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Photosynthesis regulation
I read about the regulation of Calvin cycle by thioredoxin which activates key enzymes essentially by converting disulphide linkages on inactive enzymes into sulfhydryls. Another regulatory mechanism is the pH control. The enzymes work at a slightly alkaline pH which is established as soon as the proton gradient is set up by the light reactions. But aren't these two mechanisms contradictory: at alkaline pH, the sulfhydryls $-SH$ groups, being acidic, will dissociate by giving up a proton and will be more stable in the dissociated form.
In general I fail to understand how pH will decide which bio-compounds will dissociate into proton or hydroxyl.

Your question conflates two separable events, a redox process and an acid-base dissociation.
The interconversion between disulfides and free sulfhydryls is a redox reaction, governed by the redox potential of the surroundings. The importance of redox potential to the -S-S- <> -SH equilibrium is illustrated by the difference between the cytosol and the lumen of the endoplasmic reticulum (ER). The cytosol is reducing and so free thiols are prevalent (there are usually no disulfide bonds in cytosolic proteins) whereas the ER lumen is oxidising, and the formation of disulfides in secreted proteins is promoted. The redox potentials of the two compartments is set primarily by the ratio between oxidised glutathione and reduced glutathione.
The thiol group in cysteine residues of proteins typically has a pKa of around 7, so it will indeed have some acidic character at slightly alkaline pH, dissociating to form a thiolate group. This doesn't however promote the reformation of disulfides, and in any case if it is important for a protein to have an undissociated thiol, then the environment of the specific cysteine residue can be adapted to raise its pKa. Note however that it is also possible that the thiolate form may be compatible with (or even required for) the function of the enzyme.


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Electron transport in granal stacks
See paper for distribution of PS-I and PS-II within grana
As explained in the above paper, the PS-I complex is primarily located within non-appressed thylakoid region and stroma lamella, while PS-II in the appressed regions. Now since non-cyclic electron transfer (non-cyclic photophosphorylation) requires both the photosystems, wouldn't their distribution within grana far from one another hamper their ability to carry out non-cyclic electron transport. Although there are mobile untis to account for the electron transport between marginal PS-I and the PS-II immediately below, but the electron transport to the PS-II units deep in the granal core would still be unaccounted for.

You may find useful this article.

I commented instead of answer because I hadn't understood your question precisely! Maybe the problem is mine, but can you refine this phrase?: "Although there are mobile carriers, but what about the PS-II units far in the centre of large stacks of thylakoids?"

"Although there are mobile untis to account for the electron transport between marginal PS-I and the PS-II immediately below, but the electron transport to the PS-II units deep in the granal core would still be unaccounted for." Edited in answer too.

First a clarification: the mobile units are no so "mobile". Due to (1) the high protein:lipid ratio of the thylakoid membrane and (2) the packing of protein complexes, the rapid diffusion of components along the membrane is hindered.
It has been proposed the existence of small local PQ diffusion microdomains, based upon the percolation theory:

From the percolation theory, above a critical density, immobile or slowly moving transmembrane proteins are, indeed, expected to form flexible 2D networks of closed compartments preventing long range movement of small molecules. (Kirchhoff, H et al. (2000) Biochim. Biophys. Acta 1459, 148–168)

For this reason the PQ are confined, on a short time scale, within these domains, preventing their "dispersion".
In addition of the low diffusion of mobile carriers, the geometry of the granal stacks mantains the contact area between the PSII of the appressed grana and the PSI in the margin annulus domains relatively large, enabling effective linear electron transport in microdomains.
Figure 2b of the paper cited below shows the geometrical organization of the stacked grana and its description says:

The circular border between the appressed domain and the margin annulus (ring) allows a large contact area between the PSII and the PSI domains and efficient linear electron transport from PSII via plastoquinone (PQ), plastocyanin and cytochrome b6f to PSI at a short distance of ~30–60 nm in local domain.

Further informations can be found in Albertsson, P-Å. (2001) Trends Plant Sci. 6, 349–354.

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Animal UV vision
It is reasonably well known that many species, such as bees and some types of birds as examples can see into the ultraviolet (UV).  How is the structure of their eye different to humans to allow this?
Also, how are they shielded from some of the harmful effects of ocular UV exposure?

Firstly most UV perceiving organisms only perceive far UV (~300-400nm) which is less damaging. There are different opsins, which get activated by different wavelengths. Like other light UV is perceived by opsins sensitive to UV wavelength [ref].
I am not sure about this but opsin sensitivity to UV must be high so that low irradiation is sufficient for perception and excess is filtered off.
UV filter mechanism in reported for human and squirrel eye; mostly uses kynurenine derivaties. May be similar mechanism is present in other organisms too.

Thank you for this - I was not sure of the terminology involved - but I can now find research about the UV sensitivity to opsin.

Your link [2] appears broken.

@Ruslan removed the broken link. The other reference explains the idea, I hope.

The relevant structure of the eye only differs in one way, the types of cones present, different types of cones contain different opsins (light sensitive pigments).  Reptiles and birds have 4 cone types, Mammals have 2 (primates have 3). Early mammals lost two of these as modern mammals are descended from early mammals who were nocturnal, one was the one that responds to UV light. Modern mammals as their descendants are stuck with this reduction since the genes to make those other cones is no longer present. Primates evolved a third cone, (a mutant variant of one of the two they had before) Primates did this because many a frugivores and color is excellent for determining when fruit is ripe.

Your answer doesn't answer the question. Further, it seems a duplicate of this answer -1

Also note that links can grow cold; citations to journals papers + web link are best, as these can always be found back in any university library or other search engine

@alice I did add the sources to the other answer, and this is different than the other answer, it does not require much change because the question has fundamentally the same answer.

yes I'm sorry about the sources; I saw that now; I upvoted the other answer.

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Is every cell competent?
I would like to know if every cell is competent or if there are any cells that are not competent.

Assuming that you are asking about E.coli cells being made competent for transformation using plasmid DNA, an answer is cached here from this source:

Hanahan, D. & Bloom, F.R. (1996). Mechanisms of DNA transformation. In F.C. Neidhardt (ed.). Escherichia coli and Salmonella : Cellular and Molecular Biology. (pp. 2449-2459). Washington D.C., United States: ASM Press.

The source (and it is perhaps worth emphasising that Hanahan is/was a transformation guru) states that treatment with divalent cations can achieve 10% of cells rendered competent, whereas treatment for electroporation can achieve transfer into 95% of cells.
This information was, of course, published in 1996 so it is conceivable that advances have been made in the case of the former method.


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Eye color genetics
I am trying to find a model to link the phenotype eye color to its genotypes.
I know that there exists a simple model from Davenport, which explains {brown,blue} eyes. Further, there is an extended model for {brown,green,blue,gray} eyes, based on the two genes bey2 and gey. There are plenty of articles suggesting further genes which may or may not have certain impacts.
Is there a model which is more precise than the above mentioned, but which is well applicable (i.e. does not introduce excessive complexity and has greater accuracy)? I am trying to come up with some probabilistic calculations, and could well handle one or two further genes. It would also be interesting to know about the accuracy of the model.
Many thanks!

Does this question: http://biology.stackexchange.com/questions/728/how-is-eye-color-in-humans-inherited answer your question?

Not really.. I had seen the question and also read the mentioned papers. However, what I am looking for is a still simple model, which goes into some more depth than the two gene model (also mentioned in linked questions comments: http://www.athro.com/evo/gen/genefr2.html)


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How do ants sense imminent rainfall?
I have always been told to watch to see if ant-hole mounds are built up as a sign of imminent rainfall.  My questions are,
if what I have always been told is true, then by what mechanism do ants 'sense' the imminent rainfall?  Is it a case of sensing air pressure drop, increasing humidity or both?

This article claims that ants do sense approaching rain and modify their activities in preparation. The claim is not sourced. This weather site also speaks of ant mound-building before a rain but frankly places it in the "some folks say" category. The AntBlog is associated with AntWeb, a large multi-university-affiliated database. The author of the linked blog states that ants can sense humidity with their antennae, which strikes me as a plausible means of anticipating rain.
That ants might sense changes in barometric pressure is an intriguing idea but has not to my knowledge been demonstrated.
A 2010 article in Journal of Neurophysiology reports an almost unbelievable sensitivity to temperature in ant antennae, allowing them in principle to sense minute temperature changes ($0.005^o$C) over a wide range of temperatures and over 0.2 second time intervals (5Hz). This is said to assist them in orientation in their microenvironment but I think it goes a long way to accounting for an ability to detect looming weather fronts. Humans can sometimes 'smell' rain and we can detect gross temperature changes that almost always accompany rain, but to be able to detect humidity and micro-scale temperature changes would give the ants a real advantage in forecasting. After all, not all rainstorms are preceded by a dramatic drop in temperature but probably the majority are preceded by minute step-wise drops in temperature that evidently the ants can sense.
So while I think the building activity may be anecdotal (and probably true for some species) the ability to sense humidity changes and micro-scale temperature changes accounts for their ability to sense rain ahead of time.
Ants are very well-studied and it's hard to rule out that one has missed something. There are a few "ask the expert" questions on this topic online and no one seemed sure.

An article suggests that many animals and plants have an instinctual response to seasonal cues like light levels or day length (photoperiod). Also they may be influenced by circannual clocks which depend on factors like temperature, the photoperiod and the increase or decrease in food levels available. There is also some speculation that ants may be influenced by barometric pressure changes though there is no literature available for the same (reference). There are methods that ants have devised to escape rain some of which are mentioned in this article. You might be interested in reading this article on the spread of Argentine ants being influenced by rain.

The circadian clock is a bit of a red harring here. Circadian and circannual rhythms are widely studies, and the molecular mechanism underlying them are quite well established (at least for circadian, less so for circannual). However, this does not imply in any way animals can sense changes in barometric pressure. They may or they may not, but circadian or circannual rhythms have nothing to do with that.

authors: نسمه عبدالفتاح


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How does lactulose cause the removal of ammonia from the colon?

Lactulose is also used to reduce the amount of ammonia in the blood of patients with liver disease. It works by drawing ammonia from the blood into the colon where it is removed from the body.
[Source]

How is ammonia removed from the colon?
From the quote above it sounds like ammonia removal must be some other mechanism than absorbing it into the blood, correct?

I'd imagine it would be defecated out.

@RoryM: Do you mean that ammonia would be dissolved in the liquid content of the stool? A stool with ammonia smell?

It's an interesting one, the BNF states that it "discourages the proliferation of ammonia-producing organisms" in the GI tract rather than pulling ammonia into the gut lumen, I'll perhaps write a full answer when my exams are out of the way :)

and from MRHA "Lactulose is used to
treat hepatic encephalopathy by reducing the pH of the colon causing ammonia to form
in the colon, thereby reducing blood-ammonia concentrations."

@RoryM: This sounds most logical to me so far! I believe if the colon pH is reduced then ammonia (that is alcalic) will be dissolved as ammonium ions, stay trapped in dissolved form and defecated. I would definitely accept your comments as an answer!

@RoryM: Also thanks for the sources. I found the BNF at https://www.medicinescomplete.com/. But how can I access the MRHA source you quote?

MRHA approval document though you can also just enter lactulose as a search term at mhra.gov.uk.

@RoryM Could you perhaps turn your comment into an answer? It seems like an interesting discussion and a valid answer. The question is on its way to deletion.

Excess nitrogen must be excreted by the body and can come from nitrogen in the diet (e.g. amino groups from excess amino acids) or nitrogen-containing compounds produced by bacteria in the gastrointestinal tract (GI tract).
Normally the liver and kidneys are involved in excreting ammonia ($NH_3$) and ammonium ($NH_4^+$) from the body. Ammonia can be toxic in high concentrations, but the body can detoxify it through conversion to other nitrogen-containing substances (i.e. urea) or excrete the ammonia itself.
Ammonia in the blood is freely filtered at the kidney glomerulus and can be "trapped" in the urine flow by accepting a proton to become ammonium (i.e. $H^+ + NH_3 = NH_4^+$) . Because of the positive charge the ammonium ion is unable to passively diffuse back across the tubules into the blood. This is one mechanism that ammonia is excreted. In the liver, the Urea Cycle (see any basic or clinical biochemistry text for more information) is a set of enzymes that converts most of the excess nitrogen in the form of ammonia to urea, which is a non-toxic, water soluble organic compound that can also be excreted in the urine. The body uses these processes to dispose of excess nitrogen from amino acids as well as ammonia that is produced as a by-product of bacterial metabolism in the GI tract.
Some patients with significant liver disease (e.g. cirrhosis from either NAFLD, hepatitis or any other liver-damaging disease) have lost the ability to convert all the excess ammonia to urea. In these patients, an easy way to prevent excessive nitrogen uptake in the gastrointestinal tract is by treating them with lactulose. Lactulose is a carbohydrate that that is not digestible or absorbable by the body, but is osmotically active (pulls water into the intestinal lumen) and acts to speed up intestinal transit. Since lactulose works by speeding up GI transit it makes you stool more frequently (which is why it is very useful for constipation). For liver disease patients, however, the lactulose acidifies (i.e. decreases pH) the lumen of the intestines and ammonia is protonated to form ammonium, which effectively traps it in the intestinal lumen. A lot of the excess ammonium can then pass into the feces and decrease the amount of ammonia that the liver needs to process. This is similar to the mechanism of ammonium in the urine as mentioned above. Additionally, lactulose also decreases the amount of GI bugs that produce ammonia containing compounds as well, which also lessens the amount of ammonia for detoxification by the liver. (Lactulose can also be used for a treatment for small intestinal overgrowth). These GI bacteria metabolize dietary amino acids and other compounds in the gut for energy metabolism, which liberates nitrogen-containing compounds that can be absorbed by the intestines.
Edit: Here is a link for a great reference on NCBI that explains the mechanism of action of lactulose.

This answer is good, but it could be still better with references.

Reference:  See "Mechanism of Action" - - https://www.ncbi.nlm.nih.gov/books/NBK536930/

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Why do antacids have a special importance when taking lactulose?
“Before taking lactulose, tell your doctor and pharmacist what prescription and nonprescription medications you are taking, especially antacids, antibiotics including neomycin (Mycifradin), and other laxatives.” (Quote from here)
Why do antacids have a special importance when taking lactulose?

Other laxatives can exacerbate the effects of lactulose, leading to diarrhea, and could eventually lead to dehydration and general GI issues.
Neomycin and antacids in general raise the pH of the gut, making it more basic, and reducing the peristaltic movements. Lactulose, meanwhile, is broken down to primarily lactic acid (if I recall) in the gut, and creates a more acidic environment. The acidic environment increases peristaltic movement in the bowel, and in turn the patient eliminates waste.
If you are on concomitant antacids or other drugs that raise the pH of the lower gut, you are reducing the effects of lactulose, and in a worse case scenario, making the constipation worse.

So are you saying that antacids raise the pH of the lower gut, the acidic environment in turn inhibits the breakdown of lactulose into acidic metabolites?
I guess that then less water is retained in the bowel than would be without an antacid, making lactulose less efficient against constipation.

The antacids don't necessarily inhibit the breakdown of lactulose, but they counteract the effect that would be caused by a more acidic environment in the gut. Acidity = increased peristaltic (bowel) movement. So the gross amount of acidic product from the lactulose might still be the same, but it is being neutralized to some extent by the alkaline products of the antacids.

Many thanks for your answer. In the main text you wrote “antacids … raise the pH of the lower gut”, in your comment “alkaline products of the antacids”. Isn't that a contradiction? Do I misunderstand something?

pH <7 is acidic, pH > 7 is basic/alkalinic, so the antacids (calcium carbonate, etc) would raise the pH, making it more alkalinic and less acidic, hence the "antacid"


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Why do antibiotics have a special importance when taking lactulose?
“Before taking lactulose, tell your doctor and pharmacist what prescription and nonprescription medications you are taking, especially antacids, antibiotics including neomycin (Mycifradin), and other laxatives.” (Quote from here)
Why do antibiotics have a special importance when taking lactulose?
Why is neomycin (Mycifradin) mentioned separately?

@winerd-> Sorry, you're correct. Still think you should have merged the questions though, since you are quoting the same passage and asking the same general question on two substances (feels more like a 1a, 1b question than two separate). The same answerer can most likely answer both at once.

@fileunderwater: No problem, thanks. Let's see if the answers will be similar or not. (I thought they would talk about different mechanisms, but indeed I could be wrong.)

From the Wikipedia article (I'm sure there's a scholarly reference, but I think this is well-known):

Lactulose works by relieving constipation through a number of different methods. Lactulose is made up of sugar molecules and is partly broken down by the bacteria that live in the lower part of the gut.

So, certain antibiotics affect (and reduce) the intestinal flora (and neomycin especially so, which is I believe the reason why it is mainly used in ointments), leaving the lactulose undigested and not as effective in forcing the body to retain water in the colon, which is the mechanism through which the drug acts.

Lactulose is an osmotic laxative. This means it works by drawing water into the colon (i.e. it retains a lot of water with it) and hence softens your stool in cases of constipation. As you can imagine, this interferes with absorption of most drugs including antibiotics and even food. Neomycin is especially toxic to gut flora (as mentioned above) and if taken with lactulose, it will linger in your GI tract for even longer and kill more gut flora. Your gut flora is important in protecting you against other harmful bacteria through competition for food, nutrients, etc. If you kill your flora, you are allowing other harmful organisms a field day in your intestine and they will grow and cause a condition known as pseudomembranous colitis (commonly caused by clostridium difficile infection). Also neomycin is mentioned separately because it has been associated with this condition which can sometimes be fatal (toxic megacolon, GI perforation, severe diarrhoea, etc)
In summary, you shouldn't be taking other medication whilst you're constipated anyway (especially when taking lactulose) because they won't get absorbed and may make the constipation worse.

Is there any evidence that lactulose decreases absorption thereby leading to an increased intestinal concentration?

"Neomycin ... if taken with lactulose, it will linger in your GI tract for even longer" - Are you sure about this? I thought that any laxative would REDUCE the time any substance spends in the colon.

@winerd but within the context of constipation, anything you take will linger in your GI tract for much longer. In theory, a laxative should increase your transit time but bearing in mind that lactulose interferes with absorption, this might be the case.

@AndroidPenguin, this just makes sense to me-just like having a diarrhoea which also interferes with absorption. Most laxatives will eventually cause diarrhoea which will interfere with absorption of other nutrients.

@John: I find it counter-intuitive that a laxative would increase transit time. Furthermore here it's stated for lactulose specifically and for many other laxatives that they "can cause SHORTER gastro intestinal transit time". Can you support your statement?

@winerd I meant it reduces transit time-you're right.


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What is neutral genetic differentiation?
What is neutral genetic differentiation? Presumably it's a measure of the distance between organisms in terms of their genetics, but what does 'neutral' refer to?

Seems to be discussed here, looks complicated.

Neutral genetic variation is variation that has no effect on fitness. I suggest reading more about neutral theory on wikipedia.
Neutral genetic differentiation is a way of talking about neutral genetic variation that follows some historical pattern, for example two populations isolated from each other for a long time will show neutral genetic differentiation even if they are individually in Hardy-Weinberg equilibrium. In other words, the two populations will have somewhat different allele frequencies from each other for no reason related to natural selection but rather because of random sampling and genetic drift over time.
It is generally thought that most genetic variation is neutral or nearly neutral. For example, most of the human genome is useless DNA or genomic parasites such as transposons. Almost all of the genetic variation that happens in those regions is not important to human fitness, in other words it is "neutral".


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Why do neurons have a negative resting potential?
Neurons expend the majority of their energy powering ion pumps to maintain the chemical gradients that power their electrical activity. To have a negative resting potential, neurons leak potassium across the membrane, which seems like a terrible waste of energy to me. I would like to know what benefit a neuron receives in exchange for this seemingly unnecessary metabolic load.
I am not asking how the resting potential is achieved. I am also not interested in the trivial answer: that the voltage-gated channels are configured to require a transition across the -40mV or so threshold in order to fire an action potential. It seems to me that this threshold is arbitrary; if there was no advantage to maintaining this gradient then neurons would have evolved to avoid it.
Any ideas? Or better yet, pointers to places where this has already been answered?
My best guess so far looks like this: The total range of available voltages is more-or-less fixed from -90 to +50mV. We want to avoid getting too close to either end, since the channels become less effective near their reversal potentials, so maybe the effective range is more like -70 to +30 (to go outside that range, we must sacrifice speed). Within that 100mV range, we leave the bottom 30mV or so for EPSP integration, and the other 60mV for action potentials.  Now, if the resting potential was 0mV, the available dynamic range for integration and spiking would be much smaller which probably translates to making the output noisier.

My turn to comment, lol.  The notion of membrane potential likely long predates the neuron from an evolutionary standpoint.  "Simpler" cells, e.g., an oocyte, rely on membrane potentials to gate membrane permeability to facilitate the entry of sperm. I would say it was likely due to the differential expression of membrane receptors in response to the local milieu that drove the evolution of the neuron, but I do not have a reference on hand to back that up.

(by the way, far from saying it's not an intriguing question, and the reasons you propose are plausible, so don't take any of this personally, as I implied on CogSci, you've got a good mind for this stuff)

Essentially all animal cells maintain an ionic balance causing a resting potential of about -70 mV in order to maintain their internal environment including pH, ion concentrations, osmotic pressure and volume. (Lodish, Molecular Cell Biology)  Neurons developed from existing types of cells and it's unlikely that the cost of maintaining resting potential in the neuron could have driven evolution of an entire alternative system to provide the homeostasis supported by the existing system.
Note that the depolarization of the membrane at any particular place during an impulse is very short so the impact of the ion flows have only limited effect on the cell's overall internal environment beyond requiring adjustment by ion pumps for the losses involved.  It also is not obvious how the wave-like characteristic of a nerve impulse could be generated if the membrane did not carry a nonzero potential; there would be no stored energy (in the form of ion gradients) available to make the pulse swiftly spread across the membrane.
Another point to consider is that the perhaps 15% of a neuron's energy spent on replacing leaking ions may have some hidden usefulness.  This paper suggests that neurons may actually be set up to leak at a rate higher than they would if it were minimized.

Thanks! I think your first and last paragraphs are both excellent answers. Regarding the second paragraph, I believe the bulk of the energy that drives action potentials is in concentration gradients, not electrical gradients. So it is possible that (with the right channels) one could have action potentials with no resting membrane potential (see: http://cogsci.stackexchange.com/questions/3625/how-would-synapses-behave-if-resting-potential-was-zero/3650#3650 )


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Precursor miRNA and a mature miRNA
What is the main difference between a precursor miRNA and a mature miRNA?
It is often the case that we have more than one precursor miRNA but only one mature miRNA.  The miRNA-seq data contains only precursor miRNAs, so I was wondering if we could use the expression of the precursor miRNA as the expression of the mature product or not?

precursor miRNA is ~70mer RNA with a stem loop structure. It is cleaved by dicer to generate one or two mature miRNAs (from one or both the 'arms' of the stem ; called 3p and 5p which are ~22nt long). Refer to this review. (It is an old one and some facts might have changed, but the basics are there.)
Yes, there can be different precursors giving rise to same mature form. There are a few cases like that (check for entries like mir-x-y [where y can be 1,2,3,...], in miRbase).
Usually pre-miRNA is shortlived and is immediately converted to mature form. Therefore, in small RNAseq data, most miRNA reads (more than 90% [at least that's what I get]) come from mature form (pre reads would be longer [after adapter removal] and will contain sequences not retained in mature form). Most algorithms select for the mature reads.
It is difficult to determine which precursor gave rise to a certain mature miRNA, using an RNAseq data. The usual practice is to assign the average read count to each locus. E.g., for a mature form that has 3 precursors, each precursor is assigned 1/3 of the total mature reads. However, in most RNAseq experiments, the objective is to obtain the mature miRNA profile and which precursor gives rise to it becomes immaterial.


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By what mechanism does coeliac disease cause excess fat in the feces?
Wikipedia states that “Severe coeliac disease leads to the characteristic symptoms of pale, loose and greasy stool (steatorrhoea)”. However thumbing through the causes and the pathophysiology it did not become clear to me what leads to this key symptom.
By what mechanism does coeliac disease cause excess fat in the feces?

Coeliac disease is an immune disorder resulting from a reaction to ingested gluten (a protein found in wheat, barley and rye). It is associated with inflammation of the small intestine resulting in a generalised reduction in the capacity for digestion and absorption. According to this paper:

Celiac disease is associated with pancreatico-biliary disease. Postulated mechanisms include reduced gallbladder emptying due to impaired cholecystokinin release and pancreatitis due to malnutrition.

Cholecystokinin is a peptide hormone that is produced by specialised cells in the small intestine and which stimulates the production and release of pancreatic enzymes and bile. Digestion of fat is critically dependent upon the emulsifying properties of bile salts in bile, together with pancreatic lipase. Any breakdown in this stimulatory pathway would result in reduced capacity for digestion of dietary fat.
Failure to digest fat results in fatty stools (steatorrhoea) which is one of the classic symptoms of the disorder.

I think the quoted text is quite interesting, but I'm not inclined to think that is the primary mechanism at play here.

Alan has covered some of it, but to add an illustration of the malabsorption piece of it, below left you can see a "normal" slice of small intestine, where the villi (finger like projections) are covered in enterocytes (the purple "bricks" along the border of the finger), which are responsible for the uptake of lipids (and their eventual "packaging") after they have been emulsified with bile salts in the intestinal lumen.
The offending gluten causes an autoimmune reaction over time that damages these villi as well as the enterocytes (as seen on the right side of the diagram), leaving a flattened area (hence far less surface area for absorption), and disrupted lipid packaging, so the unabsorbed lipids continue through the intestine into the stool.

from Cell Biology at Yale

So, there is no doubt that if fats are digested in the small intestine of sufferers they will not be absorbed due to the damage illustrated. However, the question remains - do the fats actually get digested at all, because if they don't then they wouldn't be absorbed anyway, even if the villi were still intact.

I always thought steatorrhea was the emulsified fats, but I may be incorrect on that.  Completely undigested fats would do a greater deal of damage to the colon and rectum, I think, as was the case when they had potato chips with Olean (sp?) in the mid 1990s.


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Are human males and females more genetically different than members of other species?
I'm looking at this Ted talk about a Saudi Arabia woman who dared to drive a car in the last few years. This reminds me that until the last century or so, women (all over the world?) enjoyed less rights and might've been pigeonholed into roles predetermined by society. Those roles might've encouraged certain traits, and discouraged others. Those who did not conform might've been punished, like the woman in the talk above received death threats and was jailed.
This sounds to me like selective pressure, did it really exist, and did it have any effect on the genetics/traits of modern women?
This makes me interested in the question - compared to other species, are men and women more genetically different because of selective pressure put on women to conform to male-dominated world for thousands of years before 19th century?

Males and females have essentially identical genomes (differing only in the very small Y and mitochondrial chromosomes), so they essentially don't differ at all.  This is true in other mammals too.

Since asking this question, I've learned that there's a massive amount of differences between male and female cognition, as explained by Evolutionary Psychology.

Females eating male spiders puts a lot of pressure on genetics too. Sea lions, lions, peacocks and hyenas also have probably as much pressure... sharia law is one of the most extreme sexual religious laws that has existed for only 1300 years, not all of human evolution. Chinese, African, etc law is 90% tribally moderate with plent of ancient civilizations having female leaders and warriors.

humans in general are incredibly genetically similar, its obvious we lost most of genetic diversity during a bottleneck.

I'm not sure I buy your premise: firstly, the degree and form of male-female differentiation in social roles has varied widely across time and culture in human history so I doubt it forms a uniform evolutionary driver such as you describe. Secondly, the degree of male-female differentiation appears to me to be much greater in species such as gorillas, lions and peacocks than it does in humans so I'm not convinced that humans would stand out on this front as a species we'd expect to have greater genetic differences.
Even so, the only genetic difference between male and female humans is the Y-chromosome. The X appears in both males and females and doesn't have exclusively female lineage so it can't acquire separate genes for male and female. The Y chromosome contains very few genes so its not capable of manifesting a major genetic gap and because there is no recombination in the Y chromosome it is not a fertile ground for new genes anyway.
So males and females have essentially the same genes. However, this isn't the whole story because how, when and whether genes are expressed is about as important as what genes are encoded anyway. It is these differences that enable big differences between the sexes not actual coding differences.

It would be interesting to check (maybe someone has already, I don't know) whether the epigenome of men and women is different!

They are different. Google 'sex differences in epigenetics' and you'll see there's quite a few papers on the subject. It's not my area so I won't claim to know the details.

If I understand your answer correctly, because most of the genes(that matter) are in the X chromosome, then selecting for a specific trait in females would also produce it in males, because it's most likely that the X chromosome would be involved. Is this correct?

Almost. Because genes can be differentially expressed you can still get differences in males and females even though they both share (almost) the same genes but there can't develop a major gap between male and female genomes because they share almost all the chromosomes. The Y chromosome is the only exception but it's not a healthy chromosome because it is exclusively passed down the male line and thus can't rely from recombination to "repair" damaged genes and shuffle genes into new contexts.

Essentially, what makes a (mammalian) man a man is a small region on the Y-chromosome called SRY. If this region is deleted, a female phenotype having XY-chromosomes develops. If this region is translocated to an X-chromosome, a male phenotype with two X-chromosomes develops. Other than that, the Y-chromosome does not carry a lot of genes.
So apart from the Y chromosome, males and females are genetically very similar and more similar compared to other species.

Are men and women not identical except the Y-chromosome (Not only similiar)?

Similar in the sense of interindividual differences in the genotype. If we were identical, we'd be clones.


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Is a "Fact" any theory for which there is overwhelming evidence in any field other than biology?
Evolution is often described as a fact, and a theory. Evolution is a heavily overloaded term, with one definition being the fact that, "changes in the frequency of alleles in populations of organisms from generation to generation." This is a measurable fact, but not the usage of the word evolution that I am in interested in.
Wikipedia has several quotes on the matter, including the Webaters definition used in this questions title, but also includes clearly observational facts like the Earth revolves around the sun.

A fact is a hypothesis that is so firmly supported by evidence that we assume it is true, and act as if it were true. —Douglas Futuyma
There is no sharp line between speculation, hypothesis, theory, principle, and fact, but only a difference along a sliding scale, in the degree of probability of the idea. When we say a thing is a fact, then, we only mean that its probability is an extremely high one: so high that we are not bothered by doubt about it and are ready to act accordingly. Now in this use of the term fact, the only proper one, evolution is a fact. —H. J. Muller
Scientists most often use the word "fact" to describe an observation. But scientists can also use fact to mean something that has been tested or observed so many times that there is no longer a compelling reason to keep testing or looking for examples. The occurrence of evolution in this sense is fact. Scientists no longer question whether descent with modification occurred because the evidence is so strong. —National Academy of Science

Do scientists refer to any theories for which there is overwhelming evidence as a "scientific fact", other than in biological sciences?
Note: Good answers will include quotes from scientific organizations or prominent scientists using the term fact to describe the theory, and will include references to the theory itself.

the definition of observation and fact (which is not often used in scientific discussions in my experience) are messier than you might think.  scientific proof is a messy business and different fields have different levels of evidence for publication, but they also have varying levels of application.  There is in practice no standard definition of these words in 'science' or 'biology' that I have seen, certainly none is taught in graduate school.

The use of the term "Law" (e.g., Newton's Laws of Motion, the Laws of Thermodynamics) seems comparable to the use of the term "fact".

@PaulA.Clayton, indeed. "Law" is an appropriate term, and is used often in Physics. I am interested in the supposed misuse of the term "fact" that scientists supposedly use according to the NAoS and others in fields other than biology. (Bonus points for not using climate scientists "fact" of the majority of warming is human caused in reference to the AGW theory.)

user1873-> Isn't the point of @PaulA.Clayton that the use of 'Law' in physics is an example from a field other than biology of a similar expression to denote a theory (in that both 'law' and 'fact' indicate a high degree of 'truth'). If you accept that 'scientific law' == 'scientific fact' then you have at least one example.

@fileunderwater, I don't accept scientific law == sci fact. The whole point of the question is that "fact" is supposedly used to indicate a high decree of certainty, and is used by scientists in this way. I cannot find any examples other than the very popular, "evolution is a fact." (And perhaps the AGW is a fact, but I am not sure if the source was a climate scientist). I doubt the claim that "fact" is used by scientists in this way.

@user1873 Is your disagreement only semantic? Or do you specifically have a problem with labelling 'evolution' or 'AGW' as law/fact? Your question seems to imply that you are asking for examples of other scientific fields where scientists are using a (casual) wording that implies that a theory is 'absolute truth'. If so, I think that the example from physics is valid. If you have a problem specifically with evolution (as a scientific theory or as as a theory deemed as'true' by most working scientists), that is a completely different question.

@fileunderwater, I suppose in a sense it is "only" semantic, since that is the root of the claim. I don't have any issue with the entomology of the word "fact" taking on this new meaning of  "any theory for which there is overwhelming evidence," my issue is with the claim that it has taken on that meaning when it appears that it only has in one specific case.  For example, If I claimed that the most women support abortion outside the womb, but insist that "abortion" meant, "to bottle feed an infant," some would take issue.

AFAIK, there are (1) evolution, (2) the Theory of Evolution and (3) Darwin's Theory of Evolution. (Other 'theories of evolution' could be counted.) The three are not equivalent. It seems that that you are asking about one of the three, but it's not clear which one.

Your question really applies to any scientific theory, not just evolution.
The problem is that, outside of the scientific world, a theory is often thought as something unproven, an unproven guess if you wish. This is not true for scientific theories, which, instead are confirmed by experimental data.
The OED defines theory as:

A scheme or system of ideas or statements held as an explanation or account of a group of facts or phenomena; a hypothesis that has been confirmed or established by observation or experiment, and is propounded or accepted as accounting for the known facts; a statement of what are held to be the general laws, principles, or causes of something known or observed.

and fact as:

Something that has really occurred or is actually the case; something certainly known to be of this character; hence, a particular truth known by actual observation or authentic testimony, as opposed to what is merely inferred, or to a conjecture or fiction; a datum of experience, as distinguished from the conclusions that may be based upon it.

So, essentially we start with an unproven idea, we corroborate it with facts (=experimental data) and we define our theory accordingly to facts.
So, why don't we say that evolution is true or that it is a dogma or that it is a fact?
Well, that is not how science work. Evolution is a scientific theory, and it always will be. Maybe (hopefully, dare I say) in 50 years from now new evidence will have make us change the theory of evolution, at least some bits of it.
Luckily evolutionary biology is not stuck at the time of Darwin and genetics is not stuck at the time of Mendel. Many new pieces of evidence have made us improve the theories that they initially defined.
Does that mean they were bad scientist or that they experiments were faked? Not at all!  Simply as their knowledge was more restricted than ours, they could not formulate a more advanced theory. Mendel's experiments still hold true, but now we know that transmissions of characters is not as simple. He was just looking at a special case. And his experiments still fit in our current theory, and will have to fit in any future one.
A scientific theory is defined by its falsifiability, that is

the trait of a statement, hypothesis, or theory whereby it could be shown to be false if some conceivable observation were true. In this sense, falsify is synonymous with nullify, meaning not "to commit fraud" but "show to be false".

The famous black swan example by Karl Popper (see e.g. Conjectures and refutations, 1963, chapter 11.6), can be exemplified by (source: Wikipedia):

One notices a white swan. From this one can conclude:
      At least one swan is white.
  From this, one may wish to conjecture:
      All swans are white.
  It is impractical to observe all the swans in the world to verify that they are all white.
Even so, the statement all swans are white is testable by being falsifiable. For, if in testing many swans, the researcher finds a single black swan, then the statement all swans are white would be falsified by the counterexample of the single black swan.

So, our theory of the white swan is accepted as "temporary true", as long as a black swan is not found. Obviously the more white swans we count (i.e. the more experimental evidence we have), the stronger our theory will be. But it will never be true.
I would like to finish quoting Richard Feynman:

It is scientific only to say what is more likely and what less likely, and not to be proving all the time the possible and impossible.

and

We never are right, we can only be sure we're wrong

I suggest to watch the full video of his fantastic lecture on scientific method on YouTube.

An biologist, a physicist and a mathematician are on a train in Scotland. The biologist looks out of the window, sees a black sheep standing in a field, and remarks, "all sheep evolved in Scotland to be black because selective forces killed off the white sheep." "No, no, no!" says the physicist. "Only some Scottish sheep are black." The mathematician rolls his eyes at his companions' muddled thinking and says, "In Scotland, there is at least one sheep, at least one side of which appears to be black from here some of the time."

@user1873: you seem to have misread my answer. I never said scientists use fact in reference to theories. I am saying that a scientific theory, or a scientific model, is based on facts, that is experimental proofs. One, however, can never be certain a theory it is true (instead one can be certain a fact is true). So, if a scientist or a journalist or anyone else uses "theory" and "fact" interchangeably... well, they are doing it in an incorrect way as the two terms do not mean the same thing.

@user1873: the example of the sheep you make is a very good example of how a theory is just an interpretation of facts. The experimental evidence (the black sheep in the field) can be interpreted in (at least) three ways. All of those three are equally good scientific theories, as they are all falsifiable. You just need to go and look at the sheep from the other side of the field, or look at sheep in another country etc etc and some (or all) of those theories will be falsified. [cont'd]

[cont'd]You can then formulate a fourth theory, which is still consistent with that data but that takes into account the new data. All of the four theories are based on facts, but they are not facts, they are interpretations of the facts.

I just reread your 2nd comment. It seems you are saying that the NAoS is indeed full of it. It is unfortunate that Wikipedia keeps such misinformation on its pages for so long.

I am indeed disagreeing with what the NAoS says (just my opinion...). I don't doubt that sometimes if a theory is proven over and over again we take the "shortcut" of calling it a fact, but I am saying this is not really correct. I agree much more with the first quote when it says: "we act as if it were true". It is a shortcut, and I understand that sometimes it is handy to say "evolution is a fact" to respond to creationists arguing that "evolution is just a theory". But really, the way one should respond to that is "evolution is a theory, proven over and over again".

A direct quote to Popper on black swans could be: That this minimum requirement cannot be satisfied ... may be shown with the help of Carnap's example, the law 'all swans are white'. This law ought to be considered *falsified* if our evidence consists of a flock of *one* black and, say, 1000 white swans. But upon this evidence, the instance confirmation, instead of being zero, will be very near to 1.. This is from chapter 11.6 in Conjectures and refutations. I have added a reference in our answer to this passage, but as a stand-alone explanation the Wikipedia quote is better.

@nico In your answer and comments you write that a theory is an interpretation of facts, and that one can be certain a fact is true. This is however (as you probably know) a very simplified view. More modern descriptions of the scientific method all highlight how observations cannot be simply decoupled from theory (see e.g. Lakatos in Criticism and the Growth of Knowledge and Kuhn's The Structure of Scientific Revolutions, or, in more extreme form, Feyerabend's Against method). Therefore, you can just as well argue that observations and "facts" are theory dependent.

@fileunderwater: Thanks for the ref. Obviously theory and observation are not independent, but whereas theory can be viewed as an interpretation of observation, the other way around seems less likely. I can have my theory that cells are triangular, and it may be as nice a theory as I wish, but that will not have the effect of making cells triangular... :)

@nico Well, neither observations nor theories will change the physical reality, so no difference there. While I agree in practice that observations and theory have a different standing, with observations being closer to "actual facts", I still think that the point of theory-dependent observations cannot be so easily written off. A classical example would be astronomy, where raw 'observations' can consist of photon recordings from a distant star. For this raw 'observation' to be made into an observation (fact?) that has bearing on a particular hypothesis (e.g. dealing with ...

contd: ... the composition of the star) an entire body of work must be assumed. Auxilary theories and methods that has to be assumed true could include recording equipment, diffraction of light in the atmosphere and in space, how electromagnetic radiation is emitted etc. The point being that these observations don't exist except in relation to a complex network of theories. The astronomy example might be seen as extreme, but I can easily envision many similar situations in biology. But I probably digress from the main topic....

@fileunderwater: surely, I agree with you on that, but that is mostly because, for practical reasons, you cannot expect everyone to repeat every single experiment needed to justify his/her theory. A scientific experiment, however, should be repeatable, so in theory all those auxiliary theories could be reconfirmed (and if they are assumed as correct by the scientific community they probably have been reconfirmed over and over again). Still, that does not make them TRUE, just not false in accordance to what we know.

@user1873 I know this is old, but I had to steal that first comment. :D


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What part of the brain controls depth perception?
Specifically the part of the brain that does depth perception based on binocular vision. I have searched all over the web and have turned up nothing. Is it the same part of the brain that processes all images from the retina?

According to the article: Scientists uncover second depth-perception method in the brain:

the neurons in the middle temporal area of the brain are combining visual information and physical movement to extract depth information

This Scientific American article states that there is a process involved:

Visual-image processing from the eye to the brain happens in stages. Rudimentary features such as the orientation of edges, direction of motion, color, and so on are extracted early on in areas called V1 and V2 before reaching the next stages in the visual-processing hierarchy for a progressively more refined analysis. This stage-by-stage description is a caricature; many pathways go “back” from stage to stage—allowing the brain to play a kind of 20-questions game to arrive at a solution after successive iterations.

This process is discussed further in this article with what is known as the Laminart model.

Some regions of primary visual cortex (V1; physically at the very back of the cortex) respond to visual stimuli present in either eye. These are called "binocular" regions, for obvious reasons. Some of the neurons in these regions are "disparity-tuned", in the sense that they respond most strongly when a stimulus is present on both retina, at a particular retinal distance apart. This has been known for cats for some time (Fisher & Kruger 1978). The suggestion is that information from disparity-tuned neurons are used for depth discrimination (Ohzawa et al. 1990).
There may be other mechanisms as well, which use relative motion and ocular convergence to estimate distance.


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Information Gene HBA2
Gene : HBA2? hemoglobin alpha 2 (Homo sapiens)
I don't find any tissues (or organs) in which the expression of this gene is strongest? What is the size of the gene (promoter off) encoding this sequence?

Hello, where have you tried to find information on HBA2?

On the NCBI site, but the site is rich in information and like I started in bioinformatics...

you could also use wikipedia as a starting point: http://en.wikipedia.org/wiki/Hemoglobin,_alpha_2 for many genes this will give you already a good overview and links to sources

GeneCards is also a decent site for these type of information.

Thank you for your answer but I don't find the size of the promoter, I know the size of the gene is 864 bases but with the promoter and i need is size without promoter

Gene size will not include the promoter. The main reason is that the exact location of the promoter is not defined (or defined arbitrarily).

not sure that I understand what is going on here, but the HBA2 gene product is 142 amino acids which corresponds to 426 nt plus a stop codon makes it 429 nt

You mention that you "started in bioinformatics", so perhaps you might feel more comfortable taking such an approach to better characterize where the promoter for HBA2 might be.
As @Bitwise mentioned in his comment, "the promoter" is not a well defined region. Often times "we" take the promoter of a gene to be some arbitrary (2-4) kilobytes upstream from the TSS. With more high throughput data coming online (especially from ENCODE), we are starting to get a better picture of where the functional regulatory elements of genes might be.
By combining data from several different high-throughput assays across a variety of cell types, the human genome has been segmented into broad regions of interest. You might start by looking for where the "Predicted promoter region including transcription start site" segment is for HBA2.
I'd also take a closer look at the DNase-seq data in this "promoter region" across as many cell lines as they have processed for you to look for regions that are differentially occupied in hopes of identifying more precisely which parts in the promoter region might be important for the gene's expression (this would, of course, require you to connect DNAseq data with gene expression (RNA-seq) data).

Thank you for your comprehensive answers that helps me a lot
I determined that the gene HBA2 had four SNPs but to find  how many allele phenotypically it is I do not know if I should take the column'' Allele origin " or the column dbSNP allele Thank you again


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Why is funnel web spider venom so lethal to humans and not so much for other mammals?
According to the information from this article,

People and other primates are exquisitely sensitive to funnel web venom but, intriguingly, other mammals such as mice, rabbits, guineapigs, dogs and cats are relatively immune and often survive 100 times the human lethal dosage.

Why is the funnel web spider venom so much more lethal for humans and primates than other mammals?

First, we need to understand that neurons have special proteins embedded in their membranes called ion channels. These allow dissolved ions such as sodium, potassium, and calcium to pass from one side of the membrane to the other. Neurons use these channels to control their electrical activity.
Peptide neurotoxins such as the one produced by funnel spiders (robustoxin) work by having a shape and charge configuration that is complementary to ion channels, and thus they will bind to these channels and affect the way they operate (often by simply blocking the channel). Robustoxin seems to operate by removing sodium-channel inactivation.
There is a bit more information about the primary toxin on the Wikipedia page for delta atracotoxin. The intended target of this toxin seems to be insects, where it interferes with potassium and calcium channels. In mammals it interferes with sodium channels, but it seems to be particularly potent in primates. Why are some species affected more than others?
Not all ion channels are built the same. From species to species, we see a huge array of genetic differences that affect both the shape and functional properties of these proteins. Ion channels which happen to have a shape and charge configuration that is highly complementary to robustoxin will adhere to it more firmly, and thus be more affected by it.
So did we just get unlucky and happen to have sodium channels that perfectly fit robustoxin? That seems to be the most likely answer, given that Australia probably has no native spider-consuming primates. Perhaps someone else can suggest other arachnid predators that might be an intended target for robustoxin?


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Keyword based literature search
I understand this is not a biological question but this is often a problem whenever I look for literature.
How to look for a reference for some fact based on keywords. For instance you know about a fact such as - Cell signaling responses are faster but short lived compared to transcriptional responses. How to find the literature which actually says this. I often end up getting irrelevant results.
In other words, how to represent a fact using appropriate keywords. Is there an algorithm which can generate synonymous statements [like MeSH terms in pubmed] and search for those.
Or is there any way of setting up a hierarchical search.
PS: If someone finds a reference for "Cell signaling responses are faster but short lived compared to transcriptional responses" then please let me know

You may want to have a look at Gene Ontology and at GOPubmed

GO is about functional annotation of genes. That's not what I am looking for. GOPubmed is cool. I need to see if it has the function of search levels

perhaps set up a 'Google alert' with those phrases.

I would either cite an advanced molecular biology or developmental biology textbook or if you must cite a paper, find the relevant chapter in the textbook and look at its references.

I think the statement above is slightly misleading. There are many many types of cell signalling, anything from RTK (at the cell surface or when its endocytosed), to steroid receptors, which operate on different time scales and produce different results depending on the type of signalling. Also it depends on what you are measuring/defining as a signal/response in lets say "cell signalling" because you could define cell signalling response as protein phosphorylation at any point in a signalling cascade or it could be the transcriptional activation itself (consider the MAPK pathway in Drosophila, at which point do you consider a response is produced? when Raf is activated? or when transcription factors such as pointed bind to their ETS binding site and start to transcribe as measured by luciferase? as you can tell the time difference between the two is quite large, well as far as I know after RTK activation in Drosophila it takes ERK 20 minutes just to translocate to the nucleus). A cell signalling response could also constitute changes in the rate of cell migration, cell shape etc, which can either be slow or fast depending on the signal in question. so I think the above question needs major rethinking and redefining.
Now getting back to your questions about key search terms, in my experience, over time you just end up developing a knack for what you consider to be key words after you carefully define the question and think bout its different aspects. A rule of thumb that I use is typing at name of proteins (e.g. JNK or RAS etc) or processes (transcription, phosphorylation etc) and use a word like rate, time-scale, half-life, turn-over or something like that if its measuring changes in time you are interested in. Just play around with words.
Also as a general advice you don't have to reference every snippet of every fact like "water is liquid at RT in standard atmospheric pressure" etc. References are meant to be there to acknowledge the work of others like "how DNA was discovered" so that people can't just lift paragraphs or pages out os someones research without acknowledging them and passing it as their own work.
Hope this helps.

Thanks Bez. What I meant by fast and slow is the response time. Protein phosphorylations are much faster than transcriptional activation. Which I know for sure. Just wanted a review sort of thing which summarizes the response times of different processes in a cell.


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What nutritious insects exist to farm that require the least attention?
What nutritious insects exist to farm that require the least attention? I'm looking to automate simply, in a self regulating way.
Edit: To add detail, I imagine the insects would live densely in a large tank and be isolated from the outside. They would be able to breed and would co-exist with a plant that is also able to propagate, that could if needs be even be an air plant, that is eaten by the insects, dead insects either return to nourish the plant, or leave through a funnel, water also evaporates and falls as rain inside the tank.
The idea is to produce food without human effort. This could be in the form of a very cheap to use coin operated vending machine. The insects could be compressed and dry fried into a block to be dispensed, maybe like a bar, the machine could be solar powered.

Nutritional? To whom or what are you planning on feeding these to?

@rg22: insects are part of the human diet in many countries and they have been suggested as an alternative sustainable source of proteins (see refs 9-12 of the entomophagy Wikipedia article).

I suppose it would depend in part as to which part of the world you live in, and what is native/endemic to that region. Also, what is the scale you're looking at - an occasional snack, a major part of your diet, a family, a commercial enterprise?

I've updated the question.

might be worth asking over on [sustainability.se] in a few days, if you don't get the answer(s) you're after, here

@nico I know, I was just wanting to clarify if they were looking for themselves or a pet lizard - the requirements would be different

The leaf cutter ant Atta laevigata is a popular delicacy in Colombia where it is known as hormiga culona (big-ass ant). The ants are usually salted and fried and play a similar culinary role (I am told) as pop corn (image source):

I can't testify as to how hard it is to cultivate them, but one difficulty will be chosing the edible ones. Apparently, only the queens are edible.

"Analyses conducted at the Industrial University of Santander about the nutritional value of the ants show high level of protein, very low levels of saturated fat, and an overall high nutritional value.", looks good.

Only the queens being edible might be a problem, it's not impossible to create an automatic filter, but does seem to add complexity, particularly if needs vary between types.

@alan2here Why do you want insects anyway? Why not algae or fungi? Perhaps even bacteria? Any kind of multicellular animal life form will be harder to grow than simple mushrooms.

Plants will be needed anyway, so an option could be not to include the insects. I suspect that the plants grow too slowly and then require a more complex process of cutting and removing from the isolated environment, particularly if they require soil, additionally insects are meat, although this needn't matter a great deal. At the risk of going off topic, do you have any ideas on this front? Simpler lifeforms also seem interesting although might be difficult to make palatable.

@alan2here there is nothing unpalatable about mushrooms, some of which are considered great delicacies. Some mushrooms grow very fast and need no care to speak of. Insects are complex and they move around. I don't see why you think they will be easier to deal with than plants.

You make good points.

http://community.theurbanfarmingguys.com might be a good place to start more of a discussion.

The silkworm Bombyx mori is farmed for silk, but the pupae are also eaten across the Far East. Since these insects (larvae) have been domesticated for centuries there are well-established procedures for growing them.

Sorry to go updating the question like this, does it affect your answer?


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Why is allolactose the LacI inducer?
For what reason(s) is allolactose, instead of lactose, the "natural" inducer of lac operon repressor?

When lactose is present in a cell, some of it is enzymatically converted by $\beta$-galactosidase from the $\beta(1,4)$ linkage (typical of lactose) to the $\beta(1,6)$ glycosidic linkage (becoming allolactose). Allolactose and other analogues can then bind LacI to induce the appropriate conformational change and unbind the lac operator (one such review here).
Why does allolactose act as a signal of lactose presence instead of just lactose? From the perspective of the lac operon, there is no operational difference between lactose and allolactose -- either way one molecule binds LacI and cannot be metabolized while bound. The full paradox is explained by Edgel and summarized by well-known biochemistry textbook author and scientist, Larry Moran, on his personal blog. The short version is that neither allolactose nor lactose are the intended substrates for $\beta$-gal and instead a different sugar entirely is the "natural" inducer and substrate.

Juers DH, Matthews BW, Huber RE. LacZ β-galactosidase: structure and function of an enzyme of historical and molecular biological importance. Protein Sci. 2012 1792-807.
Egel R. The 'lac' operon: an irrelevant paradox? Trends Genet. 1988 Feb;4(2):31.


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Can ingestion of B6 cause gastrointestinal disturbance?
Can the ingestion of vitamin B6 upset the stomach, and if so by what mechanism?

Hi there. This question is seeking specific medical advice, and as such, is against our posting guidelines which specifically restricts medical diagnoses/advice. If you edit your question to remove the last sentence, then we would be happy to try to answer your question.

However, in all cases along these lines, see your doctor rather than the internet :)  There's a lot more to be safely gained through thorough history from a professional and clinical examination than through a question asked on a website

It is not reported anywhere that Vit B6/Pyridoxine has gastrointestinal side effects.


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What do rs id, allele coded 0 and allele coded 1 mean?
So, for a project I've been working on (different story), I've been looking at the HapMap Project, and their free online files. In their README file, they talk about how for each legend file for each chromosome/region, there is an rs id, an alelle coded 0, 1, and a base pair position.
Now it's fairly obvious after staring at this for a while that base pair position means where each nucleotide is located along the genetic sequence... is this correct?
And what do rs id, and the other words mean? Any help would be greatly appreciated!
Here's the link to the README file, in that same directory are the files about the participants, only including SNPs (snips!).
HapMap Project README file link
HapMap Project sequence data link (phase 2)

rs id is reference SNP cluster ID see here. It's basically a unique identifier.
This table is taken from your link:
rs              position        0       1
rs11089130      14431347        C       G
rs738829        14432618        A       G
rs915674        14433624        A       G

The allele codes are the 3rd and 4th columns. An SNP is  site where a different base is found in different versions of the same gene (different versions of genes are alleles). For a given SNP the different alleles are referred to as the 0 or the 1 allele. So in the table the first SNP, rs11089130,  has two alleles: allele 0 has a C at the SNP position (14431347) whereas  allele 1 has a G at that position. The allele code does not imply any biological significance.
I'm not sure what would happen if there were three alleles at an SNP, but presumably there would then also be an SNP coded as 2.
Edit:
Allele 0 is the residue from the reference genome. Allele 1 is the residue being studied, the SNP.

so 0 is the standard allele and 1 is the mutated allele?

@higgs241 0 is the residue found in the reference genome and 1 is the residue found in others. Please don't refer to "mutated alleles" variation is the norm...

@terdon is the reference genome the same for every registered SNP? I mean, if you took the 0 allele at every SNP registered with a rsID, would you end up with the genetic profile of one specific individual?
It seems not: I read in http://en.wikipedia.org/wiki/Reference_genome that "the Genome Reference Consortium human genome (build 37) is derived from thirteen anonymous volunteers from Buffalo, New York". Is that the genome used as a reference for 0/1 labelling of SNPs? And what to do when there is polymorphism in this group of people? Maybe I could make a new question...

@bli It seems pretty clear from the WP page that you link to that the reference genome is a curation construct and so does not correspond to one individual. in fact the page includes this sentence: "The ABO blood group system differs among humans, but the human reference genome contains only an O allele (although the other alleles are annotated)."

@Alan Boyd Yes, I should have read the page further. So there is this "GRC human genome (build 37)" which is an artificial haploid reference. Is this the reference for all registered SNP? It could be but I have no certainty. One reason for my doubts is the following: Can it happen that a new SNP is identified in a portion of the genome not yet present in this reference genome? I suspect this is becoming rare, but when this reference was in earlier stages of construction, may be it could have happened.


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How does the human liver regrow?
I understand that there would have to be a portion of liver present to regrow from, so how much liver would the minimum to be able to regrow?
By what mechanism does regrowth occur?

At least 25% of the original liver seems to be the minimum for regrowth.
The initial regrowth is due to proliferation of hepatocytes: they exit G0 and enter mitosis. The ECM dissolves and is remodeled; the cholangiocytes and SECs also divide.
If you want to read more, you can visit the Google books link above, and the preview lets you read several pages on liver regeneration in rodents.  (If it doesn't work, try changing the URL to your current location: books.google.com is US, books.google.ca is Canada, etc.)


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Transcriptionally-mediated DNA damage
I'm researching the genetics of brain cancer, and finding a huge number of mutations in voltage-gated channels.  It stands to reason that some of this DNA damage is due to the DNA being transcribed heavily, or in an open chromatin conformation more often, leading to more breakage and damage due to environmental stress.
Of course, those are just guesses.  Does anyone know of any research papers in the area?

What is your reasoning behind your statement "some of this DNA damage is due to the DNA being transcribed heavily, or in an open chromatin conformation more often"? Just about every cell type has its portion of genes that are being heavily transcribed, even if it's just "housekeeping" genes like actin and GAPDH.

That's a good point about actin and GAPDH.  My understanding is that tightly packed heterochromatin is  more "stable" than euchromatin because it is energetically favorable to remain wrapped around histones.  Additionally, the conformation induced by the DNA/histone coil prevents many of the nucleotides in heterochromatin from being exposed to the nucleoplasm, which would decrease its exposure to DNA damage agents compared to uncoiled euchromatin.

There seems to be some solid evidence that transcription promotes mutation because the untranscribed strand is able to form secondary structures which expose bases to chemical mutagenesis.
Here is a recent paper about transcription-associated mutagenesis:
Kim H et al.(2010) Transcription-associated mutagenesis increases protein sequence diversity more effectively than does random mutagenesis in Escherichia coli. PLoS One 5(5):e10567. doi: 10.1371/journal.pone.0010567.
From the abstract:

During transcription, the nontranscribed DNA strand becomes single-stranded DNA (ssDNA), which can form secondary structures. Unpaired bases in the ssDNA are less protected from mutagens and hence experience more mutations than do paired bases. These mutations are called transcription-associated mutations. Transcription-associated mutagenesis is increased under stress and depends on the DNA sequence. Therefore, selection might significantly influence protein-coding sequences in terms of the transcription-associated mutability per transcription event under stress to improve the survival of Escherichia coli.

The authors cite a number of papers in their introduction which document the phenomenon that you could follow up. Just in case the focus on a bacterial system puts you off, the Kim et al. paper has in turn been cited in:
Wright et al. (2011) The roles of transcription and genotoxins underlying p53 mutagenesis in vivo. CARCINOGENESIS 32:1559-1567
Abstract in full:

Transcription drives supercoiling which forms and stabilizes single-stranded (ss) DNA secondary structures with loops exposing G and C bases that are intrinsically mutable and vulnerable to non-enzymatic hydrolytic reactions. Since many studies in prokaryotes have shown direct correlations between the frequencies of transcription and mutation, we conducted in silico analyses using the computer program, mfg, which simulates transcription and predicts the location of known mutable bases in loops of high-stability secondary structures. Mfg analyses of the p53 tumor suppressor gene predicted the location of mutable bases and mutation frequencies correlated with the extent to which these mutable bases were exposed in secondary structures. In vitro analyses have now confirmed that the 12 most mutable bases in p53 are in fact located in predicted ssDNA loops of these structures. Data show that genotoxins have two independent effects on mutagenesis and the incidence of cancer: Firstly, they activate p53 transcription, which increases the number of exposed mutable bases and also increases mutation frequency. Secondly, genotoxins increase the frequency of G-to-T transversions resulting in a decrease in G-to-A and C mutations. This precise compensatory shift in the 'fate' of G mutations has no impact on mutation frequency. Moreover, it is consistent with our proposed mechanism of mutagenesis in which the frequency of G exposure in ssDNA via transcription is rate limiting for mutation frequency in vivo.


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How do people who have lost both of their legs produce red blood cells?
As far as I know, just leg bones produce red blood cells. So, how people who lost their both legs produce red blood cells?

Can you point to a reference?  Any bone with sufficient marrow can produce erythrocytes.  It may be that the largest number are made in the femur and tib/fib, but they aren't exclusively the point of production.

Red blood cells are produced in the red marrow which...

"is found mainly in the flat bones, such as the pelvis, sternum,
  cranium, ribs, vertebrae and scapulae, and in the cancellous
  ("spongy") material at the epiphyseal ends of long bones such as the
  femur and humerus." - Wikipedia

So you are partly right; the femur is associated with red blood cell production, or Erythropoiesis to give it it's technical name, but there are other bones within the human body that also do this job. The process of erythropoiesis is stimulated when the kidneys detect low levels of oxygen in the blood stream and stimulate production of the hormone erythropoietin. Further, the role of the tibia and femur in erythropoiesis also decreases with age whereas...

"the vertebrae, sternum, pelvis and ribs, and cranial bones continue
  to produce red blood cells throughout life." - again from the wiki page

So I'd suggest it is unlikely that loss of the legs would have a major impact on the production of red blood cells in adults. I imagine that with the loss of legs comes some reduction in functionality of erythropoiesis but also a lower requirement of red blood cell production (less blood capacity = less blood cells needed = less blood cells need to be produced). I can't find any studies which explore the ability or needs of amputees and non-amputees with regards to red blood cell production.

While researching earlier I did find some reports on post-amputation anaemia. Clearly the compensation by other bones does not always work, but this was a minority of only about 7% iirc.

@Armatus Thanks, I guess people will be affected differently, I couldn't find any evidence of prolonged problems myself but did find cases of transfusions being required in the days/weeks after surgery but that is probably more related to the blood loss and maybe the other bones "learning" to compensate.

Red blood cells are produced in the red marrow, and white blood cells are produced in the yellow marrow. The marrow is found in the flat bones (i.e.long bones) which is the pelvis, sternum, ribs, and vertebrae. If the long bones are no longer attached the the pelvis and the ribs with have to work harder in order to produce the blood cells needed.

can you give a source for that information? Also, see comments on question that are listed above.


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Modeling yeast biochemical pathway using enzyme kinetics
I need enzyme concentration and metabolites concentration values to en-corporate these values in my model and do some simulation.
I searched through some database
yeast metabolome database http://www.ymdb.ca/
brenda and other enzyme databases for enzmye conc
and also did some literature search
but couldn't find much of data
where possibly i can get these data ??
is there any other way to do simulation without data.

You should take a look at SGD (the Saccharomyces Genome Database), and in particular YeastCyc. Some protein information pages at SGD give estimates of molecules per cell taken from this Nature paper.
Added later in response to some comments:
The question asks about levels of metabolites and of enzymes, not of transcripts. Microarray data can be, at best, only a guide to levels of proteins. Estimating the levels of metabolites from microarray data is a complete non-starter since there are entire layers of regulation that will be ignored. Just to give one example of a pitfall in this approach: you could have high levels of transcript from which you could you could infer high levels of enzyme, but that enzyme could be inactivated by a post-translational modification.

can't find much of data on YeastCyc and even

try approximating from microarray or RNAseq data.. they are available in GEO and SRA

Can you elaborate or cite a paper how to estimate concentration of metabolites mainly present in  this pathwayubiquinone synthesis from microarray RNAseq data. If any body have done similar thing and documented it please let me know.


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Statistical Analysis of Protein Folding Problem
I’m new to the field of protein folding. I’ve been searching and came across some books for predicting structures (Introduction to Protein Structure Prediction: Methods and Algorithms). Does anyone know whether I can find some code (say in C++, Java, or R) related to the prediction of protein structures? Or, do you know other good articles or books related to the statistics of the protein folding problem?
Thanks for the help.

Welcome to Biology.SE. As your question stands currently, it will likely be closed as "non-constructive." The Help page gives guidance on the types of questions to ask and not ask. We're looking for questions that have straightforward, factual answers, whereas "what's a good book to learn about ..." questions can have many, equally-valid answers. Additionally, a quick Google search will easily answer your first question.

One of the quickest ways to get oriented on what is going in the world of protein folding and modeling is to look at the proceedings of the Critical Assessment of Structure Prediction (CASP).  CASP is basically a contest, held every 2 years where anyone can use their algorithm to predict the 3D structure of a protein whose structure is known, but not publicly available.
Its been a few years since I reviewed them results much - it looks like this year was interesting, but a perennial winner has been Rosetta, which has turned into an edifice of many suites of software which each execute different tasks in protein folding and modeling.
Open source software is pretty hard to find in this field.  The software is complex.  It usually includes components of machine and statistical learning, molecular dynamics, specialized algorithms that build up the protein one residue at a time, others which manipulate blocks of the protein structure around in space, electrostatic calculations, you name it.  In addition, the software, once it gives some sort of result is quite valuable.  I don't think any of these suites has really been released.  I know that Rosetta is available to use as a web service, but you have to apply for access to the source.  I don't think its an easy thing to get.
Some of the most complicated components are available open source.  Molecular modeling and molecular dynamics open source software is quite sophisticated.  I think we need an open source protein folding suite open source.  I think David Shortle's algorithms might be a candidate for such a suite as its not so complicated and it works in some cases.
This field is pretty obscure and difficult to get around in.  There aren't any easy introductions that I know of.  Protein structures are computationally expensive and painful to work with in terms of writing software.  On the other hand protein folding that really works is a revolutionary breakthrough, at least equal to the impact of the development of computers as a technology.


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Is it true that oral sex exists in non-human animals?
For example, outside of humans, do other species of animals engage in oral sex, or any oral stimulation of others' genitals purely for pleasure, not any cleansing habits, etc.?
Basically, what I am saying is, is it true that oral sex, like in humans, exists in non-human animals?

Then of course you have the sexual deviants like this chimp.

I am not going to sugar coat this or lie folks....this is graphic.
Elephants:
https://www.youtube.com/watch?v=Q12ApVIjkD0 Then again, that is the snout so that's technically not oral...food for thought I guess... https://books.google.com/books?id=tmFJ1LhbVWcC&pg=PT53&lpg=PT53&dq=elephants+oral+sex&source=bl&ots=RYPwHuK4VA&sig=I37vEU8-GlSuE5TAVdYaOeT-C5M&hl=en&sa=X&ei=8sgpVdi6GcKdgwSUpYHYBg&ved=0CFIQ6AEwBw#v=onepage&q=elephants%20oral%20sex&f=false

Yes, it is true. Have a look at this post:9 Animals Who Are Into Oral Sex:

A recent study of fruit bats found cunnilingus to be a major part of their repertoire. While following a colony of 420 bats roosting in a fig tree over the course of 13 months, researchers witnessed 57 incidences of sex — both oral and intercourse. The female bats who received oral sex before intercourse were found to last longer during copulation.

The paper they cite is this one.


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Eye Brain Mapping
If our eyes are separated by some kind of full proof barrier/isolation, is it possible that our brain can picture/visualize two different pictures at a time?
How the brain will function in this situation?
which are the books to read to understand in depth brain behavior?
I tried to isolate my eyes with hands/paper but i am not able to do it.

I heard about yogi learning to move their eyes independently, this may be a starting point for research.

dd3 answered this already, but here's an idea how to separate your eyes: take a pair of (sun)glasses and put a different sticker on the left and the right piece. Then put them on.

First off, I should note that binocular vision is important for depth perception.
The phenomenon in which you are interested is called binocular rivalry (distinct images are presented to each eye).  You typically switch between the images, and sometimes, both at once (superimposed; this is called binocular transparency) or an averaged picture (binocular fusion).
You can find some good links at the Wikipedia page.  The Scholarpedia page is even better.  If you don't find what you're looking for, I think searching for papers on "binocular rivalry" will give you the best result.


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How do pineapples and lemongrass grow?
You can't plant the leaves, you can't plant the fruit, but, if you plant the part where leaves and fruit meet you will grow a whole pineapple plant.
The part of the pineapple where the leaves meet the stem is the point from which the whole plant seems to form. Cells below seem to become fruit and fruit skin, cells above seem to become leaves. If you look at a cross-section of this part of the plant you can see the way that the cells seem to move outward from this point.

(1)But is that really how it grows? Are the new cells added from the center or do new cells get added to the leaves at the tips and in the middle of the leaves?
(2)I know some orchid roots grow from the tip... but is this the case for all roots?
(3)I noticed that some lemongrass in my worm compost bin has grown roots! So, I transplanted it outside. Maybe I can grow lemongrass. Again, it was the part of the plant where the roots met the leaves that still had life in it.  This seems like a very powerful part of the plant. Is there a name for the part of a plant from which everything else grows?
UPDATE: http://en.wikipedia.org/wiki/Meristem
This is what the regions is called! But I still want to know if the plant "pushes" out the leaves from this central point or not... and are all root like orchid roots that grow from the tips?

First, allow me to provide the link to an old paper that deals with development in Ananas comosus, it should be freely available and answer this question in more detail: http://onlinelibrary.wiley.com/doi/10.1111/j.1469-8137.1936.tb06884.x/pdf
Now, to briefly explain the observation that a mature plant will grow from the region where the leaves of the pineapple attach to the fruit, it should be noted that the pineapple fruit develops at the top of the central stem of the plant in a developmental process known as influorescence (please see a picture of a pineapple plant). Since the top portion of the fruit is in fact the end of the primary stem, this region contains the apical meristem, a collection of stem cells that are apparently is sufficient to give rise to a mature organism. Pineapple development has apparently been a topic of constant research for nearly a century (due to its economic importance), so there are quite a number of papers that can provide much more detail, but many of these are not freely available.
In nature the primary means of pineapple propagation is the formations of lateral shoots, the growth of which consequently are accelerated by influoresence of the main shoot.
Now the actual way the plant grows is not quite as simple to answer, as plant development is often as complicated as animal development, but in general it is a function of cell division and elongation. In the root apical meristem, there is a region known as the quiescent centre which contains the actual root stem cells. Directly behind the quiescent centre is a region known as the merismatic zone, which features extensive cell division, and directly behind that is the elongation region where the cells grow, effectively pushing the root tip through the soil. In the region behind the elongation region, the maturation zone where the cells have reached full length, cells begin to form more rigid cell walls and differentiate into the different tissues of the root.
The shoot apical meristem is dome-shaped, the top of the dome is known as the central zone and is analogous to the quiescent centre of the root apical meristem, the sides of the dome are the peripheral zone, a region of rapidly dividing cells that give rise to the leaves, and the central region of the dome is the rib zone that gives rise to the stem structures. Elongation, differentiation, and maturation also occur below the meristem region, but involve the additional complexities of leaf organogenesis.
There should be considerable additional information on plant development online.


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What are the longterm effects of pancreatitis?
As the title asks, what are the longterm effects of pancreatitis?  Having one event, is the person more susceptible to have a recurrence, or are they at higher risk of other conditions such as diabetes?

Pancreatitis may cause a condition called ''systemic inflammatory response syndrome'', a immune system reaction affecting the whole body.
Also, more frequently, pancreatitis is linked with steatorrhea, which means oily fat, and it may cause malnutrition and weight loss, due to restriction of secretions containing digestive enzymes. Longer term inflammations of pancreas may cause fibrosis (scar tissue) in the organ, therefore restricting the endocrine functions including insulin secretion, so acquired diabetes is another risk.
Obstruction of the bile duct and jaundice, leading to possible liver damage is another complication of pancreatitis.


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Accurate Human Skull Model for Educational Purpose
I want to buy a model of Human skull for education purpose. However, I really want a very accurate model and at a decent price. I got the info that many of the available skulls in the market are not accurate.  Can anyone suggest me one?
Also I want to know is there any regulatory body that certifies such
educational models regarding the accuracy etc.? If not then what is the way I can ensure that I am buying an accurate (or most accurate) model.

Which location are you enquiring for?

Product recommendation are often seen as not strong questions across the network, however the second part of your question is very interesting

Maybe you can find and print a 3d model near your location?

I am unable to understand why is location important, when I can order online

@gpuguy this is very difficult to answer without knowing: what models you have been told are inaccurate, how/why they are insufficiently accurate, what you need the model for, how accurate you need the model to be, what features you need to be accurate... There is never going to be the perfect skull model because everyone's skull is different and there is considerable natural variation in skull morphology, illustrative examples: http://www.understandingrace.org/images/482x270/science/early_class.jpg and http://news.nationalgeographic.com/news/bigphotos/images/070718-african-origin_big.jpg

This question appears to be off-topic because it is about product recommendations.

The best way to ensure you're getting an accurate skull, near as I can tell, is striking the "model" part of your question, and go straight for a real skull.
A cursory search revealed, for instance, Skulls Unlimited International, The Bone Room, and The Evolution Store although other providers probably exist as well.
A regulatory board for model skulls probably doesn't exist, given the apparent ease with which real skulls can be obtained and kept.

Yuck but +1 for new info


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Is there a type of amnesia that separately affects long-term memory?
Is there a medical condition that affects the long term memory, but leaves the short-term and working memories totally or fairly intact?

If I understand your question correctly, what you are describing is retrograde amnesia.  This is further subdivided into pure, focal and isolated.
From the site:

Typically, episodic memory is more severely affected than semantic memory, so that the patient may remember words and general knowledge (such as who their country’s leader is, how everyday objects work, colours, etc) but not specific events in their lives. Procedural memories (memory of skills, habits and how to perform everyday fucntions) are typically not affected at all.


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Why is clownfish attracted to actinia?
I heard that Actinia Equina normally eats what it can catch, but this clownfish here doesn't care much about that:
https://www.youtube.com/watch?v=Ughm4mnZ1ls
Since the actinia obviously can't hold the clownfish, clownfish does whatever it wants with actinia swimming all over it. Is the clownfish having some sort of fish fun, or is there a purpose behind this playing with actinia?

It's an example of SYMBIOSIS
Clownfishes(Amphiprion ocellaris) are never found without an anemone as they have this obligate association with them. Although they can survive without them, but studies show they are much more healthier with than without.
This association is more of a survival necessity. These anemones are actually toxic and the fish is resistance to it. If being attacked they will get inside these and the attacker might be stung with this actinotoxin.
Also,

The presence of an anemone is also essential to reproduction of the
  fishes: their eggs are laid beneath the oral disc overhang of the
  anemone, where they are tended by the male.

Source:

Wikipedia on Sea anemone
INTERACTIONS BETWEEN FISH AND SEA ANEMONES
Clownfish and its mutualism relationship with anemones