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Do fat people have more chances of developing nitrogen bends?
I was reading some text on deep sea physiology. I got to know that solubility of nitrogen in fat is five times that in water. The exact text from the book animal physiology adaptation and environment by Knut Schmidt-Nielsen, was:-

The body fat, which in a normal lean male constitutes about 15% of body weight, dissolves about five times as much nitrogen per unit weight as does water

I think that having more body fat increases your body's nitrogen saturation capacity, thereby increasing the probability of nitrogen bends.
(Nitrogen bends or aeroembolism is the phenomenon in which nitrogen gas forms bubbles in the blood stream near joints and cause pain)
So can I conclude that fat people (those who have more body fat), are more likely to develop nitrogen bends in their blood stream?
I'd be grateful if anyone out there can help.

Well, you're right! First of all,

Nitrogen Bends or Decompression sickness (DCS) is a disease that arises as a consequence
  of bubbles forming within tissues. Inert gases, such as nitrogen
  and helium, enter the body through the lungs during inspiration.
Increased BMI (Body Mass Index) implies an increased fat content of the body. This
  increased body fat leads to increased nitrogen storage and hence
  possible excessive nitrogen bubble formation and thus increased the
  risk of development of DCS.

Learn more about the relation between Fat and Nitrogen Bends by reading Diving and Hyperbaric Medicine  Volume 36 No. 3 September 2006

Your Welcome, @Anonymous! Please read the link I've attached. It will surely answer your question with some more clarity.


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Osmosis vs protein-binding in preserving foods through salting
I had assumed that the preservative function of covering foods with NaCl or brine was due to osmosis killing the microorganisms on the food by dehydration.  However, I am now wondering to what extent denaturing of bacterial protein through interaction with salt ions could be responsible for killing the microorganisms.  And what evidence suggests a dominant role for one or the other mechanism.  I hope someone can clarify this matter for me.  Thanks in advance.

In addition to killing microorganisms, the salt may provide a better environment for some 'beneficial' organisms, and a less beneficial environment for other 'problem' organisms. For instance, in production of kimchi and sauerkraut, salt encourages lactofermentation to the detriment of more harmful bacteria and fungi.

This is interesting, and implies that the relative importance of osmosis vs protein-binding when preserving food with salt depends on the type of microorganism targeted.  But I still wonder about the importance of osmosis in food preservation, whether or not lactofermentation is involved.  In the latter case, are harmful microorganisms killed by dehydration?

source: Stack Exchange

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Double stranded RNA Single stranded DNA
I have seen in textbooks referring to ds RNA and ssDNA.
How a RNA can be double stranded and likewise how a DNA can single stranded  and if they do exist why are there names not interchanged?

The main differences between RNA (ribonucleic acid) and DNA (deoxyribonucleic acid) is that DNA contains a hydrogen atom where RNA has a hyroxyl (-OH) group and RNA's uracil is substituted for DNA's thymine.  The below image shows several deoxyribose molecules bound together, and off to the side, a ribose molecule. It is the OH group on the bottom right of the ribose molecule that is exchanged for a hydrogen in deoxyribose.

The structures of RNA and DNA are almost identical, so there is no reason why you can't have double stranded RNA. Similarly DNA can be single stranded. In fact, for DNA replication and transcription, the DNA strands must be separated. dsRNA and ssDNA are most commonly found in viruses. Check out these lecture slides for more about them: http://www.columbia.edu/itc/hs/medical/pathophys/id/2009/viruses2Color.pdf

"DNA contains one less oxygen atom" — please edit your answer to be more precise. The naive reader would have no idea what you mean, and the difference between ribose and deoxy-ribose is what produces different structures of dsDNA and dsRNA.

edited for clarity, though the reason I added the image originally was to provide the reader with a fairly self-explanatory comparison.

Complementary base-pairing is possible for RNA
As the poster is no doubt aware, the double-stranded structure of DNA is stabilized by A–T and G–C base pairs. He will also be aware that in transcription of DNA to RNA (in which A is replaced by U) A–U base pairing occurs. Hence, there is no physico-chemical reason why dsRNA cannot occur between suitable complementary strands.
Viruses provide examples of single- and double-stranded DNAs and RNAs
As is mentioned in another answer, the genomes of bacterial and eukaryotic viruses provide examples of dsDNA, ssDNA, dsRNA and ssRNA.
It takes two to tangle
Whether or not a particular DNA or RNA is double-stranded or single-stranded in Nature depends on whether both complementary strands are present. That depends on biology, not chemistry. Thus, a virus that is single stranded has evolved a replicative strategy whereby many copies of one strand are copied from a few copies of the complementary template. In double-stranded viruses (and organisms) the replication method starts with a double-stranded genome and makes a copy of each at the same time, resulting in equal numbers. (They are also synthesised in a way that allows them immediately to hydbridize.)
Nature is full of black swans
The fact that most DNA encountered is double-stranded and most RNA encountered is single-stranded, just reflects the nature of the genome and translation apparatus of cellular organisms. But transfer-RNA and ribosomal-RNA (and mRNAs) have double-stranded helical portions, and there are a variety of less abundant species of RNAs with individual functions that may involve helix formation. And, of course there are also DNA/RNA hybrids, for example the Okazaki fragments that occur during DNA replication.

why not link to your answer to "Does dsRNA exist in eukarotic cells?" https://biology.stackexchange.com/questions/95306/does-double-stranded-rna-dsrna-exist-in-eukaryotic-cells/97593#97593

I'll try a third pedagogical approach, the above answers are sufficient.
The typical college-entry level textbooks on biology will state that DNA is double-stranded and RNA is single-stranded. This is misleading later on, especially when you encounter an instance of single-stranded DNA and double-stranded RNA.
The posters above have already answered your question well - dsRNA and ssDNA exist all over the tree of life. However, I'd like to emphasize that they also exist transiently all the time in every single cell...
3 critical examples:

DNA must unwind and become single-stranded for DNA replication.
The same is true for transcription.
RNA has a tertiary structure too. Ribozymes rely on this. However, the most abundant RNA species in all cells is ribosomal RNA. It forms these structures:

These are 'single-stranded', but are capable of dimerizing with another RNA species if there is sufficient complementarity between local regions. Below you see many RNA hairpins and loops and locally these are double-stranded, even though it's a single molecule.
In situ hybridization is also another common technique in biology, it takes advantage of pretty much all 'exceptions to the rule' you mention. Nowadays, RNA is increasingly probed. Here is a simple diagram of how it works:

If they do exist why are there names not interchanged?

The names for RNA and DNA are not interchanged because they are different chemically! They just share features, most notably the ability to complement and hybridize to themselves and other nucleic acids, given enough complementarity.

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Is the lac operon repressed in the presence of both glucose and lactose?
In the presence of both sugars (glucose and lactose) will there be repression of the lac operon completely?
I know that more glucose means less cAMP --> less CAP --> less positive regulation, and thus less lac operon, but does that mean there will be repression of the lac operon?

There is never a complete absence of glucose in a living being; the issue is with the amount available and amount required difference. This difference determines the rate of expression of the Lac genes after the lac repressor has been inactivated due to the presence of lactose.

According to Molecular biology of the gene by James Watson, in presence of both glucose and lactose, the lac operon has a basal level of transcription. However, when only lactose is present, the operon has an activated level of transcription, due to the CAP mechanism.


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Why pellet and resuspend E. coli for plasmid prep
For maxipreps, cant you just add all the stuff that would be in P1 (RNase A, EDTA) then just add P2? Because if we pellet cells then resuspend theres got to be a reason, right? Is it slats and other stuff in the media that mess with lysis?

The reason this centrifugation/resuspension step is done has a simple reason: It concentrates the bacteria in a much smaller volume which is much easier to handle afterwards.
For a maxiprep you typically have a culture volume between 250 and 500ml, depending on the copy number of the plasmid. After centrifugation the pellet is resuspended in 10ml of Buffer P1, for lysis another 10ml of buffer P2 are added, for neutralization 10ml of P3.
Imagine doing this with 500ml culture volume - adding 500ml of each P2 and P3. This might work for a miniprep, but definitely not for larger volumes. Additionally, the centrifugation steps are carried out at high g numbers - typically something around 15.000xg. Doing this with this really high volumes is complicated and needs big centrifuges, which a lot of people are not trained anymore to operate or have available.

I want to add that there are some kits that allow direct addition of the "lysis buffer" to the cell suspension in the medium. Of course, as you said, yield would be low.


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Amino acid substitutions near the receptor binding site HA protein in type A H3N2 influenza strains?
I have read the scientific paper, "Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution" by Björn F. Koel et al (http://science.sciencemag.org/content/342/6161/976).
In the paper, important positions to influenza antigenic drift include positions 109-301, with special emphasis on sites 133, 144, 145, 155, 156, 158, 159, 189, 193.
However, nowhere in the paper does it specifically mention which positions are part of the receptor binding site and which are close to it.
The range (109-301) is a bit broad since it includes amino acid positions that are unimportant to antigenicity. I would like a list of all very important AA substitutions (that are near the receptor binding site) to involve in a bioinformatics project. The special emphasis amino acid sites list does not include all amino acids that are near the binding site.
To convey a sense of the problem, if position 155 is important, does that mean position 156 is also important?
I don't know if position 156 is considered "near" the receptor binding site.
Any help is appreciated.

I may provide a more substantial answer after reading the paper but right now I just want to point out that an amino acid substitution can affect sites that are far from it (on the sequence) because it can affect the folding. There are no general rules but some approximations can be made if we know the protein structure.

@wysiwyg that's a fair point in general but less of an issue with influenza hemagglutinin. HA is incredibly tolerant of amino variants and can include a shocking number of substitutions without drastically affecting its folding. The result is that it's usually fairly safe to consider mainly local effects of substitutions without worrying too much about major structural changes

Short answer: Yes, 156 is generally considered "near" the RBS, e.g. in this paper you can see it mapped onto the structure.
For a more general answer, you'll need to sit down and stare at 3D models of hemagglutinins (there are hundreds in the PDB), just like the rest of us. Antibody binding sites are not black and white, and interactions between influenza and antibodies are wildly complicated. What's "near" in some contexts might be "far" in others.
You might find the Influenza Research Database's Identify Sequence Features in Segments tool useful, particularly its annotation of hemagglutinin H3.
Be aware that numbering of amino acids can be confusing, since different groups may be using different starting points. There's a vague agreement on the "correct" numbering, but quite a few groups pay it lip service and then number their version however they like.


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High altitude rail travel
This question is primarily about human performance. I do know about hypoxia, hence this question.
I'm busy designing a fictional region, currently in the 1930's. I have a railway line that climbs to 15,000ft (4670m) in order to traverse a mountain range. The line was build in the 1900's, with the climb being gradual at 1:100 gradient. The town on the Eastern side is at around 5,000ft. the town in the west is at about 7,000 ft. Distance by rail is about 800km, (about 10 to 14 hour journey) with about 20 to 40km spent at 15,000ft. Using real-world data,
I only have a basic understanding of the human body, and would like to ask the following questions:
1.) With 1900's to 1930's attitudes, would it be "safe" / "wise" to send passenger trains over that pass?
2.) How would this altitude affect the drivers / firemen on the steam-engine's footplate?
3.) From a biological point of view, how do I make this journey more comfortable?
4.) Any other point which I might have missed.

The train connection (from mainland China) to Tibet is very similar to what you are describing - with exception for the time it was built. Looking into the details of that will probably give you a lot of useful information: https://en.wikipedia.org/wiki/Qinghai-Tibet_railway

For something with similar elevation changes, see the Pike's Peak Cog Railway https://www.cograilway.com/  Probablly millions of tourists rode it without any major ill effects.

People have used other modes of transport in that time without any significant health problem. Why do you think a train journey would be any different?

@WYSIWYG The train journey climbs to altitudes above 12,000ft (4,000m aprx), for several hours. In modern aviation law, oxygen is mandatory above that altitude if unpressurized. Some people (the elderly, smokers) could have reduced lung function. The high altitude may cause them illness or worse. I estimate that about 50% (if not more) of the people traveling will be affected by the altitude in some way or another.

@WYSIWYG (... continuation) I'm mainly worried about the fireman who needs to exert physical effort at this altitude. It would be bad for business if the firemen drop dead during the journey...


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Could we breed a dog to the size of a thumb?
We've gotten from a wolf to a small breed such as a chihuahua. So the question is: can we go even further and have a dog as small as a thumb (adult dog)?
If not, what are the factors that limit the smallest size of a dog breed? Is it limitations in genetics, or some physiological reasons which would prevent such small dog to survive?

I'm not sure answers to this question would need to be opinion based, so I'm voting to reopen it....It asks for a biological explanation and not conjecture. Even if the answer is "we don't know", the question could still receive a valid, and informed response.

alternatively, I'm assuming you could rephrase your question to ask specifically what genes control dog size or perhaps a question that asks about a specific physiological limitation.

You may be interested in this essay.

How long do you have, and how many individuals?  The problem seems to be that very small dogs (and purebred dogs in general) tend to have lots of health problems, so it would take many generations of many individuals to weed those out.

Whales ans elephants come from small fish, so yes, deffo, itll take 200k years only.

As mentioned above the inbreeding required to select smaller and smaller dogs would be problematic because of the myriad of health problems that would be associated with it (see inbreeding depression).
The question about physiological limitations is interesting. The main reason biological organisms often don't scale is the fact that length, area, and volume don't scale in the same way. E.g. if something is twice as big L to 2L the surface area is L to L^2 and the volume is L to L^3 which means that many systems no longer work or require more energy (see Allometry) . For example in insects the distance for oxygen to diffuse to cells is short enough that simple diffusion is possible, in humans that is no longer the case so we have whole circulatory and respiratory systems to, in effect, help reduce the diffusion distance for oxygen.
I haven't used this kind of analysis in a while so am not very confident applying it here but I would suggest that some issues that could arise due to things scaling with length versus area or volume are:

required heart rate
maintaining body temperature - many small mammals deal with this by falling into periods of cold torpor (sort of like hibernation) where metabolic rate is suppressed
fragility of bones (as Cort Ammon mentions this is actually not a problem: https://jeb.biologists.org/content/207/9/1577)

I believe bones are actually more fragile on large creatures, thanks to the square cubed law.  However, maintaining body temperature is definitely a VERY hard challenge for a small creature.

Inbreeding will defeat the goal of breeding smaller animals because genetic diversity will decrease, which will, in turn, decrease the likelihood of further change. The goal would be to select for smaller size while maintaining genetic diversity.

Compare to the smallest mammals, like bumblebee bats and pygmy shrews.


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Why are veins not blocked by plaques?
In my textbook, it is written that atheromatous plaques block the artery. This leads to heart attack and and heart failure. But my question is why do the plaques only block arteries and not the veins? Do the plaques also block the veins?

Atherosclerosis can develop in high pressure systems, such as arteries, and not in low pressure systems, such as veins. It is high blood pressure that can damage the lining of the blood vessel and initiate the process of atherosclerosis.
BUT, atherosclerosis can develop in veins that have been used as grafts instead of arteries, for example, in a coronary artery bypass surgery.
Springer: Atherosclerosis:

In this regard, we may note that atherosclerotic lesions do not
  develop in the veins in their normal environment of low pressure and
  high flow, but that the lesions do develop when the veins are used as
  arterial bypass grafts where they are subjected to high pressure.
  Similarly, atherosclerotic lesions develop in the pulmonary arteries
  only in pulmonary hypertension.


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Why are $\beta_2$ receptors present on bronchial smooth muscles , considering that they have only parasympathetic innervation?
It is well known that the bronchial muscles have only parasympathetic innervation. But they still express $\beta_2$ receptors. How does this system still cause bronchial relaxation? What is the exact mechanism?

Do you have a source for the first statement? I find that the first sentence here: https://www.ncbi.nlm.nih.gov/pubmed/11240156 seems to contradict it. Halfway through the abstract might be the answer to your question.

To be frank... I really just referred a single source .... The source is Rang&Dale's Pharmacology Ed-7 Chapter 12( Chemical mediators and the Autonomic nervous system) Pg 141. The exact statement is " Bronchial smooth muscle has only a parasympathetic (constrictor) innervation......."

The exact statement is " Bronchial smooth muscle has only a parasympathetic (constrictor) innervation (although its tone is highly sensitive
to circulating adrenaline—acting probably to inhibit
the constrictor innervation rather than on the smooth
muscle directly)."This gave the impression that there is absolutely no sympathetic innervation , when the case is the contrary! Thanks for directing me to the above paper!

Good question, but first I'll address a note in the comments.
In bronchial smooth muscle, do β2 receptors receive sympathetic innervation?
Canning and Fischer (2001) claim that bronchial smooth muscle do receive sympathetic innervation. But it would still be correct to say that β2 expression plays little role in regulating smooth muscle tone in the human airway under normal conditions.
How do β2 receptors cause bronchial smooth muscle relaxation?
You already know that this receptor is associated with bronchial relaxation. An article by Billington and Penn (2003) claims it works through Gs coupling. This binds adenylyl cyclase causing it to form cyclic AMP which activates protein kinase A (PKA) which carries out many more functions.
WHY are β2 receptors present on bronchial smooth muscles considering [minimal sympathetic] innervation?
Circulating chatecholamines released due to emotion, exercise and the like. Billington and Penn (2003) note "prophylactic bronchoprotection" as the central role for Gs-coupled receptors in airway smooth muscle.
Why ELSE are β2 receptors present on bronchial smooth muscle?
β2 receptors are important in regulation of airway smooth muscle cytokine/chemokine synthesis, and inhibition of airway smooth muscle growth (DNA synthesis/cell proliferation) i.a. (Billington and Penn 2003).

Billington, CK, Penn, RB 2003, 'Signaling and regulation of G protein-coupled receptors in airway smooth muscle', Respiratory Research, vol. 4, no. 1, PMID: 12648290. https://www.ncbi.nlm.nih.gov/pubmed/12648290

Thanks a ton for the clear explaination! It is a massive help!


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This 5X binding buffers where experiment participates in?
I saw 5X bingind buffer maded by;

100mM HEPES, pH 7.6
5mM EDTA
50mM ammonium sulfate
5mM DTT
1% Tween-20
150mM potassium chloride

which reaction helps this buffer? I don't consider to this buffer participates in which experiment by name. Although this buffer have another name but they writes just '5X bonding buffer'..

From what kind of reaction/protocol did you take this description?

I saw that recipie at pre-made buffer selling site. there's no mentioned about buffer usage.

Can you give us the link?

http://www.biosesang.com/bbs/shop/item.php?it_id=B2003 <<here. Application used by 'Applications: Suitable for molecular biology applications.'.

The description says "binding buffer" without specifying. This is pretty standard stuff, containing a buffer (Hepes), some salt and detergents. Nothing too special, but I wouldn't use a "one fits all" buffer.


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What mammal or creature dropped this? (Warning: Gross Pictures)
I'm at a loss to explain what creature dropped or created this. This giant pile showed up virtually overnight.  If someone could point me in the right direction, I'd greatly appreciate it.
The geographical area is Sparks, Nevada.

Probably a bird, or more likely a group of birds.

I know piles of poop like the one sown in your picture from swallows... Barn swallows for example. Is there a nest somewhere above?

Yep, looks like it was 2 birds hiding in the roof soffit.  Didn't think there was an opening in the soffit directly above the pile, but I guess there is.  Couldn't get a good look at what kind of bird they were.  They shan't be returning, however.  Thanks for your help!

You can see a similar pile of bird poop seen below a barn swallow nest:

 Source: deepmuckbigrake
Alternatively, if it really did appear overnight, perhaps a pile pf pigeon poop was pushed out of a nesting area in the soffit?

 Source: Scranton Times Tribune
If it's pigeon poop, you might want to be careful.


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How does vasoconstriction increase the pressure of blood?
Is the increase of pressure due to the decrease in volume? Wouldn't the decrease in volume push the components of blood closer to one another resulting in an increase of repulsive forces, thus increasing pressure? Or is the increase in pressure due to the heart pumping the blood with more force in order to maintain blood flow?

Because pressure is inversely proportional to area. If you consider a pipe, if you squeeze it's tip to decrease it's area you'll observe that the velocity of water flow becomes high due to high pressure. Same is with blood in veins.


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What does "PDPN+ cells" means?
Are they podoplanin positive cells (cells that tested positive for podoplanin)?
"...though it has been shown that podoplanin (PDPN+) cells analogous to mouse FRCs are found in human secondary lymphoid organs..." (https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2005046)
"Although rare, the few SFTPB+ observed in HLOs resemble AECII cells seen in the adult human lung, and PDPN+ cells resembled the elongated AECI cells in the human lung" "Few PDPN+ cells also showed elongated, squamous morphology seen in the adult lung." (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370217/).
Thank you.

Can you please provide some context (for e.g. excerpt from the article/book which uses this term, with proper link)?

Yes, sure: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370217/

James. We generally appreciate if a question is self sufficient. It is good that you provided a link but it would be even better if you could paste the exact sentence/paragraph that uses the term that you want to know. Use quotes or mark with a ">" in the beginning to indicate text that you have copied and pasted.

In this context, that nomenclature means "cells which express PDPN"


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Improving DNA quality and yield from stool samples
I prepared genomic DNA from pig stools but the concentration was very low — about 3~4 ng/µl, when I measured it using nanodrop. The A260/A280 and A260/A230 values also did not come out very well (0.4~0.5 and 1.0, respectively). I also tried filtering the DNA two times but it didn't improve the quality. Does anyone have experience with DNA extraction from stool samples and suggest me how I can improve the quality and yield?

Expected photometric ratios for pure DNA are around 1.8 (A260/A280) and 2.0-2.2 (A260/A230). For reference, if you are extracting pure RNA, its ratio is ideally 2.0 (A260/A280).
Often, lower ratios usually indicate low purity due to contaminants or simply a very low amount of DNA.
EDTA, carbs and phenol among other chemicals all have absorbance at 230nm. If you used TRIzol reagent to extract DNA, you may also get some absorbance from this reagent at 270nm if you incorrectly pipetted some of the phenol phase (pink stuff) or the interface (white cloudy stuff between the aqueous phase and the pink phase). If you measure a low ratio, like you did, it probably means that in your final DNA extract, you seem to have (a) things that are not DNA in your solution, and/or (b) a very low concentration of DNA.
If you suspect you have enough DNA, you can purify to try to remove non-nucleic acids. However, with ratios that low, I suspect you should extract DNA from scratch; it does not appear that you have enough to rescue simply by purifying again.
Which method did you use to extract your DNA? What do you mean by filtering?

Oh I didn't use trizole reagent. I used a commercial kit. filtering means DNA binding and eluting at column tube during experiment.

You're using spin columns, I'm sure. They contain a silica resin that selectively binds DNA (RNA is also possible), by varying salt conditions. You pass the solution with your DNA by centrifuging, the DNA gets trapped on the resin, and then elute the bound DNA with a second pass of an elution buffer. It's quite a high-quality way of purifying DNA from a solution, in my hands it works better than TRIzol extractions. I have no idea how you obtain an aqueous solution workable with columns from pig stool. In principle, it should work well if the input is good enough. Sorry that's all I got!


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Are there parasitoids of mosquitoes ? (other than nematodes)
Outside of nematodes, are there any examples of organisms that are parasitoids of mosquitoes ?
I could not find any example in literature so far. I'm notably interested to know if the most known mosquito genera (Aedes, Anopheles, Culex...) have already been described to be parasitized by other insects (e. g. parasitoid wasps), and if this is a common phenomenon in nature.

It happens I just found an answer to my question in a recent review book by George Heimpel and Nicolas Mills. It appears that for now we do not know any  parasitoid of mosquitoes.
Quoting chapter 1 :

"Most insect herbivore species are attacked by
  one or more parasitoid species, but some major
  arthropod pest groups appear to be entirely free
  of parasitoid attack. For instance, we know of no
  parasitoids that attack mosquitoes or other biting
  flies with aquatic larval stages, and no parasitoids
  that attack phytophagous mites or adelgids."

Source:
Heimpel, G., & Mills, N. (2017). Definitions and Interactions. In Biological Control: Ecology and Applications (pp. 1-18). Cambridge: Cambridge University Press. doi:10.1017/9781139029117.003


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What will be the deficits when left half of the brain is removed in adults?
Hemispherectomy is a surgical procedure to remove half of the brain. It is typically done on children with severe epilepsy. What will be the deficits when left half is removed in adults? Is aphasia a certain outcome in case of left hemispherectomy in adults?


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What restriction enzyme was used in cutting this DNA piece?
So, i was given this cut piece of dna and i was required to choose the restriction enzyme used to cut it. I had to pick either XhoI(CTCGAG) or TaqI(TCGA), where the sequence between parentheses is their palindrome sequence. Which one is it and why? I've picked XhoI since i know that the enzyme cuts in between the palindrome

GAGCT        C
C        TCGAG

DNA after the cut.

In order to keep this on topic, I will try and give a more general answer.
The most widely used restriction enzymes, and the ones typically taught first, all cut within their recognition sequences, however, this is not necessarily so as most Type I and Type III enzymes cut at a distance from their site, sometimes this is a fixed distance, sometimes it is not. It is only Type II enzymes that cut symmetrically within their sites, and even then, not all of them. However, cutting within the site is usually the most useful kind of cut for molecular genetics and thus these are the most common enzymes to encounter in the lab (see here for more).
For a particular enzyme, the best way to find the cut site is simply to google it or search directly on the NEB site (where you will likely find the top Google hit anyway), doing this for XhoI would get you a page containing information like this:

Where the little arrows in the given recognition sequence indicate where each strand will be cut, whereas as for enzymes that cut outside the recognition site you will get something like this (for AlwI) where the $(N)_4$ part tells you that the enzyme cuts four bases away on the 5'-3' strand, and the $(N)_5$ part tells you it cuts one base further away on the opposite strand.

In order to identify which of a number of enzymes cut a certain sequence you need only find the appropriate information for the relevant enzymes so you can compare these cut diagrams for the relevant enzymes.


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Confused about definition of bulk flow of water by osmosis
As a teacher of high school and introductory college chemistry, I used textbooks that defined osmosis as a flow of water (only) through a membrane that prevents other substances such as dissolved salts from passing through.  But in more advanced text, discussing osmosis through aquaporins in the plasma-membrane, bulk flow by osmosis implies that the water carries along dissolved substances.  So which is it:  pure water or a solution that moves by osmosis?  (I'm somewhat naive about biology, as my degrees are in physical chemistry and metallurgy.  Biology is way more complicated!)

Can you provide a citation or quote? I'll answer by my guess about what's being talked about, but it would be nice to be able to confirm.

Bulk flow and osmosis are different; I'm guessing your text might be talking about using osmosis to drive bulk flow, but they are occurring at different stages.
For example, if you get your water from a water tower, your house's water pressure is driven by gravity. However, the water tower could be filled by an electric pump. You could say your water pressure is driven by an electric pump, but the pump isn't really pushing water into your house, it's just pushing water up a tall tower so that gravity can act, and if you didn't realize this fact you might be confused about how you can still have water pressure even when the power goes out.
Similarly, you can drive bulk flow by osmosis. If you have a closed space (e.g., a "tube") and pump salt (or anything else water soluble) into it, it can pull water from the surrounding tissues via osmosis. As the pressure of water increases in that closed space, it can now flow in bulk through that tube. Plants can use this mechanism to deliver nutrients up a stem: they pump in ions/molecules inside the stem, which pulls in water from the soil around. Because the space is rigid, instead of expanding the water goes up the stem in "bulk": anything else carried in the water will be pushed up with it. Then, when target tissues pull in solutes, osmosis again causes water to follow, and by only pumping solutes in one place and out another you produce a bulk flow of water.

Bryan, thanks for your answer.  But please clarify the example of plants delivering nutrients up a stem.  Does this mean that the liquid that enters the roots from the soil by osmosis is essentially pure water, but once it has entered the tube-like stem it carries with it nutrients that were in a lower place in the stem?

@S.Fishman The general concept is that cells in the roots pump in any ions, etc, from the soil that the plant needs, and therefore water is pulled in via osmosis. Not totally pure water, but also anything else that can freely cross membranes. The root cells then pump those ions into other cells or cavities and water follows. The whole system is actually pretty complex and plants use a lot of combined forces to move solutes in a couple different systems, so you can read more broadly about xylem and phloem.

I should also add that I simplified a bit by talking about a "tube", because in the context of nutrient transport in plants you can also have living cells that are connected to each other via openings between cells; they aren't really just a tube anymore in that context, but from the perspective of water and stuff dissolved in water the principle is the same.


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Why can't bacteriophages survive inside the human body thus negating the possibility of using them against bacteria?
I read about the therapeutic uses of bacteriophages in Pelczar's Microbiology. It was written that it is reasonable to think that bacteriophages could be used to kill pathogenic bacteria. However, the book also clearly stated that after a lot of research it was found that bacteriophages can't be used to kill bacteria in the human body because they can't survive inside the human body. But no reason was given why.

I think it's about a claim, that bacteriophages cannot survive in the human body and can therefore not be used as a treatment against bacterial infections. The question is fine, but it would be good to give the source of such claims. You say, you have done a lot of research. Showing your sources would help understanding the question.

It would be better to quote from the book verbatim, especially as English is not your native language. The misuse of the word "sustain" is critical here. I have edited it out, but it would be better to know what exactly was written.

Well the book actually wrote sustain, yes English is not my native language but I'm not blind.

This question cannot be answered, because the assumption behind your question is wrong. I haven't found a source to claim that bacteriophages cannot survive in the human body. Bacteriophages can and are, in fact, used as a treatment against human bacterial infections, it's called "phage therapy" (1,2,3).
This is, nevertheless, a rather uncommon procedure for a number of reasons:

Availability: Compared to antibiotics, which you can easily get from any doctor/pharmacy, phage therapy requires special facilities, because very specific phages need to be produced for each disease.
Safety and regulation: Virus handling requires special safety measures and using them in humans requires a lot of paperwork, safety tests and clinical trials.
Money: Due to the reasons above, phage therapy is a lot more expensive than antibiotics.
Lack of research: Thanks to the availability of antibiotics there was no urgent need to develop the application of phage therapy. We know comparably little about how the immune system might react to bacteriophages in the blood or bacterial toxins released by lysed bacteria. We haven't found a way to e.g. quickly engineer bacteriophages for diseases.

With a growing concern about multi-drug resistant bacteria, developing new ways to combat diseases has become more important. Maybe phage therapy will be one way to deal with this more regularly in the future.

Are the special safety rules for bacteriophage treatment really needed or only a matter of paranoid bureaucratic overhead? Intuitively, bacteriophages should be the safest viruses for humans to be exposed to considering they selectively infect bacteria (fundamentally different biological architecture from human cells). For bacteriophages to infect humans, first they need to figure out infecting eukaryotes, and then they need to adapt to the different ribosome structure (which also happens to be the reason why you can take macrolide antibiotics without shutting down your own ribosomes).

While most phages are no threat for human health, they are "biological agents" falling into the biosafety level 1 regulation. When they are modified in the lab, that level might even increase. So, your lab needs to meet all safety standards to be allowed to handle them. https://journals.sagepub.com/doi/pdf/10.1177/153567601001500106


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What causes "ear rumbling"?
The video Ear rumbling happens below the range of human hearing demonstrates that the "ear rumbling" sound is actual sound and can be recorded by a sensitive microphone near the ear.
What is it exactly that produces this vibration and how is it radiated as sound waves into the air?
If it is subsonic, then why does it sounds like noise rather than being inaudible?

I'm able to create rumbling in my ears at will. Unlike the poster of the video, I don't need to yawn to do so; I can do it without my face appearing to move. I actually discovered this alongside another ability of mine when I was little: the ability to create warmth flowing from the base of my neck outwards into the rest of my body. After some research I figured out that the warmth I'm able to create is actually part of voluntary piloerection (its use for warmth is mentioned here), while the ability to create a rumbling sound is simply the contraction of the tensor tympani, a muscle in the ear. Voluntary control over either one of these things is supposed to be rare, but I've found claims of several other people online who can do both (example1, example2).
Anyways, Wikipedia gives a brief explanation of how the ear rumbling works, which also specifically mentions "yawning deeply" as a trigger:

Contracting muscles produce vibration and sound. Slow twitch fibers produce 10 to 30 contractions per second (equivalent to 10 to 30 Hz sound frequency). Fast twitch fibers produce 30 to 70 contractions per second (equivalent to 30 to 70 Hz sound frequency). The vibration can be witnessed and felt by highly tensing one's muscles, as when making a firm fist. The sound can be heard by pressing a highly tensed muscle against the ear, again a firm fist is a good example. The sound is usually described as a rumbling sound.
Some individuals can voluntarily produce this rumbling sound by contracting the tensor tympani muscle of the middle ear. The rumbling sound can also be heard when the neck or jaw muscles are highly tensed as when yawning deeply. This phenomenon has been known since (at least) 1884.

It also seems like this type of noise can happen with conditions such as Tonic Tensor Tympani Syndrome.
The tensor tympani connects directly to the handle of the malleus, so I'd assume that's why it can be heard by the person doing it. Apparently this also causes the eardrum to move. This means it's classified as objective tinnitus.
Here are some relevant studies I found:

Voluntary contraction of the tensor tympani muscle
and its audiometric effects
Voluntary Eardrum Movement : A Marker for Tensor Tympani Contraction? (paywall)
Tonic contractions of the tensor tympani muscle: a key to some
non-specific middle ear symptoms? Hypothesis and data from
temporal bone experiments (paywall)

Thank you very much for taking the time to write such a well-sourced answer. This is great!

@uhoh I didn't find it publicly, which is why I was using my school access to read it. Using that link was a mistake; I have edited it to be a link to the abstract.

That looks great, thank you! I'll stop by a library soon and give all of these a good read.

half-way through discussion Lise et. al. says "Voluntary control of the tensor tympani muscle is an extremely rare event." I can make this loud rumbling sound in both ears any time I want just as you describe in your introduction, and yes after 10-20 seconds of continuously doing it it gets difficult just like a muscle is getting fatigued.

I wonder if this is really as rare of an ability as this paper suggests, or if it's simply rarely-reported or rarely-published?

With these you may be able to finally answer What is official term for contraction induced muscle “vibration”?

The rumbling is caused by two middle ear muscles. These muscles are connected to ear drum and staples, if they are activated, they make it harder for incoming air soundwave to push the eardrum, they increase eardrum acoustic impedance so less sound gets to cochlea. This is triggered by loud sounds and it serves to prevent hearing damage, its called acoustic reflex.
All muscles when activated and under tension shiver slightly, this vibration is the rumbling you hear. The reason you hear this so loud is becose the muscles are directly connected to your middle ear bones so the vibration goes directly to cochlea. You may also hear it if you tense up your jaw muscles but it will be alot quieter becose its further away from cochlea. You can also try pressing clenched fist against ear to hear this muscle rumble.
The term subsonic is confusing and vague, its generaly considered to be sound below 20 Hz but the problem is that humans can hear down to about 5 Hz if the sound is 110db loud. Also, while its true this muscle rumble does contain sub 20 Hz sound, it extends above it too, roughly to 70Hz.

Thanks! The vibration is an artifact of some collective behavior of nerve and muscle. If the result is not a pure sine wave but instead was anharmonic and had other noise and random effects, would those end up above ~20Hz?

I am sorry I dont understand what you mean.

I'm thinking that the audible part is not a ~12 Hz (or similar) sine wave, but the random variations or noise in the contractions. Muscles have a bit of mechanical noise when they contract, in addition to the periodic vibration. I'll see if I can find a better word for it. I'm proposing that it's not the very low frequency sine wave we hear, but the random, noisy component on top of it.

Noise is just word for bunch of chaotic sinewaves. You are right, you mostly hear the 40 to 70Hz part, the 10 to 20 Hz part doesnt contribute much to audibility.

https://www.newscientist.com/article/dn11885-muscle-noise-could-reveal-diseases-progression/ links to https://aip.scitation.org/doi/10.1063/1.2737358 but I don't have access right now


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Measure of diversity, accounting for known species
I'm interested in measuring the diversity of each sample out of many independent samples. I know a priori all possible species that could appear in a sample, and expect the counts of species to be from 0 to about 10, although often times there will be none of a particular species within a sample. For example, some data might look like:
Sample # | Species A | Species B | Species C
--------------------------------------------------
1          0           4           0
2          1           1           1
3          0           1           1
4          2           2           2
5          0           1           0

The most diverse sample here is #4. The least is #5. Theoretically, #5 would also be the least diverse ever encountered (assuming there is at least one of some species in each sample).
I encountered trouble when using Simpson's Index of Diversity since that formula would make the diversities of Sample 2 and Sample 3 both 1.0. Intuitively, with this data, I am confident that #2 is more diverse. This is because I know all possible species that may show up.
I'm relying on this definition:
$$
D = \frac{\sum n(n-1)}{N(N-1)}
$$
Are there measures of diversity which account for a priori knowledge of possible species (and perhaps their bounds) and expect near-zero counts?

Without genetic data, the standard other measures of biodiversity are Shannon-Wiener index and, simply, species richness (aka. number of species). I'm afraid that both Shanon-Wiener and species richness would rank sample 2 and sample 4 equally.

There isn't a single "true" measure of diversity, and different aspects of diversity can be taken into account (abundance, evenness, uniqueness etc). Different indices also weight these aspects differently. So you need to carefully define what you are after before choosing an index.

Also, I question your calculation of D; to me the value for 2 & 4 would be 0.333 and for nr3 0.5 (i.e. 1-D equal to 0.667 and 0.5, respectively).

@fileunderwater Thanks for the comment. I realize there isn't a single "right" solution, I'm just looking for the most suitable: something that takes into account the number of unique species in addition to the overall abundance of each (perhaps with knowledge of possible species). Pardon me for not being from the biology community (this is actually a linguistics problem, but I'm reaching out to biology because there may be a fitting link)

@AlexL No worries about being from another field, especially since the diversity indices have quite wide appeal. I'm currently working a lot on scientometric data, and diversity indices (often borrowed from ecology) are common there as well. I think it would be useful for you to look at Hill-numbers, which basically are ways to rescale diversity indices (measures of entropy) into effective numbers of species. This makes it easier to compare numbers from communities/sites with differnt levels of species richness.

Simpson's estimator, which assumes that sample frequencies are not population frequencies, is unbiased on the probability scale. As @fileunderwater noted, it can be helpful to quantify diversity in terms of effective number of species, or Hill numbers. On this scale (the reciprocal of Simpson's concentration in this case), Simpson's estimator is no longer unbiased. Chao and Jost 2015 recently proposed some estimators for Hill diversity that formally rely on the total richness (of the sampled community) to estimate the true diversity of the community based on the sample, and argue that they have reduced the bias.
I sense, however, this is not exactly the same as your question. If I understand correctly, you have a known maximum diversity but not a known true cardinality/richness/total number of types within a given community/corpus whatever the pool you're looking at is called. In this case I might use maximum richness as a Bayesian prior; I might still use a Hill number as your metric but use the model to estimate that metric.
This 2014 review paper gets into these ideas a bit, or to take an Alan Turing perspective, you might find Zhang 2017 helpful.
Most diversity indices that ecologists use are not sensitive to total abundance, only relative abundance, so as Remi.b noted, classic indices (including Hill numbers) would all rank even communities with the same cardinality/richness identically; the only reason you're getting a difference between {1,1,1} and {2,2,2} with Simpson's estimator has to do with Simpson's solution to the bias in estimates of the community's diversity arising from using sample frequencies.

Thank you, this is good food for thought. The papers and book you referenced seem like valuable resources after a skim!


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How do Neurotransmitters get into the neurons?
This may be a dumb question. I'm not a Neuroscientist. I'm just trying to learn more about the brain to improve my AI learning algorithms…
I understand that there are different kinds of neurotransmitters that either increase or decrease the possibility of firing an electrical impulse through the axon. I also understand that these Neurotransmitters do not actually pass through the whole cell (Correct me if I'm wrong…), so they only travel from the Cell's terminal to the next cell's body.
So my question is: How do these Neurotransmitters get into the cell's terminal? Blood? And the more important question: How are these Neurotransmitters distributed among the different neurons? It cannot be at random, or equally distributed, because we have different "reactions" to different Neurotransmitters. For example if Dopamine is produced it gets sent to these different cells in our brain which makes the activation of its cell more likely (if I understood correctly). Dopamine is also known to increase our feelings of lust and makes us more focussed (and more). But if Dopamine got sent to ALL of the Neurons in our brain, thus make the activation of EVERY cell more likely, it would bring total chaos to our brain. (Eg. Make our fear-part of the brain activate more easily, but this is not the case.). So how are these Neurotransmitters distributed?
Thanks in advance

The general rule (though like much of biology there are exceptions) is that each neuron releases a specific neurotransmitter: neuron types are often named by this principal neurotransmitter plus the suffix -ergic: a cholinergic neuron releases acetylcholine.
There are also similar molecules that do in fact act throughout the body, but we don't call these neurotransmitters, we call them hormones. Sometimes they are exactly the same molecule: epinephrine, also known as adrenaline, is both a neurotransmitter and a hormone; it can act as both because different receptors have different affinities, and the circulating hormone levels are typically much lower concentration than the amount that can be released in a more confined space.
Additionally, neurons have receptors for different neurotransmitters, so for example dopamine does not affect all neurons, only neurons that have dopamine receptors. Different cell types can also have different types of dopamine receptors, and those receptors can do different things to the cell. The same neurotransmitter could be excitatory to one cell and inhibitory to another.
Broad simplifications of nervous function such as:

Dopamine is also known to increase our feelings of lust

really don't say anything broadly about the function of dopamine. I could similarly say that computers control airplanes: that statement is true even though you will fine airplanes not controlled by computers and because you will find the vast majority of computers don't control airplanes. However, if I turned off all the computers in the world, a lot of airplanes would have their function impacted.
How do neurotransmitters get into neurons?
Most neurotransmitters are synthesized within neurons from other ingredients. GABA, for example, is derived from an amino acid glutamate. Glutamate itself is also a neurotransmitter. All neurons that release neurotransmitters have pumps that concentrate these neurotransmitters into vesicles. Neurons often also have transporters to pull released neurotransmitter back into the cell so it can be reused, for example a common class of psychoactive drugs are the serotonin reuptake inhibitors: these drugs inhibit the protein that pumps serotonin back into serotonin-releasing cells.
General statement
Use of knowledge from neuroscience to improve AI algorithms has moved far beyond what a novice can contribute to. If you want to utilize biology in AI algorithms, you have to be prepared to become an expert in both. I'd suggest starting with a basic neuroscience textbook if you want to learn about neuroscience, for example books by Purves' Neuroscience or Kandell's Principles of Neural Science.


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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:
Is intelligence correlated with neural calorie usage?
The human brain uses a lot of calories in comparison to other species, that is usually explained by referencing the intelligence disparity between Humans and other Animals. My question is how far does that go? Do individuals with radically improved intelligence also use radically more calories? And peripherally, does that caloric need place an upper limit on human intelligence?

Have often wondered this myself. Looking forward to an answer! People say the brain atrophies without use, like muscle, and its certainly true that bigger/more active muscles use more calories, so one would think this might be the case with the brain...

Bigger brains take more calories to build, and brain size has been conclusively shown to correlate with intelligence. The relationship is not strong, only very modest, perhaps a correlation of around $r \approx .3$. There is no doubt, however, that the relationship exists.

There is also, however, some evidence that more efficient brains are more intelligent. Efficient meaning here that they use less energy per processing power. This is not quite as clear as there is inconsistent evidence. See, for example, Richard Haier's book The Neuroscience of Intelligence.


text:
How can I estimate the total number of yeast cell in a medium?
So I want to run an experiment with yeast. I want to monitor the population as close as possible in regard to its size. I am aware I could use a colorimeter or such, but I can only get a microscope. Is there a way I can estimate the population with a microscope?

Determination of cell concentration using a microscope is usually done by using a hemocytometer, also called counting chamber or Neubauer-counting chamber.
Basically, you count the cells in a defined volume within a specific area. This way you can calculate the concentration in your medium and also the total cell count.
I found a good explanation especially for counting yeast cells here.

Is there a way to find the concentration without using a hemocytometer?

@BrianBlumberg You can plate the cells after serial dilution and count the colonies. Since you mentioned that you want to use a microscope, you need to use a haemocytometer; you cannot estimate true concentration on a normal slide. Also, haemocytometer is more accurate than OD, if the cells have different sizes.


text:
What species of mushroom is this?

Growing up in Oregon I don't remember ever seeing these. There are different mushrooms growing all over my backyard right now, but these look way different than all the others and there was only a small cluster of them in the corner, which caught my eye. Searching online and trying to match pictures it keeps coming back to Psilocybe Semilanceata aka Liberty Caps, which apparently are hallucinogenic.  Like I said  I've never seen these before growing up in Oregon, so I'm curious as to what they really are. I tried to upload a better picture, but it was too big of a file, so hopefully this one is good enough. Thanks in advance.

Hi and welcome to the site. Your mushroom is a bit old for identification I'm afraid. Try to take a picture when they are fresh and preferably at the place where they grow.


text:
Does someone know of a website that keeps track of a species population?
I am planning on doing some math on population growth, but I need a reliable source of data on population growth of some species over time. Does anyone know of a resource (website/publications/public repository) that has such information?

Why a website rather than a publication who kept track of population size over time? What kind of population dynamic are you looking for (exponential growth, logistic growth, stable population size, decreasing population size, ...). Any species of preference?

A publication or such would work, as long as I can get my hands on it. I prefer logistic growth, but the others would do just fine as it does not really influence my purpose.

Humans are currently going through a logistic looking growth, where the peak of growth (growth of $r$) has been reached in the 1970s. Those would be easy data to find and always pleasant to play with.

How about human?
You will find the data of human population growth on the webpage "Our World in Data". Scroll to the second graph, click on the tab "data" and download the .csv file.
Just google for any specific species of interest
Otherwise you can just google things of interest. Look for large emblematic mammals or commercially important species.

If you google "bald eagle population growth", you will easily find these data.
If you google "moose growth population breeding pairs", you will find these data.
If you google "killer whale population growth", you will find these data.
If you google "tuna population growth", you will find these data.

COMADRE
COMADRE is a database of animal matrix population models. It can be of interest to you.

Can we ask for resource names on Biology SE like the one asked here?

I think you can, yes. As long as what you're looking for is well defined. I am a bit confused by your comment. Are Anonymous and BrianBlumberg the same person or did you forget the hyperlink on the word "here"?

No, that is not me. Thanks for the information.  Do you know of other sources which provide information on the population number of other species/organisms?

@BrianBlumberg Please see edited answer.


text:
Is it possible to see the microbes on your hand without using UV light or a microscope?
I know that black light (UV) is often used to see the microbes (colloquially referred to as germs) on people's hands but is there any way by which we can examine the microbes on people's hands without having the surroundings be completely dark (what is required for black light to work) or using a microscope? I am trying to show a roomful of people the microbes on my hand but the surroundings aren't going to be completely dark and there is no way I can use a microscope.

The term germ is generally not used in biology as it is poorly defined. In general, it is defined as a microorganism, which would mean that by definition you can't see them with your bare eyes. I don't think a black light would be of any help though. You can detect specific disease with a black light but I don't think it would help you see individual germs (as they are too small by definition, at least if you want to define a germ as being a microorganism). What make you think a black light would help?

A germ is typically defined as a pathogenic agent. Is there any reason you want to find something that is pathogenic? Or maybe, you just meant that you would like to see a microorganism?

I understand germs isn't the best use of vocabulary. I meant microorganisms/bacteria. The answer about the agar plates works perfectly but now if I kill the microorganisms in a roomful of people, how can I show that the microorganisms are killed in front of them?

@aadityak_968 You should move your comment to the answer. You are commenting on the answer, not the question.

Given your constraints, the only solution available would require some amount of preparation. If you are so inclined, you can purchase sterile, ready-to-use agar plates online, which you can then inoculate with microorganisms from your hands by simply touching the agar surface with your palms, and letting the plates incubate at room temperature. A day or two's time should be sufficient for plenty of microorganisms to grow, allowing you to demonstrate that your hands have "germs" (although some of the microorganisms you'll find on your agar plate may very well be airborne contaminants if you don't take some precautions).


text:
Does the growth in size of hippocampus of London taxi drivers affect their net number of brain cells?
In the paper, London Taxi Drivers and Bus Drivers: A Structural MRI
and Neuropsychological Analysis in the Journal Hippocampus, the authors state that changes in the hippocampus of taxi drivers in London results from their specific occupation. The authors stated this was more pronounced than in bus-drivers.
What accounts for grey matter change? Do their brains have more brain cells than other people? Or the increased in size of the posterior hippocampus means some other region of their brain must have less brain cells to have enough to grow their hippocampus?

The study you linked was very interesting, and there is a reason that the authors of this paper and many others like it refer to grey matter density or grey matter volume.
From another study on grey matter (density), Neurolinguistics: structural plasticity in the bilingual brain,

Whether grey-matter reorganization in this region is related to changes in neuropil, neuronal size, dendritic or axonal arborization will be revealed by methods other than whole-brain magnetic resonance imaging.

Meaning, there's really no way to know without autopsy and histological studies whether this means more neurons, increase in neuron size, more dendrites, more connections between neurons, etc. So, the answer to your question is, no one knows exactly.
Histopathological studies are usually done on diseased patients (e.g. Alzheimer's), not healthy taxi drivers.
However, one mouse study of loss of hippocampal grey matter did correllate MRI studies and histopathological studies, with the result that

no changes in the number or volumes of the somas of neurons, astrocytes or oligodendrocytes were detected. A loss of synaptic spine density of up to 60 % occurred on different-order dendrites in the ACC and hippocampus...

Loss is not the same as gain, however, so the definitive cause cannot be ascertained yet.
Stress-Induced Grey Matter Loss Determined by MRI Is Primarily Due to Loss of Dendrites and Their Synapses


text:
How many cells should be seeded for passaging?
Do you count cells when you passage them?
I found that many people will according to a ratio (maybe 1：2 or 1：3，etc.) to subpackage. It is so indistinct!
What is the optimal seedling density or optimal original confluent in various sizes of cell culture dishes and flasks?
that's all, thank you!

This answer is relevant in case of cell lines and not so much for primary cultures

When I first started doing cell culture, I used to count the cells before passaging. The idea is to seed enough cells to keep the population viable but not so much that you have to re-passage within 2 days. However as I became good with the technique I stopped counting as I would have a decent estimate of how much to seed. For seeding cells for some experiments (transfection/drug treatment etc) it is crucial to count the cells.
How much to seed depends on what the division time of the cell type is and how much you need after a given duration of time. You have to calculate it accordingly. For example a fully confluent well of a 6-well plate will approximately have 1 million Hela cells (this number would vary for different cell types because of the difference in sizes). Hela cells have division time of ~17h (see this post). If you need ~70-80% confluency after 17h then you should seed ~0.3 million cells.
Likewise, a T-25 flask would have ~3 million cells in full confluency. So, if you need a confluent flask in 3 days you can calculate how much cells to seed.
See this table in Nunc website for number of cells at confluency and optimal seeding density for different culture vessels.
Note that some cells (mostly primary cultures) may need to be seeded at high densities because they may need contact with other cells for survival. So, I cannot give any authoritative answer for primary cultures. Moreover, since it depends on the cell type, all examples cannot be listed here.

I'd also argue that for special cases like transfected cells, where expression is subject to drift, you have to make a judgment call (based on experience) on whether you want to maintain or expand.


text:
Where does the additional 1 proton cost of oxidative phosphorylation come from?
I've been quite confused by the source of the additional 1H+ cost right now. I know it costs the F1Fo-ATP synthase 3H+  to produce an ATP, and it is also stated that:

ADP3−cytoplasm + ATP4−matrix → ADP3−matrix + ATP4−cytoplasm //
  ADP/ATP exchange is energetically expensive: about 25% of the energy yielded from electron transfer by aerobic respiration, or one hydrogen ion, is consumed to regenerate the membrane potential that is tapped by ADP/ATP translocase.(Wikipedia/ADP/ATP Translocase)

So in some books I find out that they regard the net cost of producing an ATP as 4H+. Here is another statement:

The phosphate carrier, which works in concert with ATP-ADP translocase, mediates the electroneutral exchange of H2PO4-for OH- (or, indistinguishably, the electroneutral symport of H2PO4- and H+). The combined action of these two transporters leads to the exchange of cytosolic ADP and Pi for matrix ATP at the cost of an influx of one H+. (Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002. Section 18.5, Many Shuttles Allow Movement Across the Mitochondrial Membranes.)

And my question comes here. Why do we not consider the effect of the process of ADP + Pi → ATP on the membrane potential? It also produces a net cost of 2e-. Putting these together, this will lead to 0, i.e. no additional net cost. Or should I only consider H+ but not e-?
(This might lead to another problem about H2PO4-'s breakup.)

The energy required for the ATP production by ATP synthase is obtained from movement of ions (H+ or in some cases Na+) downstream of their potential (proton motive force). I guess, there is no exact stoichiometric exchange as in case of ion pumps. The rotation of the motor is generated by the movement of protons through a channel. The H+/ATP ratio is estimated using biophysical/biochemical techniques.
Brand and Lehninger (1977) estimated this ratio to be greater than 3.
Turina et al. (2003) recalculated this ratio using constituted liposomes and their estimate is  3.9 ± 0.2.
This is an excerpt from a more recent study on chloroplast ATP synthase by Hahn et al (2018).

The symmetry mismatch between the 14-fold Fo rotor and the
  near-threefold F1 head means that the number of c subunits rotating
  past subunit a to generate one ATP is not an integer. cF1Fo requires,
  on average, 4.67 c subunits, or protons, to produce one ATP. The
  nearest integral numbers of c subunits per step would be 4, 5, and 5,
  equivalent to rotation angles of 103°, 129°, and 129°. Surprisingly
  however, the three conformations are separated by rotations of 103°,
  112°, and 145°, or 4, 4.4, and 5.6 c subunits (fig. S5C). This means
  that the position of the c subunits relative to subunit a in the three
  conformations differs.

The structure and efficiency of chloroplast ATP synthase may be a little different but what I want to emphasize is that there is no exact exchange of protons and ATP.

Thanks! Yes, that the calculations are just estimated from experiments is a fair point. But actually it was some statements from pratice problems when I studied biochemistry that cause some ambiguity, for example the contradictory statements 'ATP/ADP tanslocase adds 1 net cost to ATP production' and 'Pi/H+ transfer adds one'. But I will bear in mind that they're all rough calculations. I really thought the F1Fo-ATP synthase was symmetric (regardless of the change in conformation) just like the honeycomb before I read your answer.


text:
What are low-accumulating genotypes?
What are low-accumulating genotypes? And how does it differ from high-accumulating genotypes?

Certain organisms and strains of organisms can accumulate certain substances, such as Cd (a toxic heavy metal). If they accumulate those compounds more rapidly and in higher amounts, the organisms can be said to be high-"substance" accumulating organisms, e.g high-Cd accumulating organisms. The genotype which causes being a high-Cd accumulating organism can be described as a high-"x" accumulating genotype, like in this paper. A high-accumulating genotype without reference to a certain substance doesn't make much sense. These genotypic predispositions to accumulation are often used with toxic heavy metals like cadmium and arsenic which persist in the body.
As another "substance" example, high-"x" accumulating organisms is also used in the description of high-plaque accumulating organisms, e.g in this paper.


text:
Size constraints on CRISPR guide RNA
I had a quick questions on the size limitations of a CRISPR guide. More specifically on the shorter end. Can I make a guide that is say 7-10bp and still have an active complex? I transfect using an RNP system.
Just curious.
Thanks in advance.

You can definitely make such gRNA, but chances of off-targeting increases as you decrease the size of gRNA. It is always better to have 17-20 bp gRNA. However, you can check off-targets of a gRNA through several online tools.


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Why are Arabidopsis plant seeds being sent to the moon and not other seeds?
The latest Chang'e-4 rover brings an entire ecosystem with it, including Arabidopsis plant seeds and silkworms.
My question is: why Arabidopsis? Is this question conclusive without having to ask Chinese sources, such as just by having an educated guess as regards to the plant's own qualities?

Welcome to SE biology, please feel free to check our help center and take info tour to find out how  does it goes on this forum. I am afraid that this question is not suitable for this forum. Nevertheless, i think that the Chinese sent the plant there just because it is plant which is biggest model organism in plant physiology . We technicly know almost everything about this plant.

Without speculating further about specific decision making processes, Arabidopsis is the standard model organism in plant biology, similar to the mouse for mammals, the fruit fly for insects, C. elegans for nematodes, etc.
It's the first plant to have its genome sequenced, it's commonly used in undergraduate laboratory experiments in part because it grows very fast, etc.
If you were going to choose a plant arbitrarily for a research project, it might as well be Arabidopsis, I'd say it would be the default against which other options would be considered.


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Blood pressure in various blood vessels and heart
What are the typical systolic and diastolic blood pressure in arteries,capillaries, veins and the heart?
I know it must be highest in the arteries. arteries>capillaries>veins
Arteries: 120-80mmHg (systolic - diastolic). I also found mean values for capillaries (30mmHg) and veins (10mmHg) but not able to find systolic and diastolic pressure specifically.

Blood vessels have "compliance": that is, they are stretchy. Mathematically, this is very similar to capacitance in electricity.
The further from the heart you go into the vascular tree, the more the oscillations are dampened and the less it makes sense to think of systolic and diastolic pressures. In the capillaries and veins, blood flow and pressure is more or less constant rather than oscillatory (except in the most proximal veins where the motion of the heart again adds some pulsatile influences).
Therefore, for those vessels, you can just stick to mean values for pressure, the oscillations around those values are small.
See another Q&A: Why do people perceive blood pressure as the force that moves the blood forwards (see details)? that has a diagram showing the dampening of oscillations in pressure.

thanks a lot! and what can be said about the pressure in heart? I thought 0 during diastole and around 120mmHg during systole ( I thought during systole it is similar to that of arteries )


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Snake with red eyes and black skin found in a plant pot
It was found dead/stiff in an empty plant pot in a kitchen.

Could it be a young Höllenotter (a melanistic vipera berus, photo in Wikimedia Commons)?
Is the reddish/brownish part an injury? And what are the greyish parts (especially at the snout)?
Size (only estimated)
Diameter: 2.2 cm
Length (in this rolled-up state): 10–12 cm
Location
Western Germany.
In the kitchen were three plants pots in a row that were used for culinary herbs, one still had basil, the other two were empty for some time. It’s unknown if the snake was already there when the pot was emptied.

Are there any pictures, which are not out of focus? Or maybe a close-up of the head?

@JulPal: Unfortunately not, this is all what I’ve got (I didn’t make the photos).

For me it looks more like a leech or a worm than a snake. a better pic of the head would be more useful.


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Convergence compared to genetic distance
Is there an information (preferably in the form of a chart, though anything will do) comparing convergent evolution to how closely related the 2 species are on the tree of life.
My searches for anything touching on this subject have returned nothing
Context:
I was having a discussion with a friend on how similar we should expect alien life to be to earth. The topic of high levels of convergence on earth being indicative of convergence between life on Earth and life with a seperate origin on another planet came up. However it appears to me that convergence tends to happen a lot more in more closely related species, but I have no solid data for or against this idea. For example I don't think any plantae have developed any significant ability to move, like animalia have, which I find surprising as it is a very broad ability.
Please note my knowledge of biology is only on a general level.

convergent evolution is a concept. It does not take a value. It is not a variable to be plotted. What variable do you have in mind?

I know it's unlikely I'll get a chart as convergence is qualitative rather than quantitative. If there is a way that it is measured even in a more fuzzy way, a chart would be great but it's not required.

Technically, it is not qualitative either. It is not not numerical, ordinal, nominal, boolean or whatever. It is a concept. The question of how to measure depend upon what you want to measure and I am afraid we cannot define that for you. Note that among examples of distantly related species that undergo convergence evolution, there are bats and birds, flying squirrel and flying lizards, Euphorbia and Astrophytum, vertebrates and insect legs, dolphins and ichthyosaurs.

Among highly related lineages, the concept of convergent evolution is a bit hard to define though. How differentiated two phenotype must be so as to consider that two lineages have undergone convergence evolution if their phenotype converges. Note that we would rarely be able to detect such small deviations anyway. Another semantic issue is that the concept of convergence evolution can be defined for both phenotypic trait and genetic sequence. I here assumed you were talking about phenotypic trait.


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Killing microorganisms on agar plates?
If I grow microorganisms on agar plates and I expose them to UV light. How exactly will I know that the microorganisms have been killed? I was watching a video that showed spots in the petri dish where the microorganisms were killed when viewed under microscope but will this be visible to the naked eye? If not, is there any way that I can show without the use of a microscope the fact that the organisms have been killed?

It would help if you speficied the microorganisms in question. Some fungi grows when exposed to certain wavelengths of UV light

Looks like this is a follow up to this question on this forum.
The short answer to your question is you will not be able to indicate that a cell or colony on an agar plate is dead even with a microscope unless you are using fluorescent dyes (i.e., some form of live/dead staining). There are quite a few ways to do this, but they will all require that you have access to a microbiology laboratory.
Now, if your objective is to simply show that UV light kills microorganisms, this is easily done as an experiment with one target microorganism (i.e., one species). I'm going to obfuscate details aplenty here, but I'll offer you a description anyway.
You'll need replicate plates of agar colonies inoculated with the same quantity of the microorganism--this is typically achieved by propagating the microorganism in liquid medium and depositing equal quantities of the medium onto multiple agar plates. Once your plates have been incubated to obtain some colonies, retain one plate as control (this will not be exposed), and expose the remaining plates to your UV source. [Ensure that you've counted the number of colonies in every plate--including the control--before you subjected them to UV irradiation.]
Now comes the hard part. You will need to re-suspend the colonies from your plates in liquid media and re-plate them on agar. You can either choose a single colony from each plate (ideally, colonies that are similar in size across plates) for re-suspension, or you can re-suspend all colonies visible to the naked eye. Either way, re-suspend your colonies in liquid media, and deposit them on agar thereafter, and incubate the agar plates.
If everything went right, the number of colonies you would observe in the re-plated control plate should be higher than the number of colonies in the UV-exposed "re-plates." What that indicates is that at least some of the colonies that were exposed to UV irradiation died, and thus did not show up as colonies upon re-plating. This would loosely "prove" that exposure to UV irradiation kills microorganisms (with many, many caveats).
All that being said, I would not attempt this at home. To the best of my knowledge, this shouldn't even be doable at home without spending a significant amount of money to obtain some of the necessary equipment (which I have not described here). Further, doing this experiment in the format I described would likely yield very noisy results--the way I've described it is more back of the envelope experimentation than something proper.
If you are keenly interested in this topic, find the nearest microbiology department, and talk to a subject expert. They might even let you try this experiment out for yourself in their lab.
Edit - the core methodology I've described here is CFU counting (CFU - colony forming units).

Why bother inoculating liquid media when you can just replica plate onto fresh plates?

You could of course, but picking colonies is already messy enough, and I just wanted to offer a solution where the user didn't inadvertently end up streak-plating and end up with even more noisier data.

There is no picking colonies with replica plating though nor streaking? And you can easily calculate proportion of viable cells by looking at the original plate and the replica.

Sorry, I misread (and also misunderstood) your comment. I read that as "replicate", and didn't catch on (and I thought you were referring to colony picking). Would this actually work though? Per my understanding irradiation would not uniformly inactivate entire colonies, and it looks to me that replica plating an irradiated plate would yield an erroneous CFU count.

I'm not sure, that's why I asked you the question. If the UV radiation does not kill off all the cells then how would culturing colonies work? Wouldn't you just be growing up the survivors?

Per my understanding, if you have x number of CFUs prior (already present as y number of colonies), and if the stress has either killed some portion of the x CFUs (or put them in VBNC state), then you would only obtain < y number of colonies, since there would only be < x number of CFUs available for colony formation. I think the important thing that re-suspension in liquid media achieves is randomization of all cells (dead or alive) prior to plating, which you would not get from replica plating, and this is perhaps more "accurate" (notwithstanding CFU counting's own issues).


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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. :)


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Choosing viruses for influenza vaccine
When scientists choose viruses for the influenza vaccine based on biological and clinical data, what indicates that a certain strain will circulate and likely be dominant in a certain season?
Does a low HI titer (meaning antigenic novelty) for a virus antigen relative to an antiserum of a virus that is currently prevalent mean that the new virus will likely dominate in the next season? OR is a high HI titer a better choice for the vaccine since it means the virus in question is very similar to currently circulating viruses?

Again, the full answer is too complex to answer here. The CDC has a broad explanation (Selecting Viruses for the Seasonal Influenza Vaccine) and the WHO has a presentation summarizing the process (The WHO Vaccine Strain Selection Process: Review of the Evidence).
The major factor for choosing a new vaccine virus is based on surveillance from the preceding season and from the opposite hemisphere's season. The surveillance data shows which virus groups are expanding or shrinking. Antigenic variation (high or low HI titers) is also a part of the decision, but every season has a number of viruses that have low HI titers to the current vaccine and the real question is whether those occasional outliers are just sporadic, or whether they're showing signs of becoming increasingly common.
Interpreting whether particular virus families are increasing or not requires a lot of familiarity with influenza behavior, genetics, and antigenicity. You can look at some of the data used in strain selection on the WHO site, e.g. Recommended composition of influenza virus vaccines for use in the 2018- 2019 northern hemisphere influenza season.

Thank you @iayork. Can you tell me how one can gain familiarity with influenza behavior, genetics, and antigenicity in order to understand as much as possible? What book(s) should I read to understand this better?

@FIREREED I don't have a simple answer. You might find some of the chapters in The Immunological Basis
for Immunization: Influenza Vaccines interesting, and Trevor Bedford's web site and his NextStrain site may be useful.


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Trying to identify the tree in this picture. Shot from the Nepenthe restaurant, Big Sur, California
I'm trying to identify the tree in this picture. This was shot from the Nepenthe restaurant, Big Sur, California.
Any help is appreciated!
Thanks,
Robert

It's difficult to make out the leaves in the photo, but the tree in the foreground appears to be a coast live oak (Quercus agrifolia).  The tree has hairy lichen growing on its branches.

Thank-you for the quick response. Much appreciated.


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Does focusing on a certain part of the body increase electrical activity in that region?
I am batting around ideas for master's thesis topics and was wondering whether or not just focusing on an area of the body would cause of boost of  neuronic activity? Not sure whether this would fall under the rubric of a self-fulfilling prophecy of the mind, or some other secondary body function. I though it might be interesting to examine the relative differences between varying parts of the body and their respective degrees of responsiveness to intentional cortical activity, as directed by a person. If anyone has an answer please respond soon as I can't quite nail down how to search for a question like this online (finding specific phrases, etc.) Also, feel free top point me to any readings related to this (would-be) phenom.
Thanks!

Gut reaction, I don't think this is a solid thesis idea. If you attach an EMG to my finger, and then I concentrate on my finger, and then my finger moves (due to stray thoughts), there will of course be a whole bunch of action potentials firing. However, that's kind of trivial and not really that interesting.
If your theme is "weird EM effects in the human body", one possible decent idea (and one that's gotten some quantity of buzz in the recent past) would be to focus on the role of electric fields in wound healing. You could even add in an intentionality/focus angle, if you really wanted to.


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Why does sympathetic activity constrict pulmonary vessels?
I don't know understand why sympathetic stimulation constricts pulmonary vessels?
I thought that the sympathetic nervous system activated the body for physical activity. Physical activity would need more oxygen supply. Doesn't constriction of pulmonary vessels reduce the gas exchange?

Short answer
The sympathetic nervous system mediates the fight, flight and fright response. It constricts the arteries and arterioles to increase blood pressure, in turn pushing the blood to the muscles and other organs vital for physical activity.
Background
The sympathetic nervous system functions triggers the fight, fright, flight (FFF) response (Fig. 1). It provides the body with a burst of energy so that it can respond to danger (source: Harvard Medical School).
The FFF response is initiated in the hypothalamus by activating the sympathetic nervous system through the adrenal glands. These glands release epinephrine (adrenaline) into the bloodstream. Epi increases heart rate and blood pressure to push blood to the muscles, heart, and other vital organs. The person also starts to breathe more rapidly and the small airways in the lungs open up. This way, the lungs can take in as much oxygen as possible with each breath. Extra oxygen is sent to the brain, increasing alertness (source: Harvard Medical School).
In blood vessels, as you say, sympathetic activation constricts arteries and arterioles (resistance vessels), which increases vascular resistance and decreases distal blood flow. When this occurs throughout the body, the increased vascular resistance causes arterial pressure to increase (Klabunde, 2012). This enhances the distribution of oxygen already present in the blood.  I don't think the pulmonary circulation responds differently than that in the rest of the body. The stress response is meant to support the evasion of acute dangers. But indeed, chronic exposure to adrenaline may eventually lead to impaired oxygen exchange in the lungs (Krishnamoorthy et al., 2012).

Fig. 1. Fight, flight, fright response. source: Freelap USA
References
- Klabunde, Cardiovascular Physiology Concepts, 2nd ed. (2012). Lippincott Williams & Wilkins
- Krishnamoorthy et al., Anesthesiology (2012); 117(10): 745-54

This is a good answer for explaining sympathetic constriction overall but doesn't say much about the specific question regarding pulmonary circulation.

@BryanKrause, true, but I don't think the pulmonary circulation responds differently than that in the rest of the body. I adapted my answer accordingly.

The stimulation of sympathetic system in the lungs causes vasoconstriction of the blood vessels surrounding the lungs and causes dilation of the bronchioles. This increases the ventilation-perfusion ratio, allowing more oxygen to enter the lungs increasing the chances of oxygenated blood. The confusion could be from what happens when blood flow to a part of the lungs is occluded, in the normal systemic circulation, we would expect the blood vessel being occluded to dilate increasing blood flow, however, this is not the case in pulmonary circulation, the blood vessel constricts diverting blood to other areas of the lungs, so the lungs acts in a way to maintain its pressure and reduce shunt.

Neat explanation, good first answer. Just a minor nit-pick, but the post could be improved by adding citations, but I'm upvoting anyhow as it stands as-is. Welcome to Biology, enjoy the site.


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Why does the DSC peak have a bell shape?
I am studying Differential Scanning Calorimetry (DSC) and am not quite understanding why most proteins have a bell shape when the heat capacity is plotted against the temperature.
Also, I would appreciate if you could provide good sources on this topic (books, articles, etc).

This is just a guess, but it's probably because the heat measurement is actually measuring the sum of many, many molecules reactions. It is a fact of mathematics, rather than natural science, that forces such phenomena to approximately follow bell curves (i.e., Gaussian functions). Basically, the central limit theorem states that if you have many instances of the same (random) variables and average them together, then the result will look like a bell curve. Here, the local thermodynamic change induced by a single individual protein molecule, as a function of the temperature, is presumably that random variable, since the thermodynamic behaviour of each protein is roughly similarly distributed. The randomness comes from the essentially chaotic random movements of the molecules.
See here or here for more.

I guess the symmetry can be explained by the cumulative states of the ensemble. However, I can't think of a no reason for this peak to be Gaussian. People often confuse most symmetric shapes (including the bell shape) as Gaussian.

@WYSIWYG True, the CLT is not always appropriate. I am not familiar enough withe subject to comment definitively, but from looking up a few curves, they are decidedly non-Gaussian far from the peak point. I had merely guessed that each molecule's "peak" (denaturation/unfolding) could be viewed as an RV (so the solution is an IID sample), and the observation was composed of the avg over molecules. This formulation, of course, only says that there should be near-Gaussianity close to that point! But even this may well be physically inaccurate. Hopefully someone more knowledgeable can jump in. :)


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What does the spectrum of Chlorophyll fluorescence look like?
I've just posted the question Which spacecraft can see plants "glow" during photosynthesis during the day, and what wavelength does it use? in a different SE site. I can't remember the details of which spacecraft this was or how exactly it worked.
My question here is simply about light produced by vegetation during photosynthesis. In this question I've shown a hodgepodge of absorption or sensitivity spectra of photosynthesis, but what I'm looking for is an emission spectrum and some details about where in the process this light is produced.
The Wikipedia article Chlorophyll_fluorescence covers the topic in general and mentions 735nm but I'd like to be able to see a fairly accurate spectrum in order to compare it against absorption lines in the Sun's spectrum.
NASA's OCO-3: Watching Plants Grow and Glow: https://youtu.be/_x-VzdEeq0c

Not to be glib, but rather as a way of clarification, a google search for “chlorophyll fluorescence spectrum” returns a lot of results. Is there something else you are looking for?

@canadianer I'm not a biologist and asking well outside of my field. It's likely that someone knowledgable in photosynthesis will have a better sense where to look for something of high scientific quality and likely to be representative of the most common kinds of photosynthesis. Googling may bring lots of results, but some may be from esoteric species with unusual biochemistry, or may represent nonstandard experimental conditions. For qualitative results this googling was sufficient but here I welcome assistance from someone more knowledgable

I think for your purpose you should start, for example, with this link:
https://academic.oup.com/jxb/article/60/11/2987/533160
UPD:
Chlorophyllous tissues emit radiation of wavelengths approximately 680-760 nm. Source: Plant Physiological Ecolgy, Second edition, Hans Lambers, F.Stuart Chapin III and Thijs L. Pons, New York : Springer, c2008, p. 37, Box 2A.4 Chlorophyll Fluorescence

That looks like an extremely helpful reference, thank you! I will read it today. To be an answer to this question, it would be better to also include a reference that contained a spectrum as well. While there may be spectra in some of the references in that paper, they are likely to be paywalled and I won't have access for several days. If you can add a spectrum to your answer, that would be best.

@uhoh I've just updated the answer adding wavelengths diapasone

If you can find a spectrum but are having trouble posting its image here, let me know; I can help you with that. If you know a book and a page number, you might try to find it in google books and take a screen shot or add a link in comments.

@uhoh I have the book. Unfortunately, there is no image for the spectrum.


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DNA of identical twins
I read an article which says that identical twins have 100% similarity between their DNA, but they have different fingerprints. Does that mean the DNA is different in the fingers? What body features can be used to exactly identify the identical twins?

DNA is not the only thing in biology that determines a phenotype (observable trait, e.g. fingerprint). Far from it.
Traits can be affected by the environment (a very good example, temperature-dependent sex determination), stochastic (random) phenomena - these are know to occur in transcription ("reading DNA") or the decay of mRNA (messenger molecules which instruct protein building) - and by epigenetic phenomena. The degree to which DNA is actively read, or silenced, does not wholly depend on the DNA. In fact, this depends on the exact state of the cell or nucleus. Roughly speaking, cells in your brain (e.g. neurons) and the cells that line your lungs have identical DNA, but they are shaped, look, behave and react differently to the outside world. This is due to epigenetics, think of it as the life history of the cell.
Here's an analogy: reading the exactly same book can have different effects on people. The book is the DNA, its information unchanging, but the person and their exact status are the complicated world of the environment and the cell that is using its DNA for some purposes. PS. Terrible analogy but it may help.
By no means is my list exhaustive. Hope you can see how that identical twins with identical DNA can have a different shade of skin color (tanning!), different fingerprints (subtle and complex differences during digit development), or a different sense of fashion (psychology, cognition, what have you).

You hit on the most important points. However, it is also worth pointing out that identical twins don't actually have totally identical DNA. They split from the same embryo and there they have identical DNA, but during development mutations occur which makes identical twins not truly 100% identical. Very close to 100%, but not exactly.

Very good point. I've had the discussion with peers whether or not to include this point in discussions with a layman on these kinds of questions. Bit of a thought experiment: why aren't homozygotic twins perfectly identical? My gut response is not to bring DNA mutations into the answer. I'm sure you'll agree the contribution of somatic mutations to fingerprints is insignificant. Incidence of cancer in twins is much likelier to be caused by genetic history rather than a lifetime of mutation accumulation. But you're absolutely right, it could influence many (inconspicuous) phenotypes!


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What does the word specific epithet mean?
Is the species for Rosa indica and Mangifera indica 'indica' as you can see is the same in both. What does this signify. It is obvious that it has different species as they have different genus.

See the last line of my answer here.

Thank You @NatWH that cleared things up nicely.