text:
What is the mechanism of reflex arcs?
When a reflex arc occurs the signal from the receptor passes straight to the motor neuron instead of being passed onto the brain.
This is a rather simplistic explanation, I was hoping to make it more detailed. How does the body know when a threshold, heat for example, has been crossed and what mechanism is able to activate the reflex?
Also where does this occur, in the receptor or the spine?

Please, see reflex arcs in the books Pocock et al. and Costanzo et al. Review Guyton if necessary. Very well written. Susan coverers only some arches. Would like to see some of your work to answer this question.

Withdrawal reflex
You asked specifically about the withdrawal reflex and the receptors that trigger this. The initiation of the reflex arc is determined at the level of the nociceptors (pain-transducing receptors) in the epidermis. For the most part, these are part of “free” (not encapsulated) nerve endings of sensory fibers. These fibers course within spinal nerves whose cell bodies are located in the dorsal root ganglia adjacent to the spinal cord. There are two types of nociceptive endings:

mechanical: with parent fibers Aδ

transduce severe mechanical deformation

polymodal: with parent C-fiber units

transduce heat, cold, irritant signals

This picture shows free nerve endings in the epidermis. The boxed portion of the big picture is expanded in the bottom right.

The withdrawal reflex initiated by these receptors is mediated by a polysnaptic (multiple neurons) arc. The sensory neuron synapses with interneurons in the spinal cord.1 Some of these use glutamatergic connections to activate appropriate muscle groups mediating withdrawal. Others inhibit the reciprocal muscle groups (reciprocal inhibition) to allow this movement to be unimpeded.
Here is a cartoon diagram showing the spinal components of the reflex arc in a cross-sectional level of the spinal cord. Notice the interneuron between the sensory and motor neurons (although it's not labeled as such here):

Stretch reflex
In order to provide a broader picture of the basic principles involved in spinal reflexes, it's helpful to also mention the stretch reflex. This is perhaps the quintessential reflex arc because it is monosynaptic, exemplified by the patellar tendon reflex. The stretch reflex is fast, with a latency (stimulus–response interval) of about 15–25 ms (contrast the polysynaptic withdrawal reflex with latency ~70-100 ms.)
The stretch is initiated at the Golgi tendon organs. These are found at the junction between muscle and tendon. The (Ib) nerve fiber splays out and intertwines with tendon fiber bundles. The  nerve endings are activated by the tension of muscle contraction (either passive (as when the patellar tendon is tapped), or active (as during voluntary movement). The afferent sensory neurons directly excite homonymous motor neurons  (i.e. motor neurons supplying the same muscles), and inhibit (via interposed “Ia internuncials”) the antagonist muscles.
I have limited the discussion here to the withdrawal reflex you asked about and another basic spinal reflex arc as an illustration of principle. There are many other, mostly more complex reflex arcs that are beyond the scope of this answer, but I highly recommend checking out a neuroanatomy or neurophysiology textbook such as the one I've listed below if you'd like more information.

Note

1. Although the discussion here is limited to the anatomy of the reflex arc, there are additional synapses within the spinal cord that connect with ascending circuits, as described in the section about afferent neurons of spinal nerves in another answer. Some of these tracts end up at the cortex and are the basis for conscious perception. However, note that this process is multisynaptic and takes longer. The beauty of the spinal reflex arc is that it does not require information to travel all the way up to the brain and back down, which would slow down the response considerably. Practically, this means that you will pull your hand away from a hot stove before you have conscious sensory awareness of the burn.

Reference

Apart from linked article and images with sources below, all information is summarized from:

MJ Turlough FitzGerald,  Gregory Gruener, Estomih Mtui. Clinical Neuroanatomy & Neuroscience © 2012, Elsevier Limited.

Image 1 from: http://en.wikipedia.org/wiki/Free_nerve_ending

Image 2 from: http://www.tutorvista.com/content/biology/biology-iv/nervous-coordination/natural-reflex.php

Dear Susan, thank you ever so much to get back to me, this is wonderfully written and informative. So you say that the nociceptors in the epidermis trigger the reflex arc.
How is there response different to stimulating reflex arcs and how is this message passed through the nervous system to the spine so that the message gets sent to the effector, as well as the brain?

@Freeman - I tried to clarify these points in the answer. Let me know if that helps.


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What is the difference between orthologs, paralogs and homologs?
These three terms are often misused in the literature. Many researchers seem to treat them as synonyms. So, what is the definition of each of these terms and how do they differ from one another?

Another pet peeve: homology is qualitative, not quantitative. So saying "significant homology" or "weak homology" is just wrong.

Regarding the function of paralogs, it should also be mentioned that in some cases they do not diverge in function but instead retain their function but work in different conditions or as genetic backups.

First, a note on spelling. Both "ortholog" and "orthologue" are correct, one is the American and the other the British spelling. The same is true for homolog/homologue and paralog/paralogue.
On to the biology. Homology is the blanket term, both ortho- and paralogs are homologs. So, when in doubt use "homologs". However:

Orthologs are homologous genes that are the result of a speciation event.

Paralogs are homologous genes that are the result of a duplication event.

The following image, adapted (slightly) from [1], illustrates the differences:

Part (a) of the diagram above shows a hypothetical evolutionary history of a gene. The ancestral genome had two copies of this gene (A and B) which were paralogs. At some point, the ancestral species split into two daughter species, each of whose genome contains two copies of the ancestral duplicated gene (A1,A2 and B1,B2).
These genes are all homologous to one another but are they paralogs or orthologs? Since the duplication event that created genes A and B occurred before the speciation event that created species 1 and 2, A genes will be paralogs of B genes and 1 genes will be orthologs of 2 genes:

A1 and B1 are paralogs

A1 and B2 are paralogs.

A2 and B1 are paralogs.

A2 and B2 are paralogs.

A1 and A2 are orthologs.

B1 and B2 are orthologs

This however, is a very simple case. What happens when a duplication occurs after a speciation event? In part (b) of the above diagram, the ancestral gene was duplicated only in species 2's lineage. Therefore, in (b):

A2 and B2 are orthologs of A1.
A2 and B2 are paralogs of each other.

A common misconception is that paralogous genes are those homologous genes that are in the same genome while orthologous genes are those that are in different genomes. As you can see in the example above, this is absolutely not true. While it can happen that way, ortho- vs paralogy depends exclusively on the evolutionary history of the genes involved. If you do not know whether a particular homology relationship is the result of a gene duplication or a speciation event, then you cannot know if it is a case of paralogy or orthology.
References

R.A. Jensen, Orthologs and paralogs - we need to get it right, Genome Biology, 2(8), 2001

Suggested reading:
I highly recommend the Jensen article referenced above. I read it when I was first starting to work on comparative  genomics and evolution and it is a wonderfully clear and succinct explanation of the terms. Some of the articles referenced therein are also worth a read:

Koonin EV: An apology for orthologs - or brave new memes. Genome Biol, 2001, 2:comment1005.1-1005.2.
Petsko GA: Homologuephobia. Genome Biol 2001, 2:comment1002.1-1002.2.
Fitch WM: Distinguishing homologous from analogous proteins. Syst Zool 1970, 19:99-113. (of historical interest, the terms were first used here)
Fitch WM: Homology a personal view on some of the problems. Trends Genet
2000, 16:227-31.

Very nice article, +1

@January, isn't it? I've been sending it to everyone who asks me the ortho vs para question for years. Thought I'd share it with y'all here :).

So given a pair of genes that have diverged by both speciation and duplication, they are orthologs or paralogs depending on which divergence event occurred first. Is that right?

now I am completely confused :)

@liyuan in that case, just use homolog and leave it at that.  Or come into [chat] and we can try and explain :)

Both orthologs and paralogs are types of homologs, that is, they denote genes that derive from the same ancestral sequence.
Orthologs are corresponding genes in different lineages and are a result of speciation, whereas paralogs result from a gene duplication. This often has important implications: while orthologs often fulfill the same role, paralogs tend to diverge in their function, so paralogy is a worse indicator of functional analogy than orthology.
This, however, is only the tip of the iceberg, since the situation can be much more complex (see, for example, the hidden paralogy problem).
There is a great article by Fitch on that subject.

Are there new ideations to address the issues Fitch had raised 20 years ago?

First, the definition: two genes are homologs if they derive from a common ancestor. Generally speaking, if two nucleotide sequences have at least 30% (or greater than 10% amino acid sequence) identity, they are likely to be from a common ancestry, however, they may not be homologous. Note the reverse does not apply: two genes can also be homologs if there is no similarity; this happens every time the drift was long enough (many genes are no longer similar---beyond random identity---after 1 billion years; only highly conserved genes keep some similarity).
In addition to the other answers another diagram and further terms:

(after W. M. Fitch, Trends in Genetics, 16, 5, May 2000, p.228)

B1 and C1 are (1:1) orthologs
B1, C2 and C3 are (1:n) orthologs
A1 and AB1 are xenologs (horiz. gene transfer)

I think (1:n) ortholog is a synonym for outparalog.
Klaus D. Grasser: Annual Plant Reviews, Regulation of Transcription in Plants (Volume 29). Wiley-Blackwell, ISBN 1-4051-4528-5, p. 37.

I am sorry but this is simply not true. >=30% nt and >=10% aa are not sufficient to demonstrate homology. For example, 2 long proteins can share a domain. They can easily have >10% aa identity and not be homologous at all. In any case, >=30% nt does not mean there is "no other possible explanation" but homology, you are forgetting convergent evolution. For a well known example, AFGP proteins from D. mawsoni and B. saida show 69% sequence identity but are not homologous.

I'm aware of convergent evolution, as well as repeating sequence parts. There is also the conservation of domains with respect to non-functional parts. That's why I wrote "in general".

Given the quality of your many other answers, I imagine you must be aware of it :). I am just saying that there is no magic sequence similarity threshold that signifies homology. I was reacting to this phrase: "there can be no other explanation than common ancestry for this fact".

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What is this beetle and what are the strange antennae for?
I found this wonderful creature in my yard (I live in the south of France) last night:

It was about 2-3cm long, with a hard carapace and wings. It also made loud hissing noises when agitated. I am curious as to what species this is, I'm quite surprised I'd never seen it before cause the beastie is quite large and last night I found it because of the noise it was making. It was upside down and hissing like a kettle.
More than the specific species' name, I am curious as to what the large antennae are for. Does their shape and size somehow increase the beetle's sensitivity to whatever stimuli these are atuned to?

Alan Boyd's comment below helped me along a bit. I seem to have found a close relative of the ten-lined June beetle (Polyphylla decemlineata) pictured below (image source)

My guess is some kind of chafer. The elaborate antennae are probably an adaptation for detection of mating pheromones during nocturnal mating flights.

From the pattern on the elytra (hard upper wings), it looks like you might have a beautiful male Polyphylla fullo. Compare your photos with the P. fullo in this illustration, or photos on the Wikipedia page.
edit to fully respond to the comments:
I suspect you're right that the antennae plates in your picture are just tightly closed up, giving a different appearance. Here's a photo I took of a related species where you can see both appearances of the antennae.
And I think that Alan Boyd is correct about the antennae being used as chemoreceptors to locate females. The wikipedia page on the Ten-Lined June Bug also mentions both of these points.

Ah yes, I think you nailed it. That does indeed seem to be it. However, whereas the specimen I saw seems to have solid antennae, other photographs (e.g. here) show a kind of brush or duster like arrangement of what looks like separate filaments. Is that the same antenna that can be fanned out at will, is this is male/female thing or perhaps an adult/juvenile difference? Also, could you shed some light on why the antennae are shaped as they are?

Thank you! The second photograph is just what I needed. So these little buggers can expand their antennae at will? I guess they do so in response to pheromones, cool!

Polyphylla = 'many leaves'. This may refer to the structure of the antennae, when fully deployed.

@AlanBoyd argh! Yes, that makes perfect sense and should have been obvious to a native Greek speaker like myself.

It's likely the this structure (the 'many leaves') is adaptive because of increased surface area / volume ratio. The more the 'frilly' your antennae are, the greater the surface area, which means more contact between the pheromones in the air and your chemosensory bits.

@Wajurgmitr yup, that makes perfect sense. Also, conversely, you would want to be able to compact them into a less fragile form.

Are we sure about this? To me the elytra look pretty different; in the OP's photo there is yellow patterning but it's relatively smooth, whereas this one is very 'ribbed' but lacks the yellow colour.

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What determines when a virus becomes a "new strain"?
The reason we cannot find a cure for the common cold is because viruses mutate rapidly. Where do the mutations occur in the DNA/mRNA of viruses and does this have any effect on the protein level? what has to change for the virus to be considered a new strain?

I don't know if this is a comprehensive enough answer, but viruses are taxonomically broken down into order (-virales), family (-viridae), subfamily (-virinae), genus (-virus) and species. This system was developed by the ICTV and is concurrently used with the Baltimore System.
A lot of species contain variations called virus strains. There are two types, serotype and genotype.
In serotypes, the differences are detected by variation in antigens. Genotypes are detected by differences in genome sequence.(1).
The reason a vaccine is difficult to create for the common cold, or upper respiratory tract infections is not only because of the frequency of mutation but also due to the large number of serotypes present.(2),(3).

Virology: Principles and Applications - Carter.
Princuples and Practice of Infectious Diseases - Mendell, et al.
E.g. Olszewska, et al. Development of vaccines against common colds. Br Med Bull. 2002. 62(1):99-111.

It is comprehensive enough for me. You have summarised the points and provided references for further reading. Thanks!


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How did viruses come to be?
My question is out of curiosity and got me thinking. How did viruses with the head, tail and tail fibres actually evolve? These viruses look more like machines than biological entities. Are there any theories to how these viruses evolved?

Does a biological entity not look like a machine? Look closer.

A bird looks like an aeroplane too...

If you look from another perspective machines resemble biological entities.

Useful book origin and evolution of viruses https://www.sciencedirect.com/book/9780123741530/origin-and-evolution-of-viruses

I found a book chapter for you here
Quick summary:
3 hypotheses to Origin of viruses

From pre-cellular world (virus first hypothesis)
From reductive evolution of parasites (reduction hypothesis)
From fragments of cellular genetic material (escape hypothesis)

Drawbacks:

virus require cells (to infect) so how can they come first
virus do not look like known reduced parasites from Bacteria/Eukarya/Archaea
unlikely that genetic fragments form complex viral structures for viral function

Because of these drawbacks, the problem of virus origin was for a
  long time considered untractable and not worth serious consideration

The rest of the chapter looks more in-depth into the 3 hypotheses

Could you summarise in your answer perhaps? It’s preferred here to preferred here to provide links for further information and references, not as the sole point of the answer.


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Is recognizing one's own mirror reflection a valid test of animal intelligence/self awareness?
I've been looking at this Ted talk on interspecies internet, and it appears that they have selected a small number of species of animals (dolphin, elephant, and some ape(?)) and are intent on developing interfaces for these animals to be able to connect with other animals over the internet.
From the talk, it appeared as if one of the criteria for animal selection was whether or not an animal recognizes itself in the mirror. This got me thinking - there are many more cats that have access to technology like the internet or TV or cats that have been interacting with touch screen displays. Yet apparently cats cant recognize their own reflection as themselves.
What is so special about being able to recognize one's own reflection? Is it a true measure of self awareness? Does it only appear in animals with larger brains?

The mirror test is definitely useful, but clearly biased toward animals with social intelligence (a notion of self is only useful if there's a notion of other) and also toward highly visual animals.  A mole-rat, no matter how intelligent, is unlikely to use a mirror for much of anything.  Using the same test for animals with very different sensory modalities is bound to fail. For example, see the comments of the following YouTube video.  The user Sluchesi notes:

sticking a piece of post-it paper on my tom cat's head where he couldn't see it without a mirror and while petting him, waited until I was sure he didn't notice it (he didn't respond to it), showed him the mirror and he instantly started trying to get the paper off his head (not the image in the mirror, his own), shaking it and using his paws.

A second user (M. Ransom) did the same test and verified it.  Not quite to the level of scientific proof that you would want to see, but certainly worth a follow-up study by someone who focuses on the topic.  If true, it would indicate that cats probably do have a conception that the reflection in the mirror is them, but place little value on introspection or visual self-concepts.  This might indicate that what cats (and many other animals) lack is not the ability to have a model of self, but to have a model of some other being modeling yourself (i.e., 2nd-order model of self).  This is actually a quite complicated level of modeling: even humans are quite bad at guessing what other people think about them.  However, basically all humans try to do it, even if their guess is often mirror-bias (i.e., other people think about them like they think about themselves).  Given that this is nearly at the limit of average human cognition (3rd order models of other/self are rare and usually limited to strategic games like poker), it seems reasonable that most animals lack this ability.
Having a model of another's conception of oneself is necessary for a being to care what they look like, for instance.  After all, if you can't comprehend that the world attaches importance to how you look, you would be unlikely to develop mechanisms to attach importance to it either.  In that second case, the mirror test may be accurate (i.e., it measures higher order thought), but it is in fact measuring something very different (and more advanced) than what it has been assumed to measure.

The sticky note on head is a good experiment, I will try it!

An interesting anecdote from the book "Merle's Door".  The dog didn't at first appear to recognize itself in small mirrors, but when the human took the dog to an exercise studio with large wall mirrors, the dog saw himself and his human together, and from then on appeared to understand mirrors.  He just needed that extra bit of social context...

To the answer above:  "I am the being in the mirror", one has to ask themselves:  Is it so strange that a cat seeing it's own paw in front of it and recognizing it as it's his OWN, and not chasing it's own tail because it knows it's his and he's not a kitten anymore?
So how much different is that when they come to understand, especially after you hold the cat several times in front of the mirror with you, making the association and he's no longer weirded out?  Many cats making this transition look in curiosity and awe and move on, never really caring that much about it -- much like kids.
Bring a cat into a bathroom with a mirrored wall behind the sinks, when he's dealing with something where the mirror is in his line of sight.  Walk in behind.  When the cat turns around to look at you to play instantly, instead of trying to play with the mirror -- it recognizes that it shows whats behind him.  I have observed this.
If a cat recognizing it's own tail out of it's "perif" is nothing special, neither is recognizing that it's him in the mirror.  He may not be cognitively advanced to think deeper than "Yep, that's me, I have THIS look.  Oh, am I getting fat?" -- they care less about that.
A good test would be to have a cat with whom you can put something on his head and he doesn't care -- unless it's something he HATES by its LOOK.  Once you've established that over and over 100%, and have been able to put it on him without him caring without him SEEING it -- put him in front of the mirror and see if he tries to take it off.
A red dot isn't going to do squat.  They don't give a shoot about things like that.  If you want to know whether they know IT'S THEM, put them in position where there's something they DON'T WANT on them -- and they try to get it off... where it's something they don't mind on them, they don't try to get it off after seeing themselves in the mirror.
Not fool-proof, though.  They may not mind it on them because it's purely how it looks.  They can just walk away from the mirror and they don't have to worry about it.
But back to the original point:  I don't think it's a big deal that they can recognize that it's themselves.  To UTILIZE that for deeper thinking in making connections is another matter.


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Does sleep duration vary for animals based on time of the year?
I'm interested in the sleep patterns of wild animals, that still use sun for controlling their biological clock.
Animals entrain their biological clock to the day/night cycle using light as the entrainment signal. The biological clock follows the day/night cycle: dim light initiates melatonin secretion, while bright morning light stops melatonin production. Melatonin is involved in sleep regulation
Here, I have plotted the day duration over the course of the year for Northeast US, around Washington DC.
My question is given the day duration plot below, would the total sleep duration for wild animals vary over the course of the year?
In other words, would animals sleep longer in the winter time and shorter in the summer time?

Yes, people, as well as animals regulate their drowsiness by light. There's a well known experiment conducted by Michel Suffre on himself in 1972. When he spent a month with no light and no information about the time, his sleeping cycles prolonged up to 48 hours.


text:
Does brain activity generate heat gradients in the brain?
I'm reading this article on guiding axon growth using temperature gradient, and it mentions that the trajectory of growth of neuron connections can be influenced by temperature gradients as little as 0.1C.
This got me thinking - does thinking generate heat or increases blood flow enough to create heat gradients within the brain? If so, this may explain how the brain rewires itself.

It is well-known that brain activity locally rises blood flow and temperature, and so there is a temperature gradient from the brain tissue (source) to the vascular tissue (sink). But this isn't what you're anticipating, probably.

I've re-read the article and it actually mentions that heat repels the axon growth(text under the photo). This is indeed not an answer I was anticipating.

Possible duplicate of How does the brain's energy consumption depend on mental activity?


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Is there a comprehensive list of human circadian-like processes, hormones or gene expressions?
I'm reading this article onblood sugar and circadian rhythms and the following question popped into my head: a lot of articles mention various diurnal or circadian rhythmicity of biological processes. Is there a "master" list of hormones, gene expressions and other processes that the modern science recognizes as "circadian"?
In other words, is there something that can give reader a clear picture of what's happening at a certain (biological)time for a human and is expected to happen tomorrow at similar time?
It would be great to take a look at such list and see what are the major processes that recur on a time-sensitive basis in humans.

There isn't a central/master website that I'm aware of, as it's still an area of active research.  I did a bit of work in the field about 10 years ago, and at that point we were still working out the circadian rhythms in the yeast mating cycle.
Since then, the field been enumerating more and more involved processes: mRNA expression, mRNA degradation, micro RNA, mRNA transport and translational regulation, then protein translation and protein regulation... Given that any single gene can be regulated at one or more of these points, and that there are at least a few different circadian cycles and they can even conflict... well, it's a bit of a mess.  Oh, and don't forget that different organs and cell types have different responses, so then you have to cross check 50 cell types.
I'd start with this review paper, which can give you an idea of what kinds of papers to search for.  If you decide you want to know about individual genes, a lot of scientists in the field have made their datasets available online in various gene expression databases.  There are several databases running currently, and maybe one of them will be specialized in circadian expression.
Circadian topology of metabolism
Joseph Bass
Nature 491, 348–356 (15 November 2012) doi:10.1038/nature11704
Published online 14 November 2012
http://www.nature.com/nature/journal/v491/n7424/full/nature11704.html


text:
What is this insect?
These photographs were taken today in Marseille, in the Mediterranean coast of France. My French friends inform me that these beasties are called cousins because they are "cousins" of mosquitoes (whatever that means).
The thing is, we are absolutely infested by them. They seem to be more active at dawn and dusk (like mosquitoes) but we have dozens flying around the house every evening. I would like to know the species' name to see if I can learn anything about them. Do they have cycles like cicadas? Are they linked to stagnant waters like mosquitoes? Why are there so many of them this year?

Here's one with my hand next to it to give you an indication of their size:

Some kind of crane fly (http://en.wikipedia.org/wiki/Crane_fly)

I agree it must be a Tipulidae. I also call them "cousins" in French, or "tipules".
I think their larvae live in the soil, not in stagnant water.
I'd bet their abundance could be related to the anormally long "winter".

i have also seen this guy roaming around in mosquito hiding places.. i used to think that it is a mutated mosquito :P

It is indeed a Crane fly, superfamily Tipuloidea, which is part of two-winged insects (Diptera). There are >15000 species worldwide. Their systematics is somewhat uncertain (used to be a single family, now a superfamily). They are placed in the same suborder as mosquitoes (Nematocera). The adults feed on nectar or not at all (they do not prey on mosquitoes), and the larvae usually feeds on litter, roots, fungi etc, but some aquatic species are predatory. Larvae of some species develop in soil and others in water. Adults of many species are attracted by light, which is why you often find them inside houses. I dont know why you find so many this year where you live, but winter conditions affecting survival is a possible explanation.

In many areas of the United States the predatory versions that prey on mosquito larvae are purposefully bred and introduced in large numbers as a non-chemical method of mosquito control. Since the predatory versions don't prey on much else (and do not prey on anything as adults) they're found in large numbers in the Summer, but are otherwise harmless. Perhaps the French government did something similar?

Didn't know that they were used as biocontrol. In the US, some introduced species are also consided pests, e.g. the European crane fly (pdf)

Nematocerans are not monophyletic, and are therefore not a valid suborder. Other than that, I agree with the answer.


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What is the mechanism of action of lithium-induced polyuria?
I was reading in my pharmacology textbook on lithium in treating bipolar disorder, and I was curious to know if there was any specific action lithium takes to produce symptoms such as polyuria and polydipsia. Any help would be great. Also, what is the most common way to monitor lithium levels in the body?

Lithium changes the effect of at least three substances that play a role in diuresis:

aldosterone:  lithium partially inhibits its ability to increase the expression of ENaC receptors on apical membrane thus increasing sodium losses [1].
arginine vasopressin (AVP): because lithium can induce hyperparathyroidism, parathyroid hormone can act as partial agonist to AVP, inhibiting its hydroosmotic action [2].
antidiuretic hormone (ADH): lithium blocks its stimulatory effect on adenilate cyclase. The result is a decrease of cAMP levels in the cells from collecting tubules. cAMP promotes formation of water channels, thus improving absorption from collecting tubules. Because lithium decreases cAMP levels, diuresis is stimulated [1].

All these result in polyuria.
Lithium levels can be determined from the blood. Usually the test should be performed 12 hours after last dose of Lithium [3].

References:

Eleanor Lederer, MD; Lithium Nephropathy on http://emedicine.medscape.com/article/242772-overview#a0104
Carney SL, Ray C, Gillies AH. Mechanism of lithium-induced polyuria in the rat. Kidney Int. 1996 Aug;50(2):377-83.
http://labtestsonline.org/understanding/analytes/lithium/tab/sample/


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Counterintuitive action of Vitamin D?
Vitamin D acts in a way which to me is counterintuitive. It functionally supplemets Parathormone. It in the intestinal tract steps up calcium absorption by altering nuclear gene expression and also prevents calcium excretion in kidneys. All of this is understandable. But it also, like parathormone, steps up osteoclast action in bone (actually steps up both osteoclast and osteoblast, but the osteoclast action is increased more to result in net bone resorption). This means that Vitamin D increases blood calcium level by increasing bone resorption.
Then how does Vitamin D help in improving bone density, bone strength and prevent rickets or osteoporosis? All of these would require bone deposition rather than resorption.

yes there are some colflicting theories.. This article says that Vit-D actually inhibits osteoclastogenesis. What I can say about it is that the action of Vit-D should be studied in a systems perspective. It may be the effect of dynamics. It allows calcium absorption, and its deficiency would cause reduced calcium leading to reduced bone-mineralization as seen in rickets. However, it also affects resorption and active modeling of the bone. It is important to take other factors (hormones etc) into consideration.

There are two pieces to this question:
a) How does bone resorption (movement of Ca/Phos out of bone into the blood) result in net improvement in bone structure?
Bones are constantly remodeling, primarily in response to mechanical stressors. Although you clearly already realize this, I will make it explicit: osteoblasts are the cells that create new bone; osteoclasts break down (resorb) bone.
Quoting Harrison’s Internal Medicine1:

Radioisotope studies indicate that as much as 18% of the total skeletal calcium is deposited and removed each year. Thus, bone is an active metabolizing tissue.…The cycle of bone resorption and formation is a highly orchestrated process carried out by the basic multicellular unit, which is composed of a group of osteoclasts and osteoblasts

Bone mineral density (BMD) can not be equated with bone quality. (This is the difference between osteoporosis – deficient bone density – and rickets – poor bone architecture.) Thus, vitamin D’s stimulation of both osteoblast and osteoclast activity is beneficial to bone structure.
b) How does vitamin D lead to overall increased bone density?
In addition to the effects above, you mentioned that vitamin D increases serum calcium by several mechanisms. This is true. Both this increased serum calcium as well as the direct effects of Vitamin D on the parathyroid gland suppress PTH production.* As PTH has powerful actions to increase bone resorption by mobilizing calcium and phosphorus to move from the bone into the blood, the suppression on its excretion applied both directly and indirectly by Vitamin D results in a net increase in bone density.
Thus, both by its effects on bone quality and quantity, vitamin D is a net boon for the bones.

*Parathyroid hormone, a.k.a. parathormone. There is a paradox here, because drugs such as teriparatide (a.k.a. Forteo, recombinant PTH) are anabolic for bone and are used to treat osteoporosis. Although the mechanism is unresolved, intermittent administration (as in the case of drug treatment) increases BMD while chronic sustained elevations decrease BMD.2

References

1. Bringhurst F, Demay M.B., Krane S.M., Kronenberg H.M. (2012). Chapter 352. Bone and Mineral Metabolism in Health and Disease. In Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J (Eds), Harrison's Principles of Internal Medicine, 18e.

2. Rosen CJ. The cellular and clinical parameters of anabolic therapy for osteoporosis. Crit Rev Eukaryot Gene Expr. 2003;13(1):25.

Nice answer, but I still am unclear about how suppressing parathormone will help out bone density. Since functionally, Vit D and Parathormone are complimentary, will not suppressing PTH be equivalent to negative feedback control, valid for most hormone systems?

@SatwikPasani Thank you for the feedback. I have added some additional explanation. This system is more complicated than a straightforward negative feedback loop, and the two hormones, while complimentary, do not have identical functions. Hopefully my addition and the reference to the pieces that remain unresolved gets at what you're asking.


text:
What is the difference between clinical and non-clinical depression, and is there a term for different severity of the bipolar disorder?
I was looking for a term which describes a bipolar disorder of lesser severity.
I know from experience from someone I know well, what a very severe case of the bipolar disorder looks like, when an otherwise very intelligent and very sane person can become completely unstable in both directions, and requires medication to basically survive it.
I'm searching for a term which has indeed the symptoms of the bipolar disorder, but is not as severe as to require medication to basically survive the mood swings. I'm not talking about being just sad for something or craving attention. I'm talking about the very real symptoms of mania, followed by depression, just not as severe to be fatally dangerous without medical intervention. A severity which I would describe of being able to cope with by learning about it and a good degree of self-control, exercise, and good eating habits.
I thought the term was clinical versus non-clinical depression, but a search of the Internet made me doubt it. They talked about it as if the clinical was a case where there is a "disorder of the brain" and the non-clinical was "just sad because of a sad event", so either were those forums wrong (I guess so, because of their apparent unprofessional writing style, and they never seemed to know about bipolar, they thought manic depression was just about being very very sad), or there is another term which best answers my question.

I found a serious-looking article which uses the term "nonclinical", but in the context of borderline and not bipolar> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772134/

vsv - bipolar and borderline are different (mostly unrelated) disorders, but the notion of "non-clinical" is widely used. I updated my answer to include this. (Sorry, I had mis-read it as "subclinical" the first time around.)

I think the main question here is:

Is there a term…which describes a bipolar disorder of lesser severity[?]

Yes. There are a couple ways to think about this, but you’re clearly accustomed to differentiating the manic and depressive phases of bipolar disorder, so I’ll start with that.
There is mania (excerpted from DSM 5*):

A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal-directed activity or energy, lasting at least 1 week and present most of the day, nearly every day...
B. During the period of mood disturbance and increased energy or activity, three (or more) of the following symptoms (four if the mood is only irritable) are present to a significant degree and represent a noticeable change from usual behavior:

Inflated self-esteem or grandiosity.
Decreased need for sleep
More talkative than usual or pressure to keep talking.
Flight of ideas or subjective experience that thoughts are racing.
Distractibility
Increase in goal-directed activity
Excessive involvement in activities that have a high potential for painful consequences

C. The mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning....

And there is hypomania:

A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 4 consecutive days and present most of the day, nearly every day. ….
B. [This criteria is the same as for mania.]
  ....
  E. The episode is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization.

I have bolded the main differences between the two definitions. You can see that hypomania is the term for the less severe form of the manic phase of bipolar depression.
Neither mania nor hypomania is likely to occur in the absence of depressive symptoms, however. Thus, there are two basic phenotypes of bipolar disorder (summarized from DSM 5*):
Bipolar I disorder: Patient experiences mania; depressive periods may not qualify as Major Depressive Disorder.
Bipolar II disorder: Major Depressive episodes are required; manic phase may be hypomanic. (This is classically considered a less severe syndrome, but this notion has been challenged in recent years.)
And finally, one more term for you:
Cyclothymic disorder: patient experiences both hypomanic and depressive periods without ever fulfilling the criteria for an episode of mania, hypomania, or major depression.
(Your other question you seem to already know the answer to, but since it's in the title.....  Nonclinical depression refers to something on the spectrum of normal (i.e. not pathological), such as situational mood disturbance. A related concept, subclinical depression is a loose term to describe depressive symptoms that don't meet criteria for Major Depressive Disorder..)

*American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.

I appreciate your effort put into this answer, it made most of the terms a bit more clear. Just so I know I understood it correctly, even though there are a lot of differences between them besides severity, if we tried to arrange them from the most severe to the least severe, we would end up with Bipolar I, Bipolar II, hypomania, cyclothymia, subclinical, non-clinical?

@vsz - I'm glad it was helpful. Mania/hypomania are phases of bipolar d/o, so conceptually it doesn't work to make a hierarchy this way. Bipolar I includes full-blown mania +/- MDD; bipolar II includes hypomania but full-blown MDD; cyclothymia includes only the milder forms of both. Subclinical and non-clinical are not strict DSM terms and can be applied to any disorder. For bipolar, "subclinical" is basically the same as cyclothymia, and there isn't really "non-clinical" bipolar d/o. Hope that's clearer.

(Sorry, MDD = Major Depressive Disorder)

Nonclinical depression is a popular term for the natural reactions to the external factors, such as loss, seasonal changes, emotional stress
http://www.depressionfree.com/non-clinical.html
while the major types of clinical depression are as follows:
Major Depressive Disorder
Major depression is a severe mental disorder that deeply affects an individual’s way of life and characterized by the inability to enjoy life fully and be satisfied.
Dysthymia
Dysthymia is a type of chronic mild depression.
Bipolar Disorder
Bipolar disorder, also known as manic depression, is characterized by constant mood changes.
Cyclothymic Disorder
Cyclothymic disorder is often described as a milder form of bipolar disorder.
Seasonal Affective Disorder
Severe mood change according to the season. Aka SAD
Melancholia
Antenatal And Postnatal Depression

can you add some links to each of those terms (preferably from a non commercial web site)?


text:
Does THC excretion increase if urine volume increases?
In regards to the body metabolizing and excreting THC: if urination is increased as a result of drinking lots of fluids, does that mean that more THC is leaving the body? To rephrase the question, is metabolism required for urination? Or can you simply urinate as a body process without metabolizing toxins from your body?

It depends on the molecule. Liver makes it water soluble if it can. After that it can be excreted with the urine. If it cannot make it water soluble, than the body can store it in fat or excrete with bile. According to wikipedia, THC is poorly water soluble and more than 55% of THC is excreted in the feces and ~20% in the urine (after processed by the liver ofc.). Since we are talking about a few amount of drug and the main bottleneck of urine type metabolism is the liver, drinking more water won't help.

This question asks about the urinary excretion of THC. Before answering the question I think you're getting at, I'll first note that cannabinoids (of which THC is one) are primarily metabolized by hepatic cytochromes rather than being excreted directly. This article is a classical pharmacokinetic paper on the topic if you’re able to access it; this one is a more recent general review accessible on Pubmed Central.
Cannabinoid metabolites are excreted both renally (via kidneys) and in the feces, so I’ll understand your question to refer to the renally excreted portion. When considering renal excretion of any substance we think in terms of glomerular filtration rate, which refers to the volume of blood filtered through the glomerular capillaries per unit time, often estimated as creatinine clearance. The question then boils down to:

Does excess hydration increase GFR?

And the basic answer is: no. The  kidneys control both volume and osmolality more distally, i.e. after the event of glomerular filtration.1
In the scenario you posit – drinking a lot of dilute fluid – osmoreceptors in the hypothalamus will sense the decreased plasma osmolality and suppress ADH (antidiuretic hormone, a.k.a. arginine vasopressin), the hormone that acts on the distal nephron to control water reabsorption. If ADH is completely suppressed, the kidneys can produce up to 25 L/day of urine with an osmolality as low as 60 mOsm/kg.2,3 This huge volume of urine, however, reflects water homeostasis achieved at the distal tubule rather than increased glomerular filtration. It does not correlate with increased excretion of THC metabolites or anything else at the level of the glomerulus.

Notes and References

1. If this makes no sense to you, you may want to check out this basic introduction to renal physiology that is available online. The referenced textbook in #3 below is more comprehensive but requires a library or purchase for access.

2. "Normal" urine osm ~300-800 mOsm/kg; plasma Osm ~280-290 mOsm/kg.

3. Christopher Lote. (2012). Principles of Renal Physiology. Springer New York.

P.S. If the question you really wanted to ask was, "Will drinking lots of water make my tox screen negative faster?".... I'm not answering that question. For reasons largely unrelated to the discussion here (but see references in paragraph #1), I suggest assuming that THC metabolites will be forever detectable via tox screen. ;-)


text:
When did our ancestors switch to a menstrual cycle instead of the estrous cycle?
The Wikipedia page on the Estrous cycle says:

Humans have menstrual cycles instead of estrous cycles. They shed their endometrium instead of reabsorbing it. Unlike animals with estrous cycles, human females are sexually receptive throughout their cycles.

The page on the menstrual cycles says:

The cycle occurs only in fertile female humans and other female primates

Do we know how many million years ago that switch happened and our female ancestors got sexually receptive throughout their cycles?

See also How is menstruation not suicide in the wild?. Although it doesn't speak to your question of when, I discussed the theorized adaptive benefits of the cycle in an answer there.

Emera et al. argue that menstruation is not directly adaptive but a side effect of adaptations pertaining to the maternal-fetal conflict.

Menstruation occurs only in most of the primates, and a handful of other mammals. It is tempting to speculate that place the switch to menstrual cycles evolved right after the split between non-menstruating primates (tarsiers and their relatives) and menstruating relatives (almost all others), which is about 63 million years ago.
There are other menstruating animals, so I am not sure if nature reinvented menstruation whenever social conditions required unproductive sex, or menses are in fact a more archaic trait.
I doubt we have material evidence about all these speculations.

Any sources to add?


text:
Converting fmri data to association matrix
I am currently working on a new tool for the analysis of (large) weighted networks. Association matrices (correlation matrices) as obtained from fMRI data are perfect examples of the kind of data I am looking for. Unfortunately I am only able to locate raw fMRI data and the task of converting them is way outside my expertise.
Can anyone point me to a place where such converted data can be found, or where I can download software which automatically converts the data? Preferably a dataset divided into control/disease.
Thanks!

Are you looking for something like this (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0040709)? GAT is a matlab package that allows for a GUI. If this is correct then please let me know and I can post it as an answer.

@Bez: I will have to take a closer look. Do you know if the software is freely available?

It says its open source so it should be! also perhaps try this (http://rfmri.org/GraphVar)

You can get raw FMRI data from https://openfmri.org/ on that website you'll also download your conditions files for the experimental design (you'll need this in creating your matrix). This is a link to an experiment(it's data) with "healthy" participants and participants diagnosed with schizophrenia: https://openfmri.org/dataset/ds000115
Raw image files from a scanner will be in .dcm format. You can use http://www.mccauslandcenter.sc.edu/mricro/mricron/dcm2nii.html to convert the multiple ".dcm" images of a scan into a 3 single 4D images for anatomicals, also known as T1 images. That converter will also convert the BOLD images into a single 4D image.
After conversion, the images you will want and need to load into whichever fmri data analysis software you're using will be in ".nii.gz".
Your question suggest that you don't need data analysis software but if you do,  I'm only familiar with FSL, you can find information on FSL from here http://fsl.fmrib.ox.ac.uk/fsl/fslwiki/
Hope this helps.

I would suggest you to learn the basics of fMRI data analysis. It is not easy to understand everything in depth, that is for sure. Anyway, luckily, you can start with some good software (e.g. http://fsl.fmrib.ox.ac.uk/fsl/fslwiki/) that does many things for you. Knowing just the basics can get you far then.
For the data, try to have a look at http://www.humanconnectome.org/data/. I think they have even preprocessed datasets.


text:
How long can a bee surive in a jar?
So, some people and I encountered an adventure game where you have a bee in a jar and need to move it from place to place before it suffocates, and someone tried to find out how long a bee would actually survive in the jar. We've found three relevant papers:

Oxygen consumption in the foraging honeybee depends on the reward rate at the food source [1]
Oxygen consumption and body temperature of active and resting
honeybees [2]
Physiological Correlates of Foraging Efforts in Honey-Bees: Oxygen
Consumption and Nectar
Load [3]

which has given us what we think is a good high-end guess of 40µl of oxygen per minute consumed.
However, we don't know at what point the oxygen level would get too low for the bee, or if carbon dioxide poisoning  would occur. Does anyone have a source for the minimum oxygen levels a bee needs to survive, or the point at which CO₂ toxicity becomes a problem?

@gopinath First thing they talk about is air holes.

@fredsbend In the game you have to transport a bee from place to place in a sealed jar, to protect it from a toxic atmosphere. However, the bee runs out of oxygen and dies very, very quickly, limiting where you can take it. We thought this was unrealistic, and wanted to work out what what the actual time was.

@fredsbend The scenario in question takes place on Mars, so I'd be more worried about the opposite situation, but that is good to know.

Assuming the jar is airtight--
I think your oxygen consumption rate may be too high and that 40$\mu l$ per hour$^1$ might be closer but since it's a high figure anyway we can use it. 40 $\mu l$ per minute would be about 2400 $\mu l $/hr.
A 12-ounce jar is about 0.355 liters. At sea level, air contains about 20% oxygen so the volume of oxygen in the jar is about 0.0709 liters.
At altitudes which are considered high for humans (17000 feet or higher) the percentage of oxygen falls to about 15%. If a bee is able to get 2400 $ \mu l$ of oxygen per hour from a jar, the volume of oxygen will fall to about 13% after ten hours.$^2$
Based on oxygen consumption alone I think a bee would be stressed at this level, especially at temperatures exceeding 32C. I would guess the bee would be stressed well before this, maybe after 5 hours (16.6% oxygen). If we factor in the likelihood that the bee's respiration is up due to the agitation of confinement I think we can shave another hour off.
Depending on the age, size, species, variety, temperature, location, etc. I think an outside limit of 4 hours in an airtight jar is a good guess.
Toxicity from CO$_2$ may be a problem but bees have a much higher tolerance for CO$_2$ than humans, according to one set of entomology notes. At 0.04% the concentration will only increase marginally due to a drop in oxygen alone but the bee itself will produce CO$_2$ and in far greater quantities under stress. A chart here shows production of CO$_2$ in reaction to a light being turned on. 400 ppm is 0.04% but in this case it is due to the bee. If the bee during respiration returns CO$_2$ as quickly as it consumes oxygen the jar could reach 7% CO$_2$ in four hours, a level that may be toxic for humans. But we have already suggested the bee is under stress from oxygen depletion at that point.
There are many assumptions in this note. A conservative estimate might be an hour in an airtight jar. I would not bet on more. There are probably other issues I haven't thought of. Bees are very fragile and the chart linked above suggests they would not fare will in such an environment.
$^1$ Respiration of Worker Honeybees of Different Ages and at Different Temperatures, Allen, 1958, J. Experimental Biology 36, 92-101. At page 97 Allen gives a chart showing log $\mu l$ $O_2$/mg body weight/hr. For a 14-23 day old bee at 32C he appears to give about .5 which means 1.65/mg/hr or about 115 $\mu l$ per hour for a 70mg bee. It may be a typo or perhaps I am misreading the chart. Also the study uses an older method of measuring respiration.
$^2$ This is a simplification. The bee will start breathing a mixture containing falling oxygen levels and this may slow the oxygen depletion a little. But if we say the bee needs what it needs this saves us a differential equation.

@WYSIWYG: "bodyweight" is not in Webster's. To edit an answer as opposed to a question is a little much, especially if the OP accepted it without comment. I usually offer proposed corrections in comments. Form for footnotes changes every few years as journals revise their style guidelines. I find this style easy to read.

Ok.. I am sorry.. Point taken.. I was trying to replace TeX code with Unicode wherever possible. Sorry that I altered the post.

@WYSIWYG: no problem and I do prefer the unicode version for microliter I'll change that back to your version when I get a chance. For CO2 I think it's easier in Latex but maybe I'm just used to it.


text:
Real time PCR normalization algorithm
When performing normalization of real time PCR results, I found two ways of doing it:

In my lab they follow the next layout: $\text{Efficiency}^{-(CT\ _{\large\text{interest gene}} - CT _{\large\text{ housekeeping}})}$ each time controls with controls and treatments with treatments. Then they divide the all values (treated and controls) each with controls.
On the other hand I found another way to normalize that follows this steps: $\text{Efficiency}^{(CT_{\large\text{control}} - CT_{\large\text{treated}})}$. Then you make the same for the normalizing gene and divide the first by the last.

The values obtained are similar but not exact. Also I noticed that first algorithm gives rather different values for most diluted when performing a standard curve.
Which is correct?

For those who are not satisfied with $2^{\Delta(\Delta Ct)}$ and want to incorporate different efficiencies of the target and normalizer PCR reactions, would this formula work to calculate arbitrary values for relative expression:
$$\frac{\mbox{Efficiency}{target}^{-(Ct{\text{target}})}}{\mbox{Efficiency}{normalizer}^{-(Ct{\text{normalizer}})}}$$
I have compared the results with that of the RTPCR instrument's own software using calibrators from a pool of tested samples, and they fit almost perfectly. But is the equation valid in a theoretical sense?

First step is the calculation of efficiency, denoted by lets say $E_{gene}$. See this post for calculation of primer efficiency.
So the fold change for that gene will be calculated by $E_{gene}^{-\Delta Ct_{gene}}$
Where:
$\Delta Ct  = Ct^{treated} -Ct^{control}$
But these Ct values are not normalized. For normalization, you take some reference gene which need not be a housekeeping gene. Reference gene should chosen such that it is not affected by the treatment. In some cases usual housekeeping genes can also get affected for e.g. in treatments affecting cell cycle or differentiation. In such cases you should use a spike-in (an artificial RNA bearing low resemblance with any known gene).
You can either normalize the fold change (Case A) or find fold change of the normalized expression (Case B).
Means the same mathematically.
Case A:
$E_{gene}^{-\Delta Ct_{gene}} / E_{ref}^{-\Delta Ct_{ref}}$
Case B:
$\large\frac{[E_{gene}^{-Ct^{treated}_{gene}}]/[E_{ref}^{-Ct^{treated}_{ref}}]} {[E_{gene}^{-Ct^{control}_{gene}}]/[E_{ref}^{-Ct^{control}_{ref}}]}$
You can rearrange the numerator and denominator to get Case A from Case B. I'm not sure how you are ending up getting different values. Recheck once. It may be because of numerical approximation errors.
Case A looks much neater; so it is best to calculate that way :)

sorry for the trouble but mistook on the query, my point 1 is edited

Answer still holds :)
Case B is what your lab people follow (point 1) and Case A is the point 2 of your question

Note: you cannot club the fractions in the numerator together to obtain the $point\ 1$ sort of form because the bases are not same ($E_{gene} \ vs \ \ E_{ref}$). It can only be done if the efficiencies are the same.

This topic could probably have it's own StackExchange, there is so much info and trial and error done with rtPCR. Here's my 2 cents:
Your adjusted calculation does not normalize your data, it just subtracts the 'background' or control. For expression studies this is not good enough. Normalizing data for gene expression must involve setting it to a scale of another gene whose expression should be not only present but consistent between your treated and untreated samples. House keeping genes (you are probably using GAPDH) make good candidates for this because their expression rarely changes. If you don't normalize than you don't know if your your expression is actually changing, or if it's simply due to a larger input of mRNA. However it must be shown that the housekeeping gene's expression is also not changing, this is usually accomplished using a different sample set. Take if from me, I've done a lot of this and this step is one of the most important in your experiment. Any reviewer who knows what he's doing will reject a paper using rtPCR without the proper statistics.
I have had a lot of success using Applied Biosystems StepOne software to provide you with accurate Ct values. Generating the variable is complication, use software to do it right every time:
http://www3.appliedbiosystems.com/cms/groups/mcb_support/documents/generaldocuments/cms_042380.pdf
What method/system are you using?

There have been several instances in which GAPDH is not suitable as a reference gene.

SYB GReen and roche, about normalizing no clue really


text:
What are the risks of elevating the legs too regularly and when tired?
I started to to think the pathophysiology of elevating legs high next to the wall too often and when you are tired.
I think possible manifestations

some damage to valves of the veins (No!)
because of collateral circulation, rhombus, heart damage, ... (No! Only in pathological situation but cannot be considered here. I think here that the risk of thrombus leaving legs is higher when you elevate your legs.)

Other side is when you should do this.
To do regularly like every evening - may not be the right way to go.
If you are tired and you do this, the vasomotor tonus is already lower so smooth muscles can less help to keep the blood so much more stress to the valves.
Cardiac output is also less because of tiredness so lymphatic drainage is less.
Elevating legs will move more lymph and blood to the middle of the body.
So less lymph and blood can be moved back to legs when you tired.
What are the risks of elevating legs for too long time in Short time and Long time?
Is there any advantage in elevating legs like increasing blood circulation of our body?
In what manner would elevating legs harm valves?
There should be no damage to valves because the direction of the blood circulation does not change.
Blood is only going from legs to heart.
I think the vasoconstriction of smooth muscles occurs first in the legs.
This returns some blood to the legs.
How is lymph made - -?
Lymph is made in lymph nodes.
After leaving the node, it is rich in lymphocytes.
After leaving digestive system, it is rich in triglycerides so called chyle.
I think after leaving legs it is also rich in triglycerides.
[W]hat is the danger of lymph leaving the legs?
I think the effective lymph (that one used in legs) is coming from the lymph nodes of the legs.
Some lymph can be made in lymph nodes of legs so no danger of lymph leaving legs.
However, some may come from the region of coxa.
How long distance can lymph travel as effective unit of immune system?
If all lymph nodes are working, there is no danger of lymph leaving the legs, I think.
If there are problems with lymph nodes of legs, then there may occur some constitutional symptoms of legs - but not sure about how fast.
Does the heart get tired like your head does, or like muscles after exercise?
No.

Valves in veins are one way. In what manner would elevating legs harm valves? How is lymph made and what is the danger of lymph leaving the legs? Does the heart get tired like your head does, or like muscles after exercise? I think if you examine these issues, you'll have a better understanding of what happens when you elevate your legs whether you're tired or not.

@anongoodnurse Thank you for your comment! I answered your questions. Do you have anything to add?

Nothing but an answer. I appreciate your improvements!

To answer your questions, one needs to address certain issues one at a time.
Veins do have valves, but they function to hold blood from settling in the legs. When you flex muscles, the blood flows towards the heart. Valve failure occurs when people stand (especially if they stand relatively still) for long periods of time every day over many years, dilating veins. You can see this on the surface of the legs as varicose veins. One way to treat varicose veins is with elevation. So, elevation does not harm vein valves.
Lymph is made at the arterial end of capillaries and is part of the interstitial fluid of tissues. It bathes cells, and returns to the circulation via the lymphatic system (which also has one-way valves), goes through lymph nodes, and returns to the blood via connections with the subclavian veins. The treatment for too much lymph in the lower extremities (also known as edema) is to elevate the legs. So, elevation does not harm the lymphatics system.
The heart was made to pump all day, every day, for many, many years. It doesn't get "tired" during a tiring day, and doesn't need to rest like we do. But it can get weak and pump inefficiently if injured (e.g. myocarditis, myocardial infarct), or if it pumps against high arterial pressure (hypertension).
As long as you have healthy arteries to the legs, I can't see how your legs can suffer by elevation.
The main effect that I can think of is on baroreceptors. The increased volume of blood in your upper body will cause an increased stroke volume from the heart, sensed by baroreceptors, and may cause smooth muscle dilation of the vascular system. In the short term, that means you will experience more pronounced orthostatic hypotension on standing (you will be dizzier). The long-term effect from elevation for a couple of hours a day are basically nil.
Since you asked about these parameters only, I won't elucidate on other possible effects.

Thank you for your answer! You can also include other possible effects. Just separate the body by "---" for clarity. I am very interested in about long-term effects because, sometimes, I hold my legs elevated more than a couple of hours - which you can feel then afterwards. I think it is a different feeling than holding for short-time. I must verify this again.  Assume you do this just before you go to sleep i.e. when your blood pressure is low, effect on baroreceptors low and also on smooth musculature.


text:
Can ovulation and menstruation occur simultaneously?
Is that possible that ovulation happens in the time of actual menstrual haemorrhage in human females - let say in a case that woman has 21 day cycle and her menstrual period is 7 days?
If yes, does it means that in this particular case the woman has lower chances to conceive?

Ovulation and menstruation don’t happen in normally cycling women at the same time. A basic outline of the hormonal cycle that triggers these events will make this clear.
Proliferative (a.k.a follicular*) phase
Beginning after menses (when the endometrium is thinned), the hypothalamus produces GnRH which stimulates the anterior pituitary to produce LH and FSH. These in turn stimulate ovarian follicles to develop. A dominant follicle produces estradiol which causes the endometrium to thicken (proliferate).
At a certain level of estrogen (actually estrogen/progesterone ratio), the feedback on the hypothalamus flips from a negative to a positive feedback loop. Thus, there is a GnRH followed by a LH surge. The latter triggers ovulation. Note that at this time the endometrium is stable due to relatively high estrogen levels.
Secretory (a.k.a. luteal*) phase
After ovulation, the high levels of LH trigger formation of a corpus luteum from the tissues left behind after ovulation. The corpus luteum makes progesterone. This hormone triggers a change in the endometrium from a proliferative to a secretory state. Progesterone also provides negative feedback to the hypothalamus and anterior pituitary, maintaining low levels of GnRH, LH, and FSH, so no new dominant follicles develop at this time.
If pregnancy does not occur, the corpus luteum will eventually (10-12 days) degenerate and stop producing progesterone. It is this abrupt drop in progesterone that triggers the sloughing of the endometrial lining. You can see these hormone shifts in an illustration like this:

The decline of the corpus luteum is correlated with a decline in serum levels of ovarian hormones including progesterone, estradiol, and inhibin A. Release from negative feedback provided by these hormones at the level of the hypothalamus and pituitary permits FSH to rise, and the cycle begins again.
You should now be able to see that:

Around the time of ovulation, the uterine lining is not fully developed and is stable due to the hormonal milieu. Menstruation does not occur.
Around the time of menstruation, FSH and LH are suppressed in a way that is not conducive to ovulation.

In theory, yes, of course there would be a lower chance of initiating a viable pregnancy (implantation rather than conception is the most obvious problem) were the endometrial lining to be unstable at the time of ovulation. The problem of luteal phase deficiency is along these lines. In this condition, the corpus luteum does not produce adequate progesterone during the luteal phase to develop the endometrial lining in such a way as to support a healthy pregnancy. However, ovulation and menstruation are still time-separated events for the reasons outlined above.
*Note that the first term is with respect to the endometrium; the second is with respect to the ovary.

Abbreviations:

GnRH - Gonadotropin Releasing Hormone; LH - Luteinizing Hormone; FSH - Follicule Stimulating Hormone

References

1. Anatomy & Physiology, Connexions Web site. Illustration is also from here.

2. Jerome Strauss, Robert Barbieri. Yen & Jaffe's Reproductive Endocrinology. September,  2013. Saunders.

Thanks for the answer, I don't understand why one can clearly say that actual hemorrhage is time separated from hormonal activity of the ovary and hypophysis - what feedback do provide endometrium itself to be independent in any way from the system? If it is not the "last" organ in the chain we should know how it itself influences changes in the chain...

I took a look at the google search from the comment just deleted. It seems to agree with this conclusion. Quoting the two sources on the front page I see that directly address this, "women who have regular menstrual cycles typically will not ovulate during their period." and "It is impossible to ovulate while having a period." I tried to provide some background on why that is so.

I added a paragraph to try to better elucidate my summary of the feedback mechanism (which is extremely complex, beyond my top-of-the-head knowledge, and way too voluminous to include here in full detail). To my knowledge, it is most at the level of the ovary-->hypothalamus/pituitary rather than the uterus/endometrium. Women after a hysterectomy may still cycle regularly.

So, we have a case of a woman with short cycle: let say 21 days + long periods ie 7days. From this we know that her ovulation is 14 before the ovulation (it's well known "fact"), thus her ovulation can come on the day 7 the last of her periods when the endometrium did not ready to implantation. So, this particular women probably has lower chances to become successfully pregnant that women with longer cycle and shorter periods.

Perhaps. Remember, though, that ovulation and implantation are time-separated events. If conception occurs ~24h after ovulation and the embryo implants another ~3-4 days later, so there is some window for the progesterone from the corpus luteum to act on the endometrium. Also, a 21 day cycle in a normally cycling woman is unusual, and it would be even more unusual for it to be associated with a long menses since the rising sex hormones prior to ovulation will stabilize the endometrium.

Of course before periods... this type of typos we should ignore %))

If you don't believe her, read the Wikipedia article on it. But stop arguing with the answerer.


text:
What factors affect the likelihood of auditory stimuli causing arousal during sleep?
I've noticed that the sound of water drops makes me wake up from sleep but other more strong sounds don't make me wake up. I can't find anything about this. The only reason I can think of is maybe because the sound of drops is continuous. Is there any research about the qualitative aspects of certain noises that affect the likelihood of causing arousal  from sleep?

Virtually impossible for us to know why water drops wake you up when other sounds don't - so that's not a valid question - but there might be some resesrch on how and why people respond differently to different noise stimuli during sleep

I think this has the makings of an interesting question with relevant research to be cited. I went ahead and cast the last VTC but re-wrote it such that I think it can be re-opened. Now voting to re-open.

The other day I was reading "Sleep soundly every night,feeling fantastic everyday" by Robert S. Rosenberg.
Somewhere in the books it was written as:
"Sound: You need your bedroom to not only be cool and dark, but also quiet. If a dripping faucet or the barking of a neighbor’s dog is interfering with your sleep, try earplugs, earphones, or generating white or pink noise to even the sound field so your ears won’t focus on the background contrast of environmental sounds. There are machines available to do so, but for some the sound of a fan will do the trick. If your partner’s snoring is keeping you awake, you should encourage him or her to be checked by a doctor for sleep apnea. Treatment can improve your sleep and also might save his or her life."
by searching more I found out that the difference between the range of frequencies from moment to moment is a more important factor than a sudden loud noise.
The idea behind white or pink noise or the natural ones like the sound of fan is that they produce a broad range of frequencies at the same level.And by doing so they can reduce or at least mask the disruption.


text:
Why do insects avoid being on their back?
I have noticed that when insects are placed on their backs, they tend to turn themselves over quickly or else appear to be in distress. Is there a physiologic, anatomic, or adaptive reason why supine positioning might be unfavorable in insects?

Because they can't get back to their legs and they therefore get stuck somewhere where they can gently wait for death to come.

Do you wish to know what the adverse stimulus is to them? Subjective perceptions, let alone feelings in bugs is mere speculation.

I'm voting to close this question as off-topic because it seems a question on  emotions in insects. Question holds potential when made objective.

@Remi.b Can you post that as an answer.

@AliceD : Is it behavioral rather than emotional ?

@AliceD The OP can roll back that edit if I'm mistaken, but it seemed likely to me that "like" was being used more loosely, intending to describe an observation about a behavioral pattern rather than emotions.

@Susan - looks OK now! Will retract close vote later (I am mobile)

Welcome to Biology.SE
Insects don't "like" being on their back because they can't get back on their legs and they therefore get stuck somewhere where they can gently wait for death to come.
Not all insects are unable to switch back on their legs but some can't do that (or can hardly do that). The reasons for which many insects are not able to get back on their legs (while mammals for example usually can do that) is that they have a exoskeleton. Their exoskeleton limits drastically their movements.

I'd guess that this varies quite a lot among different insects; in some, lying on their backs was a sign of their impending death, while others will flip over onto their backs to play dead. This isn't really surprising --- there's over a million described insect species, so some amount of variety is to be expected! Here's a video of a bunch of insects exhibiting different strategies for turning themselves over.


text:
Expanding the SETI initiative to seek intelligent data within DNA sequences?
I've recently read a couple articles dealing with long term data storage, and DNA was suggested as one of the prime candidates for long term storage of digital data additionally, there is this article which deals with decoding of long storage data. These popular articles, though simple do mention important concepts- how packets are stored in DNA use addressing schemes, redundancy of storage, writing for a recipient who may be using a different language, etc.
This made me think - we have the SETI initiative which is looking for signs of (intelligent) life in the universe. That organization was created long time ago, and uses technologies of those days - radio waves. The modern science knows that we can store a lot of data in DNA, and that most organism DNA contains only a small fraction of protein coding sequences and a large amount of non-coding material. If I understand correctly, some of the non coding material is repetitive and highly preserved. Has anyone considered expanding the search for intelligent life to include examination of DNA for messages that might've been left by other intelligent species actually visiting earth?

You suggest an interesting idea, but what's the question?

Unfortunately most of the highly conserved non coding material that you mention comes from viruses which are not really prime candidates for intelligence.

The question is about bioinformatics - is anyone looking for "long storage" data within DNA sequences.

+1: I had the idea about DNA as database too, but it didn't occur to me to marry that thought with distributed computing initiatives! Well done!

DNA as a storage medium is usually not incorporated into organisms, as I understand it. Looking at e.g. this article, they do not appear to be talking about DNA stored in an organism, but rather synthesizing naked DNA that would then probably be stored as a desalted solid under non-reactive ambient conditions (the most stable case). Organisms have an annoying habit to mutate, and there would be no selective pressure to maintain such a message (without a lot of extra complicating bioengineering).

There are now (2022) efforts in this direction, e.g.: https://www.cnbc.com/2020/02/28/how-nasa-is-using-synthetic-dna-in-its-search-for-alien-life.html ; These approaches however would be more inclusive as searching for molecules that resemble DNA (also in terms of storage) but might are formed through slightly different chemistry. Further the first step seems to be finding molecules (rather than already investigating their sequences).

@uhoh Interesting - would it be more likely to get an answer at the Bioniformatics SE, rather than here?

@bob1 That certainly could be, thanks for the reminder! This question is too old to migrate so one would have to post a new question. I don't think I'll do that but anyone else is welcome to.

@MaximilianPress "...is usually not incorporated into organisms..." *by humans. This question is about "Expanding the SETI initiative..." by searching for sequences put into earthbound genomes long ago by extraterrestrials if I understand it correctly.

@tsttst that would be worth expanding into an at least partial answer.

@uhoh All of the research referenced by OP seems to be predicated on storage of DNA outside of organisms. I don't think long-term information storage as exogenous DNA inside of organisms makes sense; we have a hard enough time with short-term DNA storage as e.g. plasmids or BACs. Willing to be proved wrong about this, just seems implausible.

@MaximilianPress yes I understand. We do have the concept of conserved sequences but resistance to mutation may require they are either necessary for life or quite durable due to some error correction or redundancy which may not be a fully explored bioinformatics concept yet. Wild speculation to illustrate a point; perhaps the huge genome of some plants contains so many copies of the same message encoded in so many different ways that it can be reconstructed even after substantial mutations?

@uhoh We're getting a little off-topic, but sure. Mutation resistance is a feature of some organisms, look at D. radiodurans. There are many error correction processes that are normal in cell biology, they just aren't perfect. Conserved sequences are usually conserved for a functional reason as you say, we usually can understand why. In terms of very large genomes like redwood, they are mostly the outcome of polyploidy or arms races between selfish elements. shrug

Let's extend your idea a bit... Ok, there are conserved sequences that we may not know what their function is. Let's assume that they are indeed not functional and are some kind of message left by an ancient form of intelligence.
How would you go about detecting that? It is already given that they are highly non-random, but this is not surprising and many "non-message" sequences have this property. Also consider that these sequences are quite short, meaning that they will have low information content. This means that if you check enough conversion codes and use imagination, you would probably be able to find several "messages" which are "hidden" there (e.g. "bible codes" etc). In other words, as I am a scientist that deals with probability and pattern recognition frequently, you will have a very hard time trying to convince me that you found a real hidden message... Formally, you don't have a satisfying background model.
The main difference from SETI is that there they know that their background is essentially random noise, so it is much easier to detect "intelligent" messages.

Very good point. What originally inspired the question was that the "data in DNA" encoding linked in the question uses very short 96 bit "packets", preceded by a 19 bit addressing sequence. While the payload can vary, the presence of the address within each packet gives hope of detection. As far as I understand, this is how genes are detected - by their promoter/terminator sites.

DNA in living creatures is just not a very good storage method. Critters can go extinct or mutate your 'message'. Theoretically you could plant a sequence of non-coding DNA in a large number of completely unrelated organisms, and that consensus sequence would last a little while. It would decay pretty quickly without selective pressure, though. In fact, you could look for these right now. Go BLAST species that are unrelated looking for highly-conserved noncoding sequences. Worst case scenario you discover a new method of gene regulation or something.

Since the initial posting of the question, the SETI institute has indeed thought about the possibility publicly.
A related question however is if aliens would also use DNA, or another chemical compound with similar properties for storing and passing information. The search for latter types of molecules is also ongoing, even with funding of a space agency (article).


text:
Does frequency of eye blinking reveal anything about human biology/nervous system?
I'm looking at an output of a single dry sensor EEG headband with the sensor positioned above left eye. As a side effect of it's placement, the device picks up eye blinks, and some eye motion as changes in the amplitude of the raw output waveform. It is clearly visible, and I can probably detect it algorithmically.
My question is - does frequency of eye blinking (not controlled) reveal anything about the state of (autonomous?) nervous system, or processes that take place within the brain? For example, what is the difference between blinking involuntary X times per minute versus Y times per minute for the same individual? Does blinking get suppressed in response to some stimuli, like loud noises, speech, etc?
I appreciate your input!

People avoid looking at what they don't like thinking about.
A feared enemy, an individual whom you have something to hide from..
Avoidance of looking/excessive blinking is a sign of fear.
It's basically a sign that the individual is not having a good time looking at what he is looking.
Sometimes people are lying and then they don't like looking at whom they are lying to... for them it would be nicer to look out the window or something that takes them away from their subject for a bit of time.
I would expect blinking to increase when lying.
Personally I have noticed excessive durational closing of eyes (a second or so), exactly at the moment of stating their lie.
Those are off course people who are honest to themselves but are trying to be dishonest to you. But some people lie to themselves as well and they may be more difficult to detect.


text:
Are lactic acid and prolactin rise after exercise connected?
I've been reading about prolactin, a human hormone. Apparently it's levels within the brain can raise after exercise, although the mechanism is not clear to me. I'm interested of there is any connection between lactic acid build up in muscles during anaerobic exercise and prolactin levels in the days following exercise. Both of these sound similar, which may be a coincidence.

Prolactin (PRL) is a pleiotropic hormone. More than 300 different functions have been described for it (Bole-Feysot et al., 1998), although probably the most well known/studied1 is the maturation of the mammary gland during pregnancy and subsequent stimulation of milk production.
One of the fairly well known situations when PRL increases is after an acute stress (Neill, 1970; Seggie and Brown, 1975; Kant et al., 1983). Although the details of this are still a bit foggy, the reason seems to be connected to the anxiolytic properties of PRL (Torner et al., 2001, Donner et al., 2007).
Anaerobic excercise is considered as a stressor, and therefore the PRL response may be important to avoid hyperactivation of the stress pathway. This has been suggested before (Ohiwa et al., 2007) and the rise in PRL may be triggered by lactic acid, as administration of lactic acid alone can stimulate PRL secretion (Sculthe et al., 2013).
Note that this does not exclude that there may be other factors involved in this response.

1 at least in female mammals, but bear in mind that PRL is present in all vertebrates, males and females alike.


text:
Would constant light or fading light be registered as more wakefulness promoting by the Supra Chiasmatic Nucleus?
During the fall and winter season, a number of people are experiencing Seasonal Affective Disorder. One of the way it has traditionally been treated is with a dedicated lightbox - a very high intensity light (5k-15k lux) that is positioned somewhere the user can see it.
One of the possible ways such light affect the brain is through being picked up by Melanopsin receptors in the eye and this info being transmitted to the Suprachiasmatic Nucleus (SCN). The SCN makes sleep/wake decisions by suppressing melatonin release.
It has been tested that melanopsin receptors in the human eye respond most strongly to the light at around 470nm wavelength.
My question is about the mechanism by which this light influences the brain - which would have a stronger influence on the brain:

A constant, high intensity source of light that is ignored by the conscious mind (fades into background)?

OR An alternating, moving or fading, less intense source of light that the eye is drawn to, such as dancing light, a moving lamp or some other form of light that the conscious mind might be drawn to watch?

To clarify my question, I know that brain has a number of self-attenuating circuits (for example dopaminergic system), where extended release of some hormone numbs the sensitivity to the hormone. I'm interested - are SCN, melanopsin receptors or melatonin suppressing process are also self attenuating, where prolonged exposure to constant light would attenuate these processes?

Did you try this over on Cognitive Sciences SE? Probably have more luck finding someone there, as it is an interesting question.

There is no light adaptation (such as Arrestin-mediated light adaptation http://www.sciencedirect.com/science/article/pii/S0896627303003908) or other negative feedback loop that attenuates melanopsin that I have ever heard of. Rodents in constant light lose behavioural circadian rhythmicity (http://www.ncbi.nlm.nih.gov/pubmed/23714074), which could technically be due to some sort of long-term depression of melanopsin-mediated signaling, but I have always hypothesized that the rhythm disruption comes from aberrant Period gene expression in the SCN due to constant light signals stimulating its transcription via retinohypothalamic tract->SCN->cAMP->PKA activation->CREB phosphorylation->PER transcription. This paper shows the rescue of rhythms in  in VIP knockout animals using constant light (http://www.nature.com/articles/srep14044), suggesting melanopsin signaling remains intact. They also claim that light may be providing tonic input to the SCN, so they are thinking melanopsin is still intact.
In terms of light influencing the brain? That sounds very vague, as light influences the brain in many ways. How would you want to delineate light input via the visual pathway from circadian light input via the RHT? Light can produce an image on your eye, and the higher thought representation of that image could evoke an emotion or an arousal state. This would be wholly different than a circadian effect.


text:
What is refractory proteinuria?
I've stumbled upon the article "Telmisartan Treatment of Refractory Proteinuria in a Dog."* What is refractory proteinuria?

*Bugbee AC1, Coleman AE, Wang A, Woolcock AD, Brown SA. J Vet Intern Med. 2014 Sep 30. doi: 10.1111/jvim.12471. [Epub ahead of print]

The article itself1  defines what the authors mean by both proteinuria and refractory:

...progressive proteinuria, with [urine protein-to-creatinine] values ranging from 0.6 at initial evaluation to 5.16 at highest (reference interval, <0.2), despite medical intervention with increasing doses of benazepril HCl (0.5-1.02 mg/kg PO q12h) and control of systemic hypertension.

Background note
Proteinuria is normally quantified as a ratio of urinary protein to urinary creatinine to account for the wide fluctuations in urine concentration according to hydration status. Normally, in humans and (apparently) in dogs, there is little to no detectable protein in the urine. In certain disease conditions (most commonly: hypertension and diabetes), proteinuria tends to increase with poorly controlled blood pressure/glycemia. Proteinuria2 may represent a novel risk factor for coronary disease in humans. Angiotensin converting enzyme inhibitors (ACEI, e.g. benazepril) and angiotensin receptor blockers (ARB, e.g. telmisartan) are commonly used to mitigate proteinuria (citing a dog article this time - this benefit is widely accepted in humans).
The point of this article seems to be that an ARB was superior to an ACEI to decrease proteinuria in this dog.

1. Sorry, I was able to access it through a library but free text is not available without such access to my knowledge. If it is, OP please post it!

2. Also sometimes measured (as in the cited article) as albuminuria - ratio of albumin to creatinine - rather than total protein. There are subtle differences is these approaches, but they are highly correlated.

Proteinuria is the presence of proteins in urine. Refractory means "persistent" or "stubborn", but in medical terms it means resistant to treatment or cure.


text:
What studies are there showing the effectiveness of any substance on canine hypertension?
Searching on http://www.ncbi.nlm.nih.gov I could only find the article titled as "Telmisartan Treatment of Refractory Proteinuria in a Dog".

Check out this consensus statement (PMID 17552466):
J Vet Intern Med. 2007 May-Jun;21(3):542-58.
Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats.
Brown S1, Atkins C, Bagley R, Carr A, Cowgill L, Davidson M, Egner B, Elliott J, Henik R, Labato M, Littman M, Polzin D, Ross L, Snyder P, Stepien R; American College of Veterinary Internal Medicine.
It includes 185 references, at least a dozen of which are related to your question. Also, if you look to the right of the article on PubMed, there are links to other relevant articles.
FYI: I located this article using search string
(canine hypertension) NOT pulmonary Filters: Review

There are quite a few others. (Canine pulmonary hypertension is apparently a popular research topic, so I found it useful to exclude those.)


text:
How does the partial pressure of oxygen affect mental focus?
On this Wikipedia page it says that lower oxygen levels can cause light-headedness. Is there evidence that higher partial pressure of oxygen can improve mental focus?

Welcome to Biology.SE. Seems like the whole question is about the definitions of percentage and concentration. This question doesn't appear to be about biology. You probably read a text somewhere which talk about precentage of oxygen in the air and concentration (of oxygen I would assume) in the air that was unclear to you. If this is the case, you should include your passage and explain what you don't understand.

@Remi.b I mean concentration as in focus. If biology.SE isn't the right place for this question, please guide me.

Oh, I got it! Ok. Your question is on-topic! I retracted my close vote. Where did you read that lower concentration in oxygen decreases abilities to focus on a task? It will probably help having the reference.

please rephrase your question, maybe expand a little. Maybe include some reference to what to talk about. Otherwise it is hard to understand

@Remi.b well I thought it was well-known, but when I went looking for it, it was harder to find than anticipated. Edited my question with a source.

Vrwim: I made a pretty significant edit to try to avert the VTC. I think you’re asking about altitude (which is the most common situation where inspired O2 is compromised), but that does not affect the percentage of O2 but rather atmospheric pressure--> partial pressure of O2. I also rephrased it so it seemed clearer to me. Please feel free to roll back whatever you don’t like.

I know that it compromises concentration, I am asking about whether higher levels of oxygen improve concentration.

Vrwim, sorry I misunderstood. I just re-edited, but feel free to restate it however you’d like.

@Susan this is great! Couldn't have said it better myself.

Long term exposure to hyperoxia actually does more harm than good. Though short term hyperoxia is recommended after brain injuries (http://www.medscape.com/viewarticle/741751_3) as a valid clinical strategy.
For lower concentrations of oxygen, there seems to be evidence that cognitive function is improved:

You can read more about that here: Chung, Soon-Cheol, et al. "Effect of 30% oxygen administration on verbal cognitive performance, blood oxygen saturation and heart rate." Applied psychophysiology and biofeedback 31.4 (2006): 281-293.
And also this:

This study aimed to investigate whether inhalation
  of the air with 30% oxygen compared with normal air
  enhances cognitive functioning through increased activation in
  the brain. The verbal and visuospatial tasks were performed
  while brain images were scanned. The results showed that
  there were improvements in performance and also increased
  activation in several brain areas under the condition of 30%
  oxygen. These results suggest that a higher concentration of
  the inhaled oxygen increases the saturation of the blood
  oxygen in the brain, and facilitates cognitive performance.

Taken from: Sohn, Jin-Hun, Soon-Cheol Chung, and Eun-Hye Jang. "30% oxygen inhalation enhances cognitive performance through robust activation in the brain." Journal of physiological anthropology and applied human science 24.1 (2005): 51-53.
Though you have to be a bit careful about oxygen poisoning.

While oxygen is an essential component for living organisms, the
  formation of reactive O2 intermediates is commonplace in aerobically
  metabolizing cells. The stability of a variety of reactive O2
  intermediates varies, but in some instances their interaction with the
  intracellular environment sets the basis for the pathophysiology of
  several disease states.

Adapted from: Cadenas, Enrique. "Biochemistry of oxygen toxicity." Annual review of biochemistry 58.1 (1989): 79-110.

Pathophysiological processes are associated with increased levels of
  hyperoxia-induced reactive O2 species (ROS) which may readily react
  with surrounding biological tissues, damaging lipids, proteins, and
  nucleic acids. Protective antioxidant defenses can become overwhelmed
  with ROS leading to oxidative stress.
The continuous exposure of newborn rats to 70–80 per cent oxygen at atmospheric pressure throughout the first 9 days of life significantly inhibited the growth of the brain which normally occurs during this period of life. The accumulations of DNA, RNA, total protein, and proteolipid protein which accompany brain growth during this period were all approximately proportionately depressed by the oxygen-enriched atmosphere. RNA/DNA and protein/DNA ratios were unaffected. The increase in brain mass in the first week of life reflects mainly cell proliferation, and since the decreased DNA accumulation occurred with no changes in RNA/DNA and protein/DNA ratios, we conclude that the effect of oxygen was to inhibit cellular division. We estimate that the oxygen exposure caused an approximately 7 per cent deficit in the cell population of the brain. These results indicate that the use of elevated concentrations of oxygen may have serious deleterious effects on the growth and development of the brain.

Taken from:* Grave, G. D., C. Kennedy, and L. Sokoloff. "Impairment of growth and development of the rat brain by hyperoxia at atmospheric pressure." Journal of neurochemistry 19.1 (1972): 187-194.*
Also hydrogen peroxide is  produced:

Thus the H2O2 concentration in brains of rats exposed to room air is calculated to be about 7.7 pM, rises 60% when O2 tension is increased to 100% O2, and increases 300% at 3 ATA 100% O2, where symptoms of central nervous system toxicity first become apparent. These studies support the concept that H2O2 is an important mediator of O2-induced injury to the central nervous system.

Taken from: Yusa, T. O. S. H. I. K. O., et al. "Hyperoxia increases H2O2 production by brain in vivo." Journal of Applied Physiology 63.1 (1987): 353-358.
You can also always read the wiki page for oxygen poisoning: http://en.wikipedia.org/wiki/Oxygen_toxicity and also hyperoxia itself: http://en.wikipedia.org/wiki/Hyperoxia

Okay, what do about slightly higher percentages? Like 25-30?

@vrwim answer edited.

that is what I was looking for! Thanks! I will look at the references in there and read up on that some more.