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How is the fluoride in toothpaste absorbed?
How is the fluoride in toothpaste absorbed by our body? Does the tooth absorb the molecule directly, or is it absorbed by the mouth?
The answers to this question suggest that some materials can be absorbed by the mouth, but fluoride is absent. Additionally, many municipalities add fluoride to tap water which I should imagine is actually absorbed in the stomach by a different mechanism than that of toothpaste.
Note that toothpaste generally comes with stern warnings not to swallow. Looking at the ingredients it seems the only thing that may be harmful is the fluoride itself. Therefore I suspect that toothpaste has a much higher fluoride concentration than tap water, which supports the notion that its fluoride is absorbed by a different mechanism than tap water.

The chemical mechanism by which fluoride protects teeth is the remineralization of hydroxyapatite $\ce{Ca5(PO4)3(OH)}$ in the tooth enamel into fluorapatite $\ce{Ca5(PO4)3F}$:
$$\ce{Ca5(PO4)3(OH) \ (s) + F- \ (aq) -> Ca5(PO4)3F \ (s) + OH- \ (aq)}$$
This reaction occurs at the surface of the enamel, i.e. directly within the mouth.  The fluoride ions participating in the reaction are dissolved in the saliva and other fluids present in the mouth.
Thus, the fluoride does not need to be absorbed into any part of the body (although, as part of the remineralization process, it can be said to be absorbed directly into the tooth enamel), and, in particular, there is no need for it to be swallowed.  Indeed, because of potential adverse effects of high levels of fluoride when absorbed into the body through the digestive tract, swallowing strongly fluoridated dental care products like toothpaste or mouthwash should be avoided.
That said, any fluoride that is swallowed and absorbed into the body, e.g. through fluoridated (or naturally fluoride-rich) drinking water, can still contribute to the remineralization of teeth, simply because some of it will be secreted back into the mouth as part of saliva.
While the fluoride levels in saliva (assuming a safe level of fluoride intake) are much lower than those in, say, toothpaste, your teeth will be constantly exposed to the fluoride in saliva, whereas they will only be exposed to toothpaste for a few minutes each day.  Thus, while the rate of remineralization due to systemic fluoride may be much slower than that due to e.g. fluoridated toothpaste, the total amount of remineralization per day may well be of a comparable magnitude.

Thank you! This is exactly the information that I was looking for, including both the mechanisms by which the fluoride gets to the tooth.

From different sources, I think that it can be safely assumed that fluoride stays in the mouth and is absorbed by the teeth while brushing unless ingested (reference). Most dental doctors agree that the fluoride is not absorbed in the mouth and that it may be retained on the surface of your oral mucosa, where it is then available to help re-mineralize your teeth after acid exposure (reference).
Fluoride levels in toothpaste differs according to the company that is producing it.

It may appear after the label "Active ingredient" or as a component
  under "Ingredients" on the toothpaste tube. Whereas previously
  fluoride content was given as a percent of volume (% w/v) or weight (%
  w/w), it is now accepted that the most efficient method of informing
  people of the amount of fluoride in a toothpaste is to give the "parts
  per million" fluoride (ppm F). Most manufacturers now give fluoride
  content in ppm F. The EU has prohibited over the counter sales of
  toothpastes with a ppm F value of 1500 (reference).

Of course ingestion of the toothpaste will lead to the fluoride being absorbed by the stomach.This could increase the dietary recommended intake of fluoride leading to fluorosis and many other issues (reference). There is also a study estimating the fluoride absorbed from toothpastes through ingestion. In the study, it states that

Measuring changing fluoride levels in saliva appears to be an
  acceptable non-invasive technique for following systemic fluoride
  absorption(reference).

The 1984 issue of Clinical Toxicology of Commercial Products lists Fluoride as "more poisonous than lead and slightly less poisonous than arsenic". Lead has a toxicity rating of 3, Fluoride has a toxicity rating of 4 (reference).
Hence it is recommended that the brushing habits of your young ones be supervised to check ingestion of toothpaste and use the appropriate amounts of toothpaste for brushing.
Health effects of fluoride can be read about in this article.
The action of fluoride on teeth and treatments with fluoride is very comprehensively given in this article.

The tooth bone directly absorbs the fluoride, then? It passes through the enamel?

@dotancohen Most articles call it absorb but I would like to say deposited. and no it doesn't pass through the enamel but becomes part of it which is why the term absorbed is used.

Thank you. If the enamel is the final destination of the fluoride, then how does digested fluoride get there? By the saliva only?

@dotancohen For fluoride in the mouth, I would have to say that saliva would be the way to get to the teeth.

I'm a bit dubious about that "more poisonous than lead" quote: it's repeated (in various mutated forms) on many anti-fluoridation websites, but I wasn't able to find anything like it in the claimed source (which, apparently, is actually a book, not a journal issue). That said, Google provides only a rather inconvenient form of snippet search access to the book, so, without an actual copy, I can't be quite 100% sure that it's bogus.

@IlmariKaronen the same thing is repeated here http://fluoridealert.org/issues/health/ and the obsevation is made in terms of acute toxicity.

Fluoride is absorbed mostly in the stomach and small intestine.

Several aspects of fluoride metabolism - including gastric absorption, distribution and renal excretion - are pH-dependent because the coefficient of permeability of lipid bilayer membranes to hydrogen fluoride (HF) is 1 million times higher than that of F(-). This means that fluoride readily crosses cell membranes as HF, in response to a pH gradient between adjacent body fluid compartments. After ingestion, plasma fluoride levels increase rapidly due to the rapid absorption from the stomach, an event that is pH-dependent and distinguishes fluoride from other halogens and most other substances. The majority of fluoride not absorbed from the stomach will be absorbed from the small intestine. In this case, absorption is not pH-dependent. Fluoride not absorbed will be excreted in feces. Peak plasma fluoride concentrations are reached within 20-60 min following ingestion. ... Many factors can modify the metabolism and effects of fluoride in the organism, such as chronic and acute acid-base disturbances, hematocrit, altitude, physical activity, circadian rhythm and hormones, nutritional status, diet, and genetic predisposition.

Source: Buzalaf MA, Whitford GM. Fluoride metabolism. Monogr Oral Sci. 2011;22:20-36. doi: 10.1159/000325107. Epub 2011 Jun 23.
Fluoride concentration:

tap water: maximum contaminant level goal is 4.0 mg/L or 4.0 ppm [1]
optimally fluoridated municipal water: 0.7 parts per million (ppm) of fluoride ion (F) [2]
toothpaste for adults: 1000 ppm or 1100 ppm F from three fluoride compounds. These are sodium monofluorophosphate (MFP), sodium fluoride (NaF) and stannous fluoride (SnF2) [2].

When ingesting toothpaste, fluoride is less absorbed from dicalcium phosphate dihydrate toothpaste [3].

References:

http://water.epa.gov/drink/contaminants/basicinformation/fluoride.cfm
American Dental Asociation http://www.ada.org/EPUBS/science/2012/may/page.shtml
Drummond BK, Curzon ME, Strong M. Estimation of fluoride absorption from swallowed fluoride toothpastes. Caries Res. 1990;24(3):211-5.

If the toothpaste is not ingested, then how does it get to the stomach and small intestine? Just whatever seeps down the throat? Why not just take a fluoride pill then, which would give a more controlled dose, instead of relying on however uncontrolled amount seeps down the throat.

Dotancohen, if fluoride is in the digestive tract, isn't the most likely source fluoridated water?

authors: евгений иванов


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Could felines live without meat?
Algae are a source of taurine and mushrooms are a source of vitamin D3. Both also contain high protein. So, it seems possible to feed a cat or other felines without any meat. Are there any concerns to have them live with this kind of diet?

This seems to have already been answered on pets stack exchange

@RoryM Already read and they always mention the same things I have search all these times, VitaminD3 and Taurine, which I present here that it could possible because there are these things contain both. And while mushroom is not meat It is very meatlike with taste of glutamic so cat love them too

Related: Is there benefit to feeding my cats food that incorporates fruits and vegetables?

@Zaralynda sorry but not so related. Because fungi and algae aren't fruit and veggie in terms of nutrition. They are composed of animal part more than plant. High protein than sugar. And no one mention about them

No, fungi are not "animal more than plant". They are a third group, independently evolved and different from either. The fact that they share a flavor component with meat that plants generally don't (umami) does noit say anything at all about their nutritional content, and the latter is what matters. (I haven't tried offering my cats mushrooms. They might appreciate the umami flavor. Then again, one of them loves fish but is apparently allergic to it, so they don't always know what is and isn't good for them.

@keshlam I have already read about nutrition fact of mushroom so I selectively use the sentence "composed of animal part more than plant. High protein than sugar" (except some species contain high sugar). And I never said that fungi is animal

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Is galvinoxyl antioxidant assay possible using NMR spectroscopy?
I would like to perform an antioxidant assay using the galvinoxyl protocol. The protocol states that we need EPR spectroscopy, but only NMR spectroscopy is available at my institution. Is there an alternate way where I perform a galvinoxyl assay using NMR spectroscopy.

Galvinoxyl is a free radical, which means it has an unpaired electron that can be detected with EPR. Antioxidants reduce the radical, which is then not detectable in the EPR anymore as it doesn't have an unpaired electron. What you need the EPR for in the assay is to determine how much of the galvinoxyl is still a radical.
Paramagnetic molecules like galvinoxyl are problematic for NMR, they bleach signals in close proximity to the radical and cause line-broadening. You still might be able to quantify the amount of oxidized and reduced galvinoxyl, but I'm not sure how reliable this would be. The oxidized galvinoxyl would probably be not visible in the NMR, while the reduced version would give a signal. You'd have to measure a few spectra to see if you can determine the percentage of reduced galvinoxyl from the NMR spectra.
EPR is the far easier method here, while I don't think doing this with NMR is impossible, there are quite a few ways it could be inaccurate. I'd strongly recommend to either use an EPR machine somewhere else, or use an entirely different assay that doesn't require such specialized equipment. I have no experience with antioxidation assays, but I'd guess that some exist that don't require EPR.

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Microscopy Book Suggestions
I've learned programming through great book recommendations; many from the Stack Exchange series of sites. I'm hoping to take this approach in order to gain a fundamental understanding of how fluorescence microscopy and sub-diffraction limit imaging tools work.
What books or reviews do you recommend that offer both a conceptual explanation of imaging biological specimens and practical advice? I'd settle for either one if you find the author to be effective.

Would also like to see a good reference!  ejstrong, would you be looking at cells, microorganisms, subcellular processes?  might be useful to you to be particular.  the game gets very different between butterfly wings and organelles.

Recommendation questions normally end up soliciting lists.  You've narrowed down your your focus a little bit, but there are still scores of books on microscopy out there.  Can you narrow it down any further (as shigeta alluded to)?

I am going to leave this as a comment, because I don't think this is exactly what you need, but the Cold Spring Harbor books about imaging are very good if you are going to use the techniques in the lab (they're very much focussed on practical issues). I own Imaging in Neuroscience: a laboratory manual but you can also find a book on imaging in general, one on live cell imaging, and one on developmental biology.

@Shigeta - sorry for not specifying. I would be looking at both cells and organotypic culture.

@jonsca - I would first want to learn about imaging live cells but would appreciate an overview of fluorescence imaging in addition to learning about specific imaging applications.

Apart from/ along with books, one can also learn through this course on [ibiology][ https://www.ibiology.org/online-biology-courses/microscopy-series/]


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Is half-a-tablet of X a substitute for a tablet of X/2?
This may be anecdotal.
At the pharmacy earlier, the prescription called for a drug with X mg of the target chemical. The pharmacy however only had stock of a higher potency of the same brand.
E.g. A prescription may call for 25mg of a particular chemical, whereas the pharmacy could only service a request for 50mg of that chemical in the same brand.
According to the pharmacist, and the medic - a proportional fraction of higher potency drug of the same brand may be substituted for the lower potency. Thus in the example above, half-a-tablet of 50mg may serve in lieu of a single tablet of 25mg.
For a given brand

Is half-a-tablet of X a substitute for a full tablet of X/2?
Does the corollary scale upwards too?

Disclaimer: all of this is not to be considered medical advice but rather a general explanation. You should talk with your physician and/or pharmacist on a case by case basis when determining whether to take a drug and how to dose it.

We should consider that most pharmaceutical forms are made up from two main components: the active ingredient(s) and the excipients.
The active pharmaceutical ingredient is:

the substance in a pharmaceutical drug or a pesticide that is biologically active.

That is, the part of the drug that actually "does the job". Note that the dosage on the package refer to this, not the weight of the pill! For instance 500mg aspirin will contain 500mg of the active principle (acetylsalicylic acid) but the pill itself will weight more than 500mg.
An excipient is:

an inactive substance formulated alongside the active ingredient ("API") of a medication, for the purpose of bulking-up formulations that contain potent active ingredients (thus often referred to as "bulking agents," "fillers," or "diluents").

This does not normally have biological effects, but allows you, for instance, to have a pill that is of sufficient size to be easy to take in your hand.
When you split a pill in half you are assuming that each half contains the same amount of active ingredient.
This is regulated by the Pharmacopoeia*. In particular when looking at the monograph for tablets we can read (bold is mine):

Tablets are solid dosage forms usually obtained by single or multiple compression of powders or granules. In certain cases tablets may be obtained by moulding or extrusion techniques. They are uncoated or coated.
Tablets are normally right circular solid cylinders, the end surfaces of which are flat or convex and the edges of which may be bevelled. They may have lines or break-marks (scoring), symbols or other markings.
If the break-mark(s) is/are intended to facilitate breaking the tablet for ease of swallowing a dose consisting of one or more whole tablets, the scoring is not critical. However, if the break-mark(s) is/are intended to permit accurate subdivision of the tablet in order to provide doses of less than one tablet, the scoring is critical. Tablets containing active ingredients having a narrow therapeutic window should generally not be presented with break-marks for subdivision. Non-functional break-marks should be avoided.

The point about the therapeutic window shows why splitting pills may be dangerous. The therapeutic window is the range of concentration of a drug which treats disease whilst staying within the safety range.
If this window is narrow, minimal changes in the dose can cause the treatment to be ineffective -if there is too few of the active ingredient- or toxic -if there is too much.
The Pharmacopoeia also lists several tests to be done on tablets. In particular, in the presence of break-marks, the manufacturer should

ensure the effectiveness of break-marks with respect to the uniformity of mass or content, as appropriate, of the subdivided parts so that the patient receives the intended dose.
A suitable test to assess the uniformity of mass during development is as follows:
Take 30 tablets at random. Break each tablet by hand and take one part for the test and reject the other part(s). Weigh each of the 30 parts thus obtained and calculate the average mass. No individual mass is outside the limits of 75% to 125% and not more than one individual mass is outside the limits of 85% to 115% of the average mass.

I will not go into further details, but there are, for instance, other tests to be done to ensure uniformity of mass and content from tablet to tablet, as well as their physical stability (i.e.: they don't have to fall apart in the box).
Note that the packaging should generally include instructions about whether it is safe to split the tablet and how to store (and how long) unused pieces.
This is for splitting tablets. The opposite situation may also arise. Are 2x2mg tablets equivalent to 1x4mg one (speaking of weigth of the active compound in the tablet, not the weight of the tablet itself)? The same reasonings as above apply, however, because tablets should be uniform and no breaking is involved, this is generally safer than the previous case.
All of this applied to a single dose of a drug. Now I would just add a word about repeated doses. I cannot stress this enough: always refer to your physician about drug dosing. Taking a pill in the morning and one in the evening is NOT the same thing as taking two in the morning and none in the evening or taking four halves during the day. Self-dosing is dangerous and should never be done.
Taking half the dose may result in sub-optimal concentration of the drug (so it won't work as expected). Taking twice the dose may result in a toxic peak concentration, which is obviously not something that you want.

* note that there are multiple Pharmacopoeias, and the exact directives may vary. For simplicity I will refer to the International Pharmacopoeia, 4th Edition, 3rd supplement, published by the World Health Organization, and available online. There are others, such as the European Pharmacopoeia (apparently not freely available?) or the Japanese Pharmacopoeia, but I guess that goes beyond the scope of this answer.

This website gives a nice overview, including how the FDA approve drugs that they expect will be spit and some practical issues of pill cutting.
Yes, half a tablet of (2x dose) is, absent other issues, equivalent to one intact tablet of (1x) dose.  The main exceptions are practical ones.. where the tablet cannot easily be cut; where the dosing is so specific that slight variations of dose (uneven tablet fragments) matter, or where the dose is in a capsule or has some special coating so that cleavage might alter the release of drug into the body.
Yes, dosing scales upwards.  Two pills give twice the total dose of one pill.
All prescriptions are dispensed with specific dosing regimens (i.e how much you take and when you take them) to ensure the drug reaches effective concentrations in the body. You should not try to 'boost' the drugs effectiveness by taking more drug, or taking drug more frequently than your physician has prescribed.  As noted in the weblink above, it can be tricky to keep track of dosing and timing if your pill bottle contains whole and cut pills.  (i.e what does "take one pill every NN hours" mean ?).
This is NOT MEDICAL ADVICE . Always consult your physician and/or pharmacist for your particular case.


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Primer design for PRP24-TAPtag
I have a problem with my proteomics homework. I was asked to design primers used to create a homologous recombination box to create PRP24-TAPtag yeast. I know that homologous regions should be 40-50nt and that my primer should include overhangs. I was told to base off of this publication:
https://www.ncbi.nlm.nih.gov/pubmed/11403571
I have designed primers before, but this time I have encountered really big problems. I have found both my plasmid, pBS1479, TAPtag and PRP24 protein sequences, but I have no idea how should I join them to create primers and how to include the TAPtag. This is my first time using this method. Are there any tools I can use for this task?
Should I add tag sequence to C end of my protein, then use plasmid seqence to create overhangs?

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Can you please help me identify this insect?

I have been trying to get rid of this bug and need help to identify it.
I found this in my bedroom first.
I don't think this is a bed bug as I saw it fly. It is black with some white spots on it.
Any suggestions on what it could be are greatly appreciated.
Thank you!

Can you please edit your question and add where you found this insect?

That is a bean weevil, family Chrysomelidae, subfamily Bruchinae. If you have dried beans at home, check for an infestation. Throw out the contaminated beans, and put your others in sealed plastic containers, or in the fridge. https://bugguide.net/node/view/13857

Thanks Karl, I checked my beans one kind of them was indeed infested with them, no rice or other grains were infested. But I still have one question how come they spread that much? Because there is a huge no of those in my house

They must have found another food source, or were attracted by the original infestation.

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You need DNA to make RNA, and RNA to make DNA, so they had to come into existence at the same time?
A statement I recently read: 'Evolution is debunked and gives no basis for morality. Natural Selection throws away info, it does not add.
You need DNA to make RNA, and RNA to make DNA, so they had to come into existence at the same time. Created.'. Who can shed a light?

I think its rather ironic to note that without question, this same "logic" (stupid as it is) could be used to "disprove" the existence of God, since no creator could exist without being created by the creator... Also, evolution has never been claimed to provide morality. Darwin was so repelled by parasitic wasps that he thought that no benevolent creator could have been responsible for such cruelty. That creationists have adopted a business model based on lies (false witness) is also pretty ironic.

What is the source of your quotation? What is your question exactly? What attempt have you made to solve it yourself? Have you searched this site for related questions?

There have been two answers that refer to the RNA World Hypothesis — which I do think is relevant — but both contain aspects I, personally, find unsatisfactory (as I commented originally). As this question has come up again from the Community, let me answer the question in a way that I, at least, find satisfactory.
I am only concerned with the biological part of the question:

“You need DNA to make RNA, and RNA to make DNA, so they had to come into existence at the same time.”

The question deals with something we do not know — the times at which DNA and RNA  came into existence — so all we can deal with is the logic of the argument, i.e. is the conclusion of contemporaneous appearance necessarily true?
To refute that all that is needed is an alternative hypothesis for a sequential appearance that is consistent with biology and chemistry.

Contemporary biological systems exist in which DNA is not need to make RNA — namely RNA viruses. Although these depend on organisms (bacteria or eukaryotes) that have DNA genomes, their replication does not directly/mechanistically involve DNA.
This, by itself, invalidates the first assertion (“you need DNA to make RNA”).
Turning to the origin of cellular life, which currently has exclusively DNA genomes, there is therefore no biochemical/mechanistic problem in envisaging that the ancestor of modern organism had an RNA genome at a time when pathways for synthesizing the precursors of DNA did not exist. Note that this does not require the other aspects of an RNA world (RNA, rather than protein, enzymes). These may be likely, but are not part of this argument.
So all that is required is a biochemically plausible hypothesis for the emergence of pathways for the synthesis of deoxyribose and thymidine, of enzymes to polymerize them, the switch to a (more stable and less error-prone) DNA genome, and the switch to this new genome encoding and transcribing the RNAs that are still necessary for protein synthesis and the like. I maintain that there is no reason in principle that this is not possible.

Whether or not the sequence of events was as in the scenario above, I argue that it demonstrates how RNA and DNA could have arisen at different times but given rise to the inter-dependent situation we see today, and demonstrates the basic flaw in the argument in the question.

I'm reading your questions as:

Since DNA and RNA co-depend on each other, which one existed first in the course of evolution

The honest answer to this is: we don't really know.
The RNA world hypothesis is a pretty good and also much studied and developed theory, but it's nonetheless a theory still. Even with solid experimental prove that a pure 'RNA world' can over time evolve to make DNA, won't let us know if it actually happened like this in the past or not.
A bit more background on why an intial "RNA world" from which DNA evolves at some point is theoretically possible:
In modern life forms genetic information is stored in DNA, then translated in RNA and a lot of functional elements are the resulting proteins. This is already a pretty complicated system so it was hypothesized that RNA might have one of the first molecules used for all of these steps. RNA can obviously store information (though not quite as long as DNA, since get degraded more quickly) and it can also have catalytic function, which is obvious from e.g. the ribosome, which still uses catalytic RNA units to build up all proteins.

The quotation in the question says nothing about which came first. It asserts both emerged together, presumably as an act of God, given the preamble. The question you want to answer has been asked and answered previously.

@David As far as i understand it the OP does not assert that DNA and RNA emerged together, but saw that statement somewhere and is now asking confirmation or further information on that - presumably from a scientific viewpoint given he is positng on this site (I'm judging from the question title and the 'who can shed light' part in the question). I purposely did not comment on the creation / act of God part since it has nothing to do with science.

According to RNA world hypothesis at some point the organisms had RNA genome only and only later DNA and transcription machinery was built to protect the genome(DNA sits in the nucleus and does not interact much with others).
RNA got both informations storage capability as well as the catalytic activity. Thus it can be concluded that at some point, RNA was the primary genome and RNA alone could let an organism survive due to its catalytic properties.
So to answer your question, it is a probability only but still, RNA appeared before DNA

Please note that the RNA world hypothesis doesn't have anything to do with nuclei - eukaryotes (and therefore the nucleus) for sure evolved much later than the DNA-RNA-protein system itself.


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Will fruit/seed of a bonsai yield another bonsai plant/tree?
With practice one can create a bonsai; no complicated modification of the DNA in a high-end lab required. The bonsai will even beget bonsai fruit.
What I am curious about is - if such bonsai fruit is planted again, will it give rise to a normal, or a bonsai tree?

No, seed from a bonsai tree will not automatically produce another bonsai tree. Bonsai are dwarfed due to restriction of root growth in their small containers - unless the offspring are also grown in environmentally dwarfing conditions, they will tend to grow normally.

Could you toss in any reference material on the subject please?

Sorry, this question will not be answered in the scientific literature. If you have any questions about specific details perhaps I can furnish answers with references for those details.

However, non-scientific sources will confirm my answer, for example the wiki page: "Bonsai does not require genetically dwarfed trees, but rather depends on growing small trees from regular stock and seeds."

Well ... according to another question on this forum I understand a sapling relies upon the food contained within the seed for it's initial growth. I assume then - for bonsai fruit to grow to average size then (a) it must exhibit a growth spurt and improved quality of tissues+chemical processes or (b) each bonsai fruit would have at most a single seed of the normal size or (c) the bonsai fruit/seed would in turn give rise to a similarly stunted plant. What am I missing?

Small seeds do not necessarily lead to stunted plants, but they will contain less resources for germination. Provided the seeds have enough resources to complete germination, which is quite likely if you are cultivating them deliberately, they will grow to similar final sizes regardless of the seed size. They might have different rates of growth during their early development.

Feel free to ask a new question if you feel there's a part of the picture you're missing. I'll try to tie it all together a bit more coherently in an answer to such a question.

@Everyone: In any case, I'd assume that a bonsai tree, if allowed to bear fruit, would produce normal-sized fruit and seeds, just very few of them. At least that's what seems to happen with naturally stunted trees growing e.g. in cracks in rock.

@IlmariKaronen yes thats right - although often when people choose a strain for Bonsai they pick one with small fruit so they don't look out of proportion. In that case the children would continue to bear small fruit, assuming the species was one that grows true from seed.


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Do any plants exhibit hormonal changes similar to puberty?
Just what the title states.
Are there any plants/trees that exhibit a growth spurt at a definite interval after the shoot appears?

In flowering plants (the angiosperms) there are several developmental transitions in the life of the plant. I won't list the plants, because the list includes pretty much all of them (although the magnitude in the change of developmental pace differs widely between taxa and environments).
First there is seed germination, which is controlled hormonally. Absence of germination is usually imposed by abscisic acid, whilst germination is caused at the appropriate time by gibberellic acid and ethylene (among other things; Holdsworth, Bentsink & Soppe, 2008).
Next, in many herbaceous species there is a transition between a spreading growth stage (e.g. rosette growth) and the flowering stage. The 'growth spurt' here is the differentiation and elongation of the flowering stem, and then subsequently the sudden flowering of buds. The transition is also controlled hormonally, by a variety of hormones including auxin (Zhao, 2010), gibberellic acid, ethylene (Schaller, 2012), and the long anticipated, recently confirmed florigen (Choi, 2012). Ethylene and abscisic acid then play important roles in the next developmental transition when seeds and fruits are produced and dehisced.
Small RNAs are also now being revealed to play a large role in controlling the timing of developmental, but they are upstream of the hormonal changes. In particular some key miRNAs are involved in auxin-based regulation of branching, and in embryogenesis (Nodine & Bartel, 2010), and RNA silencing is involved in the switch from rosette growth to flowering growth (reviewed in Poethig, 2009 and Baurle & Dean 2006).

 Bäurle I, Dean C. 2006. The Timing of Developmental Transitions in Plants. Cell 125: 655–664.
 Choi CQ. 2012. A Blossoming Field of Research: How Florigen Is Transported to Create Flowers. PLoS Biol 10: e1001311.
 Holdsworth MJ, Bentsink L, Soppe WJJ. 2008. Molecular networks regulating Arabidopsis seed maturation, after-ripening, dormancy and germination. New Phytologist 179: 33–54.
 Nodine MD, Bartel DP. 2010. MicroRNAs Prevent Precocious Gene Expression and Enable Pattern Formation During Plant Embryogenesis. Genes Dev 24: 2678–2692.
 Poethig RS. 2009. Small RNAs and developmental timing in plants. Curr Opin Genet Dev 19: 374–378.
 Schaller GE. 2012. Ethylene and the regulation of plant development. BMC Biology 10: 9.
 Zhao Y. 2010. Auxin Biosynthesis and Its Role in Plant Development.


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Are there any DNA base sequences that are fully conserved between the genomes of all humans?
That is, they don't differ throughout the entire population. I understand of course that we can't DNA sequence every human, so by "fully" I mean there's an incredibly small probability of there being a mutation retained in a living individual.
Also by the genome I'm referring to the consensus of all the cells composing in the individual.
I guess my question is really, where are the crucially important sections of DNA that are simply unmodifiable without being incompatible with life?

In 2004 Bejerano et al. identified "481 segments longer than 200 base pairs (bp) that are absolutely conserved (100% identity with no insertions or deletions) between orthologous regions of the human, rat, and mouse genomes". These were found to be mostly in/around genes related to RNA processing, which is perhaps unsurprising given that it is such a primitive/inherent biological process.
Bejerano's paper has been cited over 500 times on Scopus, with numerous papers reporting variants in such regions that cause diseases such as colorectal adenocarcinomas.

So few conserved regions exist because there is plenty of redundancy in the genome; many genes functionally overlap with others, and many genetic variants are 'silent' - they have no effect on the phenotype. Having this variability is advantageous in Darwinian terms because this increases the evolvability of the species.
There are many regions of very high homology between individuals (protein-coding regions are highly conserved even between species), but there will still be natural variation; each mutations effect will be dependent on the rest of the genome. Genes work together to produce a working organism - they do not each code for a little 'bit', and therefore a change in one portion of the DNA may be 'balanced' by a change elsewhere.
It is only in 'ultra-conserved' sequences that mutations are presumably incompatible with life because the process is so finely-tuned and indispensable.

Interesting, thanks for the research link and explanation!

ahem, "very high homology"?

@bobthejoe, thanks for that constructive comment. Is the the 'very' you dislike? Or the 'high'? Or the combination of the 2 used with 'homology'? Degrees of homology are commonly used to describe the relatedness of 2 biological systems/molecules/processes... whatever.

@LukeTheDuke. Meaning that it is commonly used doesn't mean that it is appropriate. There shouldn't be degrees of homology, just homology. Yes, I am nitpicking but it is a concept that should be better enforced.


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What are the optimal conditions for storing frozen glycerol stocks of bacteria?
The common method of storing bacteria long-term is to collect saturated liquid culture, such as LB, and mix it with sterile glycerol so as to obtain 10-30% final glycerol concentration. The resulting mixture is then frozen, usually at -80 or -20C. Bacteria stored in this way are said to be viable for years. I am curious as to what affects the success of such a storage strategy?

Obviously the temperature should be below freezing, but how exactly is viability affected? Is colder always better (assuming the tube can withstand it)? Is there rapidly diminishing returns after -80C? Is there an optimal temperature? I'm expecting something like a plot of viability after 1 year of storage vs. temperature, ideally with multiple species.
What is the optimal glycerol concentration?
How much does viability drop per freeze-thaw cycle?
Does it matter how quickly you freeze after adding glycerol?
While letting a frozen sample thawed is considered unadvisable, after it does thaw, does it matter how long? Does every second count, or is there little difference so long as it's not several multiples of the lag phase duration?

However, I found it very difficult to locate specific information about the optimal conditions for such storage. For instance, Addgene claims that optimal glycerol concentration is unknown. Moreover, a lot of the older papers on this topic are paywalled (even from my institution). But the experiment to determine it would be so trivial that I can't believe nobody has done it. I am interested primarily in data from actual experiments, and I am interested in glycerol alone as a cryopreservant.

Here’s something.


text:
Where are all the dead cockroaches?
Major North American cities are full of large cockroaches. Given their numbers and relatively short lifespan, there must be staggering quantities of cockroaches dying in a city every day. However, I never seem to encounter their carcasses in cities.
I notice a fair number of dead roaches indoors, which actually surprises me since you would think that there is more thorough cleaning and pest control indoors vs. city streets. The number of dead roaches I see indoors seems about consistent with the number of live ones.
However, outdoors I see a lot of live roaches, and hardly any dead ones. Most carcasses I notice are mechanically damaged and near heavy traffic areas, so most likely stepped on by someone who was walking by. But what about roaches dying of natural causes (or disease/poison)? Are there animals that scavenge the carcasses very efficiently (ants? birds?)? Do the roaches like to run away and die in isolation? Do they just not die naturally very often, and usually get hunted by a predator?
Note that I am asking specifically about city cockroaches, in mostly concrete areas.

Ants pretty much scavenge everything. I don't know about North America but in India ants do a good job in finishing off dead/semi-dead cockroaches. :P

I have found cockroaches live around places of low temperature, like water reservoir at my place. The huge number of outdoor cockroaches you mention of might live around underground drainage system, far from the the path you commute.

I looked up Wikipedia, according to it they need moisture and not low temperature.

In the big cities of North America (e.g N.Y), the big piles of dirt and moisture attract many hostile animals such as the ones you mentioned: the cockroaches. You should also consider that in the north there is a very common factor that attracts collonies of cockroaches: the low to mediocre temperatures. Moreover, you should reconsider the cleanliness of the sewers. The sewer and the leftovers that exist there are highly nutritional for the cockroaches. That's why you don't see many dead ones on the streets. And where is the start of the sewers? The sewers start from every house. That's why you notice more roaches in the houses than outdoors. They need a place that might provide them the sewer's environment such as the bathrooms, or an other place in the house that has moisture and is mostly dark. Cockroaches live and die to the same place and don't go somewhere else to die. The decay rate outdoors is higher of course, than indoors because every house is cleaner than the roads. With the process of cleaning many factors, such as mites are swept away to the environment.
For the second part of your question:
Outdoors there are many  scavengers and natural predators for the cockroaches. Some of them are: toads, frogs, beetles, geckos, iguanas and birds.  Entomopathogenic fungi have also been identified as lethal to roaches, as their spores attach to insects and kill them within weeks. Cockroaches affected by fungi then pass the parasite on to other cockroaches, and the cycle continues.
Ants prey on some cockroach species, but other roachess actually live with ants in their colonies. These are called myrmecophiles, meaning lovers of ants. They don't seem to offer their hosts anything in return for living with them, and are usually tiny and unobtrusive. Other species - termitophiles - live in similar fashion with termites.
And yes ants are the major factor of dicomposion in nature, because they devour almost anything.
I hope this answered your question, becaused I used very extended research :)

This is a good attempt at an answer! It would even be better (and attract upvotes) if you added some references to the research you used.


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Is this a young roach?
Looks like a roach to me, but dont know for sure or what kind. Measures about 2cm large. Location: central Mexico

short answer is that yes, it is a roach


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What is the most genetically complex organism?
I understand that new genomes are being sequenced ever day and these answers replace themselves often; although as of today, what has been proven to be the most genetically complex organism (Other than a human of course)? I keep getting a multitude of different answers like Daphnia pulex, Axolotl, Paris japonica or Adder’s Tongue all from different dates and sources so it becomes difficult to tell what is the right answer here if any. If this question is not specific enough I would be happy to revise.
Edit: I would define genetic complexity as either genome size or number of genes. Either answer  would work. If you would like give other information like chromosomes or isoforms from any other definition, that would be helpful. Whatever is the best of the best.

I think one of the biggest problem with this (type of) question is how you define 'genetically complex' - there a lot of different things one can consider (and weigh differently): genome size, number of genes, genome architecture, isoforms and/or copies per gene, (alternative) splicing, regulatory interactions of genes (at different levels). Additionally its worth to note that we know a lot more about the human (or also mouse genome) than most others - just because we haven't found things like cryptic transcripts or circular RNA's in other species (yet), doesn't mean they don't exist.

Complexity is not the length of a genome, but the amount of information encoded in it.  (See Information Theory.)  And even that isn't the whole story, since some "simplifications" like mammalian live birth & post-natal care can lead to a more complex result...

Edit: I would define genetic complexity as either genome size or number of genes. Either answer or information would work.

Largest genome: Paris japonica, a rare plant. Its genome is 149,000,000,000 base pairs large. Approximately 50 times larger than the human genome, by base pair count.
Higher number of genes in an organism: Daphnia pulex, a very common species of water flea. 31,000 protein-coding genes.
As already pointed out, the most genetically complex organism is an unclear question. Complexity can be interpreted in different ways, and I don't think we could agree on a satisfying measure (or definition, for that matter) of genetic complexity.


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Where do cockroaches go in the daytime?
Urban parks in North America teem with sizable cockroaches at night. However, in the daytime they are nowhere to be seen. Where do they go?
I know that they tend to avoid light, but how do they go about finding a hiding spot? Do they just throw themselves into any superficial crack and stay still? Do they travel a substantial distance into storm drains, water pipes, tunnels and hollow walls until they are well out of reach of larger animals? Do they have a nest that they return to every night or do they just use whatever hiding spot is nearby?
And specifically for small urban parks, flowerbeds and lawns - do they dig tunnels in the soil? Do they nest in the trees? Or do they simply leave the park and hide in nearby buildings, sewers, and similar human-built structures?
I ask because while it is obvious they must hide somewhere, I have never actually "gotten the drop on" a sleeping or hiding cockroach in a park - or elsewhere - I've only encountered roaches that were scurrying out and about. Some nocturnal insects can be found by for instance flipping over wet rocks or digging up some soil, but cockroaches despite being large and numerous are nowhere to be seen. Are they just really, really good at hiding?

Basically, yes, cockroaches are very good at avoiding detection. Since you linked to the American cockroach (Periplaneta americana), I'll discuss that species in my answer. I've only twice, in my life, seen an actual cockroach. I don't know what parks you're referring to in your question or if it's that common.
By the time you start lifting up a rock or board to look for a cockroach during the day, it will have already sensed you coming and have left.

They spend most of their time in narrow, tight cracks and spaces where surfaces touch them on both sides.
  (Cockroaches from the University of Minnesota)
Cockroaches like to be touched.
  Roaches are thigmotropic, meaning they like feeling something solid in contact with their bodies, preferably on all sides. They seek out cracks and crevices, and will squeeze into spaces that offer them the comfort of a tight fit. And I do mean a tight fit. The small German cockroach can fit into a crack as thin as a dime, while the larger American cockroach will squeeze into a space no thicker than a quarter.
  (10 Fascinating Facts About Cockroaches)

When you understand how thin a crack can be for a cockroach to wedge itself into, you get a better idea how they hide during daylight hours in the outdoors. Many trees have rough bark with enough crevices for them to hide. They could fit in the thin spaces between the bottom of concrete sidewalk pavers and soil, under leaf mulch and many other spaces you may never have noticed before. It takes very little. Best places to look for them in parks would be around trash receptacles where people toss food they didn't finish eating.

This does not provide an answer to the question. To critique or request clarification from an author, leave a comment below their post. - From Review

I bumped the submit button and quickly hit edit to finish.i wasn't sure if the beginning answer went through or not but I guess it has. ;P

Because cockroaches dislike light, they disappear during the daytime to dark places, including the undersides of appliances like stoves and refrigerators, underneath sinks or other installations, near plumbing, inside light switches and behind wall paneling or doorjambs. They also hide in the insides of bookcases or furniture, the folds of drapes or other fabrics, in piles of detritus like old newspapers, paper bags or pet food bags, and in among brooms or mops. Their hiding places are nearly endless, provided they are dark and usually undisturbed.


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Can someone identify this Lepidoptera larva?
That's from Brazilian Amazon, more specifically a small mountain (300 m high) called "Morro dos Seis Lagos" (six lakes hill), at São Gabriel da Cachoeira municipality, Amazonas state, located at 0.283 North, 66.685 West.

Can you add an approximate size? 2-3cm?

@RHA Sorry, it's been 14 long years now. But I think bigger than that, between 5 and 10 cm.


text:
Can we estimate longevity from menopause age?
This is from an answer in other question, about the age at which menopause occurs:

Aristotle's assessment was similar to those of Hippocrates and also
  Roman authors, so it seems that 2000 years ago most women entered the
  menopause in their early 40s. Mediaeval authors, however, gave the 50s
  as the age when menses ceased-much closer to the timing for twentieth
  century women.

Considering that, throughout history, menopause starts at about 40-50 years, shouldn't this point to a stable and long life expectancy? (Considering also that menopause is an adaptation.) When we read that humankind used to live much less than today, isn't it just the effect of newborn mortality, and thus adults lived just about as long as we do today?

these author may not be the best sources for anatomical/biological information. Especially for trying to gauge the average anything about women, Aristotle thought women grew fewer teeth for crying out loud. medieval "doctors" were even worse.


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Is homosexuality an adaptation in humans?
Homo sapiens have menopause - as some other mammals (e.g. some Cetacea) - a phenomenon where older females live for decades after the end of their own reproduction.
Perhaps homosexuality, that looks to hold at 10% levels in any population, may be just the same sort of adaptation?

A quick scan of global and US data on wikipedia suggests the rate is closer to 5%.

To answer this question, we need to know the 4 values in the pay-off matrix, that is nb of babies of hetero sibling of a hetero, hetero sibling of homo, homo sibling of homo and homo sibling of hetero.

Also see: http://biology.stackexchange.com/questions/7669/how-can-homosexuality-evolve-despite-natural-selection

@kmm thanks for that link. Should we mark this question as a duplicate then? unless we edit this question to focus exclusively on kin selection ?

I would put between 5 and 10%, @user137. But homophobia makes lots of homosexuals deny themselves (lowering the numbers in most researches). And other biological phenomena occurs at the 10% threshold (left-handedness, black jaguars, left-turning shells, etc.)

Is there a reason you expect black jaguars and homosexuality to occur at the same rate?

@canadianer, as I said, many minorities in Nature occur at 10% of the population. And homosexuality is also around this number. See, for instance, http://en.wikipedia.org/wiki/Demographics_of_sexual_orientation#Brazil.

Barnard's wonderful text "Animal Behavior: Mechanism, Development, Function and Evolution" offers some enlightening summary to the discussion of homosexuality in a biological context!
Brief Summary to ch 12, page 606:

What we know so far:

homosexual behavior is recorded all throughout animal kingdom
there are evidence for genetic basis to homosexuality in various species including humans

Three interrelated schools of thoughts:

Homosexuality is maladaptive - external stress creates homosexuality

reduce resource stress on family unit, youngest child tend to be gay (E.M. Miller 2000)
*** mitochondrial DNA carries male killing genes, with male being a dead-end (Hurst 1991)

Homosexuality as an adaptive early phase of development - homosexual acts are just target practice

homosexuality is just males practicing sex on each other, most homosexual acts are performed by bisexuals with just as high fertility
  as straight males (Baker & Bellis 1995)

Homosexuality advantages in other aspects of reproduction - homosexuality may imply better parenting

homosexual genes induces feminine attributes in males such as sensitivity, empathy and kindness hereby increasing likelihood of long
  term pair bonding and paternal care (E.M. Miller 2000)

*** original text:

A completely different suggestion is that homosexuality may reflect
  the interests of selfish genetic elements (see 2.4.3.2) inherited
  maternally on mitochondrial DNA for which males are effectively a dead
  end. Some insects have been shown to carry 'male-killing' genes on
  their mitochondrial DNA, so perhaps homosexuality is a similar, if
  more benign, rout to sidelining males (Hurst 1991)

keep in mind these are ot mutually exclusive either, non-exclusive homosexuality can increase reproductive success, exclusive homosexuality is rare enough it could be a side effect of this beneficial effect. homosexuality is not a single behavior.

There is a study that found that female maternal relatives of homosexuals have higher fecundity than those of heterosexuals [1]. This suggests that an allele predisposing to homosexuality may propagate because it increases reproductive success in some situations, not necessarily in the homosexual individual.
However, many factors can influence a persons sexuality, such as birth order (in males each additional older brother increases the odds of homosexuality by approximately 33%) [2], so genetics only tells part of the story, and I found no comparable explanation for female homosexuality.
Here's an interesting article if you want further reading [3].

Camperio-Ciani et al, 2004. Proc Biol Sci. Evidence for maternally inherited factors favouring male homosexuality and promoting female fecundity
Cantor et al, 2002. Archives of Sexual Behaviour. How Many Gay Men Owe Their Sexual Orientation to Fraternal Birth Order?
IFL Science. Born this way? An evolutionary view of ‘gay genes’

Genetic view of adaptation:

Do note that this is looking at the view from the POV of a gene. Please read the comments below this answer, for a small discussion on the kin selection hypothesis. Do note that I do not study evolutionary psychology, or work on the level of the population.

This is a bit of a misconception, as nature really doesn't work like that. Nature works by allowing people to pass on genes, and then selecting those genes which are the best. Now the issue with homosexuality when viewing from an evolutionary angle is that, homosexuality by definition doesn't allow for genes to be passed on. I would also quote Richard Dawkins in this issue

“That’s a very tempting error,” Dawkins replied, “not with respect to
  homosexuality, but with respect to the idea that nature does
  population control. That’s not the way nature works.”
“It’s so tempting to think that things will be best for the species,
  so nature will do whatever it takes to keep the species going. But
  that’s just not the way evolution works.”
“Natural selection,” he continued, “works at the level of the
  individual gene. So in order for natural selection to favor population
  control, [it] would have to favor a gene or genes within an individual
  that limited that individual’s reproduction.”
“Homosexuality would do that, but of course, it wouldn’t actually be
  naturally selected because the individual [who] doesn’t have children
  doesn’t pass on the genes for not having children.”
“In order for natural selection to favor population control,” Dawkins
  said, “it would have to be the case that an individual who has too
  many children ends up rearing fewer” successfully.
He noted that this is exactly what ornithologist David Lack found when
  he studied avian clutch size — those birds that laid too many eggs
  were not able to care for all their hatchlings, whereas as those who
  laid too few were not selected for the obvious reason — they didn’t
  produce enough progeny.

Taken from: http://www.rawstory.com/2015/03/richard-dawkins-explains-homosexuality-didnt-evolve-as-natural-population-control/

The OP is referring to kin selection processes (or group level processes if you prefer). Selection does not only act at the level of the gene. Homosexuality might be beneficial if sibling of homosexuals have more babies. The allele would indeed increase in frequency. From Hamilton and Nash work, we can calculate the equilibrium frequency of homosexuality from the pay-off matrix.

@Remi.b Interesting you mention that. I was reading up on [Bobrow, David, and J. Michael Bailey. "Is male homosexuality maintained via kin selection?." Evolution and Human Behavior 22.5 (2001): 361-368.]  and [Rahman, Qazi, and Matthew S. Hull. "An empirical test of the kin selection hypothesis for male homosexuality." Archives of sexual behavior 34.4 (2005): 461-467. ] and they seem to find no support for this? Do note that I am not an evolutionary psychologist, so I am not an expert in this field and am not upto date on literature. Has supporting evidence been documented ?

It's also incorrect to assume that homosexuals never pass on their genes. There's nothing about being gay that makes you physically incapable of reproduction.

@user137 Yes, I agree that homosexuals can reproduce. But do note that homosexuals, can not reproduce, unless there is a partner of opposite sex involved (which goes against the scientific definition of homosexuality). What I mean is, if a homosexual chooses to reproduce by in vitro fertilisation, surrogacy or any of the other ways that currently exist, though legally a homosexual, there has to be a biological partner of the opposite sex involved. (I mean no disrespect to the LGBT community).

Yes, I'm thinking about kin selection. Rover Eye, Bobrow & Bailey found that "homosexual men were somewhat more estranged from family members, especially from fathers and oldest siblings". This seems a consequence of homophobia, not of homosexuality itself. I don't think there was homophobia in the environment where homosexuality evolved. Rahman & Hull used a very reduced sample (n = 120) in a country well known for its historical homophobia.

Also, we don't have to think of homosexuality and heterosexuality as two isolated concepts. They're more of two extremes in a continuum.

@Rodrigo, I presume you are referencing the Samoan study, where homophobia was absent? It does make sense in an obvious way doesn't it. The inclusive fitness offered by homosexuals, is largely dependant on acceptance of society, and inversely related to homophobia. And apologies for not being able to critique the papers properly. This is not my field, and I tend to work at the genetic level, not population level.

Ok, Rover Eye, no problem at all!


text:
Is there a limit to how much concise information a human can learn adequately?
Like, I am trying to learn more chemistry, but also computer programming from the higher-level programming methodologies, frameworks, languages, APIs, XML, web development, and I'm also hoping to improve especially with computer hardware/electrical engineering, and I am trying to improve my pixel art/graphic design/animation skills all at the same time, that is no set schedule for any, and just learning whatever I get my hands on.
Is it possible to learn this way for a human, or will this eventually become too much, and I'll have to sort them/order what I learn separately?
I have not been seeing very much success, but I do keep learning. The problem? Well, I can't get a good grasp on any subject because I am interchangeably attempting to learn all of the aforementioned subjects sporadically, interchangeably, and without any fine schedule. Is this a wrong way for a human to learn, or is the human brain capable of constantly & linearly learning anything in any order very well?

You need to distinguish an ambitious learning schedule with lack of focus and concentration. What you describe in your last paragraph sounds more like the latter - try to set aside large blocks of time for each subject and read more in-depth.

if you just put in some little effort this post can become a good question.


text:
Can neurons take oxygen from air?
Why can't/don't neurons take up atmospheric oxygen or at-least dissolved oxygen (like amoeba does) to survive and do all life processes outside animal body ???

Does an amoeba (or other microorganisms) actually take up oxygen directly from the air?  My impression is that most if not all actually live in water, so they take up dissolved oxygen (and avoid drying out through loss of their internal water).

Short answer
Neurons, and in fact all cells in the body, utilize water-dissolved oxygen to fuel their energy metabolism.
Background
The brain, and tissues in general, obtain their oxygen through passive diffusion (Fig. 1). Water, carbon dioxide, and oxygen are among the few simple molecules that can cross the cell membrane by passive diffusion,  or osmosis (source: Estrella Mountain Community College).
The body uses hemoglobin to transport oxygen (Fig. 1), because passive diffusion would take too long, especially in oxygen-hungry warm-blooded animals like humans.

Gaseous exchange in fluid medium is mediated by hemoglobin. source: Kokyo

Thanks
but can neurons survive outside body ? by breathing from atmosphere ?? or swim freely in water like amoeba ??

No. Neurons are incredibly dependent on their micro-environment and require many cells to keep them alive. In many labs, neurons can be cultured outside the body but this requires very specific conditions and they do not live long.

A brief addendum: not all gas exchange in the body uses haemoglobin/blood. In fact a portion of the oxygen the cells in the cornea of the eye receive is absorbed from the air into the tear film Intro of (Leung, 2011). But note that AliceD's point about dissolved oxygen still applies in that case. Also, (Stuecker, 2004) describes how the skin can take up atmospheric oxygen but that's not to say they haven't got an oxygen supply from vasculature too.


text:
What are the limiting factors of human stamina?
What are the limiting factors of (human) stamina? Let's define stamina as the capacity to continue doing a physical activity. We clearly have our limits, so what aspects of physiology impose a limit on human physical exertion? How do these aspects work together and interact?
Great detail isn't necessary, but a concise overview is what I am looking for.

I don't have a complete answer but in some ways your question is, as yet, unanswered. It is a bit like asking, "why do we need to sleep?" Also, there are things the body needs for energy that can run out, such as carbohydrates. However, to a limited extent we can increase our "stamina" by taking stimulants such as caffeine.

@takintoolong - An answer based on our best understanding will suffice.

You might start be defining stamina, the word covers a wide variety of factors.

It seems this review has got you covered in pretty good detail: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2375555/

Since your question is being considered too broad by some members of the community, I suggest you narrow it down to "What aspects of physiology impose a limit on human physical exertion?", and/or specifically ask for physiological quantities that correlate with the onset of perceived exhaustion.

Stamina, even if you narrow it down to a capacity to continue a physical activity, is still influenced by diverse factors, including genetic, training, diet, hormonal, psychological, religious, social...It seems that one would need to write almost a book to make "a concise overview" about how various aspects work together. If you are looking for more physical factors, do you maybe want to use the term endurance instead of stamina?

There are multiple factors as already pointed out by others. You should check out a review or a book on muscle physiology. It would be difficult to explain each and every factor that affects muscular performance.

@Jan I believe Justsnilloc is looking for the more proximal factors, what physically is happening when someone reachings their limit.

@John, yes, I get it, but I still have a big problem to decide what to focus on.

It sounds like the OP is asking for an an overview more than anything, I have been looking for my book on kinesiology but have had no luck. I can't remember the actual progression after oxygen debt and running out of glycogen.

A few explanations at the cellular and molecular level:
First, for contraction to happen, muscles need signals from nerves. Replenishing the pool of neurotransmitters (used for each synaptic burst) takes a bit of time, and short-term exhaustion may happen at this level.
In the muscle cells, contraction is caused by a calcium release within the cell, from a cellular compartment called the sarcoplasmic reticulum. This reticulum can only contain so many ions, so if the muscle contracts a lot, it will eventually need to rest for a while to re-accumulate calcium in the sarcoplasmic reticulum to prepare for more contractions.
Muscles need molecular "fuel" (like ATP molecules) to contract/relax. After an intense or sustained effort, these molecules are partially consumed and the muscle simply runs out of energy; it needs a bit of time to resore the pool of metabolites needed to work properly. Conversely, muscle contraction also causes the accumulation of metabolites and ions like potassium, which partially inhibit muscle contraction. Fatigue occurs when these accumulate at high level, and they must be cleared before making new efforts.
For references see:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5668469/ doi:10.1038/emm.2017.194 (general review)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5033663/ doi:10.1249/MSS.0000000000000923 (focuses more on muscle-neuron relationships)
https://www.ncbi.nlm.nih.gov/pubmed/9232550 Green, J Sports Sci. 1997 Jun;15(3):247-56.  (at the cellular scale)
https://www.ncbi.nlm.nih.gov/pubmed/7715628 Williams & Klug, Muscle Nerve. 1995 Apr;18(4):421-34.(more focused on calcium)


text:
Will our biological bodies be changed after we’ve occupied and settled Mars?
I had this question in mind for very long time, and I could not find a clear answer on the Internet, so I was hoping that you might know the answer.
If we will bring life to planet Mars and a few years later after it turned into a habitable zone, then we will colonize it according to some rumors. But when we colonized Mars after it is turned into a green world like ours, then would our biological body be changed and new origins will be formed? I mean, it will be changed to the point where we will be able to distinguish who’s Martian and who is from Earth? Or, they would still have Earth as their origin?
Just in curiosity.
Can someone please tell me about this matter? I’m trying to understand how things work in our bodies.
Please correct me if I have chosen wrong tags.

We welcome new contributors to SE Biology, but we do ask that they take a moment to read about the scope of the site and the sort of questions that are on-topic here. To quote from the Tour, this "is a question and answer site for biology researchers, academics, and students" — it is not a discussion site. And from the Help "You should only ask practical, answerable questions based on actual problems that you face." So, though perhaps interesting to discuss, your question is off-topic here.

David, the question is not off topic. The question might need to be formed a bit better, however, it is concerning biology, human-biology, and is related to genetics and origins. I think another good tag would be evolution.

The question is making an assumption, that is is certain that humans could establish a self-perpetuating colony on Mars.  (Rather than just research bases, like the ones in Antarctica.)  It would be better asked with a very large IF.  That said, if such a thing happened, and the two populations were reproductively isolated, of course they would diverge, and eventually - a million years or so - become different species.

@takintoolong — It's not explained anywhere obvious, but you should use the @ handle when addressing comments to people other than the poster, otherwise they don't get alerted. As for it not being off-topic, I don't think "we will colonize (Mars)… according to some rumours" represents an "actual problem the poster faces". And really it is not anything that biology researchers, academics, and students are likely to concern themselves with on a serious Q&A site, which  is what this purports to be.

IF we inhabit Mars, it is very likely that our bodies will change. Separation of species is a very common factor for evolution to occur. It is theorized that our continents used to be attached in some places and when they separated animals on each continent evolved differently. There have been other forms of separation which occurred on Earth such as the formation of glaciers, rivers, and mountain ranges. https://www.khanacademy.org/science/biology/her/tree-of-life/a/species-speciation
Although physical changes in our appearance are likely, they would also likely take thousands of years to occur. The differences between "Earthlings" and "Martians" would also depend on how much the two planets interact. It would also be possible for our own future "Earthlings" to look much different than we do today.


text:
What is "bacto" peptone?
Standard recipes for yeast medium often include "bacto-peptone". Is this the same as bacteriological peptone? Is there an authoritative source that spells it out?

See here. Bacto is a brand which used to be marketed by Difco. It is a casein (milk protein) hydrolysate.

@leonardo that's a pity since it included a lot of useful information.


text:
What's the worst that can happen from eating too many spicy peppers? Can you die?
Some peppers, such as the habanero or Carolina reaper are extremely spicy, and when eaten in larger amounts than one is accustomed to, can cause some discomfort.
I've also heard anecdotes claiming that pepper spray, if applied with sufficient intensity, can cause death.
What if you were to eat as many spicy peppers as possible, despite the noxious taste? Is it possible to commit suicide in this way (and what would the cause of death)? Would you faint from excessive mouth pain? Would uncontrollable vomiting prevent you from consuming further peppers?

You can die from eating too much of just about anything so the question in the title is pretty meaningless.

@DavidRicherby Right, but at the same time, "can you die from eating too much cyanide?" is not a meaningless question (though perhaps strangely worded).

"die" or "wish you were dead"?

This is more anecdotal than an answer, but I live near a place called Munchies 420 in Sarasota, FL. The guy from "Man vs. Food" failed to eat the "Fire In Your Hole" wings.  One man so far actually did die from trying to complete the challenge. He was resuscitated in the parking lot.  Now that I read your question again, I'm going to make this an answre

The more "dangerous" properties of spicy peppers are chiefly due to capsaicin.
Sigma-Aldrich sells purified capsaicin, for which they provide safety information, including an MSDS. Most of it is the usual, unsurprising set of warnings about irritation to eyes and the respiratory system. However, there are LD50 numbers:

LD50 Oral - rat - male - 161.2 mg/kg
LD50 Oral - rat - female - 148.1 mg/kg
LD50 Dermal - mouse - >512 mg/kg

From this, we can conclude that one would have to eat quite a bit of capsaicin to die. If lethality in humans is exactly the same as rat (which it probably isn't),  a 70 kg human would need to consume about 11 g of capsaicin to reach similar levels of lethality.
The Carolina Reaper, one of the hottest known peppers, averages about 1.6 million on the Scoville scale. Capsaicin amount is related to Scoville heat units, so we can make an imprecise conversion from one to the other.
Using values given in 2 publications (Nwokem 2010 and Al Othman 2011) we can observe the following trend:

So on average, about $6.25 \cdot 10^{-5}$ mg/g capsaicin per SHU. With this, we get $(1.6 \cdot 10^5) \cdot (6.25 \cdot 10^{-5}) = 10$ mg/g, or 1% capsaicin for dry Carolina Reapers. To eat the equivalent of 11 g of capsaicin in peppers, you would have to eat 1.1 kg of dry peppers - which should be a couple of dozen.
So, I think we can conclude that it is relatively "feasible" to consume a dangerously large amount of capsaicin by eating very spicy peppers. However, there are numerous caveats with my reasoning:

Human LD50 and rat LD50 are not necessarily the same.
Toxicity is not necessarily linearly related to body weight.
Peppers have compounds besides capsaicin that contribute to hotness.
It would be very difficult to eat such a large amount of spicy peppers, and various involuntary reflexes would interfere. Even if one were force fed the peppers, I imagine the body would attempt to vomit it up - which brings up the question of how the toxicologists even managed to feed several milligrams of capsaicin to rats to measure the LD50.

This answer is quite incomplete: The quantitative aspects are inconclusive (they rely on rat values), and there is very little qualitative information on how exactly death would occur. I have nevertheless included it here as a way of collecting the relevant information I was able to find, in the hopes that it would help answerers.

1.1kg of dry peppers being a couple of dozen would be a weight of about 50g per pepper -- quite heavy, especially if you mean dried (dehydrated) peppers. These peppers don't look very big. (For reference, it seems that a medium bell pepper weighs about 100g.)

I agree with @Superbest.  This answer is based on rats.  I demand precise, demonstrated research results on what the lethal doses are for a human.  Potential research subjects might be hesitant to participate, but 50 bucks would probably seal the deal.

toxicologists even managed to feed several milligrams of capsaicin to rats to measure the LD50: Purified capsacin (wrapped in something like capsule) could have been provided in a single dose. Quite a nice answer though :)

They can also perhaps do a test in TRPV knockout rats. This would at least eliminate the instantaneous burning sensation of capsaicin. Avian TRPV channels are not sensitive to capsaicin

by TRPV I meant TRPV1.. Moreover chronic exposure to capsaicin causes analgesia. It is important to ascertain the cause of death after capsaicin overdose

If you have cardiovascular problems, then it should be quite possible for the pain cause by spicy peppers to trigger a heart attack via a spike in blood pressure. A similar scenario might occur with respiratory diseases. And of course an anaphylactic shock, if you are allergic.
Apart from such special circumstances, I imagine that it would be nearly impossible to overcome the debilitating effects of capsaicin long enough to consume a lethal dose.

Please include references

wouldn't it do the opposite instead? I would imagine that it would dilate the blood vessels lower blood pressure.


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Is it possible in modern biology to make any person's identical twin (or genetical clone) using his DNA?
I was told by a Biotech professor (who came in our college for a guest lecture) that Bio Technology has now become so advanced that if we want to make an identical twin (or Genetical DNA Twin) of a person then we can now be able to it using his DNA. I am a Mathematics Student so I don't know much about it. I just attended the lecture because I found it interesting. I am sorry, I know I should have asked this very simple question in Quora but, I wanted a precise answer which could be believed. So I asked here, where I will get answers only from the very experts. I apologize again Thank You So Much in advance
Edit 1 :- I am satisfied with @Remi.b 's answer, @Bryan 's explanation and @anongoodnurse ' references. I should also have mentioned genetical DNA Clone in the place of identical twin. Now I've added.

I will assume that by "identical twin", you refer to "clones". Individuals who share the same genetics but of course do not necessarily share the same womb. I won't pay much attention in detail epigenetic modification nor in the length of telomeres.
While it has never been done for ethical reasons, we would probably be quite able to make a clone of a human being. We can take a cell from an individual, make it totipotent again, like a zygote and then, insert this zygote into a woman's uterus. The resulting individual is a clone and therefore have identical genetics, just like two identical twins. Similar technics have been used to clone Dolly the sheep.
We cannot, however, modify the DNA in all cells of a living individual to make this individual a perfect cone of another one.

Can you add resources to we would probably be quite able to make a clone of a human being? The wikipedia pages do provide useful resources to the terminology, but the answer itself seems unsupported. (I don't question the answer in itself - you're totally right).

Has any organism been cloned by the method you described?

Isn't Dolly the sheep a bad example? If I remember correctly the sheep displayed a lot of age-related abnormalities. Take into account the age difference between it and the original then you have two sheep that would not likely pass as "identical" twins. Basically the question is if turning a differentiated cell totipotent again undoes all gene silencing?

@Cell Fair point. You are going into the details of what one might want to mean by an identical twin. I don't think these semantic details are so much the point of the question. I assumed the main point was to understand, we can clone but we can't modify the genetics of all cells in a living organism.

I am quite satisfied with @Remi.b 's answer. I apologize, I used the wrong term i.e. Identical Twin , while I should have used clone in that place. I'll try to explain clearly, what I meant by my question by giving an example; e.g. If I am an adult and I want my child to be 100% like me. Then, is it possible to get it done by Biotech?
As you said we'll make it totipotent and insert it into a woman's uterus. Will the resultant baby have characters from that woman? I was unable to understand Cell 's point & your answer on that also. People who commented here, please upvote my question. ty

Sorry, I tried you in chat, but no go. https://www.youtube.com/watch?v=meiU6TxysCg. Reminded me of your question on Parenting. See? As natural as can be! ;)

@NavedTHESheikh - They will only share genetic traits. Some behavioral traits as well, but many behavioral traits are a mixture of nature (genetics) and nurture (environment). There have been cloned dogs who were unloved by the owners because while they looked the same, they weren't behaviorally the same, i.s. "She isn't my Molly."

@Remi.b - I agree with Cell; early cloned (and even recent) do not have the vigor and lifespan of the original. Something is missing. But +1 anyway for a good explanation.

Thank you so much @anongoodnurse , your video reference was fun Watching, interesting and gave me full experience what you were trying to explain. I could not understand, what did you want to say by saying Sorry, I tried you in chat, but no go

Yeah I have completely understand. Your example of dogs was great. Thanks again @anongoodnurse

Not to belabour the point, but I don’t believe Dolly was cloned by inserting an induced totipotent cell into a surrogate mother.

@NavedTHESheikh - I'm sorry I wasn't very clear. That video was intended for Remi.b. It's an aside, unrelated to this issue. But it was fun to watch, wasn't it? :D

@canadianer - I thought I was a stickler! :) Technically you're right, of course.

Identical twins share:
A) Near-identical genetics, save mutations introduced after the original zygote splits
B) A womb/developmental environment pre-birth
and often share
C) A similar developmental environment after birth (i.e., in most circumstances identical twin humans would be raised in the same household)
Despite these similarities, 'identical' twins do develop some differences in personality, etc, and are often be physically distinguishable. Raising a newborn individual from an adult's DNA would ensure that at a minimum (B) and (C) are not fulfilled, and (A) could differ more than typical of identical twins if a somatic cell is used that has some mutations (which it almost certainly will) or if the cloning process introduces additional genetic or epigenetic changes.
Given those limitations, yes, such a thing is within the realm of possibilities, but there are technical challenges to doing such a procedure in humans, and there are ethical barriers to working through those technical challenges such that I would say our technology level is there yet we may not yet have the specific technology necessary. I think it is likely the Biotech professor you are referring to is intentionally blurring any distinction between the two.

Thank You So Much for giving your time and knowledge in answering my question. But, as I am not a Biology Student, I couldn't understand some terms that you used here. I also had used the wrong term i.e. Identical Twin while I should have used Clone instead. In other words, someone's offspring is exactly 100% like him. The only difference between them is the age difference, nothing else. Please, could you elaborate your answer towards this point in some simple words? Thanks again.

@NavedTHESheikh - A clone is even less like a twin, as Brian explained. Brian's answer was simple. See my comment above on Remi.b's answer. Genetics are only part of what makes a person unique. Environment - even microenvironment - makes a difference. That's why twins do not have the same fingerprints: because amniotic fluid flow is different for each twin depending on their hand movements.

@NavedTHESheikh An identical twin is a clone, genetically. As anongoodnurse says, I've already said this fairly simply here; we've done this with other mammals but not humans, the barrier to further development is mostly ethical, and a genetic clone is going to be less similar than identical twins are.

@Bryan Krause oh now I've completely understood it. Thank You So Much for further explanation.

@anongoodnurse Thank You So Much, your explanations gave me a very important link towards understanding the answer.


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Bug identification - Beetle, grasshopper, moth-like and it also flies
 Could anyone please help me identify this creature? It can fly and seems to like crawling as well. It has mandibles that are beetle-like.  Approximately 3cm/2inch. Location: KwaZulu Natal, South Africa

Hi Ari13, and welcome to Bio.SE! Please update your question with the approximate size of your specimen, and please provide any additional information or pictures that are possible. See [tag:species-identification] tag question guidelines here. Doing so will increase the positive voting response your question receives as well as increase the odds of receiving a good/accurate answer. Thanks!

Thanks! Updated with approximate size and location.

That is a mole cricket, Order Orthoptera, family Gryllotalpidae
https://en.wikipedia.org/wiki/Mole_cricket

Thank you! Odd that I would've found it down here though? Don't you think?

You mean in South Africa? No, they are cosmopolitan. Cool bugs!


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How can I extract DNA from horse hair?
For my project I have to find an inexpensive, quick and simple-to-use method to extract DNA from horse hair. The sample does not have to be purified because the sample will be used for LAMP and not PCR.
I will do my internship at a university so most kinds of equipment and materials are available to me. I also have a budget for my project. I searched online for DNA extraction kits but didn't have much luck because many kits were for human hair and horse hair is a little bit thicker.
Does anyone have experience with a method that would work for my case as well and can advise me?

What kind of equipment and materials do you have access to?

i will do my internship to the Wageningen university so most kind of equipment and materials are available for me, i also have a budget in terms for helping my project. i did search online to find DNA extraction kits but not that much luck because many kits where for human hair and horse hair is a little bit thicker. Do you know a method that kan help me with this, or perhaps a link where the method is explained ?


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Why are mules/donkeys aggressive when faced with predators but horses are not?
I came upon an interesting quote after going down the rabbit hole on a variety of subjects. While deep in the data, I came upon this quote

oat and farm animal owners likes to have mules with their herds because donkeys or mules will actually attack predatory animals such as foxes and coyotes.

Which raised quite a few questions in my mind. I was able to find additional sources as it relates to the predisposition of the given species.
Seemingly, donkeys and mules will act aggressively in confrontation with predators and attempt to attack to the point of killing many of them. Is there something about the physiology of a donkey/mule that makes them much less timid? Perhaps body structure? Seemingly a horse has equal or even better tools to try and defend itself.
Here are the sources (the first 2 are not the most authoritative by any means):

 Mule Behavior: Differences with horses and donkeys
Mule Facts
Donkey Behavior: A comparative study of donkey and horse behavior

I was able to find additional sources Can you please indicate these sources?

It has been completed

Different organisms evolve different behaviors, evolution is a whatever works kind of designer. it can influenced by all kinds of things, social behavior, what kinds of predators there are, offspring care needs, herd size, and a hundred other things.

We know what wild donkeys are like because they still exist in Africa, population 570, and they are more like small zebra's than horses.
Wild horses are from Eurasian grasslands and have all been captured for domestication and eaten, so current wild horses are feral.
The are completely different animals, they diverged 5-10 million years ago. They are much more genetically distant than a wolf, labrador and an alsatian, and their habitat and behaviours are completely different, including the dung strategy of donkeys and the semi-desert versus steppe habitat.

Horses have specialized in running away from predators, they are generally a bit faster than donkeys and today's horses tend to often be more slender, like deer.
Donkeys are more stout and probably adapted for different predators, terrains and climates, so they perhaps more likely to form group and kick rather then outrun the wolves/lions/tigers that would have preyed on them in the past.
It's probably best to post on a forum with people that have studied horses and donkeys for 20-40 years because they know a lot more about them.

I can’t speak for other mules but mine does not like dogs so I assume she would not like foxes or coyotes. I’ve seen her literally stomp a dog with her front hoofs. If the dog runs, I’ve seen her chase the dog and start stomping if she can get close enough to the fleeing animal. Our horse, well, he doesn’t give a hoot if a dog is nearby or not.

So horses, donkeys, and zebras are all of the genus Equus. Mules are not a species, since they are the product of the cross-breed between horses and donkeys, and are sterile (therefore do not comply with the biological interpretation of species).
Given that 2 out of the 3 species from the species of the genus Equus are aggressive against predators (zebras see reference and donkeys), it might be possible that the "aggressive" behavior is the ancestral trait of the genus, and horses evolved afterward the behavior of fleeing before fighting. Furthermore, it looks like the "aggressive" trait is dominant over the "fleeing" trait since mules (cross-breeds between horses and donkeys) inherit the aggressive trait. There are no sources that necessarily say that a dominant trait is associated with ancestral (common ancestor) provenance, but for the case of single genes, this is the most likely scenario.
So if we think that horses evolved the trait of fleeing before fighting (being the "aggressive" trait the ancestral one), then one should ask why did they evolve such behavior (why is a cringy word for evolutionary biologists, but serves the purpose here). And this is probably due to the exposure horses had to different types of predators. I wouldn't be surprised if horses had more contact with human beings than donkeys or zebras, thus they evolved this behavior as a way of coping with extensive hunting.
Alternatively, some traits are not "modular" traits that can evolve independently from other traits. More often than not, complex behaviors, like the "aggressive" trait, are determined by a large number of genes, some of which have phenotypical effects elsewhere. This means that if a species has a "selective pressure" for one trait, other traits can also be modified over time as a causal effect of this selective pressure. Horses were domesticated long before donkeys were, and zebras haven't been domesticated at all. Domestication is usually conferred by a process of selectively breeding individuals that express the least amount of aggressiveness, or show signs/traits of "neoteny". If horses were selected to produce neoteny in the species, the non-aggressive behavior might also have been selected as a causal effect of this selective-breeding.  This would explain why horses, which have been domesticated way before donkeys have, do not show aggressive behavior as donkeys or zebras do.