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Is aquafaba readily digestible?
I have always drained and tossed the water from canned beans. My understanding has been that the water that canned beans are soaked and cooked in contains raffinose, the gas-causing sugars that humans can't digest. This University of Michigan page, referred to in the answer to an earlier question, says:

Rinse beans thoroughly and never cook beans in the water they've
  soaked in. It's loaded with the gas-causing raffinose sugars.

And also advises:

Drain and rinse canned beans. That will get rid of some of the
  gas-causing raffinose sugars (and almost half of the unwanted sodium).

Now that aquafaba is all the rage, though, I'm wondering whether my understanding is wrong. I understand that the bean water would taste mildly sweet and foam up so readily because of the raffinose. But it seems to me that aquafaba would lead to severe bloating and intestinal distress, as it relies for its properties wholly on the gassy and sugary nature of the bean water.
Am I mistaken in my understanding of the need to toss the water that one soaks or cooks beans in? Or is it just that fans consider the bloating and gas a price well paid for the delights of aquafaba?

Hi Verbose, what makes a question "about health" is the knowledge required to answer it. If you ask "is it digestible", then the person answering it would have to know which compounds are digestible, and that would be physiology related knowledge. If you ask "does X contain Y", this is indeed an on-topic question, no matter if you are asking because you think that Y is tasty, or undigestible, or cures acne. The source in your text did list a compound to look for, so I changed the title accordingly.

@rumtscho This question concerned the digestibility of aquafaba. Raffinose is not the only undigestible sugar. The person answering it would have to know what compounds are digestible, but that is not prohibitive. Most questions require an answerer to know the answer. I disagree with the title change and have reverted, I believe it changes the nature of the post too much and was not the author's intent. Note also that this question is specifically not "about health". But if you choose to revert again I will not fight it. Worst case this may be a question more appropriate for the bio site.

(I.e. edit doesn't seem right, migration would seem more appropriate)

@JasonC " The person answering it would have to know what compounds are digestible, but that is not prohibitive" - that is prohibitive, because this is exactly what takes the question into physiology, and makes it out of scope here. I know that the edited question is not equivalent to the original one, but I made the edit because the original one was off-topic. Your suggestion to migrate also seems like a good one, let's try it and see what happens.

I don't see how this is a biology question rather than a culinary question; I'm not interested in the chemical structures of the sugars themselves, nor in the mechanics of digestion. The question seems a natural follow up to the linked question about using the water from canned beans. If that water is inadvisable to use for cooking because of its indigestible and high sodium nature, then that naturally raises a question about its use as aquafaba. And that is a culinary question, not a scientific one. The migration is severely inconvenient

(Whoops, inadvertent send) because it prevents my accepting Jason's answer; even joining Biology doesn't let me do that, oddly enough, and merely clutters up my app feed with bio questions of no interest to me. So yeah, I disagree with the reasoning and the migration.

@rumtscho Well, that could've gone better, lol... Whistles and moseys on home

I think after a while it let me accept the answer, which mitigates some of my sadness at the migration, but I still think biologists would be less interested in this issue than cooks would.

@verbose it doesn't matter if cooks are interested - it is off topic for cooking. We could have closed the question on Cooking without migrating, or answered the partial question of aquafaba containing raffinose sugars, or migrated here. The option "stays on Cooking as it is" was never open, sorry.

@rumtscho you're the boss; it is unfortunate that you would unilaterally migrate the question without seeking off-topic votes from other members of the community, though.

@verbose Fwiw, if it helps: No matter what site it is on, it will still come up the same in web search results. Also Google does place some priority on SE sites, cause ya know, we rock.

Much of it is not readily digestible. According to this chemical analysis:

Finally the results presented here also indicate that the amount of digestible carbohydrates in aquafaba is minimal. For families with GLUT1 deficiency, where a diet with minimal amounts of glucose and carbohydrates digestible to glucose is required, aquafaba can represent an additional foaming or emulsifying ingredient, as an alternative to eggs.

It also contains proteins, presumably digestible. The carb and protein content is significant, according to the study, which implies a fairly decent proportion of undigestable carbs.

Thanks! The linked site is useful. But I'm missing something; where does it say "the carb and protein content is relatively low"? The portion quoted in the answer says that only the digestible carb content is low. The article explicitly states that the amount of proteins and the total carb content are somewhat high: "The results showed that aquafaba primarly contains both proteins and carbohydrates in considerable amounts".  The fact that aquafaba has a high proportion of carbs but few digestible ones does suggest to me that aquafaba would cause gastric distress.

@verbose No you are right. I was passing time answering questions during a stressful wait in the animal hospital last night and wasn't all there. I misinterpreted "detectable" as "barely detectable". I can't say for certain just from that article exactly what fraction is undigestable carbs but it suggests a significant portion. Also cursory research does suggest public opinion that blaming farts on the family dog is not a big price to pay for the many wondrous and magnificent delectations of aquafaba, or at least, nobody seems to complain about it or contest it.

I mean, you could just drink it for a few days and see what comes out. For science.

Yes, for science and keep a laptop by your bedside, and write copiously as quantities so of undegestable carbohydrates entering your large intestines and bowls are fermented by bacteria. We wish you luck and god speed.  And remember, you do this so that others will never need to experience the same tragic horror. For Science.

@JasonC I'm sorry to report that the "Honey, we need to get a family dog so I can try out aquafaba. For science" ploy didn't work. I'm still pet-less.


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What causes the variable/conserved structure in the 16S rRNA gene?
See the image below for a visual representation of the 16S rRNA gene. It is composed of conserved and variable regions however I can't see to find a reasoning for why this is the case

Thanks

Are you talking about the variablility/conservation and structure of the RNA or of the gene (which would presumably include other parts of the DNA)? If it's just the rRNA, you should remove references to the gene, as this is confusing. (Also, it's "its", not "it's" for the possessive of it, the pronoun, and other pronouns except one.)

It would also be useful if you could indicate your source so that an answer can be addressed appropriately. What have you read about conserved or variable regions?

I added an image to try to be more specific to the question. I'm talking about the gene, but obviously that impacts the RNA/protein and everything else.

Thanks: that helps. I used  to follow the literature on rRNA structure and will dust off my papers (so to speak) and get back. I must say I have never seen a diagram like that — where did you find it?

OK. Found a related paper myself and answered the question.

The structure of ribosomal RNAs involves double-helical stems, on the one hand, and loops or junctions, on the other. A comparison of small-subunit rRNAs of different sizes shows that, despite increasing complexity, a basic core structure exists. The is illustrated in the diagram below is adapted from Brimacombe, Trends in Biochemical Sciences (June 1984) 273–277.

From a structural (3D) point of view, both stems and loops are conserved, but as far as the nucleotide sequence is concerned, the helical stems are less conserved than the loops and junctions. This would appear to be because the main function of the helices is structural — so an A–U base pair can generally be replaced by a G–C (or U–A or C–G) base pair, whereas the loops are involved in interacting with various species — tRNA, initiation, elongation and termination factors, ribosomal proteins and the 50S subunit — which may involve more specific bases.
The main thrust of research on ribosomal structure (and what has interested me) is the relation of structure to function, but Carl Woese realized that, because of its ubiquity, rRNA was an excellent molecule for phylogenetic studies. Although, if one compares, say, mitochondrial ribosomes with mammalian ribosomes the sequence conservation is small, with different strains of bacteria it is much larger. This has led microbiologists interested in bacterial phylogeny to analyse the best regions for comparison in 16S rRNA, in terms of their degree of conservation, resulting in the concept of variable and conserved regions in the diagram in the question. (I find this terminology rather unfortunate because of its similarity to the totally unrelated immunoglobulins.) It appears that this is due to van de Peer et al. (1996), from whose paper I reproduce the figure below.

[Figure 3 of van de Peer *et al.*The most variable positions are in red, the most conserved in blue. Absolutely conserved positions are indicated in purple. Nucleotides present in E.coli but absent in >75% of the bacterial sequences considered are indicated in pink.]

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What is the purpose of the incus?
The three bones in the middle ear -- the malleus, the incus, and the stapes-- play a role in transmitting sound waves to the inner ear (the cochlea). I understand that the malleus is the bone closest to the tympanic membrane (and therefore the primary receiver of information) and I understand that the stapes is responsible for transmitting the information to the cochlea... so why even have an incus bone?

The incus is there in humans because it is there in our mammalian ancestors, and it is there in our ancestors because the mammalian three-bone ossicle system was inherited from early amniotes.
The synapsid ancestors of mammals had the ancestral jaw articulation between the articular (later called malleus) and quadrate (later called incus). This is the bottom image below. There are fossil species with a transitional form in which there are two jaw joints (e.g., Pachygenelus). In extant mammals, the jaw joint lies between the dentary and squamosal (part of the temporal bone), while the old articular and quadrate are part of the ossicle system (top image below).
There is a lot of material on the web about this:

http://crompton.oeb.harvard.edu/publications/transformation-quadrate-incus-through-transition-nonmammalian-cynodonts
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552421/
http://www.zoology.ubc.ca/~millen/vertebrate/bio204_labs/Lab_3__Skull.html

So in short, the incus is there because there was no other way for the mammalian ear to evolve from the ancestral system. It doesn't have a purpose per se, except that it's always (at least going back to jawed fishes) been attached to the stapes and articular (malleus).

Great answer thank you, so would there be a serious problem if a human was born without the incus, or if they had an ear infection that caused the incus to malfunction?

Nice answer +1. Interesting yet complicated material. I've added an answer from a functional perspective. Thanks for this excellent overview of the evolutionary perspective. I refrained from answering initially, given the dreaded duality in the "why is there X" anatomical questions. Kudos

Short answer
The incus forms a lever with the malleus, thereby amplifying incoming sound and aiding in the impedance-matching function of the middle ear.
Background
In addition to kmm's excellent evolutionary perspective, I'd like to add my two-cents worth in terms of the functional advantage of the incus.
The tiny bones in the middle ear (ossicles) constitute an important mechanism to increase auditory sensitivity. The auditory receptors of the inner ear (the hair cells) operate in a fluid environment, but acoustic stimuli enter the ear via air. When sound in air strikes a fluid boundary (i.e., a boundary between media with different acoustic impendances) 99.9% of the energy in the incoming sound may be lost due to reflection. This loss equals 30 dB, which is a substantial reduction in stimulus intensity and quite noticeable to a listener.
For what it's worth, as a personal anecdote - I have around a 30 dB loss in the 125 to 500 Hz frequency range due to genetic reasons and that substantially reduces my speech understanding, especially in noisy environments.
In order to overcome the mismatch in the impedance of air and fluid, the middle ear, which is interposed between the tympanic membrane and the oval window, is designed to amplify the incoming sound. This process is referred to as impedance matching.
There are two major middle-ear structures in place that passively amplify sounds:

The tympanic membrane;
The malleus-incus lever.

The effective area of the eardrum is about 21 times that of the stapes footplate. Thus, the force caused by a given sound pressure in the air acting on the area of the eardrum is concentrated through the ossicles onto the small area of the footplate, resulting in a pressure increase proportional to the ratio of the areas of the two structures which, in humans, is about 21:1.
It also happens that the lever arm formed by the malleus in rotating about its pivot is somewhat longer than that of the incus, giving another factor of about 1.3 in pressure increase.
The 21x of the drum/footplate area ratio, multiplied by the 1.3x lever arm factor, yields about a 27.3x increase in pressure, which is 29 dB, thus just about overcoming the theoretical 30 dB loss due to the air/liquid interface. Hence, the middle ear matches the acoustic impedance between the air and the fluid, thus maximizing the flow of energy from the air to the fluid of the inner ear (Fig. 1).

Fig. 1. impedance matching properties of the middle ear. source: Wisconsin University
Impairment in the transmission of sound through the middle ear creates a conductive hearing loss.
Source
- Wisconsin University

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Cytochrome Oxidase activity in neuronal cells
The abstract of this article says
"...the entire neuron is often not metabolically homogeneous; most of the oxidative activity is usually found in dendrites."
Why would the activity of cytochrome oxidase be localized in the dendrites of the cell? Is it because it has a greater surface area (more channels and such) compared to the rest of the cell?

How would oxidative activity mean only cytochrome c oxidase? It could mean more oxidation of glucose, which could be due to presence of more channels in dendrites than axon.

@Metroplex I do not know, the article is talking specifically about histo- and cytochemical methods for mapping activity of cytochrome oxidase. I do not have access to the full article (I'm working on finding it), but I thought asking "where's the full article" would be an inappropriate question.


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Being able to write/type different texts using each hand respectively, at the same time?
Has there been any documentation of being able to either write down (jot down) or type in (key in) different texts using the left hand and the right hand respectively, simultaneously?
So, I'm interested in whether or not it has been documented that certain individuals can do this, and I would be greatly interested in any literature on the subject. For example, have there been any pedagogics who have argued this exercise would be beneficial for the development of individuals?
Note: Of course, many people could do this, if they would do it extremely slowly; so obviously I am interested in the maximum velocity.
See also: Being able to read one text in braille using sense of touch and, at the same time, read another text visually?

If so I'd also be curious to know if said texts were arbitrary, since some, or perhaps even many, people could probably learn to type a very specific sequence quickly with a lot of practice. Also curious to know about keystroke timings, I imagine the ability to type two texts completely independently is very different than, say, alternating keystrokes. Former is much more multitasking, latter is coordination. For instance, one who can type on a regular keyboard effectively with either hand could imagine both hands were on the same keyboard and type arbitrary msgs, but that's not impressive.

US President James Garfield is the first person who pops into my mind. I believe Leonardo da Vinci also could, but I might be wrong...


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What does DNA taste like?
I've seen plenty of speculation online, but does anyone know of a scientific study or have a definitive argument?
I'm thinking probably not sweet, because the deoxyribose sugar is bound in the structure of the helix. Salty, due to group I counterions? Bitter due to the alkaline phosphate groups? I'm guessing not sour, because despite the name nucleic acids are in their conjugate base form at physiological pH. I've read some nucleotides can activate the umami/savory taste, would this be significant?
I am aware essentially everything we eat contains DNA, but I'm interested in the taste of DNA itself, pure/isolated if necessary you like.

I'm voting to close this question as off-topic because it is not about biology in the terms of this list.

Where can the list be found so I can review? I feel it is a question about a biological sensation of a significant biomolecule. Is there a SE site that is more applicable?

This is a valid question. It asks for objectively verifiable answers. Tastes are not subjective. Nobody in the entire universe tasets glucose to be bitter. Even if we have deseases that cause deviations in taste, we still can resort to statistics. Most of people would taste the same, because that's statistical mode.

Youtube chemist NileRed chemically extracted DNA from strawberries in this video, he also tastes it if I remember correctly: https://www.youtube.com/watch?v=araeHtN_3Lk
TL;DW: He gets the DNA from the strawberries and says it has a slimy texture as it isn't soluble, and it tastes salty more than anything. Note though that this could be from leftover reactants from the reaction, so take this with a grain of salt.


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Why don't all organisms reproduce asexually?
According to a comment at Why are not all species hermaphrodites?, asexually reproducing species go extinct more easily. However, I don't think sexual reproduction is a true evolutionary stable strategy. Since humans reproduce sexually, somebody with resistance to malaria and no sickle cell anemia can produce a kid with sickle cell anemia. For any sexually reproducing species, if a mutant asexually reproducing individual that happened to have the right genome arose, her clones would outcompete the rest of the species because almost none of them would produce an offspring with a bad trait, because they have weaker genetic drift against advantageous traits and so have a larger amount of some of them, and because they would be so slow to evolve by genetic drift to be unadapted to all those future sudden changes in the environment that they're already adapted to. Wouldn't an asexually reproducing snail from a species that snakes eat with the mirror image form from most of its species have the advantage of being harder to be eaten without having trouble finding a mate. Maybe just like humans could evolve to have resistance to malaria without the risk sickle cell anemia if they reproduce asexually, maybe if a mutant asexually reproducing cheetah with the genome that would make its clones spread arose, its clones would evolve to be furless poikilotherms that can thrive the low night temperatures because that would enable them to chase their prey longer before they became too hot to continue the chase because they would start at a lower body temperature, and individuals with that trait would never produce an offspring with any costly trait that comes with it except for a tiny costly trait.
In addition to that, if a mutant female asexually reproducing individual arose in a sexually reproducing species with the right genome and the species currently was in an evolutionary stable strategy with monogamy with each couple just able to get food fast enough to rear two children, the mutant female would also get a mate and with his help still be able to get food fast enough to rear two children both of which have entirely her genome, and then her asexually reproduced clones would spread very quickly. Once the species reaches a new evolutionary stable strategy where each individual can only get food fast enough to rear one child because there are so many females taking the available food, they may still have a slight evolutionary advantage over other species that's not nearly as high as the evolutionary advantage of asexually reproducing individuals was over sexually reproducing individuals of the same species earlier.
Source: https://www.ncbi.nlm.nih.gov/pubmed/16217668

The overwhelming majority of species in the animal kingdom reproduce sexually, yet you don't think sexual reproduction is a true evolutionarily stable strategy?  Is it just a fad that will be abandoned within the next billion years?

The question at http://biology.stackexchange.com/questions/5148/why-are-not-all-species-hermaphrodites is a good question. I don't see why this one wouldn't also be. I think a lot of people who can answer that question can also answer this one.

Please link to the comment you are referring to in the other question. If it does not contain a citation supporting the claim that asexually-reproducing species go extinct more easily, please provide your own citation supporting it.

The evolution of sexual reproduction is a big and very common subject in evolutionary biology. As your question is not very specific, you should probably just start by reading the wikipedia article to get familiar with the main hypotheses.

Read about Muller's ratchet. If you think sexual reproduction is not an ESS but it exists in nature then perhaps your model is wrong and you need to revise it. Also look at this post

Just because a mutant with a certain trait would spread if it arose doesn't necessarily mean it's going to just happen to arise in the first place. When I say sexual reproduction is not a true evolutionary stable strategy, I mean that if a mutant asexually reproducing individual with the right trait arose, it would spread and resist going extinct after the next sudden change in environment. Most of the existing asexually reproducing species went extinct because they didn't have the trait that made them already prepared for those sudden changes in environment that happened later.

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What are the different causes for a snail species to have chiral dimorphism or speciate into a new species of the opposite form?
One way for the snail species to have complete chiral dimorphism where one form is an identical mirror image of the other form is if one form can't reproduce with the other form and it's predator is a species of snake that also has chiral dimorphism. If the snail species has chiral dimorphism and and one form can't reproduce with the other form but the species of snake that eats it does not, that means each individual snake of that species can eat either form and the evolutionary stable strategy is to have a mixture of both forms of snail in unequal proportions; if one form becomes more common, the snake will evolve to change a tiny bit in shape to be better at eating that form and less good at eating the other form so that form will evolve to be less common again. If the species of snail reproduces asexually and has chiral dimorphism and the species of snake that eats it also does, then the evolutionary stable will also be for both forms of each species to be identical mirror images occurring in equal proportions, even if it's very rare for in individual snail of that species to be eaten by a snake. If an asexually reproducing species of snail has chiral dimorphism and the species of snake that eats it doesn't, then both forms of snake will still occurr in equal proportions but the random fluctuations from that equilibrium will be larger because it will be the snake's brain adaption that makes it better at eating the more common form but its brain will already be so well adapted to eating both forms. According to Remi.b's answer at Does the species of snake that eats Amphidromous inversus have chiral dimorphism? and https://www.ncbi.nlm.nih.gov/pubmed/16217668, Amphidroumous inversus has chiral dimorphism occurring in very nearly equal proportions and one form can reproduce with the other form but the species of snake that it's it doesn't have chiral dimorphism. Maybe it can be treated very much like the case where the snail species reproduces asexually and the snake does not have chiral dimorphism but one form isn't quite an identical mirror image of the other form because the identical mirror image of either form would be less able to reproduce with that form and the species of snake that eats it is very close to symmetrical but isn't quite because the two forms of snail aren't identical mirror images. How can predation cause mutants of the rarer form of snail to arise and evolve into a different species entirely? Is it really because no mutants of the predator species of the mirror image form arise getting it into the evolutionary stable strategy where the predator and prey both have chiral dimorphism occurring in equal propertions?


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Why aren't more prostate glands just removed?
Some 80-90% of men have some problem with their prostate gland as they get older. Beyond about age 60 it is unlikely that men will need the prostate to contribute to seminal fluid, so there seems little point in keeping this troublesome organ - yet a huge proportion of older men end up with either benign prostate hyperplasia and/or prostate cancer. So why isn't the standard treatment just to remove the prostate altogether?

Are you saying men older then 60 don't need sexual lives?

Apart from the 0.4 to 3.0% of people who aren't interested in sex (depending upon who's survey you believe) sex is, of course, important. But the prostate only produces about 30% of seminal fluid, whilst at the age of 60 the chemical components generated by the prostate are unlikely to be needed to impregnate anybody.

Almost all men will experience erectile dysfunction for several months to a year after a radical prostatectomy - http://www.harvardprostateknowledge.org/achieving-orgasm-after-radical-prostatectomy

Your question is along the lines of "Many women will develop breast cancer, especially later in life. Why don't they just remove their breasts after menopause, because they won't need them for breast feeding?" There are a lot of disadvantages and only questionable advantages.
Chief among the effects of removing the prostate are urinary incontinence and erectile dysfunction. That area of the body is very highly innervated, and it is nearly impossible to just remove the prostate without damaging anything else. While it is true that many men will develop prostate problems as they get older, they can frequently be treated medically, or just observed for any dangerous changes. Benign prostate hyperplasia is just that - benign - so there's no need to undergo a major operation with significant side effects. Additionally, many prostate cancers are so slow-growing that they never metastasize or pose any threat, so they are simply monitored and treated medically as needed.


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Why are there relatively more predators on the land than in the oceans?
Our biology teacher told us that among worse conditions one of the reason that intelligent life had actually evolved on land is that there is a more important selective pressure due to the bigger number of predators.
Is there really relatively fewer predators (in numbers) on the land? What is the cause of this phenomenon?

I wouldn't say that conditions are poorer on land, but it's definitely more diverse (as you say). But I'm not sure that this is the cause, as I think many of the fish species are predators to other fish species or marine organisms and microorganisms. And although I don't agree with the term "intelligent life", we do have marine organisms, such as dolphins, for which we give anthropocentrically intelligent characteristics.

Check this out. It won't answer your question on the predators, but maybe give some more ideas and opinions on the matter of intelligent life (just found it looking after I saw your question): http://www.pbs.org/wgbh/evolution/humans/intlife/index.html?fy

@BioGeo Thanks but I actually argued that marine is more diverse (I imagined harsh conditions such as a desert or polar areas :) but you're right, maybe I can imagine better that there are lot more diverse climates due to the changing climate on the land

Is the question "Are the more predators on land? (In (relative?) number of species or in (relative?) number of individuals?)" or is it "Why are there more predators on land?". If the question is the second one, then a citation is needed but I guess you are rather asking the first (on of the first actually) question.

I wouldn't say conditions on land are poorer... just more unstable, less predictable over a span of a million years. And an unstable environment appears to be one of the factors in the evolution of human intelligence. ie the environment changes faster than evolution can adapt the body... so one solution is to adapt the animal's behavior which requires intelligence.
That said, dolphins too are plenty intelligent. Octopus also are quite good puzzle solvers.. but are short lived.
As for predator -prey ratio https://www.mcgill.ca/newsroom/channels/news/why-arent-there-more-lions-254873 Here is something to read. Predator-prey ratio appear to be govern by the rate of growth of prey items
And prey in the ocean has a faster turn around in the ocean.. so there are more predators in the ocean than on land. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4240998/.

Sorry, I think you haven't answered the question (I'm sorry for bad formulation) if there is bigger predator-prey ratio on land.

The ratio of predator to prey is higher in the ocean than it is on land. So the predator prey ratio is not the cause for intelligence.


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What is/are the effect(s) of altering the Tris concentration on polyacrylamide gels?
Why do we use two different concentrations of Tris (i.e. 1.5M Tris in resolving gel and 1.0M Tris in stacking gel)? For the gel to run properly there needs to be a different pH, but that can be done with with same Tris concentration and altering the HCl concentration.


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DNA Structure and Function
In a strand of DNA, why does identifying the 3' side and the 5'side matter? Or the 3' --> 5' strand and the 5' --> 3' strand? Also, what is a single strand of DNA called, is it just a helix, or is the helix just the backbone?

These are basic questions that a careful reading of a textbook can answer. If you post to this list you need to show evidence of having made an effort to find the answer to the question. I suggest you refer to Wikipedia or, better, texts available in NCBI bookshelf and then edit your question. The link is: https://www.ncbi.nlm.nih.gov/books/?term=dna+structure. Biochemistry by Berg et al., Molecular Biology of the Cell by Alberts et al., or Molecular Cell Biology by Lodish et al. are all well-written and authoratitive.

A double strand is a helix, as the basepairs move with a horizontal angle with each step to the next basepair. Identifying the sides is important for DNA-replication and RNA synthesis as the way DNA is read is from 3' to 5' so that the complementary bases can be ''glued'' together from 5' to 3' in which the phosphate groups bind to the OH groups of the other molecule by a polymerase reaction.
Disregard first answer.
There.

Well, a single strand of DNA is called a denatured chain ... Basically, it has the structure of RNA

A single strand is a helix, as the basepairs move with a horizontal angle with each step to the next basepair. Identifying the sides is important for DNA-replication and RNA synthesis as the way DNA is read is from 3' to 5' so that the complementary bases can be ''glued'' together from 5' to 3' in which the phosphate groups bind to the OH groups of the other molecule by a polymerase reaction.

Welcome to SE Biology. When you answer a question here you need to back up your assertions with references. Otherwise nobody can determine whether or not they are correct. In this case you are certanly incorrect in stating that "a single strand is a helix". There is no reason for a single strand of DNA to adopt a helical conformation and it is unlikely to do so. It certainly will not adopt the double-helical formation as that requires base-pairing between two strands.


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Are there any animals that get smaller as a normal part of their life cycle?
It seems that at any given moment in a creatures life, it either grows bigger or has stopped growing.
The only exceptions I know of are extreme events like insects undergoing metamorphosis or evolutionarily irrelevant effects like humans shrinking a bit at old ages due to their spine getting compressed (I consider it irrelevant because for most of human history, people old enough for this effect to be significant enough were either dead or long done with reproduction).
Are there any animals that are known to "grow smaller" over some period of their lives as a purposeful part of their biological functions?

Are you asking about decreases in length, volume, weight, or all of the above?

In holometabolous insects it is quite common for the final larval stage to be heavier than the adult stage. For instance, Goliathus beetles, which are among the largest insects on earth, the adult stage often weighs about half of the final larval stage (which weigh 80-100 grams).
The same situation can be seen in the Hercules beetles, which this picture of both larvae and adult of Dynastes tityus clearly shows:
.
(picture from http://harrellhouse.com/in-the-museum-eastern-hercules-beetles/)

Sorry, I just saw that you mentioned metamorphosis in your question, which I managed to overlook. I'm leaving the answer either way, since some might find it useful.

here's some, a jellyfish and a frog: https://www.reddit.com/r/askscience/comments/5lse3t/are_there_any_animals_that_get_smaller_as_a/

Animals behaviour may lead to a weight reduction, although this is not a reduction of the structure itself: the number of organs (for sure) but also of sub entities within organs (number of brain lobes e.g.) remains the same but some of these may reduce in size in a regulated manner.
This is most obviously the case in hibernation, but has also been evidenced in non-hibernating mammals and is termed Dehnel's phenomenon.

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RNA interference
If dsRNA is produced through a mutation (such as forming of a hairpin structure) in a particular gene and RNAi has become possible because of that, will an organism which is a heterozygote to this gene (whereby one of his alleles has the mutation and one doesn't) have his healthy allele be partially unaffected by the dominantly mutated allele when the siRNA doesn't fully bind to the healthy allele?

Josh - try editing your question... you have written one extremely long run-on-sentence that is difficult to follow (if you break it down and edit it will make it better)


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Why don't we build up an immunity to sore throat?
We often get sore throats once or twice a year, and it clears in a few days sometimes without any antibiotics. I was wondering why doesn't our body become immune after clearing a sore throat?

Sore throat is mostly a symptom of viral infection. So this post is relevant.

 Short Answer

It should be noted that there are many non-pathogenic causes of sore throat, and I would suspect that you are not always distinguishing these causes from actual illness.

In most cases, it would not be possible to build a response (immunological or otherwise) to avoid reacting to these stressors.

Bacteria and viruses mutate frequently in ways that make your immune system unable to properly recognize them to ward off initial infection.

Your immune system recognizes specific pathogens based on structural characteristics. If those characteristics change when pathogens mutate (which happens fairly frequently), your immune system will not recognize it as readily (or initially at all).

 Long Answer
Sore throat is most commonly attributed to pharyngitis, or the inflammation of the back of the throat called the pharynx.
Causes
Sore throats can be caused by many things. (e.g., see here, summarized below):
First off, a sore throat can be the result of many things unrelated to illness:

Allergies
Dryness
Irritants
Excessive talking,singing,shouting,etc.
Muscle Strain
Gastroesophageal reflux disease (GERD)

As a result, at least 30+% (higher in adults) of reported sore throat cases (and supposedly many more unreported cases) are not due to any type of illness.
Further, a number of pathogens can cause a sore throat:

Viruses

Rhinovirus, coronavirus, influenza, parainfluenza, adenoviruses, Epstein–Barr, etc.
(see here for one estimate of relative etiologies).

Bacteria

A number of bacterial infections can cause a sore throat. The most common is Streptococcus pyogenes (aka "Strep A").

It turns out that pathogen-caused pharyngitis is fairly common. Supposedly 10% of adults with sore throats have strep, and around 70% of children pharyngitis cases seen by doctors are either virally or bacterially caused.

However, it should be noted that only 20-30% of children and just 5-10% of adults have bacteria to blame for their sore throat, with viral infections being much more common. (source: IDSA).

Sore Throat Frequency
It turns out that sore throats are fairly common; Jones (2004) determined that about 7.5% of people have a sore throat in any three-month period. Further, on average, adults get a sore throat two to three times a year and children about five times a year (Tamparo 2011 and Rutter & Newby 2015), so your personal experience is fairly average.
Because viral causes and non-pathogenic causes make up an overwhelming percentage of overall sore throat cases, it shouldn't be surprising that most sore throats clear up without the use of any antibiotics.
As for those that are caused by pathogens:
Why no Immunity?
Bacteria and viruses both mutate fairly quickly (see Antigenic Variation, Antigenic Drift and Antigenic Shift), so it shouldn't be surprising that you're capable of having an immune response to pathogens throughout life.

If we consider just strep alone, it mutates/reemerges with improved fitness frequently (e.g., see Bao et al 2016 and their citations)
And see Sanjuán et al. (2010) for a reviewof viral mutation rates.

So not only are there a number of pathogens that can cause sore throat, but each of these pathogens can mutate. That leaves you with a fairly sizable number of potential invaders that can illicit a sore throat.
Let's See How Your Immune System Responds:
Your immune system contains cells that can be split into two broad groups: cells that belong to the adaptive immune system, and cells which belong to the innate immune system. [See here for a simple explanation].

Innate Immune system: consists of cells responsible for initial detection of pathogens, recruitment of other immune cells, activation of the complement system, engulfment and (more immediate) destruction of pathogens.
Adaptive immune system: consists of cells which coordinate to develop a memory of the infections they've seen previously in order to mount a faster, more pronounced immune response to repeat pathogens.

Depending on the kind of foreign invasion, two different immune responses can occur in either of these 2 broader "systems": either a humoral response involving antibodies or a cell-mediated repsponse.

A general feature of the immune system is that these mechanisms rely on detecting structural features of the pathogen or toxin that mark it as distinct from host cells (see Chaplin 2010 for a review). The mechanisms permitting recognition of pathogenic/toxic foreign structures can be broken down into two general categories:

hard-wired responses encoded by genes that recognize molecular patterns shared both by many microbes and toxins that are not present in the mammalian host. This is the innate system described above.
responses that are encoded by gene elements that somatically rearrange to assemble antigen-binding molecules with extreme specificity for individual unique foreign structures. This is the adaptive system described above.

Antibodies recognizes a unique/specific molecule of the harmful agent, called an antigen, and binds to it to tag it for immune attack.

Because the adaptive system is composed of small numbers of cells with specificity for any individual pathogen the responding cells must proliferate after encountering the antigen in order to attain sufficient numbers to mount an effective response against the microbe or the toxin. [Source: Chaplin 2010].

This means that you can still experience some mild symptoms due to the invading pathogen.

The important take-away from all this, though, is that your immune response relies on structural "markers" on pathogens in order to recognize them. This is true for both innate and adaptive immune responses. If the physical/structural properties of a pathogen change (due to antigenic processes and mutations as mentioned above) your immune system will be slower (and possibly ineffective) in responding to an attack.

The result, then, could be another one of those sore throats...

Citations

Bao, Yun-Juan et al. “Phenotypic Differentiation of Streptococcus Pyogenes Populations Is Induced by Recombination-Driven Gene-Specific Sweeps.” Scientific Reports 6 (2016): 36644. PMC. Web. 17 Mar. 2017.
Chaplin, D. D. (2010). Overview of the immune response. Journal of Allergy and Clinical Immunology, 125(2), S3-S23.
Jones, Roger (2004). Oxford Textbook of Primary Medical Care. Oxford University Press. p. 674. ISBN 9780198567820. Retrieved 4 August 2016.
Rutter, Paul Professor; Newby, David (2015). Community Pharmacy ANZ: Symptoms, Diagnosis and Treatment. Elsevier Health Sciences. p. 19. ISBN 9780729583459.
Sanjuan, R., Nebot, M. R., Chirico, N., Mansky, L. M., & Belshaw, R. (2010). Viral mutation rates. Journal of virology, 84(19), 9733-9748.
Tamparo, Carol (2011). Fifth Edition: Diseases of the Human Body. Philadelphia, PA: F.A. Davis Company. p. 356. ISBN 978-0-8036-2505-1.


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Quinone A, Quinone B, Ubiquinone, Plastoquinone: whats the difference?
I am getting very confused about this. My understanding so far is that ubiquinone is used as an electron (and proton) carrier in oxidative phosphorylation in the mitochondria whereas plastoquinone is the carrier in the light dependent reaction in photosynthesis in chloroplasts. My guess is that these carriers are similar because it is a highly conserved carrier that was present in many of the original life forms (including those that formed chloroplasts and mitochondria).
My first questions are:

is the above distinction correct?
do we find ubiquinone and plastoquinone elsewhere in cells, other than in mitochondria and chloroplasts, or in other prokaryotes?

Then I am not sure about quinone a and b. My lecturer said that quinone b is present in photosystem II and it accepts the two electrons from the lysis of H2O and then it accepts two H+ ions from the stroma to enter the membrane of the thylakoid
But I have also read that it is plastoquinone which shuttles the H+ ions in the thylakoid membrane in the form of plastoquinol. So could it be that quinone B turns into plastoquinone on accepting the electrons, and plastoquinone accepts two H+ ions to form plastoquinol?
If so, how is the quinone B from photosystem II replenished?

Difference between Ubiquinone (UQ) and Plastoquinone (PQ)
Structural Difference: Structurally, UQ and PQ are very similar. They only differ in a methyl group and 2 substituents on the benzoquinone ring (Liu et al, 2016). See the image for comparison:

Functional Difference: Functionally, PQ and UQ are very different. I'll give some differentiation points:

PQ is located on thylakoids of chloroplasts (Millner et al, 1984), whereas UQ is located primarily on the inner membrane of mitochondria, though it is found in all cells and membranes (Turunen et al, 2004).

Half-life of PQ is 15 hours while that of UQ is 30 hours in spinach cells (Wanke  et al, 2000).

UQ10 influences expression of hundreds of human genes involved in different cellular pathways, and UQ10-mediated gene-gene networks are involved in inflammation, cell differentiation, and peroxisome proliferator-activated receptor signaling (Schmelzer et al, 2011).

On the other hand, the redox state of PQ pool controls the NADPH dehydrogenase complex activity and further influences on cyclic photosystem I (Ma et al, 2008).

Although UQ has more widespread effects than PQ, most of their effects are restricted to their corresponding organelles i.e. UQ mostly influences mitochondrial activity whereas PQ mostly influences chloroplast activity. This can be understood on the basis of endosymbiotic theory since mitochondria appear to be related to proteobacteria whereas chloroplasts appear to be related to cyanobacteria (Mereschkowski et al, 1905). These two are thought to be taken in by cells about 1.5 billion years ago. We can suppose that at that time, both these organisms had similar carrier molecules (since they are very crucial for metabolism). This can justify why UQ and PQ are so similar in structure. Thus, your way of distinction can be considered as correct.
Difference between Quinone A (QA) and Quinone B (QB)
Structural Difference: In many cases, both QA and QB are structurally identical. For example, both QA and QB are ubiquinone-10 in Rhodobacter sphaeroides (Laszlo et al, 2004). Thus, the main difference between the two is functional difference.
Functional Difference: The distinct physical properties of QA and QB, including redox potential, are controlled by interactions with the binding site environment. Studies have shown that the 3-methoxy oxygen of QB interacts with the reaction center backbone (specifically amide of GlyL225). This interaction pattern serves to break the symmetry of neutral UQ between QA and QB by locking the 2-methoxy dihedral angle of QB in a position conducive to electron transfer from QA to QB (Vermaas et al, 2015). In short (not going in further details), QB interacts with the amino acid residues in reaction center in such a way that QA and QB acquire large difference in redox potentials. Apart from this, since QB is more loosely attached to the membrane, it is easily detached on being reduced to QH2 for transferring high energy electrons taken from QA to cytochrome bc1-complex8.
Thus, it is hard to differentiate QA and QB on structural basis, although QB and QA have different redox potentials due to different environmental conditions. Also, it is hard to tell whether QA and QB are structurally similar in all organisms; it is only known that they both are UQ10 in Rhodobacter sphaeroides. So, there is no simple answer (yet) on whether QB converts to plastoquinone or not. But since, in Rhodobacter, QA and QB are UQ10, thus it is not possible to convert QB to plastoquinone by this species. On the other hand, in a photosynthetic bacterium Rhodopseudomonas viridis, both QA and QB are plastoquinone molecules (Deisenhofer et al, 1994). Here, there is no need of conversion of QB to plastoquinone since it is already a plastoquinone. This finding only strengthens the fact that it is not easy to give a simple answer on whether conversion of QB to plastoquinone actually takes place or not. A much similar reaction center, from a thermophilic cyanobacterium Thermosynechococcus elongatus, looks like this (Ferreira et al, 2004; Loll et al, 2005; Umena et al, 2011):

Talking about replenishment of QB, when QH2 reaches the cytochrome bc1-complex, it is oxidized back to QB. This oxidized QB can again participate in the process of transfer of high energy electrons. Thus, QB easily gets replenished in cyclic photophosphorylation.
References:

Liu M, Lu S. Plastoquinone and Ubiquinone in Plants: Biosynthesis, Physiological Function and Metabolic Engineering. Frontiers in Plant Science. 2016;7:1898. doi:10.3389/fpls.2016.01898.

P.A. Millner, J. Barber, Plastoquinone as a mobile redox carrier in the photosynthetic membrane, FEBS Letters, Volume 169, Issue 1, 1984, Pages 1-6, ISSN 0014-5793, http://dx.doi.org/10.1016/0014-5793(84)80277-X.

Mikael Turunen, Jerker Olsson, Gustav Dallner, Metabolism and function of coenzyme Q, Biochimica et Biophysica Acta (BBA) - Biomembranes, Volume 1660, Issues 1–2, 28 January 2004, Pages 171-199, ISSN 0005-2736, http://doi.org/10.1016/j.bbamem.2003.11.012

Wanke M., Swiezewska E., Dallner G. (2000). Half-life of ubiquinone and plastoquinone in spinach cells. Plant Sci. 154 183–187. 10.1016/S0168-9452(00)00200-4

Schmelzer C., Niklowitz P., Jürgen G., Okun J. G., Haas D., Menke T., et al. (2011). Ubiquinol-induced gene expression signatures are translated into altered parameters of erythropoiesis and reduced low density lipoprotein cholesterol levels in humans. IUBMB Life 63 42–48. 10.1002/iub.413

Ma W., Deng Y., Mi H. (2008). Redox of plastoquinone pool regulates the expression and activity of NADPH dehydrogenase supercomplex in Synechocystis sp. strain PCC 6803. Curr. Microbiol. 56 189–193. 10.1007/s00284-007-9056-x

Wikipedia contributors. "Symbiogenesis." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 26 Mar. 2017. Web. 14 Apr. 2017.

Laszlo Rinyu, Erik W Martin, Eiji Takahashi, Péter Maróti & Colin A Wraight (2004). Modulation of the free energy of the primary quinone acceptor (QA) in reaction centers from Rhodobacter sphaeroides: contributions from the protein and protein–lipid(cardiolipin) interactions. Biochimica et Biophysica Acta (BBA) - Bioenergetics, 1655, 93 - 101.

Vermaas JV, Taguchi AT, Dikanov SA, Wraight CA, Tajkhorshid E. Redox Potential Tuning Through Differential Quinone Binding in the Photosynthetic Reaction Center of Rhodobacter sphaeroides. Biochemistry. 2015;54(12):2104-2116. doi:10.1021/acs.biochem.5b00033.

Wikipedia contributors. "Photosynthetic reaction centre." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 22 Oct. 2016. Web. 14 Apr. 2017.

Yocum, Charles Photosynthetic Reaction Centers, Univ. of Mich. 5 Sept 2008. Web. 14 Aug 2014


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What kind of fish is this, caught in Cape Coral, Florida?
What kind of fish is this?
It was caught in the canal in Cape Coral, Florida. The canals are clean brackish water — a mix of saltwater from the Gulf of Mexico and freshwater from the Caloosahatchee River — but the canal where the fish was caught has gulf access so it should be saltwater. The fish was about a foot long, a little less maybe.

Please provide approximate size if possible. Also, please comment whether this fish is fresh water or saltwater, since the canal is fed by the Caloosahatchee River. Thanks

The canals are clean brackish water (a mix of saltwater from the Gulf of Mexico and freshwater from the Caloosahatchee River bu the canal has gulf access so it should be saltwater, the fish was about a foot long.

It looks like the spotfin jawfish, Opistognathus robinsi. The larger ocellated spot on the foredorsal fin is a key identifier for this species. They are not so common in Florida, but do inhabit sandy bottoms, such as canals. Are you sure about the length? It looks about 5 inches from the photo provided, when compared with the the size of the hole on the dock. This species grows to about 5 to 6 inches.
See here for more info.

Thanks a lot, that should be it, you are right about the size.

Hi @johan, thank you for your reply. Jawfish are pretty amazing fish and many species keep their fertilized eggs stored in their large mouths until they hatch! If this or any other future answer has solved your question please consider accepting it by clicking the check-mark. This indicates to the wider community that you've found a solution and gives some reputation to both the answerer and yourself. There is no obligation to do this.


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Redox potentials in photosynthesis light dependent stage
In my lecture notes, it states

...there is a significant thermodynamic problem due to the respective redox potentials of the half reactions:
H2O<--> 1/2 O2 + 2H+ +2e-      pE=+0.82V
NADP+ +2H+ +2e- <--> NADPH +H+      pE=-0.32V

Could someone please explain what the 'pE' is? I thought it would be just ordinary redox potential, however the redox potential for water is apparently +1.23V not 0.82V. I cannot find anywhere a source stating the figures given above or what they mean (I have also consulted Biochemisty, Stryer et al)
Could it have something to do with this being the potential in the conditions present in a typical chloroplast as opposed to standard conditions?

You are right about the conditions in the chloroplast stroma vs. standard conditions. The pH is high (i.e., low H+) in the chloroplast compartment where the reaction takes place (within the stroma), so the pE is shifted from the nominal "pE0", which is +1.23V (effectively you push the equation to the right by low concentration of H+).
See this for a textbook-like summary of the important reactions and this for a quick problem on the math behind pE in different conditions, as well as this for more on the stroma.


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What is the derivation of the rules of proportionality between axon conduction velocity and diameter?
We have been told that in myelinated fibres, conduction velocity is proportional to the diameter of the axon. In unmyelinated fibres, velocity is proportional to the square root of the diameter.
Can this be derived from use of the length constant? The length constant being the distance over which the voltage drops to 37% (1/e) of its original value.
length constant = sq.root(transmembrane resistance/longitudinal resistance)
I understand that longitudinal resistance would (if analogous to electrical resistance in a wire) be inversely proportional to the cross-sectional area, which would lead to being inversely proportional to the square of the diameter (from area = pi.r^2).


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Why is it said that bacteria have no membrane-bound organelles, when they often have one or more flagella?
Why is it said that bacteria have no membrane-bound organelles, when they often have one or more flagella?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3386205/  "Cilia and flagella .. are membrane-bounded organelles with unique membrane,"
Also, there is a biological motor (I don't know whether it's considered part of a flagellum or considered to be outside the flagellum, driving it?), but the motor surely has parts, e.g. a flagellum motor -like some mechanical motors, has a part, a "stator".  And surely these parts have membranes.
I understand there's one bacterium discovered, that does have a membrane-bound organelle mentioned here "There is at least one species of bacteria that has a clearly membrane-bound structure inside it called an acidocalcisome (I think that's how it's spelled). This organelle was.. discovered.. this is obviously a minor (albeit important for that bacterium) exception to the rule...that prokaryotes lack membrane-bound organelles."
Note- Alcamo's Fundamentals of Microbiology: Body Systems p124  this link from google books mentions other cases of membrane-bound organelles in bacteria including a discover as early as 1994. here
But putting aside the bacteria that have been discovered to contain membrane-bound organelles and going back to before those discoveries.. The texts that describe bacteria as having a flagellum, say that they don't have membrane-bound organelles. Why is this?
I suppose an answer might be that when people say that a bacterium contains no membrane-bound organelles, they mean except for any flagellum that it has.  They're referring to the main body of the bacterium, like one might refer to the torso of a human.

Let us continue this discussion in chat.

Explanation of my edits to the question. 1. Some words in biology are of Latin origin and if they end in -um in the singular generally form their plural with -a. Hence bacterium / bacteria, flagellum / flagella. 2. When a noun such as membrane is being used as part of a compound adjective such as 'membrane-bound' (describing organelle) it is hyphenated to avoid initial confusion when reading. This may appear pedantic, but clear communication of ideas is important in science, and if nobody points this out, people remain ignorant.

This question is unclear. Your question is underpinned by a question like"what are the differences between bacterial and eukaryotic flagella?". The literal question being asked "The texts that describe bacteria as having a flagellum, say that they don't have membrane-bound organelles. Why is this?" is subjective since each text may have different reasons and qualifiers.

The question boils down to 'what is an organelle'. I remember a heated yet interesting discussion in the past in the chat room about this topic. I think the lead was this question. But it's closed. Perhaps OP ('you') can edit the question to make it more clear. I'll vote to close but I'm happy to re-vote to re-open it again once edited.

@AliceD  the question you link to shows no research whatsoever. My question is far more specific and researched and is asking about a very specific contradiction.  It is possible to write a general question what is an organelle and to research it well, but there would be other questions within that. My question is very specific and asks about a specific contradiction

@James The question of "what are the differences between bacterial and eukaryotic flagella" may be a big question that doesn't answer specifically the question here.. Though it's possible that an answer to such a question might cover my the question of membranes in relation to the flagella - outside it and inside it,   it's possible that it might not cover that detail.  BTW can you offer any insight into my comment question on  Gerardo's answer?

Prokaryotic flagellum is very different from eukaryotic flagellum: it's not surrounded by a biomembrane (as in eukaryotes) and its composition is distinct. Actually, they only have in common the name and the function:

The term flagella is ambiguous. It refers to bacterial structures composed of flagellin protein and to eukaryotic structures composed of microtubule proteins.

Source: https://www.ncbi.nlm.nih.gov/pubmed/7378551
It's clear that prokaryotic flagellum is just a protein-made structure that crosses the membrane and grows outside it, as represented in this image (notice the TEM at the bottom right):

though that picture is not a cross-sectional view, and this wikipedia page on the flagellum, showing a cross-sectional view, identifies this one as being with bacteria i.e. prokaryotic  http://i.imgur.com/JZVXEbc.png and it has a part labelled as stator and it looks quite elaborate. Also it says "The depicted type of flagellum is found in bacteria such as E. coli and Salmonella, and rotates like a propeller when the bacterium swims. "    and "The bacterial flagellum is driven by a rotary engine (Mot complex) made up of protein, "

The picture I shared is a cross section. 2. What does all this has to do with the answer?

well, do you think the picture I linked to in my imgur link in my comment is a prokaryotic flagellum? if so, it seems to have parts, and do you not think those parts have membranes?

That's the plasma membrane! Bacteria lack endombranes, or membrane-bound organelles. That's the definition of prokaryotic cell, it's quite simple.

Let us continue this discussion in chat.

I guess you're saying yes the imgur link I gave is indeed a prokaryotic flagellum as described. And I asked about those parts of the flagellum e.g. its rotary engine.. and I asked about its stator. And how those things can't have a membrane. And you just said that's the plasma membrane. I'm sure it's not. I just looked up about plasma membrane, and a plasma membrane is around the whole of the outside of the cell.. Not around an individual part within a cell.

For most bacteria the flagella are not bounded by the plasma membrane (e.g. E. coli), but some do have a sheathed flagellum which is covered by the plasma membrane (e.g. H. pylori).

Yes, they do, but it makes no difference: neither eukaryotic flagella nor prokaryotic ones are organelles.

First, this is of some relevance..
https://www.karger.com/Book/Home/258738  says "The traditional view of biology divides living organisms into two major groups, the eukaryotes and the prokaryotes, the former having membrane-bound organelles, the latter lacking them. However, recent research has revealed that this view is blatantly in error. "  (so that is a link confirming one of the things the question said).
Though, a knowledgeable biologist I spoke to said while indeed, that above mentioned distinction between prokaryotes and eukaryotes, is mistaken, there are still distinctions, a genetic distinction(nowadays the distinction would be genetic), and also observable distinction that prokaryotes don't have a nucleus and eukaryotes do. So the terms prokaryotes and eukaryotes are still relevant and not in error.
It may be that texts that say "membrane bound organelles" may mean "membrane bound organelles within the cytoplasm" But it seems even so, as I mention below, a bacteria's flagellum doesn't have a membrane.
Now, to elaborate in answer to the question itself -
I have spoken to a biophysicist familiar with microbiology, that seems pretty knowledgeable.. and he gave an answer that went straight to the point.
He said that the bacterial flagellum has no membrane, and none of its intricate internal components have any membranes.
As to what holds them together(given that it's not a membrane) - all the flagella stuff is protein, held together with protein-protein interactions, the same stuff that holds all protein complexes together, such as salt bridges, hydrophobic effect, etc.
Also the question mentions this

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3386205/ "Cilia and
  flagella .. are membrane-bounded organelles with unique membrane,"

It appears the above statement is wrong or misleading, see
https://www.ncbi.nlm.nih.gov/pubmed/7378551
"The term flagella is ambiguous. It refers to bacterial structures composed of flagellin protein and to eukaryotic structures composed of microtubule proteins and ATPase (tubulin and dynein). The fact that cilia are nearly identical to eukaryotic flagella and have nothing in common with prokaryotic flagella is not apparent from the terminology. It is proposed that the 30-year old suggestion of Smagina and reiterated by Kuznicki and others, be adopted: that cilia and eukaryotic flagella be called "undulipodia." The term flagella ought to be restricted to prokaryotic organelles, bacterial flagella and spirochaete axial filaments: solid structures composed of flagellin which protrude through the plasma membrane and lack intrinsic motility throughout their length. Undulipodia are defined as intrinsically motile intracellular structures showing a 9-fold symmetry in the pattern of arrangement of 24 nm diameter microtubules. They are limited to eukaryotes, members of the protoctist, animal and plant kingdoms."
The knowledgable biologist I spoke to then said that the distinction between eukaryotes and prokaryotes nowadays is done mainly by genetics. Nevertheless, (as mentioned), an observable distinction between eukaryotes and prokaryotes is that eukaryotes have a nucelus and prokaryotes do not have a nucleus. Furthermore, if any prokaryote was ever discovered to have a nucelus, then it'd require a reorganization of phylogenetic trees. Also, while phylogenetic trees use the term eukaryote, they don't tend to use the term prokaryote, though the term prokaryote is still relevant, and there is an organization called the  ICSP(International Committee on Systematics of Prokaryotes), that deal with the naming of groups of prokaryotes.
Also, while it's not entirely clear to me if there was at any time a shift from observable characteristics, to genetic characteristics, in determining the difference between eukaryotes and prokaryotes,  this page mentions something about the origin of the terms prokaryote and eukaryote. And I understand from the knowledgable biologist I spoke to that nowadays the distinction is genetic or mainly genetic. http://www.madsci.org/posts/archives/2000-04/956011333.Gb.r.html
added
I have spoken to another microbiologist.  He thought that the term prokaryotes is not useful, it doesn't have an evolutionary basis.. And at least the term eukaryotes, cells with a nucleus, the cells may be quite related.. Whereas prokaryotes  - cells without a nucleus - is defining something partly by what it's not, and it doesn't group organisms phylogenetically/evolutionarily.   Prokaryote refers to bacteria and archaea, both generally unicellular. But archaea are evolutionarily and biochemically more similar to us(eukaryotes) than they are to bacteria. There's no valid reason to lump them with bacteria.  Not evolutionarily or biologically.   The most recent development is that eukaryotes likely evolved from archaea.  Some newer models show the eukarya lineage as rooted in the archaean lineage.  All of them show that they're more close than either is to bacteria though That's universally agreed Phylogenetically and also cytologically.  The three domains of life are Bacteria, archaea, and eukarya. Eukaryotes still make sense as a grouping as they are a group of organisms more similar to themselves than to bacteria or archaea.  And indeed they are identified genetically.

There are some interesting topics here for discussion, particularly in the discussion with the microbiologist on how prokaryotes is often an unhelpful term for describing evolutionary distance.  The key point is ...the bacterial flagellum has no membrane, and none of its intricate internal components have any membranes. This is already in @GerardoFurtado's succinct answer.

@James I notice Gerardo wrote "It's clear that prokaryotic flagellum is just a protein-made structure that crosses the membrane and grows outside it, "  So what is a membrane made of then that distinguishes it from just protein, is a membrane..protein+fatty acid?   Or is the definition more abstract like is it something that surrounds something, so e.g. in a sense the body has a membrane that is skin?


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What motivation is there to create general, cross-species neural models which account for the variation between species in different environments?
The main components of human neuroanatomy have been mapped out. What attempt has there been to map a broad (many-species) spectrum of functional parts of the nervous system? Such a mapping could be useful in behavioral ecology, which associates functional behaviors with driving environmental forces.


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Can any systems biology model be complete?
In systems biology, models identify the primary actors in the body system, but can any model which does not include all secondary actors be said to be complete?
The current sysbio paradigm is to identify and study biological subsystems. However systems and interactions are subtle and numerous, and no scientist will be able to identify and describe, by hand, how the system works in its entirety. What attempts have there been to model a complete ecological system of internal chemical dynamics?

"All models are wrong but some are useful". This goes for both mathematical and experimental models.

That's right, but some models are less wrong than others.

@Jamie Your comment reminds me of George Orwell's quote from Animal Farm - "All animals are equal, but some animals are more equal than others"

Your question is quite broad. People are constantly making efforts to make better models. With increased computational power, simulation of complex models is no longer difficult. However, you should also keep in mind that if the question that you are asking can be explained by a simple model then no need to complicate things. Choose the model with the least number of parameters.

True, what I am looking for is a discussion of "completeness" of a chemical-biological model. If you consider the human body as a complex system, what reduction can be made to computer data? Clearly there is no representation which recovers the entire system, but if you model a human as a cellular automaton, what data and rules of evolution could capture a smaller system that works on the same principles?

Here's another way to phrase: A biological systems model is a reduction of the entire biological system, which is exactly the positions and velocities of all atoms. How is it that we can make such reductions, and how can we define the notion of a biological model? Are some models more complete than others?


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Does the red blood cell in frogs undergo amitosis?
It is a notion particularly popular among Chinese high school Biology textbooks, that the red blood cells in frogs can undergo amitosis (not mitosis), a claim which I have not been able to find reference. A search on Pubmed led me to this article, which states:

The nucleus of the frog erythrocyte is not a regular ellipsoid; ... a single nuclear invagination located at one end of the long axis is frequently seen in the phase microscope.

However I have also been unable to find more recent researches on the nature of this observation, and whether it is related to amitosis. Can you help me find some?

Unlike mammalian blood cells, blood cells in Amphibia are nucleated (as the paper in your link explains) and can perform cell division (here is an old paper from Acta Haematologica, 1954: https://www.karger.com/Article/Pdf/204534).
Your question is: is this division a regular mitosis or the so called amitosis? According to Barni et al., 1995, amphibian blood cells can perform amitotic cell division:

The proliferation of haemopoietic cells, detected by the anti-BrdU labelling index, was accompanied by absence of mitotic cell division and the appearance of cells showing features of amitosis (e.g. nuclear constrictions with bundles of electron-dense chromatin)

Source: Barni, S., Fraschini, A., Prosperi, E., Vaccaronel, R. and Bernini, F. (1995) ‘Possible occurrence of amitotic cell division during haemopoiesis in the Urodeles’, Comparative Haematology International, 5(3), pp. 183–188. doi: 10.1007/bf00368042.

"Circulating" Red Blood cells are terminally differentiated cells, and cannot divide further. What appears to be the notion is that ejection of nuclear content is biased to one daughter cell (which is then eaten up by macrophages), and some researchers have dubbed it as amitotic process, instead of defining it as a maturation process. In case of humans the process of losing the nucleus from erythroblasts occurs prior to entry in circulation (in adults). You can read this if interested.
However, exceptions do exist... in newborns (and even in foetuses) nucleated red blood cells can be seen in circulation (although the count maybe low). In foetuses, this count is usually high when the oxygen demand increases (hypoxic/acidemia conditions). Read here.
The process from normoblasts to reticulocytes and finally RBCs is one of the setting points in evolution. In frogs (or amphibians in general), and other lower vertebrates (like fish, reptiles etc.) the presence of nucleated blood cells just identifies them as less advanced on the evolutionary-tree. Since higher order vertebrates have smaller blood vessels and complex respiratory organisation, evolution decided to squeeze out the nuclei from these cells to allow easy passage even via micron-thin vessels without compromising oxygen transport.
In short, the presence of nuclei doesn't necessarily determine the mitotic capability. RBCs have long been considered as terminally differentiated cells, and do not divide. If there are any studies reporting "circulating" RBCs as (a)mitotically active, I am unaware of it.


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Taxonomy: Categorising Collembola
Observe: In some rows (Order, Family), the third column reveals a discerning physical characteristic or body type (Elongate, Slender).
What are the discerning characteristics, missing from the other rows (Superfamily, Subfamily, Genus, Species)?
Basically I want this knowledge so I can work towards being able to separate, categorize (catalogue) and/or identify new or unknown species, etc.

Imagery
Exhibit A

Entomobrya unostrigata
(aka. Cotton Springtail)

Taxonomy
Domain      | Eukaryota        | (Eukaryotes)
Kingdom     | Animalia         | (Animals)
Phylum      | Arthropoda       | (Arthropods)
Subphylum   | Hexapoda         | (Hexapods)
Class       | Collembola       | (Springtails)
Order       | Entomobryomorpha | (Elongate)
Superfamily | Entomobryoidea   |
Family      | Entomobryidae    | (Slender)
Subfamily   | Entomobryinae    |
Genus       | Entomobrya       |
Species     | Unostrigata      |

Sources:
Image; photographed by myself. Text; transcribed from my own hand-written notes. Most likely (originally) gleaned and adapted from publicly available, online information. It may contain errors or inaccuracies.

Resources: Check out Bugguide.net and Collembola.org.

Reprise
Okay, the question has been put on hold, preventing answers from being posted (very irritating and obstructionist policy for those seeking answers, I might add). So I will attempt to clarify.

Exhibit B

Orchesella cincta

Exhibit C

Willowsia nigromaculata

Exhibit D

Entomobrya multifasciata

Exhibit E

Seira bipunctata

The diversity of these specimens; span not only multiple species, but multiple genera. Yet, despite the fact that they each exhibit relatively distinctive combinations of patterns and colours across their cuticle (epidermis, surface epithelium), setae, scales, etc. they all look pretty much identical.
This seems to be the equivalent of declaring a homo sapiens of African descent; a different species to a homo sapiens of Irish descent, on account of their superficial aesthetic differences (most notably regarding melanin; the pigments that determine the colours of a human's skin, hair[s], and iride[s] (eye[s]), and so on). Which, at first seems absurd. But for those of you who disagree, observe the differences between (for instance): Exhibit X vs Exhibit B & Exhibit Y vs Exhibit E. Similar variations between individuals of the same species are not uncommon in the least.
Thus, my question: What are the discerning taxonomical differences between various species and genera of the Arthropoda known as Collembola (aka Springtails)?

Exhibit X

Orchesella cincta

Exhibit Y

Seira bipunctata

Don't know the answer to your question, but I have had the same problem as you; feeling like there should be a set of criteria for each and every binomial systematic group (otherwise what's separating them?). Also, I sometimes find that once you get to Order, Superfamily, Subfamily, Subfamily, they groups tend to change from resource to resource making them unreliable, there doesn't seem to be any one official resource of all the known species in all of their groups. So, yes, I agree, being a bit of a perfectionist myself I find it annoying that there isn't always a criterion for every group.

Is the third column supposed to contain characteristic features? At the moment, this is not really the case (its a mixture of common names of taxonomic groups and physical descriptions). I also doubt that "slender" can be used by itself as a trait to separate Entomobryidae from other families. Are you looking to construct a dichotomous Identification key of springtails, or what is the exact purpose of the question?

Continued; If the purpose is a determination key, you need to decide whether your key is supposed to mimic the phylogenetic situation (which your table implies), or if it supposed to be easy to arrive at a species determination. For a key that moves along with the phylogenetic tree, you will need to find good "taxonomic characters" for all taxonomic levels, that are easy to diagnose. If you are only looking for a way to determine species, there might be better ways to structure the key (even though it is in many situations preferable that keys follow the phylogeny).

The third column is just for notes, including common names, etc. But if you're really getting hung up on that, you're probably missing the point of the question.

@LucasDyson-Diaz is on the right track. Some kind of key or matrix would be nice, for instance; a discerning characteristic of arachnidae VS insecta, might be something like 8 legs VS 6 legs, or something of that nature.

Yeah @tjt263 , also I've tried to make a chart, as you describe, but I've only succeeded to make it to phylum level since there are many in the prokaryotic kingdoms, still to that level it's difficult to distinguish organism from organism at such a high (phylum) level let alone order, class, etc.

The third column doesn't contain distinguishing characteristics at all -- they are the first word of the vernacular (or common) names for those groups on Bug Guide. Specifically, Bug Guide lists order Entomobryomorpha as Elongate-bodied Springtails, and family Entomobryidae as Slender Springtails -- so I think you're just looking at truncated data that's misleading you!
What you're looking for a taxonomic or identification key, which gives you set of yes-or-no questions that will allow you to identify an individual to a particular taxonomic group. Know Your Insect has a taxonomic key that allows you to identify insects to order Collembola, which provides exactly the sort of distinguishing characteristics you're looking for: "This illustration shows two characteristic features of members of this order: the collophore (center), a tube-like structure used to secrete fluids; and the furculum (lower left arrow)." Note that this resource refers to this group as an order, not a class -- that's not uncommon among different taxonomic resources. Wikipedia refers to this group as subclass Collembola!
Unfortunately, it doesn't look like there's a freely available taxonomic key for species within this group, unless you buy a specialized guide like A Key to the Collembola (Springtails) of Britain and Ireland.

You're wrong; elongate and slender are discerning physical characteristics. For example: The Poduromorpha and Entomobryomorpha have an elongated body, while the Symphypleona and Neelipleona have a more rounded, globular shaped body. But yes, the taxonomic rank of Collembola has been disputed, given the more recent genetic evidence that suggests any similarities between springtails and insects are a matter of convergent evolution.

Sure, but they aren't very helpful characters (how slender? Elongate how?), and the first couple of values are clearly not characters at all (What sort of characters are Arthropods? Springtails?), which is why I'm pretty certain that third column is common names, not characters. I think you're looking for are apomorphies -- characters shared by individuals within a group but not found within its close relatives, like hair in mammals or hollow bones in birds.


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Sections Of DNA
I know what major (2.2 nm) and minor (1.2 nm) groves are, but what is then name for:

a 360-degree rotation of DNA (3.4 nm)
the gap between each base pair (0.34 nm)?

The term for distance covered in a 360° rotation of helix is known as the pitch of DNA helix, though there is no special name for distance covered between 2 base pairs. It can be called as rise per base pair of DNA. See the table below from this article:

Reference: Nucleic Acid Double Helix

458 views :) wow !

It turns out that the gap between (heterocyclic nitrogenous) base pairs is called 'adjacent base pair width'. Also, the pitch (10 base pairs long) is also known as 'one helical turn'. Just a bit of additional information...

it is (kind of) mandatory here to give some references to your answer (even if its on your own question) so that other readers can have a source for more information.


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(A)sexual reproduction of plants
Are all plants capable of sexual reproduction? Some can do asexual reproduction as well but I haven't found any plants that aren't capable of sexual reproduction. Is it correct to say all plants are capable of sexual reproduction?

No, it's not. There are common plants that can only reproduce asexually.
It's likely you can buy produce from several plants which are unable to do so at your local supermarket. The most famous example is, of course, the banana which is a sterile mutant and all bananas of a particular variety are clones, but some seedless varieties of grapes and oranges would also count (although most seedless fruit you find in the supermarket are actually produced with hormonal treatments rather than being asexual varieties).
These plants are examples of artificial selection but there are also examples of plants that have lost the ability to sexually reproduce in the wild. The evening primrose is a good example, with some 30% of species in the genus Oenothera having evolved to be asexual (Hollister et al, 2015), but this is not the only example. It is likely that, just as in animal species, asexuality has short (on an evolutionary timescale) term advantages but results in lower fitness in the longer term.

How come bananas lost their ability to reproduce sexually?

Because bananas with seeds are nowhere near as edible, humans have selected the varieties without for cultivation.

Did some plants also lose their ability to reproduce sexually due to natural (non-human) circumstances?

@Koekje: Yes, see updated answer.

Thanks 1000 times for answering my questions! (I've been looking on the internet for at least 2 hours without finding any evidence for plants that solely reproduce sexually)

So it turns out that what I said about seedless fruit in the supermarket is largely incorrect, while some are produced from seedless varieties most are produced with hormonal treatments that induce normal seeded plants to produce seedless fruit and these plants can reproduce normally when allowed to do so. Bananas are an exception to this, and really are obligately asexual.

Does "heterosis" fit into your context? From Hollister who you link to I got, e.g. Dorken, M.E. and Eckert, C.G. (2001) Severely reduced sexual reproduction in northern populations of a clonal plant, Decodon verticillatus (Lythraceae). Maybe "banana" is just an example for all sorts of plant losing their capability when: inbreeding. "Obligately" could even, conversely mean: all other forms extinguished.

Actually, I think you might be referring to apomictic plants.
Apomictic plants are those plants that are unable to complete the normal process of sexual reproduction and have to use another alternative pathway to produce an embryo. One way out is through asexual reproduction, and another is called Agamospermy.
Agamospermy is basically the process of formation of seeds without sexual reproduction. Agamospermy is further of two types, sporophytic agamospermy and gametophytic agamospermy.
In sporophytic agamospermy, the embryo is directly formed by diploid sporophytic cells such as those of the nucellus of the ovule, and this is also known as adventive embryogeny. More often than not, in adventive embryogeny, multiple embryos are formed(this is called adventive polyembryony, but i will not go into that for now).
However in the case of Gametophytic Agamospermy, the nucellus cells first develop into a diploid egg cell( the egg cell is normally haploid, however, in this case meiosis is not possible so egg cell has to be diploid). This diploid egg cell now undergoes parthenogenesis(i.e, formation of embryo without fertilisation or syngamy) to produce an embryo which is a clone of the parent.
Now coming to the examples. Apomixis is really well marked in Citrus plants like oranges, lemons, etc and also in Mango.
Also, some varieties of apple are known to show parthenogenesis(DO NOT confuse with parthenocarpy!!)

Even Rubus shows the same.

Refering to question, are those plants not capable at all of sexual reproduction; have they completely opted out of or lost their sexual way of reproduction?
I think your definition of "sexual reproduction" is based on gametes as special cells being a prerequisite. Some authors may consider Apomixis sexual reproduction as the term implies crossing over of genes. I think the  question: "Can parthenogenesis be considered sexual reproduction?" pretty much relates to your answer.


text:
Can you eat enough to make your stomach explode?
Background
After eating a large meal last night, I noticed that my tummy had significantly enlarged. After that, I started wondering if eating too much could cause a stomach to explode. Could this actually happen?
Question

Are you able to explode your stomach by eating too much? Can it pop or break?

I assume your body would just regurgitate the extra food.

What if you held in the regurgitation? Then would you explode?

It is obvious that you will make yourself to vomit... The human organisation isn't created by nature to be self-destroied.

Perhaps better suited to the Health S.E. site.
Eventually vomit will become projectile... You can't hold that in I don't believe.

Here's a simple cross-section of the stomach (from here):

The stomach accomplishes much of its function by mechanically breaking down the swallowed food particles and mixing them with acid and enzymes into a sort of slurry. To do this, there are three major layers of muscle surround the stomach - from the outside, the longitudinal layer, the circular layer, and the oblique layer. The stomach also has two holes in it - the gastroesophageal opening, coming from the esophagus with the swallowed food/saliva mix, and the pylorus, where the food/acid/enzyme slurry exits into the duodenum, which is the beginning of the small intestine.
Due to the three layers of (rather strong) muscle, the stomach doesn't have a lot of expansion capability once it is filled completely to capacity. Fortunately, this almost never occurs (despite how we may feel after a large meal) because material is always leaving the stomach on its way to enzymatic digestion in the intestines. Additionally, once the stomach is filled to a certain extent, hormones such as leptin are secreted that give you the feeling of being sated, or full, triggering the brain to make you stop eating.
Of course, as we can see with the current epidemic of obesity around the world, the stomach can change its size over time. However, this is a rather slow process (weeks to months to years) of adapting to continuously consuming large meals.
But what would happen if you completely ignored these internal warnings, or were being force-fed, or whatever? Instead of rupturing (the biological equivalent of "exploding"), food would most likely be expelled either into the small intestine or back into the esophagus and back up the way it came down, i.e. causing vomiting.
For this answer to be complete, however, I should point out that stomach or gastric rupture is technically possible, although it is an extremely rare occurrence. Cases have been described in the literature (1, 2, 3, etc.), but they are rarely correlated with overeating or eating disorders like bulemia. In cases that are, other pre-existing conditions such as gastric ulcer have been found on autopsy that likely weakened the stomach wall in the first place. The bottom line - if you're an otherwise healthy person, a single instance of massive binge eating is very unlikely to end in stomach rupture, as vomiting will most likely begin well before you are in significant physical danger.

Stomach rupture is a known rare cause of death in those with eating disorders

http://www.medicaldaily.com/breaking-point-when-does-eating-too-much-one-sitting-become-deadly-362856

@GrahamChiu it's incredibly rare, which is why I didn't mention it. I guess I will for completeness.

"Four reports of unexpected mortality due to gastric rupture and necrosis were found in 152 reported deaths, accounting for 3% of the causes of mortality. Four additional individuals were suspected to have gastric rupture. " in Pradi Willi syndrome .. 3% in at least this population is not incredibly rare as per your 3rd reference.

First of all, you must understand the way that our(human like) digestive system, simply digests the food. Here is some information about what happens when you eat:
Digestion is the process of changing food into a form that the body can absorb and use as energy or as the raw materials to repair and build new tissue. Digesting food is a two-part process that’s half mechanical, half chemical.
Mechanical digestion begins in your mouth as your teeth tear and grind food into small bits and pieces you can swallow without choking. The muscular walls of your esophagus, stomach, and intestines continue mechanical digestion, pushing the food along, churning and breaking it into smaller particles.

Chemical digestion occurs at every point in the digestive system, beginning when you see or smell food. These sensory events set off nerve impulses from your eyes and nose that trigger the release of enzymes and other substances that will eventually break down food to release the nutrients inside. The body then burns these nutrients for energy or uses them to build new tissues and body parts.

ALSO HERE ARE THE COORDINATES OF YOUR "TUMMY":
Your stomach, a wide, pouchy part of the digestive tube, is located on the left side of your body above your waist and behind your ribs.
Now, lets get to your main body of your question:
Like the walls of your esophagus, the walls of your stomach are strong and muscular. They contract with enough force to break food into ever smaller pieces as glands in the stomach walls release stomach juices — a highly technical term for a highly acidic blend of enzymes, hydrochloric acid (HCl), and mucus. The stomach juices begin the digestion of proteins and fats into their respective bodily building blocks — amino acids and fatty acids.Churned by the stomach walls and degraded by the stomach juices, what started as food — apples, pears, potato chips, steak, cake, you name it — is now a thick, soupy mass called chyme (from chymos, the Greek word for juice). The stomach’s wavelike contractions push this messy but still intact substance along to the small intestine where your body begins to pull out the nutrients it needs.
Moreover you should consider that the stomach is made from muscles; that makes it strong and immune to HCL. So, if even a very strong acid like HCL can do any damage to the stomach, will a very big meal make it to explode? Simply it will force yourself to vomit just because the very big ammounts of food can't be digested.

Oh, oh, I know how digestion happens. This is a hypophetical question. Isn't the stomach the actual sciency name of the actual stomach section, but the general area with the skin there is called the tummy?

@DanielCann "tummy" is not a scientific term by any stretch of the imagination. In American English, it's a childish name for the abdomen.