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How are primary monoclonal antibodies for screening mutant cells made, physically?
I'm working with a fairly common protein expressed in a large numbers of organisms, let's say a keratin-associated beta-protein. I'm trying to develop a process which requires primary-secondary antibody screening for the keratin-associated beta-protein. Trouble is, it's expensive. Very much so.
I can't find the antibody for any less than $778/mL, and after accounting for dilution and volume required for the recommended protocol, I can't imagine I'll be able to finish designing the process with any less than 20mL. The protein can't change as a design constraint, so there's no reason I'd ever need to change my antibody, but if I need so much... is there any way I can make it myself?
How are these antibodies actually manufactured? Would I need to get ahold of actual B cells and use those, or could I isolate the cellular machinery that produces the antibodies and use that?

If it is not that difficult in your organism, then you can create a transgenic with your protein of interest with a HA or a FLAG tag. The anti-HA and anti-FLAG antibodies are cheap.

Monoclonal antibodies are typically manufactured from a hybridoma cell line. If you are able to obtain hybridomas already made for your antibody (not very likely), or another antibody against your protein, then it's quite easy to produce the antibody yourself. The hybridomas secrete the antibodies into the media, so after growing a bunch of cells, you can purify the antibody from the media with a protein G column.
However, there are not very many hybridoma cell lines available. It's a lengthy and expensive process to make your own (several months and thousands of dollars), even with the help of a core facility/company. You would provide the facility with several milligrams of your protein, they would use it to immunize mice, then after 1-3 rounds of screening, you could obtain hybridoma clones.
There are some banks with hybridomas available for research, for example:
http://dshb.biology.uiowa.edu/
http://www.cellbankaustralia.com/ecacc-hybridoma/


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Is autoimmune disease associated with self-reactive B cells?
I'm a bit of an amateur, so excuse what may be a very naive question, but I somewhat understand how B cells that are self-reactive (bind to endogenous epitopes) are selected out during development. I also know that autoimmune disease is caused by the immune system persistently attacking specific components of the body, which sounds a lot like self-reactive B cells.
Is autoimmune disease associated with (dare I say caused by?) errors in this self-reactive B cell selection process? Any useful references so I can hopefully become less amateurish?

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Interpretation of genetic results
Result of genetic testing indicated: c.341del, p.Thr114Lysfs*37.
The c.341del probably means:deletion at the cDNA 341 nucleotide.
Buy what does the second part:p.Thr114Lysfs*37 ?

I think this question could use additional context. Please update with some more detail. Also, we ask that all question aksers do some of their own research and report what they've already learned or tried. Please take the time to see what you can find on your own, and the community can try to help you if you get stuck.

You are right about the cDNA 341 nucleotide deletion.
It is an exon deletion, meaning that the deletion is part of a gene that encodes to a protein.
This corresponds to the second part - the protein level (annotated with p.).
The mutation that is caused on the protein level is a frameshift mutation (corresponds to the fs).
A frameshift mutation changes the reading frame of the protein.
You can find more information on frameshift mutations annotations on the HGVS nomenclature website.
In your case (p.Thr114Lysfs*37) the annotation indicates that the cDNA 341 nucleotide deletion led to a frameshift mutation of the protein with a Thr amino acid residue being replaced by a Lys amino acid residue. Furthermore, this also altered when the protein terminates: there is a new translation termination (stop) codon after 37 amino acid residues instead of terminating at the end of the protein where it normally does.

Great additional information. You are right about all of your questions, according to the ref.

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In my DNA sequence for one sampling site there're W's; Y's; R's and K's?
I also just experienced the same thing with my DNA sequences, there are w's, Y', R', s' and k'. This is the very first time I've seen this. I am used to N but not these ones. Please kindly assist with knowing what might have caused these. Thanks in advance.

These are the so called "DNA ambiguity codes", when the sequencing result allows to bases at the position but it cannot be decided which. This can happen for example when you sequence genomic DNA and you have two different alleles present.
The code is the following (taken from this website):

Thank you so much. I was really confused and now you've given me some light. Thanks a million!

@AudreyVanya You're welcome. What is easy for one person, is not necessarily for the next. That's why we have this community.


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What kind of Caiman is this and what is on it's nose?
I was able to snap a good picture in the Manù Parque Nacional in Peru. When I reviewed the pictures in more details I noticed something on it's nose, that resemble insects. What are those? Is it a known symbiosis? What do they gain?
Also our guide called it a "white river caiman", is this accurate?
And lastly: It seems one teeth is sticking out on top of it's mouth. By looking at the shape of the jaw it looks pretty natural. Is this common for caimans?
Picture for reference:

I took the picture around here:

Nose only:

Photo taken around May 2018.


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Why is the ingestion of salt and water beneficial to muscle cramp
According to Wikipedia, muscle cramps are caused by the inability of myosin fibers to break free from the actin filaments during contraction, resulting in a prolonged contraction.
A lack of ATP would obviously produce cramping, as myosin requires ATP to become free from actin.
However, I have heard that potassium and sodium are useful for treating cramps and that their deficiencies can lead to cramping.

Your title says salt and water; your last line says sodium and potassium; presumably you mean electrolytes and water in general. The only reason this level of vagueness can be answered is that there's not much evidence for any of it.

After answering this, I see the question is very similar to https://biology.stackexchange.com/questions/7847/what-is-the-cause-of-muscle-cramps by the way, which however I think has a very bad accepted answer.

Magnesium!!! it's the most common mineral defficiency in the world, 40% of humans are magnesium deficient! Water and Salt are abundant. Magnesium is also used in nerves, and it known to reduce cramps. in fact, in hospitals they inject pure magnesium solution into asthma attack patients because it has an immediate effect. it also helps with deep sleep.

Maybe it isn't.

The standard theory: muscle cramps are caused by loss of fluids and electrolytes, which alters fluid balance in the body and increases the excitability of nerves.
The "new" theory: muscles cramps result from "altered neuromuscular control," which can be triggered by a variety of factors, including genetic predisposition, damaged or fatigued muscles, starting too fast, and not tapering enough -- none of which have anything to do with hydration or electrolytes. [...]
A few years ago, researchers at North Dakota State University published a study showing that dehydrating subjects by 3% of their initial body weight didn't change their susceptibility to muscle cramps (as measured by threshold frequency). Now, in a new British Journal of Sports Medicine study, they've extended those results to a greater degree of dehydration: their 10 subjects reached an average dehydration of 4.7% (greater than 3% is "significant" dehydration, while greater than 5% is "serious") after almost four hours of exercise in very hot conditions. Crucially, they exercised only with their non-dominant limbs, while the cramp testing was performed on their dominant leg, so that muscle fatigue/damage could be eliminated as a triggering factor.
The result: no difference in cramp susceptibility or intensity, despite an extreme dehydration protocol that saw them lose about 4 g of sodium! The researchers conclude that their data supports the "altered neuromuscular control" theory.

Even the older research that did find it more plausible that electrolytes were a cause wasn't very adamant that's the [only] cause, e.g.:

Consumption of a carbohydrate-electrolyte beverage before and during exercise in a hot environment may delay the onset of EAMCs [Exercise-associated muscle cramps], thereby allowing participants to exercise longer. However, it appears that dehydration and electrolyte loss are not the sole causes of EAMCs, because 69% of the subjects experienced EAMCs when they were hydrated and supplemented with electrolytes.

There are a few [not very well controlled, IMO] experiments from the 1920s and 30s (three papers to be more precise) that did find a role for sodium depletion in some cases of mild cramping. The most controlled of these (published in 1936) involved sodium depletion for 10 days (daily sweating and virtually no intake), which  is hard to argue is that common in most cramp suffers. The original paper notes that the level of sodium depletion involved led to quite a few other symptoms:

Such deprivation led to aberrations of flavour, cramps, weakness,
  lassitude, and severe cardio-respiratory distress on exertion. The nitrogen balance became negative and the blood urea rose.

And despite the severe sodium depletion, the cramps were mild but generalized:

These muscular cramps were not of the very severe localized type which are
  said to affect stokers and miners (Moss, 1923-24), but were widespread,
  frequent, not very painful, and generally controllable. Any muscle in
  the body was liable to go into spasmodic contraction, especially if some
  little effort was demanded of it (Moss, 1923-24). “ Coughed a little
  over something, cramps round chest, mild.” * R.B.N. experienced
  occasional cramps in the muscles lining the floor of the mouth but the
  extremities were most affected, and it was possible sometimes by suitable
  movement of the toes to alternate the spasms for hours on end between
  the extensor and flexor muscles. Perhaps the most characteristic of all
  were the manual cramps. R.A.M. experienced “ constant mild cramps
  of the fingers and thumb when using forceps at the balance,” * and R.B.N.
  found that he “ cramped quickly when working, telephoning, or using
  pipettes.” *

So that's why I say these types of cramps probably have little relevance for those experienced by most people.
I'm not sure there any studies for potassium. The paper reviewing the sodium evidence notes:

Mechanisms in heat cramping remain murky. Sodium loss contracts extracellular fluid space and may alter ion channels to make neuromuscular junctions or muscle units hyperexcitable, thus evoking
  involuntary and sustained contractions, or heat cramping. And, not all camps buy salt loss for  cramps. Bananas, for example, remain popular in some football camps, to prevent heat cramping by ‘replacing potassium’. But here, bananas are yellow herrings because little potassium is lost in sweat. The same applies to calcium and magnesium. Sweat after all, is mainly water and salt (sodium chloride).

And do note that his latter paper is written by a Gatorade consultant.
One 2009 review in clear opposition to relevance of electrolytes-water for the usual exercise-related muscle cramps notes:

In summary, dehydration and electrolyte depletion are often considered together (and recently together with muscle fatigue) as the “triad” causing EAMC. The key components of this hypothesis (fig 1) are that electrolyte (mainly sodium) depletion through excessive sweat sodium loss together with dehydration causes EAMC. However, results from prospective cohort studies consistently show that athletes suffering from acute EAMC are not dehydrated, neither do they have disturbances in serum osmolality or serum electrolyte (notably sodium) concentrations. Furthermore, sweat sodium concentrations measured during exercise in 23 reported cases with a past history of EAMC are not higher than those reported in many other studies. Both electrolyte depletion and dehydration are systemic abnormalities, and therefore would result in systemic symptoms, as has been observed in other clinical conditions. However, in EAMC, the symptoms classically are local and are confined to the working muscle groups. Thus, the available evidence to date does not support the hypotheses that electrolyte depletion or dehydration cause EAMC — therefore an alternate hypothesis for the aetiology of EAMC has to be considered.

Suffice to say that this field is still quite contested... and plagued by conflicts of interest. Witness a 2019 paper finding that a magic electrolyte formula (contents not disclosed) from a pharma company absolutely does lower the risk of cramps after exercise compared to water. Study funded by aforementioned pharma company, of course. And the press reported this as "water after exercise increases risk of cramps" (by diluting the electrolytes in your body, of course), arguably due to the authors' summary.

And while most of the previous material was about exercise-related cramps, even for the nocturnal cramps more often experienced by the elderly, the role of electrolytes appears uncommon; according to a 2007 review:

Muscle cramps, notably nocturnal leg cramps, are common symptoms experienced by general medical patients, particularly the elderly. Their etiology is varied; most commonly, these cramps are idiopathic. With the notable (and relatively rare) exceptions of serious electrolyte imbalances including hypokalemia, hypomagnesemia and hypocalcemia, these cramps are typically benign in nature. [...]
The second recent study to challenge the notion that diuretics [which promote a loss of electrolytes through urine] are a common cause of muscle cramps was a cross‐sectional survey of 365 general medical patients. Although the prevalence of leg cramps in this cohort was 50%, no associations were found between these cramps and any medication except analgesics that were used to treat the cramps. [...]
Nevertheless, a review of the Physicians' Desk Reference database (available at www.pdr.net) suggests a consistent association between diuretics and muscle cramps. [...]
The mechanism of diuretic‐associated cramping (if such an entity truly exists) is likely related to hypokalemia, hypomagnesemia, or volume contraction (with or without metabolic alkalosis). Hypocalcemia is a possible cause during therapy with loop‐diuretics such as furosemide, but is unlikely with the hypocalciuric thiazide‐type diuretics. Interestingly, potassium‐sparing diuretics, such as amiloride, are also associated with cramping. Thus volume contraction appears to be the one mechanism that is common to all classes of diuretics.

A 2012 new large-scale investigation did point to some epidemiological associations between cramps and diuretics:

Cramp treatment was substantially more likely in the year following introduction of LABAs [long-acting β2-agonists], potassium-sparing diuretics, or thiazide-like diuretics, and 60.3% of quinine users (individuals experiencing cramp) received at least 1 of these medications during a 13-year period. In contrast, statin and loop diuretic associations were small. Physicians should be mindful that the use of these medications may worsen symptoms in patients experiencing nocturnal leg cramps.

And they also have some comments on putative mechanisms:

Physicians may be surprised that potassium-sparing diuretics have a stronger link to cramp treatment than loop diuretics. Yet, hyperkalemia facilitates neuronal excitation, and hypokalemia suppresses motor neuron activity. β2-Agonists are known to have a stimulatory effect on motoneurons, and β2-adrenergic receptors are found on peripheral nerves.


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Identifying a mysterious bird in the writings of Hebrew prophet Jeremiah
In Jeremiah 17:11, the verse states:

קֹרֵ֤א דָגַר֙ וְלֹ֣א יָלָ֔ד עֹ֥שֶׂה עֹ֖שֶׁר וְלֹ֣א בְמִשְׁפָּ֑ט
  בַּחֲצִ֤י ימו [יָמָיו֙] יַעַזְבֶ֔נּוּ וּבְאַחֲרִית֖וֹ יִהְיֶ֥ה נָבָֽל׃
Like a 'korei' hatching what she did not lay, So is one who amasses
  wealth by unjust means; In the middle of his life it will leave him,
  And in the end he will be proved a fool.

I am trying to identify the mysterious 'korei'.
Various commentators, including Rabbi Shlomo Yitzchaki, Rabbi Meir Leibush ben Yehiel Michel Wisser and Rabbi David Kimhi all indicate that this is a species that has a habit of hatching eggs that are not its own.
Rabbi Meir Leibush identifies it as a "perniz" but it is unclear to me what language he is using.
Rabbi Shlomo Yitzchaki identifies it as a "cuckoo glontzant" - but he obviously cannot be referring to a regular cuckoo because cuckoos are brood parasites or obligate parasites, but do not bother sitting on other birds eggs.
Are there any birds known to science today with this odd habit?
Are there any birds with latin names (or names in any other language) that correlate to those provided by Rabbi Meir Leibush or Rabbi Shlomo Yitzchaki?

This may be a better for https://judaism.stackexchange.com.

The specific bird doesn't seem to be at all important to the passage; it seems most likely to be referring to a bird that has been a victim of a cuckoo: it's the other bird that is sitting on cuckoo's egg. I think this is not really a biology-relevant question because there is nothing in this passage that would allow a biologist (as opposed to a Hebrew scholar or perhaps linguist) to answer it.

Also in your link on sefaria the translation says "partridge" - doesn't that seem like a reasonable translation?

this page adds to your discussion. However, I agree w/ Bryan, that ultimately this is not a biological question -- understanding the passage likely doesn't rely on a specific species. If you're strictly interested in the biology of the bird, then see my answer, as it should give you some initial info. To ID to specific species, however, cannot be done without further details about the bird. Just answering based on the name is really more of a translation question, not one about bio

I'd also ask whether the passage applies to wild birds (where it doesn't seem to make a lot of practical sense), or the practice of farmers having one kind of bird hatch out eggs of other species,  e.g. chickens hatching duck eggs/

The korei must be a victim of a brood parasite.  It likely refers to a then-current story or common reputation of some such bird (perhaps a domesticated bird as jamesqf suggests).

L.B., thanks for your suggestion, I posted here because I was looking for a specific biological species. Thanks Bryan Krause for your comments, yes, it is likely to be referring to the victim of a cuckoo - but the commentaries I quoted seem to name a specific species, so I wondered if it was known to science. I wouldn't place much faith in the "partridge" translation, these can be arbitrary or mistaken unless sources have been quoted. Does the partridge have the habit of sitting on other bird's eggs? I supposed that if it did, someone would identify it as such anyway.

jamesqf, very interesting point, however, commentaries across the board clearly present it as a habit of the species.

Cowbirds lay their eggs in other bird nests to have the other birds rear their young.
According Cornell's All About Birds informational page on the brown-headed cowbird:

Over 140 host species of the Brown-headed Cowbird have been described, from birds as small as kinglets to as large as meadowlarks. Common hosts include the Yellow Warbler, Song and Chipping sparrows, Red-eyed Vireo, Eastern and Spotted towhees, and Red-winged Blackbird

So, to answer your question, there are many birds that will do this.
More generally, birds such as the cowbird that rely on others to raise their young are considered to be brood parasites.

Sometimes this involves intentional egg mimicry and sometimes it's not so secretive.

There are countless numbers of brood parasites and even more species that act as their "hosts." Your bird could be any number of them.
According to Wikipedia:

The subfamily Cuculinae are the brood-parasitic cuckoos of the Old World

So perhaps their host species would be a good place to start looking...
For example, a quick Wikipedia search reveals that the common cuckoo is one such member of the Cuculinae, and they have more than 100 host species:

More than 100 host species have been recorded: meadow pipit, dunnock and Eurasian reed warbler are the most common hosts in northern Europe; garden warbler, meadow pipit, pied wagtail and European robin in central Europe; brambling and common redstart in Finland; and great reed warbler in Hungary

Thanks for this. According to the helpful link in your comment above, Maimonides writes "The korei is called alhajel (in Arabic...), and in this species the males hatch the eggs just like the females." - another clue. And the "perniz" that I mentioned from Rabbi Meir Leibush is the latin "perdrix" which indeed is the partridge family. Sefaria seems to be on the mark - this source identifies the korei as a sand partridge or a rock partridge. Biologists, does that fit in with what you know of the species?

Trying to be biologically relevant: to the best of my knowledge there are no birds that exists that deliberately want to incubate the eggs of other birds. From an evolutionary perspective, raising offspring is costly. However, like you mentioned there are birds that can act as brood parasites such as cuckoos, some duck species etc. The brood parasites then invest their time on other activities such as foraging and producing further offspring.


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Does the mutation CCR5-delta 32 increase the genetic info?
My understanding is that the mutation CCR5-delta 32 caused the CCR5 co-receptor to be of a different shape, resulting HIV virus to not be able to attach itself to it.
My question, this shape/mutation, is it a result of a more or less information in the genetic information of the person with the mutation as compared to one without it?

your going to have to clarify what you mean by "more or less information in the genetic information" and "increase the genetic info"

"Increasing genetic information" is a creationist buzzphrase, most recently popularized by "Intelligent Design" fraud Michael Behe in his most recent book; Behe claims that it's impossible for mutations to add information, only subtracting it, and that therefore evolution is impossible.

Whether or not a mutation changes the 'amount' (meaning the size of the genome) of genetic information present in an individual depends on the type of mutation and is independent on which gene is affected.
In general there are 3 types of mutations:

point mutation: this is the change of one base pair to another (e.g. A to C). The total amount of information/the size of the genome is unchanged.
deletion: this means that a certain stretch of DNA is missing, likely disrupting what was there before. The total amount of information/the size of the genome is reduced.
insertion: this means additional DNA was added at a certain place in the DNA and probably disrupts something that was there before. The total amount of information/the size of the genome is increased.

The CCR5-delta32 mutation is caused by the deletion of a few (only 32) base pairs, however this deletion causes a frame shift in the gene and therefore leads to an early stop codon, which renders the protein inactive.


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What type of insect or bee is this?
First time with Mason Bees here in Tacoma WA. We had three come out of their cocoons today. One female is working in a tube. But we had one insect who flew up to near the bee house, shook off their wings and is now wandering all over the bee house.
Is this a mason bee or something else? Should I be concerned?

What is the approximate size of your specimen? Please update your post using the [edit] button to include at least an approximate size. Thanks. See here for how to write a well-received [tag:species-identification] question that has a better chance of getting a good (and correct) answer.

Black garden ant and associated image from its Wikipedia page.

Ants and bees don't get along so if you want the bees you should get rid of the ants.

I've downvoted b/c many ants look similar, & your post hasn't done anything to convince readers this is an accurate ID. It appears as a guess w/ a picture. You should indicate explicitly what characteristics of L. niger you find to match the OP's specimen. You could also address why it's not other related or similar looking species. Finally, please examine & mention the likelihood of your answer based on known range info...For example, the range map for L. niger from antsmap.org suggests it's an exotic with few records in WA...

@theforestecologist Thank you for the guidance, I should wait until it is "well asked".

Rob, I agree -- getting more info from a better asked question is ideal. In the absence of an update to the question, I recommend 1 of two things: 1. just move on. or 2. Write a darn good, detailed answer being very clear about why you think it is what it is. Even if you're not correct, your reasoning will be valuable and might encourage discussion, question edits, or additional answers. You could also present various species options and "teach" us why it's unclear which is correct and which characteristic to look out for and how specific traits would be indicative of specific species.

For example, see my answer to  this post. I wasn't sure of the answer, but I present the likely group and try to narrow based on characteristics and ranges.

@theforestecologist The cephalothorax of blackjack75's spider looks different than your two examples, but I may have found you a better photo, a 'my guess is better than your guess' discussion isn't productive unless one of us is a myrmecologist. What is really helpful, is this Meta post of yours, a comment from the Moderator might assist Susan and be better received than a random person's comment (mine). Thanks again. Moving on.

@theforestecologist - Perhaps "I found a bug" questions should go to our The Great Outdoors site. More upvotes per effort expended.

I'd rather they stay here where both the question and the answer will be held to higher standards and therefore likely result in a more accurate (vs seemingly close-enough) learning moment for the OP and future visitors. You can see a previous issue I had concerning the robustness/accuracy of effort taken by previous TGO ID posts here

I'm all for correctness and accuracy, but the last couple of askers haven't been interested in providing a better question they don't want TMI, only JEI (just enough info). I agree, this being the biology site, that a high standard ought to be adhered to; the question is, what kind of answer do they need/want (much as on Physics, Stats, Math, etc.SE). A simple "I found a bug" question might only want a "it looks like this" answer. While the other asker has earned a few points they filled out their profile: "In 9th grade".


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While in motion, why do closer objects appear to move faster?
When I look outside the window while travelling by a car, why do closer things seem to be moving faster and appear unclear but the farther ones seem to be moving slower and appear clear?

@BagiM no answers in the comments please

@AliceD Sorry i thaught the question is going to be moved/deleted since it is not biology so i just left a comment. I can repost the comment as an answer.

@BagiM: the 2nd half of the question/answer clearly involves some biology.

@BagiM this is all about perception. Ontopic as can be. Only problemis that OP hasn't gone through any prior effrt, so that would, for me, be a valid reason to put it on hold.

@Fizz you are probably right. I didn't think of it that way since the same effect of motion blurr would happen for a camera and I thaught of it in terms of physics. But now I see you are right.

Why do closer things seem to be moving faster?

This is due to parallax. A very simple phenomenon exhaustively explained on wikipedia.

Why do faster moving things appear unclear?

This is primarily due to retinal persistence also well detailed on wikipedia.
It takes time for the retina to detect a change in light at a given position on the retina. Things that move quickly across your visual field (i.e. retina), or that reflect very low amounts of light tend to blur or simply be invisible. Car headlights moving close to you will blur because it takes time for photoreceptors to 'switch off' and the headlights would appear as a streak or trail of light for you. And similarly, if a car were to move at an incredibly large speed, the car wouldn't reflect enough light to trigger a response in the retina, so it would be unseen by you. Remember that what matters here is how much range of your visual field an object crosses, not the speed of the object itself. For example, a fast car in the distance does not blur since it's crossing a tiny fraction of your visual field, but a slow car right in front of your nose will be crossing your entire visual space very quickly.
These are properties of the retina. It is also possible the encoding of visual information in the brain also plays a role in how your perceive something. However, the illusion you describe is entirely explained by these retinal phenomena due to sensory neuron biology.

It also works the other way around.  Flying in a passenger jet at 30K ft seems excruciatingly slow, even though you're moving at ~600 kts, while a single-engine plane doing ~100 kts at treetop level seems quite fast :-)

This is not entirely correct. Because of motion parallax an object twice as close moves twice as fast on your retina, correct. But retinal information are next to useless. The whole point of your visual system is to infer what exists in the real world by interpreting retinal inputs. If your visual system was perfect, you would in fact compensate for distance and perceive the 2 objects move at the same speed. What this illusion demonstrates is that vision is not perfect and fails to perfectly take the distance of the objects into account.

Take this demonstration: put your right thumb at arm-length, and your left thumb and half arm-length. They look the same size right? On your retina your left thumb is in fact half the size of your right thumb. This is not useful information for interacting with the world. What you want to know is the real size of the object. Your visual system compensates for distance and makes you perceive your 2 thumbs at roughly the same size. Speed works the same way.


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Are there specific theories as to what causes cold[-water] muscle cramps?
The field of what might cause cramps is quite contested with a lot of controversy around the heat/dehydration cramps, but I find it surprising that no specific theories appear to have been proposed (or tested) while swimming, usually in cold[er] water. There's one governmental site that does acknowledge cold and cold water in particular as a risk factor. I for one never get cramps in a pool/water over 18 degree C, but I am quite likely to get them below that, no matter what I do in terms of stretching, drinking etc. (There's one other site that mentions that "muscle spasms" occur during cold-water shock, below 15 degreed C.) Am I correct that no specific theories have been proposed or tested for cold-related cramps?

Interestingly, the cutoff temperature I found experimentally for myself is perhaps reflected in one article:

during swimming at a water temperature of 18 [deg] C, it is noted that
  esophageal and muscular temperatures tend to decrease, below 37 [deg] C. [3 refs cited for this fact]

So below 18 C water temperature it appears that consistent cooling of the muscles occurs. So I guess one could ask, equivalently, why muscle cooling [below 37 C] can lead to cramps.


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What was the biological mechanism that allowed Tarrare to eat so much?
Are there any conjectured mechanisms that cause Tarrare's extremely oversized stomach and abdominal cavity? Along with his superhuman appetite of course.  Whether from a medical perspective or a genetic one (I.e a potential diagnosis that is perhaps quite similar or the genes that would be at play).
Even correlated genes and their subsequent mechanisms that are being affected could be an interesting addendum.
*I would like to make sure that any answer is also trying to explain the enlarged esophagus and abdominal cavity(seen during autopsy) along with the appetite, sweating, and other observed manifestations of an underlying condition(see Death section of Wiki for info and associated source material in book "Two-headed Boy and other Medical Marvels").

Typically questions about symptoms and medicine are closed. Since this is a famous case study, I think it should stay open. It is, however, a historical case study meaning that there will be speculation about a definite cause. Personally, I think there is enough evidence to discuss biological concepts of disease in relation to Tarrare, but I understand why there are votes to close the question.

@James yes, this is why I also tried to focus on the genetic aspects involved. If you'll look I updated my post to also try and get some more info on the deformities seen at autopsy. If you want to expound upon those I will go ahead and select your answer.

It's a good question, and I like the idea of considering this as a genetic disease case study. I've found what I can from the source material on the autopsy.

Recently there was Mr Mangetout also... he ate a plane. https://en.wikipedia.org/wiki/Michel_Lotito#Death

@LifeInTheTrees I don't think Mr Mangetout is a useful comparison, he was purely a snowman, if perhaps one with a psychological eating disorder, and didn't consume excessive quantities of digestible material as Tarrare did or share any of Tarrare's other symptoms, Tarrare's daily consumption of vast quantities of ordinary digestible food coupled with a lack of any obesity and the reported high body heat suggests some form of metabolic condition,, was

Tarrare had these symptoms:

Grossly increased appetite, eating raw meat and other inedible things
Excessive sweating with bad body odor
Chronic diarrhea, which was "fetid beyond all conception"
Wide jaw, abnormally large esophagus and stomach
Loose skin around his cheeks and stomach
Heavily stained teeth
Unusually soft fair hair
Apathetic temperament

He didn't vomit excessively and he was not overweight.
Description of his skin and internal organs:

When he had not eaten, his skin would hang so loosely that he could
  wrap the fold of skin from his abdomen around his waist. When full,
  his abdomen would distend "like a huge balloon". The skin of his
  cheeks was wrinkled and hung loosely, and when stretched out, he could
  hold twelve eggs or apples in his mouth.
At the autopsy, Tarrare's gullet was found to be abnormally wide and
  when his jaws were opened, surgeons could see down a broad canal into
  the stomach. His body was found to be filled with pus, his liver and
  gallbladder were abnormally large, and his stomach was enormous,
  covered in ulcers and filling most of his abdominal cavity. (Wikipedia)

Possible causes:

Constant hunger and excessive eating was obviously due to chronic diarrhea that resulted in loss of most nutrients he consumed, which also explains why he was keeping relatively low body weight.
Saggy skin, large esophagus and stomach can be explained by a combination of eating large amounts of food at once and lax connective tissue - the later could be genetically predisposed. It is known that eating huge amount of food at once can result in acute gastric dilatation.
Enlarged liver (hepatomegaly) and gallbladder were likely due to abscesses as part of purulent infection in his abdomen discovered at autopsy.
Chronic diarrhea could be caused by a gastrointestinal infection or intestinal parasites, which may also explain his other symptoms: eating inedible things ("pica"), excessive sweating, bad smell of the skin and stools, apathy (due to anemia) and ulcers and pus found in the gastrointestinal tract at autopsy.
Excessive sweating could be a combination of:

Chronic infection
Diet induced thermogenesis due to eating a lot of meat, which is high in protein, which releases a lot of heat when metabolized (see also "meat sweats"). This same effect can explain why the other man, Charles Domery, who was eating huge amounts of meat, was sweating profusely at night (after eating), despite having no diagnosis of infection, diarrhea or other health condition.

Comments are not for extended discussion; this conversation has been moved to chat.

Tarrare
Tarrare was a showman who was renowned for his insatiable appetite including eating cats, dogs, and snakes sometimes raw.
He is also said to have eaten many inedible items.
At the time, he was alleged to have committed cannibalism of a 14-month-old baby and was caught in the act of cannibalising cadavers by hospital staff.
He was given away as a child by his parents and served in the French Revolutionary Army.
Tarrare died at the age of around 26.
From the book "Anomalies and Curiosities of Medicine" originally published in 1896 by Gould and Pyle:

He was of middle height and was always heated and sweating. He died of a purulent diarrhea, all his intestines and peritoneum being in a suppurating condition.

This record is 100 years after Tarreres death and is largely based on the 1819  London Medical and Physical Journal.
The earlier record claims:

At seventeen years of age, Tarrare weighed only one hundred pounds,
  and was already able to eat, in twenty-four hours, a quarter of a
  bullock of that weight.

From these accounts, I form the opinion that Tarrare ate an incredibly poor diet of raw meat and offal and countless inedible objects.
There are references to throwing up after consuming raw animals and chronic diarrhoea. There are references to sleeping for large periods of time after eating large quantities of food.
Autopsy
A passage from the 1819 London Medical and Physical Journal:

This is the closest article we have to a contemporary record.
From this account we gather that his stomach was enlarged and ulcerated, his gall bladder was enlarged, and his liver was diseased and enlarged.
Also, it might be a factor that his appetite was lost during these final days, common among patients with diarrhoea.
The record at the time, as quoted above, attributes the cause of death to diarrhoea.
Although the picture is painted that the autopsy occurred soon after death, we have no idea if this was hours, days, weeks, and conditions were much less sterile than modern morgues. I am not sure if the  "corruption" mentioned is significant.
One source claims Tarrare died of TB, however, I cannot find any corroborating evidence.
Another source recounts Tarrare blaming his demise on eating a golden fork.
These post mortem observations could have developed from 20 years of eating an exceptionally poor, unhygienic, and often inedible diet and may or may not have been the cause of his underlying condition.
Summary
So we have a few things to consider.

Polyphagia including inedible object consumption
Died young
Gastrointestinal abnormalities identified post mortum
Chronic fever and sweating
Chronic diarrhoea and vomiting
Periods of prolonged sleep

Polyphagia
The London Medical and Physical Journal describes Tarrare as having polyphagia which in his case could not be cured by acids, opium, or tobacco.
Colloquially, polyphagia means ingesting a wide variety of items.
However, if they meant "polyphagia" medically, it could be a symptom.
Polyphagia is a medical symptom defined as excessive hunger.
In modern times, this can indicate a disorder such as diabetes (improper production or reception of insulin) or Kleine–Levin syndrome (a disorder of the hypothalamus).
It could also indicate a genetic condition Prader–Willi syndrome and Bardet–Biedl syndrome.
The full list of causes from Wikipedia is:

Anxiety
Stress
Depression
Orexigenic drugs
Diabetes mellitus
Hyperthyroidism
Hypoglycemia
Fatigue
Premenstrual syndrome
Prader–Willi syndrome

From the
NHS:
Prader-Willi syndrome is a rare genetic condition that causes a wide range of physical symptoms, learning difficulties and behavioural
problems.

Bulimia
Graves' disease

Autoimmune thyroid disorder that can lead to an intolerance of heat

Kleine–Levin syndrome

A sleep disorder

We cannot know if Tarrare's polyphagia was brought on by his stressful exhausting life, his poor diet, or some genetic condition.
We cannot even be sure if his condition was responsible directly or indirectly for his death.
We cannot know if his sweating was related to; his underlying condition, or a chronic state of infection.
The only cause for his eating we can rule out from the above list of underlying causes is premenstrual syndrome (PMS) and orexigenic drugs (which are not documented).
There could be a case made for most of the other causes.
Concluding remarks
Given the scarceness of good quality medical records, the anecdotal nature of what was recorded, and the relatively poor diagnostic power of medical practitioners of the time, it would be, in my non-medical opinion, impossible to conclusively form a diagnosis.

Comments are not for extended discussion; this conversation has been moved to chat.


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Effects of tobacco smoke on plant health
We know that tobacco smoking is associated with a wide range of negative health effects in humans, which holds for active smoking, second hand smoking and probably even third hand smoking.
What are the effects of second hand smoke exposure on plants?
For example the german wikipedia page on nitrogen dioxide claims that exposure to nitrogen dioxide leads to reduced yield in apple and pear trees, white birch, barley and salad. It is also stated that first physical signs of alterations can be detected with one time exposure at levels as low as 3 ppb for less than one hour. However I cannot access the source because it is a book.
Bonus: How does cannabis smoke differ from tobacco smoke with respect to plant health?

I think you should see the words "start a bounty" right below my comment - clicking on it, I think, will let you set a bounty

Plants have varied reactions to smoke of different kinds, either to grow differently or to fall ill. this page says that tomatoes and peppermint contain nicotine and nicotine is used to treat plants, so the nicotine can't be that detrimental to them, but the other many smoke compounds can make them ill, but only in very high levels of smoke. http://www.takepart.com/article/2015/04/15/nicotine-plants-second-hand-smoke

https://www.vidarholen.net/contents/junk/nicotine.html

@CuriousIndeed Your question seems to be asking about the gaseous components of cigarette smoke and their effects on plants, but, considering a house plant exposed to concentrated cigarette smoke, I think the particulate matter in secondhand smoke is likely more immediately harmful to plant health. Consider the effect that any particulate matter will have:  residue or tar that settles on the leaves will both inhibit photosynthesis and clog stomata, reducing the efficiency of gas exchange.

Results from the peppermint plants study show that all the peppermint plants contain minor amounts of nicotine before treatment, but the experiments revealed that the plants also incorporate nicotine considerably from the soil as well as from tobacco smoke. These findings demonstrate for the first time that the reported occurrence of nicotine indeed may originate from tobacco. The incorporated nicotine was subsequently metabolized by the plants.
Effects:
Apart from the nutritional aspects, the results on nicotine uptake may also affect basic plant biology, because they demonstrate that alkaloids can be transferred from one plant, after its death, to another plant species.

The plants, said Dirk Selmar, the study’s lead author, appeared, at
  first, to be unchanged. “As far as we have seen, there have been no
  negative effects on the growth,” he wrote in an email. Yet, tests for
  nicotine, conducted at various stages in the plants’ life, found that
  they had “tremendously elevated nicotine levels,” Selmar said.

References:
https://link.springer.com/content/pdf/10.1007%2Fs13593-015-0298-x.pdf
http://www.takepart.com/article/2015/04/15/nicotine-plants-second-hand-smoke
https://www.ehow.com/info_7987584_effect-cigarette-smoke-house-plants.html
some anecdotal answers (to be taken with a grain of salt) on your 2nd bonus question: https://www.rollitup.org/t/is-smoking-weed-around-a-growing-plant-bad.182179/

The answer focused too much on nicotine an ignores the rest..considering smoking, the health hazards of nicotine are negligible compared to the other constitutes of smoke..e.g Polyzyclic aromatic hydrocarbons (PAR), Nitrosamines, Aldeshydes, Arsenic, Nickel, Cadmium..Thus I'm not particularly happy with the answer however because its the only one so far the bounty goes to you if no one else answers...


text:
CRISPR/Cas9 edited E.coli on AFM?
I am doing CRISPR/Cas9 experiment on E. coli. I am introducing recombinant plasmid  BPK764 (which carries Cas9 + sgRNA designed and added later in that plasmid) into compentent E.coli cells which already carries another plasmid with GFP gene. sgRNA will be designed so that it corresponds to that GFP gene becouse my main point is to cut out GFP gene. The main result of this experiment will be E.coli cells that do/don't express GFP gene (depending on CRISPR/Cas9 efficacy), therefore, the resultant cells will or hoply won't light green. I will see that under UV lamp, and by fluorescent microscopy.
Now I'm getting to my question.
Is there something on those resultant cells (some trait, like membrane structure, youngs modulus, that differs from CRISPR untreated cells) that can be visualized on AFM (atomic force microscopy)? Something that changes on cells after inserting plasmid that can confirm efficacy of this experiment?
Or maybe some other idea on this experiment using AFM?

Welcome to Biology.SE, Mila99. I think there is a good question here, but it's not entirely clear. Are you asking for a suggestion for a control that you can use to evaluate whether the plasmid has been successfully incorporated? Does it need to involve AFM?

Unless you're specifically targeting genes involved in the physical morphology of the cell, I doubt you would find any differences with CRISPRed vs non-CRISPRed cells that is measurable via AFM.
Perhaps you should instead target genes known to contribute to the structure of the cell wall, which I would expect to be the dominant material contributing to the Young's modulus. Since you mentioned GFP as a tool for selecting for "successful" cuts, it might be worthwhile looking into generating a multiplex plasmid that allows you to target several loci with a single construct. Such kits are available on Addgene and contain associated publications and manuals on how they can be used.
So to summarize, no, I don't think there is anything physically different about cells that have been CRISPR treated compared to a control group. If you did want to use CRISPR to effect a knockout of the fluorescence in the competent cells you described and alter the cell mechanics, you would likely have to generate a multiplex CRISPR plasmid with multiple gRNA cassettes for both GFP and perhaps some gene involved in cell wall formation. Keep in mind that your efficiency percentage is compounded with each new target in the same multiplex – instead of a single cut being deemed successful, you will have raised the bar to 2 cuts being deemed successful without doing anything to improve the efficiency of a single cutting event.
Hope this helps, and I'd be happy to discuss this more.


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Antibiotic resistant genes
Can someone help me find be it an article or journal that has the conventional PCR method for the detection of antibiotic resistant genes?
Thanks in advance.

Do you have in mind any specific antibiotic resistence gene? Which antibiotic?

I tested my isolated bacteria against 10 antibiotics, namely: Tetracycline, vancomycin, cephalothin, ciproflaxin, chloramphenicol, ampicillin, erythromycin, kanamycin,trimethoprim, and neomycin.


text:
Are inadvertent environmental catastrophes also examples of natural selection?
I just want to understand the concept of natural selection and its relation to evolution.
Evolution by natural selection occurs when we have hereditary trait(s) that causes an effect on reproduction rate of a population, either towards the positive, and thus deemed as beneficial or towards the negative and thus labeled as harmful.
Evolution by natural selection would result in keeping the beneficial trait(s), and wiping out the harmful ones.
The idea according to Darwin is that the slightest harmful effect a hereditary trait(s) would bring to a population then with time it would result in extinction of the population with that trait(s). [On the origin of Species, p.78, chapter: natural selection: "On the other hand we may feel sure that any variation in the least degree injurious would be rigidly destroyed"].
Therefore natural selection could be viewed to result ultimately in washing out of injurious traits, and only promoting beneficial traits. So natural selection can be the cause of extinction of some genotypes, and ultimately of some species.
In this sense natural selection can be considered as a creative natural tool, like a rubber wiping bad intermediate solutions, and only keeping the correct steps, thereby facilitating reaching into a solution.
Now suppose that we have a population of living subjects with varying heritable traits on an Island, and those had equal fitness over a very long period of time, so they were pretty much adaptive to their environment. Now suppose a volcano erupted or a big comet stroked that island that ended all life in it. Lets suppose that the genotypes of that population is not present outside of that Island. So these genotypes became extinct.
Here this event doesn't have the same functional genre that natural selection had, it actually didn't act in a differential manner promoting those genotypes with better fitness and wiping out those with lower fitness. No it actually was NOT fitness dependent at all, it simply squashed all life forms without regards to whatever feature was brought up by the different genotypes, all were simply extinguished.
Now can we label this event of indiscriminative extinction to be the work of natural selection also? Or we just label it as inadvertent environmental factor?
If the latter, then are those inadvertent environmental factors part of the mechanism for evolution?

Let me give another example:
The beetles stochastic example
Suppose we have a population of brown and green beetles, now suppose that we divide the place they live in into two territories A,B, now suppose that the movement of beetles across those territories is random, so at some moment of time all brown beetles happen to be in territory A, other times they have different distribution, and as said the movement pattern is totally random, i.e. there is no significant difference in the pattern of movement of both genotypes of beetles across territory A and B. Now suppose by the act of randomness a moment came where all brown beetles were located at Territory A, while some of the green beetles were in territory A and others in territory B, and suddenly came a big comet and hit territory A at that time that caused all the brown beetles to die, and also caused all green beetles on territory A also to die, but since territory B was not hit, the green beetles in B remained a life.
Now a moment of evolution did occur, since a change in the heritable characteristics of the beetle population did occur. But that change was merely accidental, there was no role attributable to fitness of the green beetles that resulted in their survival, it was a mere random event that caused all of the brown beetles to die. In some sense it's a kind of a stochastic environmental factor that caused that extinction. Fitness of the green beetles didn't have any role in that case of differential survival.
This can be called selection, it is environmental kind of selection, BUT it is NOT the outcome of differential fitness of the genotypes in that environment.
Now this moment in evolution is it described as an event of evolution by natural selection?
More broadly speaking, is it the case that any point of change in the heritable characteristics of a population (i.e. evolution) that is merely due to an environmental factor [like the above example], would qualify as a case of evolution by natural selection? or only those points where the resultant change is attributable to fitness differential that is genotype determined?

FYI, you misunderstand the quote: "On the other hand we may feel sure that any variation in the least degree injurious would be rigidly destroyed". This does not suggest that any deleterious variation would result in extinction of a species.  It's a restatement of what selection is.

if you read the whole chapter of natural selection in Darwin's book "on the origins of species" then you'ed definitely get the impression I'm speaking about. In the struggle for life, Darwin highly adheres to Malthus principle that resources are not enough that ultimately even the slightest disadvantage a heritable trait would bring with it then this would be enough [over sufficiently long period of time] to cause extinction of that trait. Any variation that causes negative shits in balance in the struggle for life, would cause extension. That's what I mean here, and what Darwin meant.

DO NOT read Darwin expecting to understand the concept of natural selection and its relation to evolution. Darwin wrote over 150 years ago, and is entirely irrelevant to modern evolutionary theory. You are not educating yourself; you are simply confusing yourself, and wasting everyone's time by expecting people to explain obsolete, irrelevant concepts as if they're currently important. Darwin was a great thinker and set some foundations for modern evolution, but he is now important only as history, not science.

You can find good courses on-line, such as the one from Yale: https://oyc.yale.edu/ecology-and-evolutionary-biology/eeb-122/lecture-3 (Look at the next lecture on drift as well)

Is a change in allele frequency resulting from a catastrophe evolution by natural selection?

The catastrophe itself is an example of a change in environment that brings with it a change in selective pressure. The events you describe (a volcano eruption, or a comet strike) would select for existing variation in the population. Heritable traits that are more common in those surviving the event would have been selected for. This represents natural selection.
Consider the description of natural selection from the UC Berkeley Understanding Evolution Course. We need the following things: variation, differential reproduction, and heredity.
Provided there were some variants that are able to survival, and their survival is the result of some heritable trait, this certainly fits the bill.
What if nothing survived?
This is highly implausible. I'm not aware of any event where this has occurred. Volcanic eruptions are colonized by microorganisms, and the K-T extinction certainly benefited us. If you are focused on, e.g., a specific population that happens to not have enough variation to survive the catastrophe, then that particular population has become extinct. This becomes more plausible the smaller and more homogeneous the population is.
To be honest, I'm not sure if complete loss of a heritable trait that made the population susceptible to the catastrophe (e.g., limited flight range in a bird population that was entirely unable to escape an eruption) would be considered natural selection in the event that the entire population was lost. From a framework of a larger population of birds that included that trait in some birds not on the island in question, I suspect it would, despite the fact that the birds without the trait may not have been exposed to the selective pressure. I would argue that, because there is a decrease in the frequency of a trait in the population due to selection against that trait. Perhaps I should ask a question about it. I welcome any comments or edit suggestions on this point.
Changes that are not due to natural selection
As discussed in a chat with @BryanKruase, changes in allele frequencies that are associated with, but not on the causal pathway to failure to reproduce, would not be considered natural selection. So, selection of birds with a longer flight range, provided that flight range is heritable, would be considered natural selection. If those birds also happened to have more green feathers, an increase in the frequency of that trait would not be due to natural selection. One need not invoke a rapid change in environment (seen from one perspective as a catastrophe) in order to see both types of changes (the trait under selection as well as those associated with that trait). From my perspective, that may have obscured the question. As Bryan pointed out, one should be careful not to overestimate natural selection as the principal cause of evolution.
Your green/brown beetle example would be an example of a change in a heritable trait that is not evolution due to natural selection. Here a random event led to all the brown beetles failing to reproduce, but the brown trait itself was not selected for or against. Speaking of the trait, then, and accepting your hypothetical, we can say that the change in this trait was not due to natural selection.
A few additional comments on your question:
On reading Darwin: I'm glad you're carefully reading Darwin. It's been a while since I've done that. I would recommend you not get too caught up in whether something fits with his description. That was the state of things 160 years ago.
On an "inadvertent catastrophe": this phrase is a little confusing. Your examples are natural phenomena. I'm not sure you mean to distinguish your examples from purposeful changes, e.g., for an experiment.
On changes "merely due to an environmental factor": selective pressures in natural selection are always due to an environmental factor of some sort or another.

The event killed ALL the living population in the island, where is the selection?

@ZuhairAl-Johar if that happened, that's the selection. I'm not sure what is unclear there? No traits allowed for survival under that selective pressure.

evolution by natural selection occurs when we have variation in heritable traits that cause differential fitness that would result in extinction of the less fit genotype. In other words "natural selection" is a function of differential fitness. But here the catastrophe caused extinction was not a result of variation in heritable traits, definitely this point in evolutionary history (i.e. the catastrophe causing this massive indiscriminate extinction) is not the result of what Darwin was speaking about in his chapter "natural selection".

Its true that the catastrophe had resulted in a change in the heritable characteristic of the total living population on earth, since that would lack the ones that became extinct, and a moment of evolution had occurred yes, but that was not due to evolution by natural selection, i.e. that change in hereditary characteristics didn't result from a change in fitness of completing genotypes. It was a blind force having no direction at all. The natural disaster didn't select for anything that it acted upon, it destroyed them all.

@ZuhairAl-Johar the catastrophe is the environment, not the selection. In a hypothetical and extremely implausible case that has never occurred (100% of life everywhere is abolished), absolutely everything was selected against because there wasn't a variant that allowed survival in that environment. In any other case, something is selected for.

I think there is a problem in terminology here about "selection" itself, to me selection cannot be "totally selected for" and cannot be "totally selected against", to me those are example of NO selection, because there is no differential effect of that environmental factor on genotypes. If you look at Darwin he explicitly says that no selection occurs if the there is no extinction of one of the genotypes, similarily to me if it results in extinction of all the genotypes under its effect, then no selection had occurred under effect of that factor.

@ZuhairAl-Johar consider that your hypothetical (all life is abolished) never happens and you will see that selection does occur. There are organisms that survive the catastrophe. If they have heritable traits that allowed them to do so (mobility and ability to predict or detect the event, so they were out of the primary blast area, heat tolerance, tolerance reduced light after the fact), then those traits were selected for. Those organisms without those traits were selected against.

Yes of course, under this scenario there is indeed an example of selection that occurred due to the heritable characteristics of some genotypes, that enabled them to evade the catastrophe, definitely this would qualify as an example of natural selection. But that's not the question of mine really, its another scenario. In my scenario there was no differential output, truly there is some life remained outside the Island, but this is not due to the beneficial traits of those genotypes, it was merely due to the comet not striking them, so their survival is not attributable to their fitness.

what I'm trying to say here, is that I think [I might be quite wrong of course] that it would be more plausible if we restrict "natural selection" to situations where "differential survival" [remaining in existence] resulted from "differential fitness", and preferably under a predictable setting! If some genotype survived some environmental impact not because of its own characteristics, but just because of mere chance that this environmental impact was directed away from it, then this better not be regarded as an example of natural selection, call it inadvertent environmental selection.

@DeNovo In my view, which I would accept a challenge to, the key for natural selection is that there is differential survival because of a heritable phenotype. Living on a particular island is not a heritable phenotype by itself, and an event that kills every organism is not natural selection. I might be wrong to lump it in with genetic drift, but I contend it would be more similar to drift than selection, there's basically just been a bottleneck if some subgroup is wiped out.

@bryankrause I should edit to clarify. I don't believe there has ever been a case where survival or failure to survive a catastrophic event would not depend on at least some trait with some heritability (other than in the marvel comic universe)

@thanks for this informative answer, but can you please answer the beetles example question, this is a later edit to my question, in that particular example, it appears that natural selection is not playing any rule, since the survival of the green beetles is not attributable to their fitness at all.

@ZuhairAl-Johar your welcome. I've addressed the beetles question.

thanks for your very informative answer, I now know matters better. But I just want to make sure of one point as regards my beetles example, you said it is an example of change in heritable traits of a population that is not due to EVOLUTION. I thought that a moment of evolution is a moment where a change in the heritable characteristics of a population occurs, so my example defines a moment of evolution, but that moment is not caused by natural selection. I mean that's my understanding of the matter. But when I saw you saying that it is not due to evolution, I need to fathom this.

@ZuhairAl-Johar that was a word finding problem/brain fart. In a bit I will edit to fix.

The idea according to Darwin is that the slightest harmful effect a
  hereditary trait(s) would bring to a population then with time it
  would result in extinction of the population with that trait(s).

Citation?  I certainly don't think any modern biologist would claim that a single deleterious allele will doom a population.

Therefore natural selection could be viewed to result ultimately in
  washing out of injurious traits,

In real life, there is no infinity far away "ultimate" point to be reached.  What's deleterious today might be beneficial if the environment changes.  And the environment is always changing.

Now can we label this event of indiscriminative extinction to be the
  work of natural selection also?

I don't see why you would, since survival was not influenced by genetics.

If the latter, then are those inadvertent environmental factors part
  of the mechanism for evolution?

Well, if it kills every single organism, I don't think we can say that population is evolving any more.  But bottlenecks randomly and radically changing allele frequencies are hardly an unknown mechanism for evolution.

I've given the citation, according to Darwin, he believed in Malthus rule about geometric growth of populations with arithmetical growth in supply of food that eliminating that abundance. So over time any slight injurious trait would result in extinction of that genotype, due to that struggle for life, since by Malthus law its impossible for all of them to remain extant.

+1, I think a key issue here, which you point out, is that there is no inherently "good" or "positive" trait, the value of the trait depends on the environment, which is changing.

Simply citing Maltheus does not mean that Darwin really believed that a single deleterious variation would destroy a species.  The strength of Origin of Species was all the work Darwin had put into observing variety across a number of different organisms.  I don't think he ever said "Well, these barnacles are going to be extinct soon, because I observed this undesirable trait in one of them"

@swbarnes2, I've given a clear reference to Darwin, and the tone of his speech clearly imparts what I've said here, "the least injurious"a trait would be then this would cause extinction, but I did NOT say "soon". I didn't cite Malthus, I've cited Darwin account and Darwin's own claims about malthus principle in relation to the struggle for life, that's not my citation, that Darwin's citation himself, read his chapter on natural selection very carefully. –

You are missing many points. Darwin is almost entirely irrelevant to modern evolutionary theory and has been since the modern evolutionary synthesis in the 1940s (and even more so since Kimura and other modes of evolution), so arguing about what Darwin said is a waste of time. It's like claiming Egyptian hieroglyphs disprove internal combustion. Further, trying to map Darwin's arguments onto modern genetics is silly; Darwin had no clue about genetics, and entirely misunderstood heredity. Your reading of Darwin is wrong, too, but I won't bother explaining why since it's so irrelevant.

Natural selection is an important part of evolution, but not the only part
Evolution is described as changes in heritable characteristics over time: you can look at changes in allele frequencies and call that evolution.
Genetic drift, for example, describes genetic changes that are caused by random sampling rather than selection. A natural disaster (if we assume it acts only to kill off some individuals, rather than changing the environment), could hypothetically contribute to genetic drift.
Consider some population of a species of birds on a group of islands. The birds can fly between islands, so they interbreed but not at the same rate (i.e., they are more likely to breed within their island than between islands). Therefore, if we look at allele frequencies, they are not identical. They will be especially likely to drift apart if they aren't especially important to survival (an example in humans could be something like eye color).
One day, all the birds on one of the islands die by some disaster. If we look at allele frequencies across the whole population across all the islands, those frequencies just suddenly changed: any alleles that were more common in the doomed island were just reduced. Evolution just happened (heritable characteristics just changed), with no selection.
These effectively random changes can be quite important evolutionary forces over the long run, especially when population bottlenecks occur, in which case a small population survives rather than is wiped out.

I'll concentrate on your sentence .., with NO selection.  So the above is not an example of natural selection. Is that correct?

@BryanKrause on closer reading, I disagree. If the birds suddenly died due to stochastic effects, this is not natural selection. If the birds on one island suddenly died because of a natural event, this is natural selection. The fact that the event is a catastrophe or sudden does not make it any different from the rare visit of a particular predator, a change in tide patterns, extinction of some food resource, or the sudden presence of antibiotics, complement, or antibodies.

@DeNovo It's only natural selection if a heritable phenotype is involved in the process, by my view. An island that is randomly destroyed by disaster is in fact stochastic. If some survivers remained because of protective heritable phenotypes then that would be natural selection. I'm curious how RemiB would weigh in.

@BryanKrause I would agree that if the phenotype wasn't involved in the selection process it wouldn't be natural selection, but I can't imagine a case where that would be true

@DeNovo I agree it's a bit of an artificial scenario, but read the OP's scenario: by random chance, individuals of different phenotypes are in two regions. One region is destroyed at random by a natural disaster. Maybe a hurricane floods an island and kills every member of a species on that island but not other islands. Allele frequencies are changed subsequently by this random event, which did not target one region or the other based on anything related to the heritable phenotypes of the individuals affected.

@BryanKrause neither of those events are random, though. I think the tendency to see the effect of rare events as something other than natural selection has to do with the simplification when evolution by natural selection is taught, that an environment is constant over many generations. Some regions are susceptible to hurricanes. Some aren't. Arriving and staying in that area is going to be associated with some heritable trait. Not being able to detect and leave or find shelter is also going to be associated with some heritable trait.

@BryanKrause the fact that the hurricane is rare, or causes a sudden change, doesn't prevent it from exerting selective pressure when it occurs.

@DeNovo " Arriving and staying in that area is going to be associated with some heritable trait" - not necessarily. Europeans are more likely to have blue eyes than people elsewhere. Nothing about blue eyed people made them up and migrate to Europe. If Europe got hit by a meteor and the fraction of blue eyed folks in the population was therefore reduced, I don't find it appropriate to call that "selection." That isn't to say that such an event couldn't also involve selection, but the trait I described does not provide fitness against meteor strikes.

Let us continue this discussion in chat.


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How does bonding between non-complementary bases occur?
My teacher told me that when DNA polymerase makes an error (roughly every 10 million nucleotides?) that if, for example, it matches an A with a G that the error remains and is the main cause of point mutations. How do the two bases that aren't complementary remain bonded?

How do the two bases that aren't complementary remain bonded?

Non complementary bases can only form non-Watson-Crick bonds, which are very unstable and noticeably different.
Therefore any mismatch in the DNA of the genome will form a recognisable disruption of the DNA helix. This disruption is usually removed very quickly by the cells, since it makes DNA much more unstable.
Most cells have multiple mechanisms to detect and repair these sites, with one system specifically dedicated to DNA mismatch repair.
This system acts on mismatches directly after DNA replication, since at this point specific markers (sometimes DNA methylation, sometimes not fully understood) can differentiate between the newly synthesised DNA strand (which may contain an error) and the old one.
The repair mechanism will remove the mismatch and replace it with a properly bonded base pair, so that mismatches in the DNA are always short term issues - it is still possible though that 'wrong' mismatching base is replaced, which then (finally) leads to a mutation.
The error rate of DNA polymerase (1 in 10^7 sounds about right, this is the combination of the initial error rate and the DNA polymerase proof-reading mechansim) therefore has to multiplied with the error rate of this repair mechansim, which is around 10^3 (I can't find a source for this right now), to get a final error rate of DNA replication in cells.

"They do not" is incorrect. Non complementary base pairs do form, and remain until they are removed. They are less stable, and produce a detectable change in the 3-d structure of the duplex. The rest of your answer is correct.

@DeNovo edited the answer accordingly


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The Viceroy Evolution Paradox
The viceroy butterfly generates a toxin compound which make it distasteful to predators.  Biologists agree that the viceroy must have developed this trait as a passive defence mechanism to prevent being eaten.
Let’s look at it from an information point of view.
For this to work, information about the bad taste of the viceroy must be known to the predators.  This can happen by a predator eating one viceroy, discovering the bad taste, learning and never doing it again.  Unfortunately, the unpalatable butterfly had to die in the process.
The second, and most important, information path is the genetic one.  One way, evolution work is by the survival of the fittests. In this case the important trait of “tasting bad” dies with the butterfly and is less likely to have been transmitted to a new generation, unless (and this might be part of the answer) we consider the local population of butterfly as the evolving organism.
The question:
If a successful gene is only proven successful when removed from the gene pool, how does the species evolve a trait involving this gene?

Possible duplicate: https://biology.stackexchange.com/questions/24312/how-can-natural-selection-occur-at-species-level-whilst-not-occuring-at-the-indi see also: https://biology.stackexchange.com/questions/66081/how-does-natural-selection-explain-how-organisms-that-are-poisonous-evolved

@BryanKrause Thanks for finding the duplicate. I think your second link is probably more clear, but since that points to 24312, I used it as the dupe.

OP the reason this isn't a paradox is the title of the duplicate (natural selection occurs at a species level, not an individual level). The mechanism by which a toxin would be selected for is discussed specifically in this answer. If it helps, you should remember that natural selection acts on existing variation. So the toxin is already present in the population at some frequency.

I think the problems your two points. bring up can be summarized as evolution does not act on the level of a single organism.

The post marked as duplicate talks about species/lineage selection. This is unlikely to be a good explanation for the process asked by the OP. Instead, the other post @BryanKrause suggested as duplicate (How does natural selection explain how organisms that are poisonous evolved?) is a much better duplicate IMO (and talks about kin selection among other things).

@Remi.b the problem is the second post is closed as a duplicate of the first. I think we're not supposed to close a question as a duplicate of a closed question, but rather close both for the same reason.

@DeNovo Oh yes indeed. Good point. I just nominated the post for reopening as I personally don't think it should be closed as a duplicate of the other one. Thanks


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Origin of different brainwaves
I'm creating a project in which I can measure brainwaves (more or less like EEG). Since I'm not a medical student im having a problem finding the origin or most prominent regions for measurements of alpha and beta waves. I have researched on the internet but can't find a definite solution. So can  someone please tell me the exact origin or the most prominent region (active region) of our brain where  the alpha and beta waves can be measured reliably??( Like ocipital region or frontal temporal etc)

This is probably not off-topic here but I personally think this is an excellent question for the psychology & neuroscience SE. Also, the first search engine link I stumble on states that alpha waves mainly "originate from the occipital lobe during wakeful relaxation with closed eyes" and beta waves are "general over the whole cortex and occur during normal wakefulness". I think this checks out but I'm not entirely confident this answer is as satisfactory as one you could get from a cognitive neuroscientist.

If I ask the question now on nueroscience then it will be marked as  duplicate right??

It wouldn't. It's a completely separate stack exchange. Please try to search whether an answer already exists there. Also, put in a little effort using a search engine, I'm sure this information may exist already on online educational pages. If you are still lost, feel free to ask there!

@infottie Does this answer your question? https://psychology.stackexchange.com/questions/20075/why-do-brains-oscillate-within-specific-frequency-ranges/20086

No it doesn't..it doesn't say which wave is most prominent in which part of the Brain..

Alpha and beta brainwaves are just two of several arbitrary, named frequency ranges for a brain-wide phenomenon. See Types of Brain waves. These so-called brainwaves are big electrical events that sweep across the entire brain.
My recommendation for electrode placement is based on my engineering experience. Pick any location on the scalp. You could start with the temples. Take your measurements. Then move the electrodes to a different location and repeat the measurement. Continue this experimentation until you discover by observation which location yields the best results. When you have finished with the experiment, you can post your experimental results on SE Biology and answer your own question.
I suspect that electrode type and method of contact (dry versus conductive gel) will be more significant than actual placement on the head.


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A cure for radiation exposure?
Some of the greatest inventions of my lifetime have been from looking at nature and copying. I found out tadigrades in outer space have the ability to repair their own DNA when exposed to radiation thousands of time higher than what it would take to kill a human being. Can the tardigrade's genome be mapped and the section of DNA responsible for repairing radiation damage be duplicated? Would that be a good thing? Could a stem cell with that section of DNA make our astronauts safer?

Would that be a good thing?

Recent research from the Samson lab at MIT suggests that there are side effects from amplifying the DNA repair mechanism.
Hyperactivity of a base-excision repair (BER) protein called AAG in mice caused a positive feedback loop in DNA repair signaling that triggered macrophages to attack retinal cells, leading to a cycle of increased inflammation, photoreceptor (PR) necrosis, and ultimately blindness.
From the linked paper:
In this study, we demonstrated that programmed necrosis and subsequent inflammation are important mediators of AAG-dependent alkylation-induced PR cell loss in male mice... We showed that PR cells present necrotic morphology and oxidative DNA damage after the induction of PR cell death with alkylating agents; furthermore, we observed that PARylation in the PR nuclei is associated with the release of HMGB1, increased macrophage infiltration, and elicitation of an inflammatory response.
Another research project looked at a DNA repair protein called ATM in mice, where hyperactivity or overexpression may be implicated in Alzheimer's and Huntington's diseases. Knock-down mutants show reduced expression of this protein and reduced neural damage.
Ignoring the larger ethical questions of splicing genes into human beings, and the technical questions of how to get said genes inserted, transcribed, and translated in the right place at the right time in the right way, it would likely require considerable study to see what the systematic effects might be from expression of tardigrade or other organisms' DNA repair genes in humans.
At the very least, these papers suggest that the biology is complex enough that turning up the dial on repair machinery could cause serious health problems downstream, as much as it might confer greater protection from radiation or other environmental damage.

My first thought is that, if we were able to introduce such a mechanism, we'd essentially stop natural mutations and therefore natural improvement and diversification of our species. Perhaps, this would only be useful for Human 3.0.
(Tardigrades have ~1300 known species and been seen in fossils as old as 530 Myr.)


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Is it trivial to assume a version of Hamilton's rule that applies for numerous generations?
Is it trivial to assume that a version of Hamilton's rule that applies to numerous generations is:
C > rB
C = lineage fitness lost by an actor,
B = lineage fitness gained from the act, and
r = relatedness between actor and those that gained lineage fitness?
Or does this rely upon a particular derivation of Hamilton's rule?  If so, does anyone know of a citation in which this derivation is made?
Thank you very much.

I am not sure what you mean by "applies to numerous generations". If the following does not help, can you please clarify what you meant?
Hamilton's rule expresses the condition for which, under a prisoner's dilemna game (see game theory), the stable equilibrium that will be reached is the one where everyone is cooperating. Hamilton's rule is, therefore, a condition to determine the directionality of a dynamic system (the system is dynamic because the state of the system varies over generations).
EDIT

what if the values of B and C differ depending on [the generation]

In other words, you are asking

What if the (social or not) environment is changing over time?

Well, under such circumstance, of course, the simplistic rule that consider B and C as constant won't hold.
You could not simply replace B and C by the the arithmetic mean (or by the geometric or harmonic or any other mean) as the system as two stable equilibriums and upon reaching one there would be no way to get out of it (at least as long as the game remains a prisoner's dilemna).

Hamilton's rule states (according to Wikipedia, for one):  A gene responsible for an altruistic act should increase in frequency if rB > C, where:
B = additional reproductive benefit gained by a recipient
C = reproductive cost to the actor
r = the genetic relatedness of the actor and recipient
My question is, what if the values of B and C differ depending on how many generations have elapsed since the act because of a disparity in the number of, for example, grandoffspring or greatgrandoffspring?

For example, what if after 1 generation, B is F offspring and C is H offspring and after 5 generations, B is G descendants and C is J descendants?  And what if H > rF but J < rG? Is it trivial to assume the act will gain frequency after a long number of (> 5) generations because J < rG?  Is it still Hamilton's rule even if it deals with C and B in the form of descendants rather than offspring?

@sterid Thanks for clarification. Please see edit.

I am not asking about the environment changing.  Here's an example.  Consider Jim relinquishes resources and they go 10% to Bob and 90% equally to all individuals (so, r = .1).  Consider that Jim would have 2 offspring from the resources and Bob would get 9 offspring from them.  But after 5 gen, Jim would have 8 descendants from the resources and Bob would get 100 descendants from them.
2 > .19 but 8 < .1100
Then after 1 gen, there is less of the variant responsible for the act than at gen 0, but after 5 gen, there is more of the variant than at gen 0 (the variant has evolved).


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human body in an environment where temperature is above body temperature
What would happen if humans were to live in an environment where the temperature is above the body temperature?
Does the human body have a mechanism to cool the body?
When the surrounding temperature is below the body temperature, the body has a mechanism to heat up. When the surrounding temperature is above the body temperature, the body would require some mechanism to cool down since there will be a net heat transfer into the body.

Temperatures greater than ~37C occur commonly on Earth where people live. Have you thought about possible ways that people keep cool that you already know about? Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure.

My bad. I wasn't clear enough. I was looking for specific active metabolic processes for cooling. I'll edit it in a few hours.

There are many ways by which a healthy human body deliberately dissipates heat. First, it is important to note bodily temperature is not uniform. Our skin is generally colder or warmer than the rest of the body, which is the reason why we place the thermometer between our armpit or inside our mouth, instead of just placing it in our say, fingernails.
Vessel dilation
Arterioles can tighten or relax, increasing or reducing blood flow. High CO2 concentrations and heat cause the arteriolar diameter to increase, allowing larger blood flow. High oxygen concentration and cold cause the opposite effect. At normal conditions, about 0.2 to 0.5 liters of blood pass through the skin. But under stress, this can rise up to 8 liters per minute. What this response entails is an increase in cardiac load.
Sweating
We have up to 4 million eccrine sweat glands. Normally, they secrete an extremely filtered version of blood plasma, which is odorless. Exercising or heat changes this. As it is mostly water, which has a specific heat of 4.2 joule per gram, its evaporation releases quite a bit of heat. So what this mechanism requires is greater hydration, or else there is risk of hyperthermia (increase in core body temperature unrelated to fever).
References
This text is a very resumed version of this article:
Physiological Responses to the Thermal Environment


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How atom works and it's different from DNA?
I am studying atoms recently because I am writing a short story and the characters would talk about it for a bit. And I wish it's scientifically accurate.
So I read a lot of articles about the atom and here is something that I saw:

Around three-quarters of a human body is water, made from oxygen and
  hydrogen atoms. These atoms, along with all the others in the world,
  have been around for eons, shifting through any number of organic and
  inorganic processes, or simply hanging about in the atmosphere.
  Anybody could have some oxygen or hydrogen atoms in their constitution
  that had once been part of Einstein, Elvis Presley or Mother Teresa.
  On the other hand, an atom could have once been part of a decomposing
  piece of rat offal.

So, if I really got some atoms of Einstein, it doesn't work like DNA which I might have curly hair right?
Thanks!

If you recycle plastic or metal then does it mean that it will retain the properties of the the object that it had been in the past? Think about it. I don't want to be dismissive but your question is super elementary! You must do some reading on your part before asking others.

you should probably read what is DNA, this should clear things up

DNA is a complex molecule which contains the genetic information. DNA, just like any other molecule, is made of atoms. However, the atoms themselves do not contain any genetic information.
To be more accurate, DNA is made of a double strand (themselves made of atoms) and among those two strands are a succession of elements that we call nucleotides. The 4 four possible nucleotides; Adenine, Thymine, Cytosine and Guanine (usually, just called, A,T,C and G). Nucleotides are simple(-ish) molecules. The genetic information is in the succession of four nucleotides. For an analogy, consider the nucleotides to be letters and the succession of letters make words and sentences. The letters themselves don't hold information but their succession does. For example, the letter "r" in itself does not have much meaning but it is essential for the sentence "The door is red" to make sense.
So, whether one of the atom found in a given nucleotide (or anywhere else) has been in Einstein's body or not, does not change anything in your genetic information.


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Why are the grey matter structures of the inferior medial frontal lobe not directly (not via white matter) connected?
I have recently been trying to understand the three dimensional nature of the brain for a neuroanatomy class. Part of this strategy has included learning about structures such as the falx cerebri, tentorium cerebelli, anterior dural girdle, etc in order to understand the physical barriers that surround different parts of the brain and therefore separate them from one another. For example, the reason that the cerebellum and floor of the occipital lobe are not directly continuous is because of the tentorium cerebelli.
One issue that I have recently come across is understanding why the inferior medial component of the frontal lobe, in the region just anterior to the pituitary gland and optic chiasm, are not directly continuous (i.e. the left cortical hemisphere at this location is not continuous with the right cortical hemisphere). I have attached some photos to clarify my confusion:

As you can from this image, the falx cerebri's anterior extent leaves a small opening (indicated by the red line) that would, presumably, permit grey matter from the left hemisphere to be directly continuous with grey matter from the right hemisphere. However, no such connection exists. This is readily confirmed using an inferior view, such as that indicated in the following picture, boxed in red:

As you can see from the boxed area, the medial inferior cortical grey masses from the left and right hemisphere (which are likely the subgenual division of the anterior cingulate gyrus) are distinctly separate. This separation is clearly not related to the falx cerebri, as the anterior descent of the falx cerebri occurs further in front of this area (as indicated by picture 1).
Could anyone offer an explanation as to why these structures are distinctly NOT continuous at this point? Further, if anyone could confirm whether any part of the cortex exhibits grey-matter-continuity (i.e. not via white matter tracts) between the left and right hemisphere, that would be greatly appreciated.

Could anyone offer an explanation as to why these structures are distinctly NOT continuous at this point?

The crista galli physically separates the straight gyrus.

Click to zoom

Click to zoom

... that would, presumably, permit grey matter from the left hemisphere to be directly continuous with grey matter from the right hemisphere. However, no such connection exists.

They are not physically touching in that location, elsewhere the two hemispheres are not connected (even though physically touching) by gray matter.

Further, if anyone could confirm whether any part of the cortex exhibits grey-matter-continuity (i.e. not via white matter tracts) between the left and right hemisphere, that would be greatly appreciated.

Except in rare cases, for example agenesis of the corpus callosum (ACC), communication between the hemispheres is via the anterior commissure and the corpus callosum.
The two halves are separated by a deep longitudinal fissure, see this animation:

sorry, but I do not believe the crista galli separates the WHOLE straight gyrus...it only separates the anterior portion, by virtue of the falx cerebri, which is illustrated in the very first picture I posted.

That's OK. I didn't claim that it does nor do my images show that, as explained in my second paragraph it's not the only factor; watch the animation, where it pauses.


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Is there a known mutation of an insertion type that prevents being infected by a virus?
Recently there was big news about the mutation CCR5 delta 32, that prevents HIV from infecting white blood cells, that was a deletion type of a mutation.
Do we know of an insertion type of mutation that have similar affect? i.e prevents being infected by specific/some virus(s)

Not an insertion but a gain-of-function mutation which causes virus resistance: https://www.ncbi.nlm.nih.gov/pubmed/16306606 Are you looking for human examples or mutations in any organism?

I am happy with any organism


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Creatinine excretion
Creatinine accumulates in blood if kidneys fail to excrete it.  Does this unexcreted creatinine ever get thrown out of body? What prevents creatinine from continuously rising in the blood?

Welcome to MedicalSciences.SE! Please take the [tour] and read the [help]. For reasons mentioned in this post and in [ask], we require prior research information when asking questions. Please help us to help you and [edit] your question to provide more information on what you have read on this subject, what made you ask this question, and any problems you are having understanding your research. This helps to provide an answer which will be more helpful. If you found nothing, what did you Google?

This is better suited to Biology as it is a fundamental science concept.  On that site as well, prior research (what you've found so far) needs to be demonstrated to avoid closure.

Your question has the answer.

Creatinine is formed irreversibly and non-enzymically from creatine and phosphocreatinine and is usually assumed to be metabolically inert in humans (Wyss & Rima Kaddurah-Daouk, 2000, Creatine and Creatinine Metabolism): no human enzyme is known to metabolize creatinine, and this compound is normally eliminated from the body via the kidneys

In chronic liver failure, however, "a significant quantity of creatinine is excreted into the gut, as is true of urea and uric acid, and is metabolized by gut flora" (Jones & Burnett, 1974, Creatinine Metabolism in Humans with Decreased Renal Function: Creatinine Deficit.

This was 'news to me', and the observation about urea is also surprising, but it looks to be a very good paper.