My research is not going to be as well founded as many of the people on here.  I don't have any references to what I have hypothesized but would like to know if there is a better explanation.  If you know anyone that has studied the subject extensively please make them aware of this post and let me know what they think.  The thought came to me and I wanted to share it with the universe.

Then post it as a question not an answer.

I have never heard a good explanation on why coconut water exists.  My explanation is simple and makes sense.  If you can reference a better explanation, please do so.