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What is a cortical circuit?
I have read about cortical circuits in the context of connectomics (e.g. any example here) and computational neuroscience (e.g. any example here), but a simple Google/Wikipedia does search not show an exact definition.
What exactly is a cortical circuit?

Could you maybe give an example of one or two places where you read about them?

I may be simplifying this, but I think it's just a fancy schmancy way of referring to the electrical "circuits" found in the brain, in this case the cortex (overall, or more specifically motor, visual, etc., as the case may be).  Connectomics tries to map the connections between neurons, mainly in the brain, building what is, in some sense, a circuit.  For some sentences in context:
http://www.jneurosci.org/content/32/31/10562.short

These results indicate a tight correlation between the effects of sensory drive and maturation on cortical neurons and provide a new set of cellular mechanisms engaged in the postnatal refinement of cortical circuits.

http://www.jneurosci.org/content/32/32/10982.short

...spontaneous cortical activity provides a recurring template of functional cortical circuits within the developing cortex and could contribute to the maturation of integrative connections between sensory and motor cortices.

+1 as it is correct, although I don't really see how it is fancy... a series of cortical neurons connected between each other forms a cortical circuit. Doesn't seem too fancy to me :P

Thanks Amory and @Nico. So does the term "cortical circuits" refer to circuits found anywhere in the brain, or in a specific place?

"the cortex (overall, or more specifically motor, visual, etc., as the case may be" I meant to imply that "cortical circuit" appears to broadly refer to the cortex, but there are instances of more specific uses.  Visual cortex circuits, motor circuits, etc.

@user815423426: In general you can speak of a "circuit of neurons" anywhere in the brain. For instance you can talk about hypothalamic feeding circuits, in reference to the circuit of neurons controlling feeding in the hypothalamus (a region at the base of the brain).

Thanks nico. I think I understand that "circuit of neurons" refers to circuits anywhere in the brain, my question was more about "cortical circuits. I guess that refers to circuits within the neural cortex (grey matter), probably excluding circuits in the white matter. Is that correct?

@user815423426: I don't think a distinction between white and gray matter is really necessary in this case. The fibers that compose the white matter come from neurons, so they can still be part of a circuit. "Cortex" refers to the outer layer of the brain, which is connected to many other parts of the brain (for instance connections between neurons in the cortex and neurons in the thalamus will form cortico-thalamic circuits, and so on). Of course you can also have purely cortical circuits (i.e. connection of neurons in the cortex between each other)

The term "cortical circuit" refers to the generalization that the neocortex is a uniform structure. For the most part, the outer sheet of the brain (the neocortex) is the same structure of neurons all the way around the brain.  It consists of the canonical six layers and it generally looks something like this.  Different research will emphasize different aspects of the circuit.
Anyway, it's quite an interesting evolutionary step for mammals.  The neocortex.. or "associative cortex" as it's sometimes called... is a very dexterous structure.  Someone born without sight will still make use of their occipital lobe to process nonvisual sensations.
Of course, as a I qualified above, it's not strictly true that the neocortex is uniform all the way around; there are exceptions.


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Why is venom more common in fish and snakes than other vertebrates?
Reading this question, I wondered why is it that we associate vertebrate venoms so often with snakes and fish, and more rarely with lizards, amphibians, mammals, and birds (apparently never, in birds?).
Are venoms more advantageous for snakes and fish, or more expensive or dangerous to produce for the other taxa? Or is it connected to evolutionary history – is venom somehow more 'evolvable' for snake and fish lineages?
Or, perhaps, is it just chance?

This write up by Carl Zimmer basically covers anything I could have said.  He links to a number of resources, in particular Casewell et. al. 2013, which at a cursory glance looks utterly fascinating and very well done.  Zimmer recapitulates figure 1, which sums it all up, or to quote Carl:

"Each lineage of venomous animals became deadly on its own, independent of all the others. And yet, in the end, their venoms echo each other... These results show that there are a limited number of ways to kill your victim quickly. No matter what genes you borrow for the evolution of venom, they will end up very similar to other venoms."

Another Zimmer piece specifically points out research purporting to show that snake venom genes are much older than snakes, maybe 200 million years old.  That gets around but doesn't quite answer your question.  An older review tried to coalesce things (as best as he could in '92), spending time focusing on insectivora and dealing with mammals.  The theory is that while venom is an excellent advantage, it requires a significant investment and is often slow-working.  In a world with sharp teeth capable of tearing, venom may not be necessary.  Mammals, for example, might evolve to not use venom, as it may not be suitable for their high daily energy demands.  The pdf linked above briefly touches on the concept of "reverse recruitment," where venom genes may be usefully re-purposed for other biological processes.
Reference:
Nicholas R. Casewell, Wolfgang Wüster, Freek J. Vonk, Robert A. Harrison, Bryan G. Fry. Complex cocktails: the evolutionary novelty of venoms. Trends in Ecology & Evolution
Volume 28, Issue 4, April 2013, Pages 219-229

+1. Your "this pdf" link is broke. Would you mind providing the titles and authors of the articles you cite in case the links break? Thank you.

From the Zimmer source, it's this 2013 paper by Caswell, et al: https://www.sciencedirect.com/science/article/abs/pii/S0169534712002935 (https://doi.org/10.1016/j.tree.2012.10.020)

Old answer:
Venom production is a "hard" adaptation to achieve**. So it is conceivable that simpler organisms had enough evolutionary time to get the adequate mutations for this to happen, which would explain why venom is almost absent (I know only of a platypus as being poisonous) in mammals and birds, and seemingly abundant in fishes, amphibians (such dart frogs) or reptilians.
Also, as I understand there should be great selective pressure and mutation in simpler organisms is more likely to produce viable offspring than in more complex ones, which can be a contributing factor.

**UPDATE:
It has come to my attention that the answer I gave is not exactly correct. Upon investigating venomous mammals many more came up (not only platypus - male platypus to be more precise),  such as vampire bats, solenodons, many types of shrews (thanks @releseabe), moles and even primates (the slow loris , being the possible single candidate)
There are no birds know to be venomous, but some (such as the pitohui, the ifrita and the roufous) can be toxic to eat.
My initial belief that toxicity is hard to achieve (this is hardly my area of expertise, and perhaps I should have refrained from answering something incomplete), does not seem to be really substantiated by literature, where lots of different organisms seem to have developed toxic/venomous adaptations.
Maybe it should be noted that many of these animals have evolved poisonous glands from salivary glands/sudoriferous glands and that they are described as presenting convergent evolution. Another caveat is also that most(all?) poisonous birds have Batrachotoxins that comes from their diet (which they concentrate on their skin and feathers), not something they produce themselves and are not as potent as the ones produced by dart-frogs. In this sense they are maybe less toxic than other animals, and the intensity of this effect may be related to co-evolution of those organisms and their prey/predators.
It's also worth mentioning that the slow loris, while considered venomous, has the poison from its gland that resembles a cat salivary allergen, and maybe would be better described as allergy inducing, rather than a poison, or perhaps cats could be considered venomous (my opinion, hardly worth anything). Another possibility is that the substances used in marking territory are the same and eliciting allergy is an unintended consequence (from the paper: "Rather than possessing a brachial gland like the loris, small cats directly add salivary allergen proteins to inanimate objects (... ) The idea that species recognition systems share a close relationship with immune recognition").
My opinions about toxic and venomous animals changed as I was reviewing this subject and, as I view it now, it is a property that is ubiquitous on many different branches of the tree of life .
Wikipedia link about venomous mammals. it is not very good to reference because people may change it at some point and the information to which I am refering would no longer be there, but it is strongly peer reviewed see here
shamelessly stolen from wikipedia about slow loris venom characterisation Talking Defensively: A Dual Usefor the Brachial Gland Exudate of Slowand Pygmy LorisesLee R. Hagey, Bryan G. Fry, and Helena Fitch-Snyder
pitohui:     JP Dumbacher, BM Beehler, TF Spande, HM Garraffo, JW Daly. Homobatrachotoxin in the genus Pitohui: chemical defense in birds?
slow loris paper:  Nekaris, K. Anne-Isola, Richard S. Moore, E. Johanna Rode, and Bryan G. Fry. 2013. “Mad, Bad and Dangerous to Know: The Biochemistry, Ecology and Evolution of Slow Loris Venom.” Journal of Venomous Animals and Toxins Including Tropical Diseases 19 (1): 21. https://doi.org/10.1186/1678-9199-19-21.

also shrew is a mammal with venom.

I note that both fish and snakes lack limbs and in fact many venomous and poisonous creatures would be almost helpless without venom/being poisonous to eat or touch. There are cases of poisonous creatures whose sole defense is their coloration advertising their poisonous nature and the poison itself (and of course their are false advertisers); these creatures rely on predators choosing not to eat them, not any kind of active defense at all.
So I suggest lacking limbs and/or being slow and/or being small/fragile favors evolving toxins as a means of self-defense or for killing.

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Any food crops that could grow in a desert provided that they get fertilizer and water
I am working on an idea to provide nearly unlimited amounts of water in desert regions. To make this commercially viable. I would use the water to irrigate desert sand and grow crops. Given my extremely limited understanding of biology, I cannot find an answer to the following question:
Are there any food crops (preferably high valuable/low maintenance ones), that can grow in a desert, given that I can just provide the seed, water and fertilizer and stop sandstorms.
My motivation for investigating this is the following map showing regions that are either already deserts or at risk of becoming deserts:

Source: http://en.wikipedia.org/wiki/Desertification

I think the people behind seawater greenhouses have been exploring this very question

Just look at whatever grows in hot areas. If you can provide unlimited water and protect from the elements, then it is no longer a desert and desert plants will probably not even survive.

With respect to nutrients, there is a big difference between pure sand deserts and ones with higher contents of clay and organic matter, and this will affect which plants can growth there.

@fileunderwater I am considering pure sand deserts mainly. If that is not viable, then I have to go for especially suited areas.

I think many projects have shown that desert is self-reinforcing (so deserts expand b/c plants have trouble surviving at the margins), but also that non-desert is self-reinforcing (so if you're able to get a patch of forest that survives in the desert, it can also naturally expand to convert desert to forest). So it seems like a first step might be focussing your water/shelter/fertiliser etc. on giving an initial boost to a robust plant community that once established will work for you (ie. not need more external inputs). Cf. http://en.wikipedia.org/wiki/Gaviotas.

You might want to check what food crops grow easily in hydroponics. Those crops require little soil nutrition as long as they are fertilized and watered. Also perhaps what grows in sandy soils(Watermelon, I infer coconuts,etc)

Following up on Jeremy Kemball, does your idea even require that the plants be planted in the desert soil? Or can they just be grown hydroponically above the water or in, say, keyhole gardens (which are becoming common in some sub-Saharan countries).

Even if you have unlimited water available to the plants you'd still have to worry about the high temperatures and light levels of these areas. In the hot periods I would look into any plant that uses c4 carbon fixation like millet, sorghum, corn, sugar cane... In the cooler periods maybe look into rotating to a cool season legume crop like the cowpea that would help fix nitrogen. Another really important thing to do would be to find cover crops that will hold down the soil and build up some life in the otherwise sterile sands of the desert.

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Utilising Mycorrhizal Association
We know that mycorrhizal association helps the plant to absorb nutrients.
Why can't this association be exploited in agriculture ?
Can't we add spores of the specific fungi to specific plant and enjoy the benefit of this association as we would not have to add many fertilizers ?( We could add organic manure whose main drawback is the time it takes to release nutrients. The fungi could probably solve the problem.)

Mycorrhizal fungi are often used in small-scale agriculture for just that reason.  If you search mycorrhizae on amazon they sell it by the tub.  I think its especially used in organic gardening for just what you said, the slightly less-processed organic fertilizers are harder to take up by plants without their mycorrhizae partners.
I'm not sure about how widespread the practice of applying mycorrhizae is in large-scale non-organic farming.  Judging by how big of a problem fertilizer runoff is, my guess is that a lot of companies have decided that their bottom line is best served by just swamping everything with artificial fertilizers.  I'm not sure how mycorrhizae is produced either, it might really be prohibitively expensive to scale production of it up that much.


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How are the paranasal sinuses linked with the capillaries in the ear canals?
Sinus congestion often seems to be accompanied by excess pressure on the outer ears (as anyone who has shared a transcontinental flight with an infant can attest to) or fluid buildup in the canals.  An increase the capillary pressure within the ear canals would explain the pressure, but what is the physiological connection between the sinus pressure and pressure in the ears?
The most obvious answer I can think of is that any direct drainage from the sinuses would cause a backup of fluid into the Eustachian tubes.  This would only explain pressure coming from the other side of the eardrum, but is such pressure simply relieved by blood pressure transfer to the capillaries in the ear canal, or is there a non-trivial mechanism by, e.g., a vagal circuit which governs the relationship between the sinuses and the outer ear?

There is no direct link between the capillaries in the sinuses and the ear.
The Eustachian tubes drain the middle ear (between the eardrum and the inner ear) into the nasopharynx, the part of the throat that is just behind the nose.

The para-nasal sinuses drain into the nasal passages themselves at different points. The sinuses and middle ear constantly produce some fluid, which is either reabsorbed or drained.

Often what happens is that in the case of a common cold or other upper respiratory tract infection, the nasopharynx and nasal mucosa are both infected. The inflammation causes swelling and blocks off the Eustachian tubes and the drainage pathways of the sinuses and the trapped fluid itself causes sinus & ear pain and can get infected causing sinusitis and otitis media. Alternatively a viral infection can also go up into the middle ear and sinuses causing direct infection.
The process that occurs when you go on a plane is slightly different. The Eustachian tubes and sinus openings collapse due to pressure and thus the natural fluid that is produced accumulates as well as there being an inability to neutralise the internal and external pressure (thus why making your ears 'pop' works- you force the Eustachian tubes open via positive pressure)

Regarding blood supply of the paranasal sinuses and the ear:
The ear is supplied by the posterior auricular and superficial temporal arteries of the external carotid artery.

The paranasal sinuses are supplied by various branches of the internal and external carotid artery including the maxillary artery, anterior and posterior ethmoidal arteries, ophthalmic artery, supraorbital and supratrochlear arteries


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Species Identification - small insect: is this a bed bug?
I found this bug in my apartment in Chicago.  We had bed bugs in our house the previous year (but we thought we got rid of them).  This bug was very small - maybe 2 millimeters in length.  These photos are all of the very same bug (just different lighting).

Can you smell almonds? Bud bugs have a distinctive smell usually described as being "like almonds".

No noticeable smell.

See my answer to Insect identification - Is this a bedbug?

This is a really old thread but just in case someone happens upon it, this isn't a bed bug.
I am not an expert but it looks like it's likely a book louse or psocid.
See comparison photos of unfed first instar bed bug nymphs vs. psocids/booklice here: http://bedbugger.com/2008/03/04/booklice/
It's all about the shape of the head and body.

I agree, I've had book lice in my Fly lab before and this looks rather like it!

Thanks for following up with this.  I think you're right, the photo you linked to looks spot on.  Actually, the lady in the apartment above us had lice one or two times during this period - so that must have been what I found.  Actually, I'm relieved, I'd rather fight lice than bed bugs.  Either way, our apartment seems to be bug free now.

This is deifnitely a psocid species. See here for another SE example.

Also book lice are not the same as head lice (and are in fact in totally different orders)

Wow, the internet is weird!  Can't believe that I took a photo of a very tiny bug with my phone and then someone across the world identified it.  Modern society is pretty trippy man.


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Cell state and cell function
I have read many papers that refer to cell type, cell state and cell function, but I haven't found an explicit definition for each of these terms.
For example this paper (Brown et al. 1994. J General Virology 75: 2367-2377) refers to cell type and cell state without providing an explicit definition of both terms.  I have a vague idea of what these terms mean but a more explicit definition would help me greatly in understanding them.

Mainly cell type refers to the differentiation degree to form a cell population whose characteristics are identifiable by using simple microscopy, stains or immunological methods. Examples of cell types would be T8 lymphocytes, peripheral astrocytes or hepatocytes. Cell types can be pathological too, like tumor cells.
Cell state makes references to the current physiological condition of a given cell. A given cell type can be found in different proliferation states, metabolic conditions (i.e: An adipocyte or a hepatocyte will have different metabolic profiles depending on the insulin and glucagon balance), electrophysiological state (The human oocyte rapidly changes its membrane potential once a spermatozoid has entered) or even degree of differentiation (The typical example are B lymphocytes, which can be in a "naïve" state if they haven't found an antigen, or into a mature state. Once they have matured, thay can be subdivided into cells that actively produce antibodies and cells that divide actively).
A cell function usually refers to a process that occurs inside a cell, or to the physiological function that cell type has in the whole organism. Cell functions could be metabolism, signaling, cell division, etc.; while also could be the likes of detoxification (hepatocytes), hormone production (Langerhans cells) or contraction (myocytes).

I'm busy writing a section on this topic for a dissertation and have run into the following useful definition, which I'll write here for posterity:

Cell type and state can be thought of as a location in "state space", a virtual landscape covering all possible cell states and types.
Each point in this space represents a combination of various configurations in the cell: its genomic arrangement (physically and chemically), its transcriptomic profile, its metabolic state, the arrangement of its organelles and cytoplasmic components.
Configurations which are similar will confer similar functions to cells (having gene expression skewed towards energy production and lysosome formation will probably be associated with phagocytosis, for example). Phagocytic cells thus might be near each other in this space.
Cell type and state can be thought of as snapshots of this cell space with different resolutions - cell type being a large zoomed out version, and cell state being a granular view. For example, the T lymphocyte cell type is a broad but useful classification of cell, but the cell states within that type could include naïve and activated T lymphocytes.

Some nice references here: an easy blog post by M Bernstein, and a more in-depth article referenced therein by C Trapnell.

As it’s currently written, your answer is unclear. Please [edit] to add additional details that will help others understand how this addresses the question asked. You can find more information on how to write good answers in the help center.


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Is it possible to clone a Neanderthal?
As Neanderthal DNA has been sequenced, is it possible to create a living Neanderthal?

Not any time soon.  By far the greatest challenge is getting the DNA sequence from the computer into a form that could be implanted into an embryo.  Craig Venter's team was able to build a bacterial genome from scratch, but that was incredibly painstaking work, requiring the assembly of many small fragments of DNA into a single circular chromosome.  With current technology that process becomes prohibitively difficult for a human-like genome.  You would have to build each chromosome from scratch, these chromosomes are linear, and you'd need to associate with them the various histones and other proteins help tightly fold them together.
Another huge problem is epigenetics.  The next generation sequencing methods used for the neanderthal genome just give you DNA sequences, not what epigenetic modifications are present on that DNA.  Genomic imprinting in mammals is very important, and presents problems even in normal cloning efforts where genomes are taken wholesale from live animals.
Not to mention that 1% of the current genome is contaminated with human DNA (not meant as a criticism, its amazing what they have been able to do with a toe bone if this work stands up to peer review).
And none of this takes into account the ethical problems associated with this.  Would you clone it in a human?  Chimp?  Either way its got serious ethical questions.
Dont take my word for it though, here is the leader of the project commenting on this question a few years ago:

Paabo said because the Neanderthal DNA was scattered in imperfect
  fossils, the notion of cloning a Neanderthal was far-fetched.
"Starting from the DNA extracted from a fossil, it is and will remain
  impossible," he said. "There is not really an improvement on current
  technologies that would make that possible.


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Is diabetes mellitus a sex-linked disease?
There are two types of diabetes mellitus.
a. Type 1 diabetes mellitus
b. Type 2 diabetes melliuts
Is either of them a sex linked disease? Can either one be inherited? My book says, "this disease is transmitted as a recessive genetic characteristic." What does this mean?

You seem to be confusing inheritance with being sex linked. The two are not related. While sex linked characteristics are indeed inheritable, not all (or even most) inheritable traits are sex linked. As for what a recessive characteristic is, have a look here (the first hit when you search for "recessive genetic characteristic" in Google.

Is either of them a sex linked disease? Can either one be inherited? My book says, "this disease is transmitted as a recessive genetic characteristic." What does this mean?

Neither are sex-linked. Type 1 can be directly inherited (in a non-Mendelian fashion), but Type 2 genetic factors mostly increase risks. "Recessive genetic traits" are traits that only express themselves when ONLY the recessive alleles are present in the organism (a dominant allele, if present, will 'overpower' recessive one).
Longer info:
Diabetes mellitus Type 1 (Juvenile Diabetes) is inherited, but it is autosomal with complex dominant/recessive rules:

Type 1 diabetes is a polygenic disease, meaning many different genes contribute to its onset. Depending on locus or combination of loci, it can be dominant, recessive, or somewhere in between.

That results in some interesting, albeit complex, expressions:

The risk of a child developing type 1 diabetes is about 10% if the father has it, about 10% if a sibling has it, about 4% if the mother has type 1 diabetes and was aged 25 or younger when the child was born, and about 1% if the mother was over 25 years old when the child was born.

Diabetes mellitus Type 2 does have genetic components, but the vast majority merely increase the risk of developing Type 2 Diabetes. Environmental factors play a large role in Type 2.

Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60-80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.

Fascinating and complex indeed! So even though there are different risk factors for Type 1 based on mother or father having it, you still wouldn't term it "sex-linked"?

@Oreotrephes: sex-linked just means that it depends on some gene present on the sexual chromosomes (chromosomes X and Y), so that it is not passed equally in the progeny (e.g. a gene on the Y chromosome will not influence females, who are XX). I would also like to add that epigenetics plays a very important role in the development of diabetes.

I understood from your explanation that type 1 is inherited but the defective gene is on autosome not on sex chromosome. But didn't understand what you said about type 2. Does the same explanation goes for type 2?

Actually the genetic component of type 2 diabetes is much higher than type 1. See this link http://www.diabetes.co.uk/diabetes-and-genetics.html

@Snipergirl - That doesn't contradict what I said. The genetic components of Type II increase risk of getting the disease, with the development left up to environmental factors. You can directly inherit Type 1 regardless of environmental factors. At least, as far as I'm aware.

@MuhammadRafique - The genetic components for Type II would be mostly autosomal, though if I recall correctly it's development is more prevalent in women so there may be some sex-linked genetic factors, but I have not read anything directly stating that.

@MCM the way in which your answer is worded is somewhat misleading; the comparisons between type 1 & 2 are not comparing the same thing (you don't list the absolute or relative risk of 1st gen relatives of type 2 diabetics for example, but you do for type 1)

I'm not aware of any of the genes implicated in either T1DM or T2DM being sex-linked. However, there is maturity-onset diabetes in the young (MODY, for short). MODY is a subset of T2DM that are caused by an autosomal dominant mutation in one of a few genes (e.g., glucokinase, KCNJ11, ABCC8, INS). These are all rare, heritable forms of T2DM with various responses to traditional T2DM therapies.


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What kind of insect is this?
Found in Russia in the kitchen. It is about 3 mm long.

RelatedTiny dark-colored bug ID in Amman-Jordan

That is a flour beetle, the two most common and likely types are the confused flour beetle and red flour beetle but to identify look at the antennae. I'd suggest it is the confused flour beetle because the antenna go from thin to fat quite gradually, though the pictures may not be good enough for that to be certain.
Other commonly used names are tribolium (the genus name) or flour weevil. They are also used in labs as a model organism, groups in my last two labs have used them. They are a pest and you should probably get rid of them.

"Both types of beetles are often found not only in infested grains,
  but in crevices in pantries and cabinet, as well. Damage to food is
  caused somewhat by the beetles' feeding, but also by their dead
  bodies, fecal pellets, and foul-smelling secretions. In addition to
  creating a foul odor, the beetles' presence encourages the growth of
  mold." - Wiki.

Can we agree that "confused flour beetle" is a fantastic name?

@Oreotrephes definitely, never heard of that name before, but are now curious how it came about.

@damien it's because people often confuse the two when identifying them.


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Are there any pathogenic archaeans?
Most textbooks seems to restrict pathogens to the domains bacteria and eukarya. Are there any pathogenic archaeans?

To date, there isn't a single species that may be considered pathogenic to animals or plants. There are archeon who live in association with animals (in the case of human, they have been found in the gut microbiota aswell as certain skin surfaces) that are mainly methanogens. This could lead to think that archaons could produce "pathologic farting", but that condition has never been described.
In the case of ascidians and other marine invertebrates, some archeon have been found living in symbiosis, with the microbe aiding the animal by means of nitrogen fixation. One could think that, since they're able to live inside the organisms, they could behave as opportunistic pathogens, but none has been described.
Furthermore, it actually exists at least one known species who could be classified as parasitic, the nanoarchaeota Nanoarchaeum equitans, which has been described as a symbiont of some hyperthermophilic archaeon. Despite that description as symbiont, Nanoarchaeum cannot live by its own, while its companion does. Moreover, its genome contains the typical traits associated to parasitism, with great reduction in genome size and loss of many key pathways and cell functions, including methabolic pathways an even some key components of its transcriptional and translational machinery. Since there is no known function of the Nanoarchaeum itself, it should be considered as a parasite.
However, the lack of evidence may be biased, since few people has used metagenomic approach to look for archeon in clinical samples, and some rare cases may be found in the future.

I have to disagree with the comment "Since there is no known function of the Nanoarchaeum itself, it should be considered as a parasite." It is an obligate partner of its Ignicoccus host, and genome reduction occurs in beneficial symbionts as well.  There is currently no evidence either way, so it should not be assumed to be one way.  In the original papers on its discovery it was shown that Ignicoccus growing with Nanoarchaeota reached the same cell densities as Ignicoccus alone.  It is quite possible that in their natural environment nanoachaea play a positive role in the symbiosis.

Actually, there exist at least one reference to a negative effect of Nanoarchaeum towards its host. Jahn et al (2008) describes that single Ignicoccus cells wich had more than two Nanoarchaeum cells attached were unable to grow, while those with two or less could form a colony.
It's true that there isn't strong evidence to considere Nanoarchaeum as a parasite in the traditional sense, provided this is the only reference I have found to a negative (or positive) effect of this archeon. It's also true that even traditional symbiots such as micorhizic fungi can be harmful in certain conditions, and because of that, this lonely example wouldn't be representative. However, untill this reference there were the same evidence to consider this archaeon as a symbiot or as a parasite, and for unkown reasons the first hypothesis was assumed by default. This results sugest that Nanoarcheum is potentially harmful and, since there still isn't any evidence that demostrate that Nanoarchaeum has any benefit, I strongly believe the consideration of a putative parasite should be encouraged and used as the default hypothesis.
Some authors prefer to use the term "intimal association", and they define it as "a highly specialized system combining characteristics of symbiosis, commensalisms, and parasitism" wich tries to be something neutral beween the two hypothesis. However I find that expression unnecesary, confuse and with an strong lack of meaning; mainly because that kind of relationship can be described with classical ecologycal terms.

The conclusion to the paper you are referring to states: "However, the fact that I. hospitalis and N. equitans build a stable coculture without sustained damage to the Ignicoccus population clearly distinguishes N. equitans from the bacterial parasites mentioned above. Therefore, we propose that the association of I. hospitalis and N. equitans represents a highly specialized system. Consequently, assignment to the classical category of symbiosis, commensalism, or parasitism might not be possible even in the future."  It is confusing, but thats the nature of the system.

I agree that their isolation experiments are interesting, and point towards a negative interaction, but their data shows that: "N. equitans had no inﬂuence on the doubling times, ﬁnal cell concentrations, and growth temperature, pH, or salt concentration ranges or optima of I. hospitalis."  This does not seem like the characteristics of a parasitism, and I don't think there is a reason to choose a default when there isn't enough data either way.  For others: http://jb.asm.org/content/190/5/1743


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Is there a preferred sleeping position for humans?
I remember hearing various sleep related advice as a child, like "sleep on your right side", or " have your head pointed in X direction".
Is there any biological reason why sleeping on one side versus another, or with a head pointed in some direction is beneficial for humans?

The enWikipedia article summarizes the best/only real research on positions that I am aware of.  I read a book in high school (that is to say it was old and I have no idea what the title was) that claimed that the semi-fetal position was the best, as it supposedly maximized protection without compromising breathing too much.  I can't say I've seen anything that would indicate your head's direction actually matters, except as it depends on the position of the rest of your body.  Do you mean facing North or the door?  That's some Feng Shui stuff or something similar, which is meaningless.
In terms of which side to sleep on, there is actually an answer!  Well, maybe.  Sleeping on your left side aggravates heartburn more than sleeping on the right side1, but sleeping on your left may be somewhat associated with heart problems.2  From what I can read from the studies, the heartburn one sounds more causative, but then again dying is worse than a little heartburn...  In the end, though, about the only thing that matters is that sleeping on yours side can lower the amount of snoring (annoying) and sleep apnea (unhealthy).

By head direction I meant compass orientation like north or east

Disclaimer: Not in any way my area of expertise. Maybe someone else can expand

In relation to pregnancy, there exist one australian study (Stacey et al. 2011) that reports an increased risk of still-birth for women that sleep on their back at the later stages of pregnancy. The purported mechanism is pressure from the uterus on the inferior vena cava and aorta, restricting blood flow. Lowest risk was found for women that sleep on their left side (less pressure on the liver). Another recent study from Ghana (Owusu et al. 2013) has found similar results, with associations between sleep position (supine position) and birth weight or risk of still birth. However, the studies are relatively small and the results must be further corroborated.


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Molecules and human memory
Has it been demonstrated that the memory of human brain is just connections between neurons, not "long" molecules such as RNA or proteins?

The idea that memories could be stored as RNA or proteins is an old one.  It got a lot of attention decades ago when James McConnell did a number of experiments where he conditioned planarian flatworms to respond to certain stimuli, ground them up, fed them to worms that hadn't gone through the conditioning.  He claimed to have observed that the worms fed conditioned worms learned to respond to the stimuli faster.  This supported the idea that memories were just RNA or proteins, and thus survived the grinding up process.  His results were not readily reproducible, and so the idea fell out of favor.
There have been a number of studies at this point that have been able to look at the firing of individual neurons and shown that there are unique patterns that respond to different stimuli, for example Category-specific visual responses of single neurons in the human medial temporal lobe. So I think it is pretty well established that there are certain connections between neurons that are critical, sometimes even individual neurons.
That doesn't necessarily rule out that there are unique RNA or proteins in those specific neurons, and they are what's actually storing the memory.  I'm not a neuroscientist, but I think the biggest argument against such a storage system is simply the speed with which you can recognize something.  When you see a face you know you nearly instantly recognize the person, and have a flood of memories about that person.  If the memories were somehow stored in RNA or protein structures, I think it would take much longer to somehow "read-out" that data from the molecular structure.  The only thing that really works that fast are the action potentials in neurons.
An interesting comparison might be made to the system in our bodies that DOES have molecular-based memory, the immune system.  When you get sick with a cold you've never been sick with, your immune system doesn't immediately recognize the antigens that come from that virus.  Through the process of somatic hypermutation, your body produces B- and T-cells that have protein receptors that recognize the viruses and the cells infected by the viruses and go and kill them.  A small subset of the T and B cells that have the molecular recognition of that cold become 'memory' cells.  These memory cells that go into a quiescent phase, waiting around until the next time that cold infects you.  But that time they 'remember' it immediately, and you don't get nearly as sick, if at all, because the genes for those recognition proteins are stored in the memory cells.  The activation of immunological memory cells takes a long time as compared to remembering a face, or some other normal memory function, so such a molecular system couldn't be responsible.

cf. http://biology.stackexchange.com/questions/2875/can-rats-pass-on-memories-of-a-maze-to-their-offspring

ah, thanks, I thought I remembered there were some old papers on rats but couldn't find any reference.

The study with the cannibalistic planaria has never been replicated, after many attempts.


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Do people with colorblindness have less cones or no cones of a certain type?
https://en.wikipedia.org/wiki/Color_blindness#Red.E2.80.93green_color_blindness

Protanopia (1% of males): Lacking the long-wavelength sensitive retinal cones,

Deuteranopia (1% of males): Lacking the medium-wavelength cones,

Do they lack all those cones, or are they just (severely) short?

This is a complicated case, as it can have multiple causes.
The genes which are coding for the long (L, yellow) and medium (M, green) wavelength photopigments are located head-to-tail on the X chromosome. This is the reason why this colors are affected much more and especially in men (which only have one copy of this chromosome).
What seems to happen mostly is that the photopigment of one type of cone cells (and their neuronal connectivity) is missing, while the density of the cone cells is still the same. This means that the cells are they, but are not functioning. See these publications (when you have problems getting the articles, let me know in the comments, I can help):

The density of cones in the fovea centralis of the human dichromat
Color-deficient cone mosaics associated with Xq28 opsin mutations: a
stop codon versus gene deletions.
Functional photoreceptor loss revealed with adaptive optics: an
alternate cause of color blindness.

What can additionally happen in some cases is that these cones have a different pigment than they should have. See the third paper above for details.

You need to have faulty cones or be completely devoid of the cones that help you perceive a particular colour. If you do possess cones to visualize a colour, you aren't technically colour blind because you should still be able to detect the colour slightly (reference).


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If people with colorblindness lack one type of cone cells, shouldn't they be unable to recognize one particular color?
The 3 types of cone cells in normal humans allow them to view 3 types of colors and any color made from mixing and matching those 3.
So, 2 types of cone cells should only allow to view just 2 types of colors and any colors made from those two.
But that is clearly not the case.
https://en.wikipedia.org/wiki/Color_blindness#Red.E2.80.93green_color_blindness

Protanopes, deuteranopes, and tritanopes are dichromats; that is, they can match any color they see with some mixture of just two primary colors (whereas normally humans are trichromats and require three primary colors).

Also, from personal experience, I'm colorblind and can see and differentiate all 3 red, green, and blue. It's just the hues between red-green and green-blue I can't distinguish much...
How exactly do dichromats see all three colors when they lack one type of cone cell?

Cones do not literally interpret colors.  The three cones work together to encode a signal that is abstractly interpreted by your brain in higher processing centers.  Here is what neuroscientists currently think the decoding scheme looks like:

This leads to what's called opponent process, an antagonist mechanism whereby the perception of green/red are a matter of the contrast between the two.  In a deuteranopes, the mechanism of antagonism is missing, so the colors can not be differentiated.
What this implies is that (to some extent) a single color has no meaning.  Colors are only meaningful in the context of other colors.

Based on that decoding scheme, the problem of green/red colourblindness (assuming lack of "green" cones) should be that there is a lack of information in green and red areas. For both the only signal would be low levels of "red" stimuli (since the overlap of "green" stimuli is missing). However, this should also cause multiple correspondence pairs along the "red" stimuli curve (light green to dark orange; yellow to orange etc) at similar levels of "red" stimuli. Is this the case in green/red colourblindness? I thought that only green and red were mixed up.

The decoding scheme is direct measurement of cone activity in the presence of light.  But how the higher processing centers interpret signals from the cones is not as straightforward as you might imagine; it's actually still an open question! Opponent process is a current theory about how it works, but the experiments consist of more psychology than neuroscience so we're on the outside looking in.  But notice that the evidence suggests that R-G relies on only two cones, while Y-B relies on all three.  So there's probably some loss in YB, but not to the point where you can't differentiate them.


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Green feather-like formations in tap water - what is it? (with pictures)
These things recently appeared in my tap water Copenhagen Denmark, this summer 2013. They are very small, and have a feather like structure. I've called the water supply, and they thought that it was some tracer put in there by humans to trace if the warm water supply leaks into the tap water. But I could not show them the pictures.

What are they? Are they dangerous?
For size comparison: the green stuff is located on the top right of a piece of A4 paper.

Some sort of algae? You might need (somehow) an even closer picture to get a good identification.

I'm also thinking algae or moss (overall apperance could match species in Dicranaceae?). Better picture probably needed though. Would be strange for something like a moss to find its way through your tap water supply though.

I have had a biologist out taking some samples of the water. She examined them in a microscope, and identified the algae as blue-green algae/cyanobacteria. She could not identify the species further.
She said the reason probably was that my pipes where exposed to sunlight, and also that the pibes with hot and cold water ran too close to each other, creating a nice lukewarm temperature for the algae to thrive in.
I'm of course going to change the pipes :)


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What areas of the brain are involved in doing arithmetic operations?
Do neuroscientists already know what areas of the brain are involved in mental calculations? Has any fruitful research been done on that or not yet? Do you think that if we understand what areas of our brain are responsible for doing arithmetical tasks we may one day have the ability to improve someone's calculation skills by non-invasive methods?

neurosynth is a useful tool for answering these kinds of questions.  Go there and enter "arithmetic" in the search bar and you can find a number of studies through meta-analysis and their relevant brain regions on a brain map.  Note it's in beta, so use the "studies" tab to confirm with the literature.

This is a part answer to your question.
According to "Arithmetic processing in the brain shaped by cultures" (Tang, 2006), the parts of the brain that are activated while doing arithmetic is to an extent, governed by culture, in the article, the authors assert:

Using
  functional MRI, we demonstrated a differential cortical representation
  of numbers between native Chinese and English speakers.
  Contrasting to native English speakers, who largely employ a
  language process that relies on the left perisylvian cortices for
  mental calculation such as a simple addition task, native Chinese
  speakers, instead, engage a visuo-premotor association network
  for the same task. Whereas in both groups the inferior parietal
  cortex was activated by a task for numerical quantity comparison.

(The article also includes fMRI imagery examples).
It also seems that recognition of simple arithmetic starts at an early age, according to "Infant brains detect arithmetic errors" (Berger et al. 2006).


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Can one die from pain?
Is it possible that a human or any other creature can die from pain?
I googled and found different answers. Some articles say Yes while others say No.

A related disease http://en.wikipedia.org/wiki/Fibromyalgia is not fatal.

This is probably very hard to study, since it will be difficult to disentangle pain and the reasons for pain (e.g. injury). However, I can imagine that extreme pain can lead to heart attack and death. In that case the direct cause of death would be heart attack but pain would be the underlying cause (probably along with other underlying risk factors). See e.g. http://www.nhlbi.nih.gov/health/health-topics/topics/heartattack/causes.html

@fileunderwater - Cause of death would be complications of shock, not pain. Can pain cause shock? absolutely.

Sure, f pain makes an organism not want to live, then I would consider it fatal. You can link it to satiety or whatever, diabetes put the body is a state outside of homeostasis. So does pain

I very much doubt it. You may however die from whatever's causing the pain. The reason you feel pain is so you stop doing whatever is causing the pain. Hence someone knows not to touch a hot fire because it is painful. But the pain itself is not actually the danger — it's the fire burning away skin. So pain is actually a good thing, a survival mechanism. So for something that is meant to prevent death it's hard to imagine it doing the opposite.
Perhaps if you were in SO much pain you may be unable to breathe and paralysed — but even then I still think you'd go unconscious before that would happen, and you'd start breathing again, etc.
The only other thing I can imagine is having a cardiac event, and the heart stopping. Again, this would be because of stress. Other than that — you may commit suicide on account of insufferable pain, however it's a different situation.
However pain never comes on its own for no reason, just like smoke needs a fire. In this case it's the fire, not the smoke, that will kill you!
People who've ever been in a desperate or life threatening situation like a car accident have often walked on a broken leg for example — feeling no pain. In this case the body was giving them a chance to escape what might have been a lion, etc.
In short, no, I don't think you can. However I cannot give a 100% correct answer. It would take just one example to prove that however!

One could imagine sending signals through the nociception system to cause pain perception without any actual physical danger to the body.

great answer! though the fire/smoke analogy is not so apt: "50–80% of fire deaths are the result of smoke inhalation injuries" http://en.wikipedia.org/wiki/Smoke_inhalation

Yeah, that's what I was saying - "in this case it's the fire that kills you". So it's essentially a reverse analogy, retrospectively I realise it was confusing!

Totally wrong answer, -1

"feeling no pain" because they're in shock.

The evolutionary functional answer here is probably not right. 'Expecting biology to behave a certain way is not a safe bet!'
Its a common misconception that all living things are designed to endure regardless of cost.  You can die from pain.  One can definitely die from fear.
This report tries to make a case though the diagnosis is not causal: Sudden, Unexpected Death in Chronic Pain Patients pretty much says it all.  "Unexpected, sudden death due to severe pain is poorly appreciated, since many observers still view severe pain as a harmless nuisance rather than a potential physiologic calamity."
It goes to further note the physiological stress of constant pain:
"Severe pain is a horrific stress. Severe pain flares, acute or chronic, cause the hypothalamic-pituitary-adrenal axis to produce glucocorticoids (cortisol, pregnenolone) and catecholamines (adrenalin and noradrenalin) in an effort to biologically contain the stress. Catecholamines have a direct, potent stimulation effect on the cardiovascular system and severe tachycardia and hypertension result Pulse rates may commonly rise to more than 100 beats per minute and even rise to more than 130 beats per minute. Blood pressure may reach more than 200 mmHg systolic and more than 120 mmHg diastolic."
Just to further the discussion of our evolved defiance of death.  I've long heard that rabbits can die from fright.  They don't put up much of a fight.  This is a typical experience with rabbit owners:
Rabbits Can Die of Fright!
It is possible for a rabbit to die of fright. Loud sounds, such as cats, dogs, loud music, or screaming can lead to a heart attack and put a rabbit into shock, causing sudden death. It can take several days for the rabbit to die this way, and it does not happen often, but it is quite possible.
And yes, People can die from fear too.

I refer the honorable gentlemen to James Harriet. He reports discovering by accident by ending the pain he was in some cases able to reverse the pathology by ending the pain with anesthetic drugs, thus allowing the body's natural healing abilities to take over.
He first discovered it in a sheep by accident (insufficient dose to put it down) and later used it effectively on dogs.


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Randomness in living systems
The point of my question is not to talk about events that are uncontrolled by living organisms. My question is about controlled randomness, or I'd like to say adaptive random process. Process that are random because it was selected in order to be random.
The first thing that pop in my mind when thinking of "adaptive random process" in biology is Fair Meiosis. Do you have other examples of "adaptive random process"? An individual might display a random behaviour in order to avoid that others to predict its future behaviour. Is there any evidence for such things? Do you know any other evidence on what I called "adaptive random process"?

Randomness might arise due to ever changing chemical composition of cells and the environment where the process takes place.

I find your computer example inconsistent with the rest of the question. If you are not interested in randomness at the molecular/sub-mulecular level, then you can say that, as PRNG in computers, also biological processes are deterministic. You make a "random" choice between A and B because (as an extremely simplistic example) your neuron "A" fired more than your neuron "B"...

@nico Thks for the comment. I'm not sure I get your point though. Would you think my question to be improved if I asked what type of PRNG does nature use?

@nico I modified my post shortening the computer example.

@nico After more thinking, I kinda aggree that my question might not make much sense. I'll shorten it to keep only the "Do you have other examples?" part

@Remi.b: don't get me wrong, I find the question very interesting. I think at the end it all comes down to the definition of "randomness" which one wants to use. Is a random event something that is too complex to predict? Or is it something even with infinite computing power we could never predict?

@nico Yes I understood this philosophical issue in your previous comments and I had a hard time to know how to deal with it. So that I decided to shorten my question. I might repost the second part of my question later on. Thanks nico

We use the word "stochastic" often in ecology / community biology. Is this the same as "random"?

In an evolution mutations are often random and lead to differences in phenotype that can be adaptive under certain pressures.  A lot of times mutation is a random process, but here are three cases I can think of off of the top of my head where I would say the organism is 'trying' to do it:
HIV is a retrovirus, which means in its viral form its genome is single stranded RNA, which is then converted into double stranded DNA within the host.  That conversion is carried out by a virally encoded reverse transcriptase.  This enzyme has a much higher error rate when making the RNA into DNA because it cannot proofread like our DNA polymerases.  This means that HIV mutates incredibly fast.  Many of these mutants are not very fit, but since there is so much selective pressure against staying the same due to attack from the immune system, some mutants will be much more fit if they can avoid that attack.  Its a numbers game, and by making lots of random mutants HIV is very good at it.
A related, but different case is found in the diversity generating retroelements of certain bacteriophages.  These are double stranded DNA viruses that infect bacteria.  The bacteria these viruses infect could mutate to escape the viruses by losing a certain receptor that the virus binds to.  It was observed however that the the virus would mutate incredibly quickly to bind to a different receptor, a lot faster than would be expected for a DNA virus.  Also, it was found that these viruses contained reverse transcriptases, which is bizarre, since there is no reverse transcription step in a dsDNA viral life-cycle (so we thought).  To make a long story short, this virus will transcribe the DNA that codes for its binding proteins into RNA, then use its reverse transcriptase to turn that RNA BACK into DNA, but uses a sophisticated targeting strategy so that it only mutates the region that is used for binding to the bacteria.  It will only mutate adenine residues, leaving the C's, T's and G's alone.  This is a much more clever system than HIV, because this virus uses site-specific mutations on its binding feet, and doesn't mutate its core proteins, the mutation of which would probably just lead to viruses that couldnt replicate.  Here a reference for the interested: http://www.nature.com/nature/journal/v431/n7007/abs/nature02833.html
Just so you dont think this is reserved to viruses, we do this as well with our immune system.  In order to recognize antigens in attacking pathogens, our immune cells have two methods for making diverse, random, receptors.  First is V(D)J recombination, where the multiple diverse copies of the V, D and J regions of antibodies and receptors are combined at random to make one set.  Wiki says theres 3x10^11 possible combinations here.  After that, theres also somatic hypermutation during the proliferation of B cells.  In this process, the random mutation rate is hugely increased in the region of the B cell receptor gene, specifically for making slightly different versions of the already 'OK' receptor to make it a great receptor.
General theme: raising your mutation rate, either across the board(HIV) or specifically (DGRE and SHM) is a good way to intentionally add randomness for a beneficial purpose (to the extent that you can attribute 'intent' to a viral particle).

Thks a lot for these examples. The article for which you provide a link seems very interesting btw. You examples are interesting. As you say at the end, all the examples you provided are examples where the mutation rate (which is a non-adaptive random process) is raised (which is a non-random adaptive process). It is interesting though. But I would call an "adaptive random process" a process which adaptative process which is directly random but does not use an underlying already existing process. Does it make sense? Thks

Hmm, sorry, I'm not exactly sure what you mean then.  In Meiosis you get the random segregation of chromosomes, after a random cross-over that makes hybrid chromosomes.  In the DNA mutations you randomly change a basepair to one of the other three, and in V(D)J recombination you randomly splice together one of each of the segments.  Each process seems fairly random, and results in an offspring or cell or virus that is slightly different.  Whether that random difference is a good adaptation is for the environment to decide.

I know of an example in development biology. Here is an example where noise in retinoic acid gradients is required for the boundaries in the developing hindbrain to sharpen. A related result is that the zebrafish hindbrain has a protein to modulate noise, but does not reduce the noise to zero. Together these results show that noise in the retinoic acid gradient is beneficial to hindbrain development. So in some sense the amount of crabp2a (the noise modulator) evolved to control randomness (noise/stochasticity) in the morphogen gradient, but was selected to not eliminate it.


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Why did Fair Meiosis evolve?
How and why did Fair Meiosis evolve?
I can hardly think that it provided a fitness advantage to the individual carrying the mutation. Why would it? Or did it evolve through lineage selection? Or was it some kind of pre-existing characteristic of meiosis that have no energy cost and therefore never disappear?
UPDATE:
I call fair meiosis the process of meiosis in which each chromosome has an equal chance of transmission.
I'm trying to make my questions clearer.
Is there any selection pressure in favour of alleles causing a fair meiosis? If yes, why? It doesn't seem to me to provide any advantage to the individual carrying this allele.

It would be helpful if you defined what you mean by 'Fair Meiosis'.

I do not understand what you mean with the last sentence.

I think you mean 'segment of a chromosome' if a chromosome's missing that's usually fatal in animals!

There's a more meta-level discussion on meiosis, which is that there is an advantage for genes which can get themselves selected in meiosis more often would prosper.  This is a prediction of the biologist Robert Trivers, working with Bill Hamilton in the late '60s, known also as the 'selfish gene'.  In fact the reason the selfish gene theory was so successful was that selfish genes - individual genes which propagated to offspring more often than 50% of the time. The Dawkins book 'The Selfish Gene' discusses this whole idea and its ramifications in great detail.
So at different times in evolutionary history, its hard to imagine that meiosis was completely 'fair' (50/50% change of any segment of DNA being chosen). In fact its pretty clear from genetic analysis now that some longer segments of DNA tend to be transmitted in one piece, though overall its still felt that the propagation if 50% likely for any given segment.
Over the long run, its been shown, mostly through game theory, that honesty is the best and most profitable policy.  The most famous of these experiments was the Prisoner's dilemma competition where all comers have been invited to submit computer programs which can either betray or cooperate.  Overall cooperative programs with some safegaurds which punished cheaters win overall.  Over time its been shown that systems tend to defend themselves from cheaters and that cooperation and 'fairness' do much better than mobs of cheaters running amok.
Cheaters and unfairness still continue to happen though - systems which are fair tend to invite in a small number of cheaters.  Say what you will about the income tax as a system!  there is variance over time as to how 'fair' a system can be.
Dawkins has even said he sometimes thinks he should have titled the 'selfish gene' something else instead: 'Nice Guys Finish First'.  I doubt that the book would quite have done as well though... we all should be fair, but it doesn't seem to invite book sales.

Thanks for your answer @shigeta. Now that I think of this question again, I think that something goes wrong in your answer.

I think the use of game theory doesn't bring much explaination for the fair meiosis. Whatever the game, altruistic behaviour may evolve thanks to genetic relatedness (Hamilton) or reciprocity (Trivers). For both of them it is important that the behaviour is not expressed toward any random individual/unit (therefore you need population structure, recognition or whatever). But such non-random interaction is not possible for alleles (at least under the assumption of random mating). Moreover, one might argue that the concept of relatedness does not stand when looking at two alleles. Am I right?

well the chromosome can be viewed as a highly structured community which plays a game every time it reproduces offspring.  that's the formulation that game theory might use look at meiosis. there are other ways, but this is I think a common view now.

I think that Fair meiosis (I assume that you are referring to that chromosomes have an equal chance of transmission) can be seen as a byproduct of recombination at meiosis, which makes every chromosome a mosaic of maternal and paternal chromosomes. Therefore, selection does not act on chromosomes as a single unit, and "unfair" meiosis becomes meaningless. The "value" of "fair meiosis" most likely lies in the adaptive value of recombination.
Addition: To expand on the value of recombination, it has been suggested that the specific value of recombination is to break up linkages and thereby prevent meiotic drive (Haig & Grafen 1991, also see Okasha 2006). Haig & Grafen 1991 also specifically discuss selection for recombination. For an interesting analogy between economy and fair meiosis (veil-of-ignorance vs fair meiosis) see Okasha. 2012. Okasha notes that:

In both, randomization is used to deprive self-interested agents (genes and individuals) of information about their identity, forcing them to adopt an impartial perspective.

In summary he also writes that:

A gene that distorts segregation in its favour can spread despite reducing its host’s
  fitness. This harms genes at unlinked loci, who are thus under selection to
  restore fair meiosis if they can. One effect of fair meiosis is to equalize the
  interests of all the genes, thus ensuring they work for the common good.
  One way of achieving this is to destroy linkage, given that segregation
  distortion typically involves linked genes working in concert.

Okasha's paper also has a nice and accessible description of the biological process, and of the selective forces that are operating to counterbalance meiotic drive/segregation disorders.

Thanks @fileunderwater! I updated my question, hoping to make it more understandable. Does your answer mean that there is no selection in favour of fair meiosis (as fairness is an inveitable consequence of meiosis)?

My point is that I think it is likely that the main "target" of selection is recombination, and that fair meiosis is a byproduct. However, I'm not a geneticist and there are maybe experiments showing selection for fair meiosis. Also, you should look into meiotic drive (preferential selection of certain gemetes), e.g. in sex-chromosomes; see http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0050293 and http://www.annualreviews.org/doi/abs/10.1146/annurev.ecolsys.32.081501.113958.


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Difference between viral and human genetic material
I have heard that there is a difference between viral and human genetic material. What is that difference?
If I take my cells and take DNA out of them and insert only a small part of it having a sequence, say, AGTTC, and viral DNA with the same sequence, can my body distinguish between the two? If so, how?

It is not at all my subject but here are some differences. bacteria's DNA are circular and does not look like our chromosomes. Bacteria don't have epigenetic variation. They don't have histones (which are proteins aroung which DNA forms 2 loops). Bacteria have no introns (no pre-RNA splicing). Bacteria have almost no non-coding DNA.

In the gene (DNA) there are sequences that are called exons and sequences that are called introns. Exons are those that will code for the protein amino-acid sequence and introns will be spliced (=eliminated). Before splicing the mRNA is called pre-mRNA. You can have a look to the wikipedia page as well, you'll get more information. http://en.wikipedia.org/wiki/RNA_splicing

not having methylated CpG is a big difference, and a red flag for the Tol-like receptors that a certain bit of DNA might be invasive: http://en.wikipedia.org/wiki/CpG_site

Additionally, a virus genome is not necessarily DNA. There are (lots of) RNA viruses. There are viruses with single stranded DNA and double stranded DNA. But your "AGTTC" is just an oligonucleotide and could come from anywhere. At least if the original C in the human sequence was not methylated, replacing it with AGTTC from a virus should not make a difference. (If this is the only thing happening, replacing exactly this sequence with the viral equivalent, and nothing more. Which is unlikely.)

To sum up: If we are not talking about chromosome organization, nucleotide sequences and overall genome architecture (which are incomparably different in eukaryotes and [even their] viruses) the differences in the genetic material are as follows:

viruses are much more diverse in their choice of genetic material, which is in the cornerstone of viral higher systematics. It can be DNA or RNA, single- or double-stranded, circular or linear. Animals, in turn, possess only double stranded DNA as their genetic material: linear dsDNA for the nuclear genome and [usually] circular dsDNA for the their mitochondrial genomes.
DNA termini pose a special problem for the maintenance of the molecule and show very unusual organization in terms of DNA sequence and structure. Repetitive terminal sequences of eukaryotic chromosomes have 3'-overhangs, which form a special quadruplex form of DNA. Termini of viruses are naturally much more diverse and are (nearly?) never of the same structure as in Eukaryotes. [Circularization/decicrularization is one of the mechanisms recruited by viruses]. (Deng et al 2012)
DNA methylation is normally present in varying degrees in animals and in vertebrates most of the cytosines in CpG dinucleotides are methylated. Viruses differ considerably from one another in this respect, but it seems that smaller viral genomes are generally under-methylated and larger genomes do not show under-methylation, although it depends on the stage. This conclusion is based partly on indirect evidence that CpG motifs are considerably much less frequent in smaller viruses. Integrated "genetic parasites" like retroviruses are normally rich in CpG and are highly methylated. (Hoelzer et al 2008)
although I couldn't find relevant literature, I'd hypothesize that the highly packed genetic material in viral particles may potentially exist in more compact forms of the DNA helix (in dsDNA viruses). Most of the dsDNA in cells is present in a so-called B-form, but there are more compact A-form and less compact left-turned Z-form (there are other forms, most of which are biologically not relevant). (cf. Wikipedia for an introduction)


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How can sex ratios remain Fisherian (1:1) in species where only the dominant male gets to mate
In certain species only the dominant male gets to mate (or given strong preference), and yet the sex ratio remains 1:1. (I'm thinking in particular of gorillas). How does this happen? It doesn't seem like Fisher's argument should apply in this case.

The average reproductive success of males is what counts, when a parent is 'deciding' whether to make a son. A low probability of your son getting to reproduce, can be balanced by his high output if he does reproduce. It's like a lottery (and at equilibrium, it's a fair lottery).

Fisher's principle applies to such cases as much as it does to species where only pairs mate.  Consider a species where a successful male has exclusive mating with a harem of 20 females, and for each such male, 19 other males are not able to mate.  A female has 100% chance of mating, and a male has a 5% (1 in 20) chance of mating. Assume a female has two offspring.
In this scenario, an equal sex ratio would mean having a female offspring would lead to an expected number of grand-offspring of 2 (100% chance of 2 offspring from that female).  Having a male offspring would also lead to an expected number of 2 grand-offspring (95% times 0 offspring plus 5% times 20 harem females each having 2 offspring).
What would happen if the ratio of births was off from 1 to 1, say 5 females were born for each male? Then expected number of grand offspring would be for a female is still 2, but for a male it is 25% (chance of taking a harem of 20 females against the 3 other males born alongside those 20 females) x 40 (20 harem matings x 2 offspring) = 10. Hence with a lopsided sex ratio in this situation, having a male is much more valuable genetically than having a female.  If a mutant arose which produced more male offspring in this imbalanced situation, it would have success until the population sex ratio became close to 1:1.

as a very belated comment on something I stumbled upon this assumes all children are equally fit.  If, for some reason, you are less likely to raise a fit child, capable of competing and besting other males for mating rights, you would be better off having a female with a far more likely chance of reproductive success despite her overall lower level of fitness.  In deed I believe studies have confirmed that there are slight variances such as this in many species.

mgkrebbs has already covered the maths that leads to the preservation of ratio, so I'll not recap.
You might have noticed that the argument only remains true if you don't know whether the particular male you produce is likely to be the dominant male or not. If you could "know" in advance that your particular son was more likely to be dominant it would make sense to skew their sex ratio towards male and vice versa. It may interest you to know that this actually happens.
Males born to high ranking females are more likely to succeed than males born to low ranking females. This makes intuitive sense as they'll get better access to food and the same genetic traits that help a female become dominant may help the male become dominant too. What's fascinating is that this actually leads to top ranking females having a male-skewed sex ratio among their offspring, and low ranking females having a female-skewed sex ratio.
See Great expectations: dominance, breeding success and offspring sex ratios in red deer for the original paper. I do not know what the mechanism behind the sex selection is.


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What decides the position of the node of Ranvier?
The oligodendrocytes makes the myelin sheath in CNS and schwann cells make it in PNS. What decides where the oligodendrocyte or Schwann cell will attach and start forming myelin sheath? Is it genetically determined? Is it random? Is there any disease associated with improper positioning of node of Ranvier?

A combination of differentiation site, chemical guidance during migration, and signaling cues form a variety of sources.

The final step in the generation of an oligodendrocyte is the
  development of a mature myelinating phenotype, and this is largely
  regulated by axonal signals. It seems likely that both soluble and
  cell mediated signals from adjacent axons are integrated into the
  developmental profile of oligodendrocyte precursors resulting in cell
  differentiation, up-regulation of myelin gene expression and formation
  of the myelin organelle. Candidates for axonally derived soluble
  factors include FGFs (Bansal et al., 1996 and Qian et al., 1997) and
  thyroid hormone (Barres et al., 1994a and Barres et al., 1994b), while
  axonal cell surface molecules such as L1, MAG, NCAM and N-cadherin may
  regulate formation of the myelin sheath (Payne and Lemmon, 1993 and
  Trapp, 1990).

http://www.ncbi.nlm.nih.gov/pubmed/12385864
I don't know of any diseases that just mess with positioning but there are diseases that kill oligodendrocytes (like multiple sclerosis).

Thank you ! My question is actually not about how oligodendrocytes develop and migrate to neurons but rather about how , once they have reached their ,know where to form myelin sheath along the length of an axon.

Ah, ok, this is the same paper, but I have changed the quote to the more specific discussion of myelination;  short story: the axons themselves cue the oligodendrocytes.


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Use of pigs for obtaining transplant organs
It is being said that organs can be obtained for transplant from the pigs. What is special about pigs that we are using them? Why can't we use monkeys or chimpanzees with whom we share a more recent common ancestor?

Here's the answer: http://en.wikipedia.org/wiki/Xenotransplantation#Potential_future_animal_organ_donors

Monkeys and many other primates are too small to provide organs that will provide the needs of a human host. The fact that primates are so close to humans physiologically is not always a win as transplanted organs will bring diseases into the host that can be quite dangerous.
Besides, because even human human transplants induce immune rejection of organs. Its typical that immune suppressants will be a lifetime treatment for the patient.
Finally, the cost of a pig organ is negligible and their organs are about the right size, and I would bet that activists don't protest pig transplants nearly as much as primate donors.


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Are SLC52A2 and GPR172A really the same?
The official HUGO gene nomenclature page says that GPR172A (Gamma-hydroxybutyrate receptor) and SLC52A2 (riboflavin transporter, member 2) are the same. The sequence reported by Andriamampandry seems to be the same, but I find no other evidence. Can anyone enlighten me?
(I'm wondering if I should add the SLC52A2 information to the GHB receptor Wikipedia page.)

This isn't a case of gene splicing causing different protein variants.  In the studies that identified these two functions (GHB sensitivity and riboflavin transport), they were using DNA derived from mRNA (cDNA), which means what was being expressed in their experiments did not have introns, so there was no chance for alternative splicing.
This gene has a weird history, here is the summary:
Takeda et al. 2002: Identification of G protein-coupled receptor genes from the human genome sequence
Takeda and co. download a copy of the human genome and translate it looking for GPCRs.  They look at all the ORF that DIDNT have introns: "We collected intronless open reading frames (ORFs), which were long enough to cover GPCRs from the human genome". They also only look at things with 6-8 transmembrane helices as determined by the prediction program SOSUI.  One of the GPCRs they found was named hGCRP41 (hypothetical protein similar to GPCR) accession number: AB083623.  They report it probably has 8 transmembrane helices, and 418aa.  This protein probably doesn't exist because they read straight through two introns in their analysis.  The protein also terminates in the middle of a frame-shifted exon.
Ericsson et al. 2003: Identification of receptors for pig endogenous retrovirus
Next, Ericsson et al come along looking for receptors for the pig endogenous retrovirus and find this gene.  They used cDNA to make a bunch of transduced cell lines that had difference human cDNAs expressed.  They found two related proteins that could serve as receptors to the pig endogenous retrovirus.  They named the first one HuPAR-1, which is 445aa long and has 11 transmembrane helices.  This is the length of one of the proper splice variants of this gene.
Andriamampandry et al. 2007: Cloning and functional characterization of a gammahydroxybutyrate receptor identiﬁed in the human brain
Andriamampandry is looking for gammahydroxtbutyrate (GHB) receptors by using cDNA and seeing which cDNA-transduced cells become sensitive to GHB.  They find two nice proteins that are sensitive to GHB, GHBh1 and C12K32.  GHBh1 is identical to HuPAR-1, it has 445aa and 11 transmembrane helices.  C12K32 is a frameshifted version of GHBh1 that is slightly longer, but has the same number of helices. They had previously found a 512aa ortholog in rats, in 2013.
Yao et al. 2010: Identification and Comparative Functional Characterization of a New Human Riboflavin Transporter hRFT3 Expressed in the Brain.
Finally, we have Yao et al, who searched for homologs to their Riboflavin transporters.  They found one in a cDNA library, and it was 445aa long.  But they noticed upon BLASTing it that people had been calling it a GPCR.  They point out that this is weird since it has 11 transmembrane helices, and go on to show that it is a Riboflavin transporter, concluding: "The molecular function of GPR172A has yet to be determined. We designated it hRFT3 (GenBank accession no. AB522904) based on its functional characterization as shown below."  This paper is in pretty poor form, because somehow they don't address the Andriamampandry paper which presented data supporting its function as a GPCR.

So this protein, in this specific spliced formation, has been shown to be a virus receptor, a GHB G protein-coupled receptor, and a riboflavin transporter.  It is very weird that it is a GPCR with 11 transmembrane domains... they very rarely have more or less than 7.  I'd wait for more studies to confirm both of these findings before I'd accept that this protein is an XXL GPCR moonlighting as a riboflavin transporter.

Its fairly common for a gene to have multiple names. I cant say for certain, but Jax and GeneCards also lists them as being synonymous so I would say its safe to say they are the same
http://www.informatics.jax.org/marker/MGI:1289288
http://www.genecards.org/cgi-bin/carddisp.pl?gene=SLC52A2
Edit in reply to comment:
In higher level Eukaryotes the vast majority of genes have more than one isoform as a result of alternative splicing, and this can drastically change the protein sequence and function of that protein. So even if it comes from the gene, two different isoforms can have completely unrelated functions.
According to ensembl, this gene has 14 isoforms.
http://useast.ensembl.org/Homo_sapiens/Gene/Splice?g=ENSG00000185803;r=8:145577795-145584932
Of course there could also be some type of post translational modification that could also change the function, but Id say mostly likely if the same gene produces two different functioning proteins its because of alternative splicing.

the functions just seem to be so diverse that I have a hard time believing it... but you never know, I guess


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Determination of gene direction
I have one sequence that composed of sequences of three genes. I should determine the direction of each gene, but two of these genes are disrupted, and I can't determine the initial codon. Does anyone knows how I can determine the direction of genes?

I'd first try translating it and looking to see if there are big regions that jump out at you that do not have stop codons in them.  I normally use this tool for quick and dirty translations, it gives you all 6 reading frames.  Also, you could just try BLASTXing your sequence if it is short enough.  BLASTX translates your DNA in all 6 reading frames and will search the protein database for matching proteins.  Most anything will have a hit in there, and if you get a hit it will show you the DNA sequence and reading frame that got translated.  If your sequence is too big, break it down into smaller chunks until BLASTX works.  One of your chunks will have your gene in it, and it will get a protein hit.  You'll also need to break it up if you have two genes in one chunk, but you only get results for one of them because its longer and gives better hits.


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What is genomic imprinting?
What is a  genomic imprint? How does genomic imprinting take place?
If I say that "this" allele is maternally imprinted does it mean that the allele of the gene is passed only by the mother? If a pedigree is given, how can we identify whether the trait is paternally imprinted or maternally imprinted?
Please try to explain all this in as simple words as possible.

Is this a homework question? If so, please tag it accordingly.

Have you read the wikipedia entry for genomic imprinting?

@Biogirl here is a new review paper all about genomic imprinting http://www.nature.com/nrg/journal/v14/n9/pdf/nrg3543.pdf?WT.ec_id=NRG-201309

**** "What is a genomic imprint? How does genomic imprinting take place?"**

Genomic imprinting is an epigenetic mechanism  of inheritance which allows genes to be expressed differently depending on which parent they come from. This means it is modification of the genome, or changes what the genome produces, without changing the nucleotide (DNA) sequence. The result of imprinting in diploid organisms is that one of the two alleles is silenced.  This page provides a good overview of imprinting.
Two major mechanisms are proposed called DNA methylation and histone modification though others may yet be discovered. DNA methylation silences a gene by adding methyl groups to nucleotides (it modifies the nucleotide but not the sequence) which affects how they are expressed, whilst the exact mechanism is unknown (at least I can't find one on scholar) it does appear to be a key factor in some cancer growths. Genes can also be silenced by histone modification, binding a gene to histones reduces its activity, ie it produces less product.
Genomic imprinting was first described in Mealy Bugs (or at least this is one of the first described) which silence half of their genome in males. Whilst females are fully diploid, the male is also diploid but one half of the genome is silenced, making them effectively haploid. This is done by turning one half of the genome heterochromatic.

****"If I say that "this" allele is maternally imprinted does it mean that
  the allele of the gene is passed only by the mother? If a pedigree is
  given, how can we identify whether the trait is paternally imprinted
  or maternally imprinted?"**

Specific control of a gene, rather than entire chromosomes described above, is only known in plants and some mammals. In this case, when a gene is imprinted, the gene is silenced. An example is Igf2 in mice described in the below diagram which is maternal imprinting (ie the mothers allele is silenced). When the mother has a mutant allele and the father a normal allele and normal offspring is produced. When the male passes on the Igf2 mutant the offspring is mutant because the mother's normal copy was imprinted.

The Igf2 gene can be seen in the above diagram. This is the one of the
  first evidences of genomic imprinting discovered. In the first part of
  the diagram a mutant gene trying to make the mouse offspring dwarf is
  passed from the mother. It can be seen that the mouse is not dwarf
  because the allele for size in this mouse is an imprinted. The
  maternal allele is not expressed, so the dwarf trait is not expressed
  in the offspring, only the normal size trait from the father is. In
  the second part of the diagram the father passes on the mutant gene
  and therefore all the offspring will be dwarf because the size trait
  is completely dependent on the paternal allele, which in this case is
  dwarf. - Creating Variation

The page this diagram and quote comes from also has a good section on genomic imprinting.

It is incorrect to say that a trait is imprinted, although the phrase is often used.  I will simplify this by talking about just two chromosomes.  A mammal will have one chromosome from mother and one that is nearly identical inherited from the father.  The genes on each chromosome typically have an equal likelihood of being expressed.  An imprinted allele creates silencing on one chromosome and gene expression from solely the other parent. There are many more complexities and Wikipedia is a great source as well as Geneimprint http://www.geneimprint.com/site/what-is-imprinting
See the link regarding Parental Imprinting, the definition is concise.
http://groups.molbiosci.northwestern.edu/holmgren/Glossary/Definitions/Def-M/molecular_imprinting.html

So if I say maternal imprinting , does it mean the maternal allele has been silenced ?

No, it means that whatever imprinting was effected, it came on the maternal gene. It could have been silenced, activated, or something more complicated.


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Why does the stomach ache if you take a brisk walk after lunch or dinner
After eating your lunch or dinner, if you take a brisk walk, most of the time your stomach aches. Why does that happen? What happens with respect to the body metabolism?

Maybe the acid can go to places through the sphincters (because you move) where the epithel is not accustomed to that kind of acids and then it hurts. And also there is more blood while you are digesting in the stomach and the inervation is more sensitive at that time. But I don't have any proof at my hands right now, so only a comment ;)

The reasons for Exercise-related Transient Abdominal Pain are unknown. The current theories are:

Irritation of the parietal peritoneum, a structure lining the abdominal wall as it rubs against the visceral peritoneum, which lies against it and over the top of the abdominal organs
Strain on the ligaments that suspend the abdominal organs (however somewhat unlikely as it occurs during swimming

It used to be thought that blood was diverted away from the diaphragm during exercise causing pain however that has been found to be incorrect.
See this link: http://www.ausport.gov.au/ais/nutrition/factsheets/hydration/cramps_and_stitch


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Do insects respond to the detection of dead insects?
Are there insects that change their behavior upon detecting the nearby presence of other dead insects? If there are, can you provide an example?

Yes, it is a common behaviour and is called necromone signaling (Yao et al 2009, see references in paper for many examples), and is probably used to avoid predators, parasites and disease. The chemicals used are often similar (unsaturated fatty acids), and seem to have an old evolutionary history (~400 million years). Many groups of species can also detect infected, not yet dead, conspecifics. Removal of dead individual is also common in e.g. ants (necrophoric behavior).
The paper referred to earlier (beside reviewing earlier evidence) also provides experiments of detection/avoidence in isopods and Tent
caterpillars (Malacosoma americanum), where they show avoidance based on crushed conspecifics, unsaturated fatty acids and (for isopods) intact corpses.
Naturally, the same type of compounds are used by e.g. species of carrion beetles (Silphidae) to find their animal hosts, but then for the purpose of reproduction.

Ants respond by eating the dead insect, except if it is one of their own, most of the time.

True. I originally read the questions as asking about detection of dead individuals of the same species, but I now see that this is not entirely clear.

The experiment where a live ant is 'painted' with necromones is one of my favorites. The painted ant is repeatedly carried out of the nest (and will aid other workers in carrying itself), and then walks back into the nest.


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Known MicroRNA - Gene Systems?
Have there been any experimentally-verified systems of microRNAs targeting a gene set (e.g., in cancer, perhaps)?

Yes. Below is a link to a review of ncRNA (non-coding RNAs) and their role in disease. There are many examples in this review in all sorts of diseases, one of which is miR-200, which is thought to play a role in some cancers.
There are also some tables in the paper that list the miRNA and the disease they are linked to. They also have a reference for each one, so you could read more about that particular miRNA and its function, including the gene it regulates.
http://www.nature.com/nrg/journal/v12/n12/full/nrg3074.html
Im not sure if that article is open to the public or not. If you cant access it you could always check out the wikipedia entry for miR-200
http://en.wikipedia.org/wiki/Mir-200


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Why is duck fat less saturated than cow fat?
Why does the composition of fat in animals vary?  Is there an evolutionary advantage to producing fat that is less or more saturated?

I can't reply in-full at the moment, but yes. There are plenty of advantages. Saturated fat is (slightly) more energy-dense, makes cell walls more rigid (bad in a cold environment - like polar waters), and have higher melting points (which also means they can insulate better).

Because ducks need to float and cows don't. If there was a densely fat duck it wouldn't float or fly very well and it wouldn't survive to reproduce.
To answer your question, the composition of fat varies because of the different conditions in which the organism needs to thrive. Fur is different as well. Bear in mind nature is a cruel place and any tiny edge you can get is vital for your survival.
My answer is a bit general but I hope it addresses the question.


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What causes sinus pain and congestion?
When the sinuses flare up, it can get very painful.  Thus, my question - what biological mechanisms cause the congestion and especially the pain associated with sinusitis?

Inflamed sinuses are often associated with some kind of illness or irritant such as flu, the common cold, or hay-fever. As an example the cold causes sinus pain and inflammation because the virus is attacking/located in the nasal passages which causes swelling in the mucus membrane (the mucus membrane lines the sinus cavities). The swelling, along with increased mucus production, combines to create clogging and the pressure associated causes pain. Humidity will help loosen the mucus and anti-inflammatory medication should help reduce pain by reducing the mucus build up and swelling - thus relieving pressure.
The increase in mucus production is because of the role it plays in our bodies - it is produced to trap foreign bodies and help keep our system clean. The more mucus we produce the more our bodies are trying to clean up. This can cause an excess which is difficult to clear such that our sinuses become blocked and dried mucus becomes an irritant.
Sinusitis is the painful condition of swelling in the mucus membrane. Sinus comes from the latin for bent or curved surface, and -itis is from greek meaning swelling or inflammation linked to disease.
In summary: Painful sinuses, aka sinusitis, are painful because of infection in the mucus membrane producing swelling and excessive mucus build-up.

@Damien does this answer your question?

Yes it does, very nicely!  (just got to wait 30 minutes before I can give the bounty).  Thank you for this.

@damien that's ok, I was just wanting to check if it did actually answer your question otherwise I would have done more work on it, rather than bounty hunting :)

That's cool :)  Your answer is ideal and provides many good links (and links in links)


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What's the difference between Cytoplasmic pool and Granular storage pool?
What's the difference between Cytoplasmic pool and Granular storage pool when speaking about neurotransmitters and synaptic cleft. I encountered this here:

Amphetamine’s mechanism of action
  thus depends on the cytoplasmic, newly synthesized, rapidly metabolized pool of dopamine.
  Methylphenidate’s mechanism of action depends
  on the granular storage pool (Brust, 2004)

Reference
Brust, J. C. M. (2004). Neurological aspects of substance abuse. Philadelphia, PA, Elsevier.

Neurotransmitters like dopamine are synthesized in the cytoplasm and then imported into synaptic vesicles.  When the neurotransmitters are released it is by a fusion of the synaptic vesicle with the neuron's cell membrane, emptying the contents into the synaptic cleft.  Re-uptake of the neurotransmitter back into the pre-synaptic neuron's cytoplasm is done by active transporters, in Dopamine's case by DAT.  The cytoplasmic pool refers to the dopamine in the cytoplasm, while the granular pool refers to the dopamine stored in the synaptic vesicles.