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Cleavage of RNA by restriction enzymes?
Six restriction enzymes discussed in Sequence-specific cleavage of RNA by Type II restriction enzymes (Murray et al.) have the ability to detect and cut RNA strands with that enzyme's recognition sequence.
As you know, restriction enzymes come from a system carried by some bacteria referred to as a restriction-modification system.
With this fact in mind while reading the paper above, I wondered how the bacteria carrying one of these six systems protects it's own RNA from restriction. Do the corresponding methyltranferase in each system methylate DNA as well as RNA? Would this not greatly sacrifice gene expression rates seeing as the methyltranferase surely cannot methylate all the RNA sequences being produced?
Perhaps I misunderstood the paper somehow. Could it be only in some circumstances outside the cell that these restriction enzymes have this unique ability?

When you take a look at Table 2 in the article, the activity to cleave RNA–DNA substrates is quite low. This means you should be careful to think that the enzymes actually cut RNA–DNA substrate in bacteria. The activity could be just artificial and may not happen physiologically.

This paper found that these enzymes recognize RNA:DNA heteroduplexes. Such duplexes are unlikely to be encountered in vivo. They are present when DNA is primed for replication, but these duplexes are relatively short and thus are less likely to randomly contain a recognition sequence. Furthermore, if the recognition sequence is found in the primer, the gDNA will be methylated specifically to protect it from degradation. RNA:DNA duplexes are also found during transcription, but they are also short and the gDNA would be methylated. Additionally, the transcription bubble where the heteroduplex forms is protected by RNA polymerase, which subsequently displaces the transcript from the gDNA as it leaves the elongating complex.
It's also important to note that this paper found that these enzymes don't cleave RNA:DNA as well as they do DNA:DNA duplexes and these results occurred under experimental conditions with relatively high concentrations of enzyme and substrate. The lower catalytic efficiency is likely due to lower binding affinity, which could be caused by:

presence of uracil in RNA (this was explicitly mentioned in the paper)
2'-OH presenting a steric barrier
helix shape (RNA tends to adopt an A-form helix)

Further into the paper they discuss the ability of these enzymes (specifically TaqI and HaeIII I believe) to also cleave RNA alone.

@CDB Duplex RNA? I shall read the paper later and delete my answer if it's incorrect.

Again, I could very easily be wrong, but that is my understanding of the paper. Feel free to correct me.

@CDB Are you referring to the paper by Molloy and Symons that was discussed in the introduction? TaqI and HaeIII were found to cleave the RNA strand in RNA:DNA heteroduplexes. I skimmed the paper and didn't find any mention of cleavage of ssRNA or RNA:RNA homoduplexes.

RNA:DNA heteroduplexes are encountered in vivo fairly regularly during replication. The RNA primer created at the beginning of DNA replication must be removed, and this is done with RNAse H, an enzyme that cleaves the RNA strand of RNA:DNA double helices. Though the abstract seems to indicate that these enzymes are cutting both RNA and DNA strands, so they would not be like RNAse H.

@user137 That's a good point about primers, but they are short and less likely to contain the recognition sequence and, if they did, the DNA strand would be methylated to prevent gDNA digestion.

@canadianer It would appear that you are correct. I must say though, this paper really confused me as to the results of the experiment. However, now I have another question. Perhaps I should post this as a whole new question, but I wonder why these restriction enzymes cannot cleave duplex RNA. I understand why uracil would present a problem, however HaeIII has a recognition sequence of GGCC, so nothing would really change with that... maybe something to do with the different RNA ribose backbone?

@CDB I don't know that they can't cleave dsRNA, it's just that this paper doesn't talk about it. I would expect that the 2'-OH presents a steric barrier since these enzymes evolved to recognize dsDNA. It seems from this paper that RNA:DNA duplexes lower the binding interaction so that, with RNA:RNA duplexes, the interaction may not be strong enough for efficient catalysis.

@CDB The shape of the helix may play a role as well, RNA double helices tend to favor the A form of the helix, while DNA double helices tend to favor the B form. The A form might be just different enough that the binding sites don't like it.

As to why they don't recognize RNA-DNA heteroduplexes (which are present during transcription, for example), I suspect that the methylation which protects bacterial genomic dsDNA (see the DNA modifying enzyme section of this Columbia University lecture for more info) also protects RNA-DNA hybrids, as the genomic DNA would still be methylated.
Note that most of the enzymes featured in the paper are listed by New England Biolabs as methylation sensitive (for example: AvaII, BanI, HinfI, TaqI).
@canadianer and @user137 provide a host of reasons that these restriction enzymes cannot cleave ds/ssRNA in the comments on canadianer's answer (different helix form, different interaction strengths between strands).

RNA-DNA heteroduplexes (which are present during transcription) are transient and are unlikely to be targeted by either RNAse-H or these restriction enzymes.

True, but it also doesn't take very long for a restriction endonuclease to cleave dsDNA

I just modified my comment. If such heteroduplexes really formed then the RNA will be first degraded by RNAse-H which is abundant. That, however does not happen

Yes, that was basically canadianer's answer. I wanted to provide additional insight based on bacterial self-methylation of its restriction enzyme recognition sites

@WYSIWYG Maybe this justification is clearer. Q: Why don't bacterial restriction enzymes degrade RNA? canadianer: That paper talks about RNA-DNA heteroduplexes, which are rare in vivo. me: Also, a RNA-DNA heteroduplex would likely not be recognized for the same reason that bacterial genomic DNA isn't recognized.

I imagine that the RNA:DNA duplex formed during transcription would be protected from  degradation by RNA polymerase. Assuming that the RNA doesn't reanneal to the template strand after it leaves RNAP, the duplex is only ~10 nts.


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The ermine's colour and geographical range
Ermines turn white during the winter, with only the tip of the tail remaining black. However, in the southern regions of the ermine's range it clearly doesn't get so white. Encyclopedia of Life says that:

However, in the Netherlands, the animals are often only partially white.

Ermine's range is clearly much more southern than the Netherlands:

Wikimedia, stoat range
So I was wondering where does the border go, north of which the ermines are completely white and south of which they remain more brown? I understand it necessarily is not a clear cut line, mountains have impact and subspecies may differ, but I would assume someone must have mapped this. Or is it just weather related, will a southern ermine turn white if the winter is really cold?
I'm just asking this out of curiosity, but the question is rather relevant. Ermine pelt has a long history as an important trade item, and the most valued pelts must have originated on the white side of this line.

The color change of Mustela erminea (more commonly known as ermine/stoat/short-tailed weasel) is both temperature-dependent and photoperiodic (depending on the length of the day). Bissonette 1943 and King and Moody 2012 show that the molting of the ermine happens as a result of the change in daylight lengths.  The King and Moody paper addresses the temperature dependence, using stoats (ermines) in New Zealand as an example:

In temperate countries such as New Zealand, stoats frequently fail to complete the full change to white. Such animals are not necessarily all caught in the process of moulting. If ambient temperature fell below the threshold for whitening of the lower part of the body but not the rest, new hair would grow white on the tail and flanks and brown on the head and back.

This is a chemical effect of lower temperature (King and Moody):

Experimental work has established that production of brown hair depends on melanocyte-stimulating hormone (MSH); in cold climates in autumn the synthesis of MSH by the pituitary is inhibited.

They don't provide a specific temperature at which the white color change does or doesn't occur, but I suspect that in nature it'd be very difficult to create a map since temperature is not constant year-to-year. There would most likely be an intermediate zone of partially white animals (both in terms of a mixture of brown and white animals, and a single animal that is not fully white).

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Double stranded nucleic acids are more 'durable' than single stranded nucleic acids?
I'm struggling with a question I've been asked.
"Why is double stranded genetic material more 'durable' than single stranded one?"
I know that double stranded genetic material is more stable due to multople strands. The single stranded isn't as stable as the double stranded since it lacks the second strand and therefore the bases are open.
Stable isn't the same as durable, and I've never heard in class that one is more durable than the other one. Did I miss something or is this just a mistake?

I'm having trouble understanding the question right now, but I do know that single stranded RNAs are more likely to be digested by RNAse enzymes than double stranded RNAs. From an error correction viewpoint, the second strand provides a template for fixing the first strand, so single stranded genomes would be more likely to mutate, or just get cut in 2.

A similar question has been asked in the past: http://biology.stackexchange.com/questions/23851/importance-of-double-helix-dna-structure

I don't know what one means by durable. For example it could be a simple question of stability as you mention, or is this in reference to DNA data storage where the double stranded nature can be used to identify or recover areas that are damaged over time.

I'm having troubles as you. I don't know what is meant. I asked my teacher today, and she said that the sentence is totally correct. She meant it like that. Furthermore, she added that it has nothing to do with stability. I don't find anything valueable in my book, nor in the internet. Any help is appreciated.

Do you mean durability against physical stress (shearing etc)?

This sounds pretty close. I would be happy to see an answer according to this idea.

I'm interpreting "durability" as the DNA's resistance to physical stress, such as shearing. The Bustamante lab at UC Berkeley does a lot of very cool single-molecule biophysics looking at forces involved in protein-protein interactions and protein-DNA interactions. This Bustamante et al. review paper, Single-molecule studies of DNA mechanics includes a look at the force required to break ssDNA and dsDNA:

Single molecules of dsDNA were broken
  with a receding water meniscus [26] at forces estimated
  to be 960 pN (correcting Young’s modulus doubles the
  published scission force of 480 pN). Short dsDNA molecules  pulled  with  an  AFM  tip  [27]  sustained  forces
  over 1700 pN.

pN = picoNewton
AFM = atomic force microscopy
dsDNA is more resistant to stretching/shearing forces because the double helix arrangement is "springy". I recommend giving the paper a read for more info. Very cool stuff.

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Is Araucaria fruit toxic?
I've had an Araucaria tree in my garden for more than 30 years.
Today a fruit fell off the tree. It looks just like this one:

I want to know if it is toxic?
Can I eat it? If so, how?

A very simple Google search should have told you that the seeds are edible.

Araucaria araucana is an evergreen. The pictured "fruit" is actually more of a cone (which I don't think you'd want to eat). However, the seeds are edible, and look like this:

Let the cone dry and it should open up.


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How to visualize the ECM?
Specifically, I'd like to look at changes in HA (hyaluronic acid) production. Most often you only see people staining the cell surface or removing cells from culture for fixation and then imaging. Does anyone know how to analyze the ECM (extracellular matrix) and proteoglycans that surround a cell if you're looking to see if a condition may be changing the way a cell remodels it's ECM? Is it even possible with some fluorescent tags?

Can you define some of those acronyms? I'm assuming ECM is extracellular matrix, and HA is hyalauronic acid, but I could be wrong, and I could have spelled hyalauronic wrong.

Yes, sorry---ECM = extracellular matrix, HA = hyaluronic acid.  I know that a typical hematoxylin and eosin stain (H & E) will pick up things that are negatively charged, such as HA, but how can you fix cells without disrupting the ECM?  Also, I was wondering if methods exist to analyze cell ECM production via fluorescence or some other method that utilizes a probe that I could observe with a microscope.

Interesting question. Afaik ECM is much more than just HA, it contains chondoitin and other glucoseamine related stuff as well. Some of them is capable to regulate immune reaction, for example chondroitin-sulfate can reduce TNFa production and so inflammation by arthritis.

http://www.naturebiotech.com.tw/Fluorescent%20ECM%20Proteins.pdf
I guess this study uses the same stuff: http://figshare.com/articles/Degradation_of_fluorescent_ECM_networks_by_SPARC/404676 it is probably possible, but I never worked with ECM.

There have got to be some antibodies against ECM components you could use for immunohistochemical labeling.

Different components of the ECM can be stained differently but since you asked about hyaluronic acid (HA) I'll limit my answer to its staining.
See this paper. They use Hyaluran Binding Protein (HABP) as a specific probe for HA.

Because HA has a very simple, conserved composition and is
  ubiquitously expressed in all animals that have a developed immune
  response, HA is not immunogenic. Therefore, there are no antibodies
  that specifically recognize HA, and traditional immunohistochemical
  methods of detection of HA are not possible. Fortunately, a very
  specific and tightly binding protein, the hyaluronan binding protein
  (HABP), which is composed of the HA binding domain with the link
  module from aggrecan, was isolated (Hascall and Heinegård 1974;
  Tengblad 1979) and adapted as an HA probe (Ripellino et al. 1985).
  HABP is now widely employed for specific detection of HA.

Biotin tagged HABP can be used for IHC based visualization procedures.

The book "Basic Histology" by Junqueira and Carneiro acknowledge the problem in histologic fixation of ground substance. They recommend freeze drying in liquid nitrogen and  then removing water by high vacuum at a temperature of -30 celcius, which will cause sublimation (ice-->vapor). Then fixing the sample with a nonpolar solvent. Afterwards you can use stains like PAS technic.
I've never done this, I'm just copying from the book. If you already happen to have liquid nitrogen, high vacuum, and PAS in your lab this might be cheaper than HABP.


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T7 vs pBAD promoter strength
How do pBAD and T7 promoter strengths compare when pBAD is induced under conditions which would lead to its highest strength? Are there any papers that compare the two inducible promoter systems?

The exact numbers depend on the protein.
In my hands, I would say between the pAraBAD and a pLac-T5 you can expect some fold improvement and pAraBAD and a pT7 promoters you can expect about an order of magnitude… but there are two big caveats.
First, pET and other T7 driven plasmids do not work in K-12 strains (without the pTARA) so BL21 is generally used. BL21 is much better generally than K-12 strains (more primary metabolites cf. omics paper) for a lot of things including protein expression. The chaperone balance is difference, so you will get differences from that too —if you have used the TAKARA plasmid team you will have notice how quirky protein expression optimisation can be.
Second, if your protein has a cofactor you have a major problem. FeS clusters, PLP, heme or even O2 (for maturation of GFP, say) become rate limiting and overexpressing the protein can make it highly toxic and you might be in a bigger pickle than with a lower level promoter. In my thesis, I added pyridoxine to a pBAD expression, because it gave an improvement.
Footnote: If the expression levels are really bad, changing promoter might not be that great as the assumption of linearity might not hold.
If heterologous and not codon optimised, consider using pRARE.
If insoluble, consider using ethanol shock and the TAKARA chaperon plasmid team.
If oxygen sensitive, alas, doing expression and purification anaerobically.

thanks for taking a stab at this old question... I know that it may be difficult, but do you think you could add some links/references to some of the details you mention in your answer? We always appreciate references/links on BiologySE - and it will definitely improve the strength of your answer. Thanks!

The best reference I could find is a book chapter (available here as a .pdf) from a book on optimizing the expression of membrane proteins that argues for T7. Although they don't appear to reference a source for that specific claim, some of the references close by could be helpful. It seems as though this applies in general, not just to membrane proteins. They bring up limitations of the araBAD system as well:

However, careful studies of the araBAD promoter by Siegele et al. [20] and Giacalone et al. [21] both agreed that at subsaturating levels of l- arabinose, protein expression cultures contain a mixed population with only some of the cells expressing protein. In addition, the potential for protein overexpression is generally lower when a pBAD vector is compared to T7-mediated expression from a pET construct.

In general, T7 is stronger in producing mRNA. However, the final amount of protein produced depends on other factors like protein solubility, stability, and toxicity.
Here, https://microbialcellfactories.biomedcentral.com/articles/10.1186/1475-2859-12-26, is a study that compares T7 and other promoters for the production of few different proteins.


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Are there yearly variations in HIOMT (HydroxyIndole-O-MethylTransferase) availability?
I'm reading a booklet on melatonin published in 1996, titled "Melatonin and the Biological Clock". And see the following statement:

HIOMT (HydroxyIndole-O-MethylTransferase), one of enzymes of melatonin
  synthesis, rises and falls in an annual rhythm, with troughs in March
  and October and peaks in January and July.

Seeing how HIOMT is the last methyltransferase involved in Melatonin synthesis in humans, I'm interested in learning if there's indeed a yearly variation in this MT production in humans, and if it is regulated by genetics or photoperiod duration.
Thank you for your input!

usually the author of a book gives references for all quoted statements.

This isn't really a complete answer but I can't fit it into a comment.
I've found that there is a large body of literature on seasonality of melatonin levels in various vertebrates, particularly livestock, because of its interaction with breeding patterns. Similar studies in humans are however, difficult to find, but the review paper cited below looks at a link between seasonal variations in melatonin levels and seasonal variations in immune system functions. It cites a few references that might be worth following up.

Srinivasan, V. et al. (2008) Immunomodulation by melatonin: Its significance for seasonally occurring diseases. Neuroimmunomodulation 15: 93-101 DOI: 10.1159/000148191
Abstract
Melatonin is not only synthesized by the pineal gland but also in many other organs and tissues of the body, particularly by lymphoid organs such as the bone marrow, thymus and lymphocytes. Melatonin participates in various functions of the body, among which its immunomodulatory role has assumed considerable significance in recent years. Melatonin has been shown to be involved in the regulation of both cellular and humoral immunity. Melatonin not only stimulates the production of natural killer cells, monocytes and leukocytes, but also alters the balance of T helper (Th)-1 and Th-2 cells mainly towards Th-1 responses and increas- es the production of relevant cytokines such as interleukin (IL)-2, IL-6, IL-12 and interferon-γ. The regulatory function of melatonin on immune mechanisms is seasonally dependent. This fact may in part account for the cyclic pattern of symptom expression shown by certain infectious diseases, which become more pronounced at particular times of the year. Moreover, melatonin-induced seasonal changes in immune function have also been implicated in the pathogenesis of seasonal affective disorder and rheumatoid arthritis. The clinical significance of the seasonally changing immunomodulatory role of melatonin is discussed in this review.


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Does human digestive system benefit from eating same kind of food consistently?
Here's the reason why I'm asking: I've heard that it takes some time for pets(cats/dogs) to adjust to a different dry feed, where the new feed has to be mixed with the old one, slowly replacing the old one. I'm wandering if this advice has any truth in it, and if so, does this apply to humans as well?
For example, a cat eats the same kind of food for months at a time, but humans vary their diet  much more dramatically. Are there any benefits to eating the same kind of food over extended period of time? I'm interested in knowing if the digestive system/symbiotic bacteria in the gut adapts to the food, resulting in better digestion/absorption of nutrients.
Thank you for your input!

I think it would depend on the benefits you are looking for.
If you ate the same thing everyday, it's possible your intestinal flora, and the rest of your GI tract would optimize themselves for maximal nutritional extraction. It is known that the flora in you GI do affect nutrition. I recall reading about obese patients who had gut-bacteria which made more nutrients available.
However, if you were in an environment where your diet could change unexpectedly, this optimization could actually be detrimental, since you wouldn't be ready to switch foods when necessary.

well they do adpat to how food is prepared.  https://news.harvard.edu/gazette/story/2019/10/study-finds-gut-microbes-adapt-quickly-to-changes-in-food-preparation/

When I first clicked that link it didn't lead to article. After hunting it down, and reposting the link, I realize now it works! That's a strange link.

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How is propagation of action potentials terminated once the "message" has been sent/received?
I'm thinking about neurons in the brain that are used for "thinking". As I read about action potentials, I see that an Axon is connected to a Dendrite of a neighboring cell and that there are neurotransmitters involved in the signal propagation from cell to cell.
I'm interested in learning how action potential propagation gets terminated. Let's say a message from the brain region A to brain region B has been delivered through action potentials.

How does the region B know not to "route" the action potential further down the chain of neurons?
How does the region A know that the message has been sent, to stop sending more messages?

Note that the same mechanism is valid for any neuronal type, not only those "used for thinking"

related question: http://biology.stackexchange.com/questions/3831/what-protocol-does-the-nervous-system-use

Action potentials do not travel from neuron to neuron. They travel from the body of the neuron to the end of the axon, and then stop because they've reached the physical end of the cell. To transmit a message from one neuron to another, we need to use neurotransmitters.

I'm not a Neurologist or Neuroscientist, so I can only share what I know about the subject!
TL:DR

Cease sensation
Neuronal recovery period prevents further signaling
Neurotransmitter inhibition prevents ligands from binding to receptors (usually Feedback mechanisms)
Neuronal hyperpolarization prevents signaling
Creation of signal (can be perceived as cessation of signal)

It's important to note, first and foremost, that a cessation of stimulation will result in a cessation of the propagation. This is one of the simplest ways that neurons can stop firing - you're no longer touching, tasting, hearing, seeing, smelling, or thinking of what you were previously.
Because of the way Neurons are constructed, and as far as I'm aware, signal propagation will persist as far down the line as possible. I don't believe there's a discrete point where an Axon will simply not send a signal once a dendrite on the same neuron has received the order.
What can happen is that a competing signal has exhausted the propagation potential for the next neuron in the chain (the neuron is still recovering), or a competing signal has released inhibitors that prevents the neurotransmitters from another Axon from affecting the target neuron. Competing signals is particularly common in the neurons of your eye, since the Amacrine cells fire depending on the competitive input of the Cones if I'm remembering everything correctly.

Then there are also substances like Benzodiazepines which block propagation by opening Cl- channels and hyperpolarizing a neuron's membrane, which prevents it from firing. Only a subset of GABA receptors have sites for benzodiazepines, but it's one more way that signals will cease.
Another way to cease a signal, or at least the perception of a signal, is to actually induce propagation. The Rods in your eyes only fire below a certain lumination threshold. What you perceive as light is them not firing, and darkness is what happens when Rods fire at full strength.
I'm not the last word on neurobiology, but I hope I've given you a good start!

You may want to add that GABAergic signalling is physiologically very important in the brain, without need to bring up benzodiazepines. GABAergic and glycinergic neurons in the brain (plenty of them) secrete GABA or glycine and will hyperpolarize their targets by acting on GABA receptors. The amacrine cells you talk about are a very good example of GABAergic or glycinergic neurons.

The neuron doesn't need to know "not to "route"" an AP because this is not necessarily it's default response.
Upon receiving an AP from another neuron (via either an a chemical synapse or a gap junction) the next neuron receives a signal. The nature of this signal depends on the nature of the connection between the two neurons - the proteins and neurotransmitters involved - and is therefore context specific. Also context specific is the sensitivity of the receiving cell. If the connection is strong and activating and the receiving neuron is sensitive, then it will fire and the AP would be "routed" as in your question.
However, there are other possibilities. For instance, the connection may too weak, such that it can only activate the receiving neuron given sustained activity, or in conjunction with another neuron (in effect forming an AND logic gate). The connection may also be inhibitory - meaning that it deactivates, rather than activates the neurons.
Analogies between neurons and electronic systems are useful, but it's important to remember just how drastic a simplification they are. Individual synapses are complex. Cells have thousands of them, and a good deal of other moving parts besides.

Nice answer! What is sustained activity, is it a pulse train(multiple spikes) on top of tonic activity, or tonic activity alone?

I just came across this answer when I was answering another related question. Although this is closed there is a strong claim from the accepted answer which needs to be toned down.
Cessation of stimulation does not always mean cessation of propagation. Once an action potential(AP) is fired it does not necessarily stop its propagation in the next cell. Also cells can make synapses onto themselves which can cause further AP firing without stimulation.


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Does increased calorie intake cause increase in libido in humans?
I'm interested in the effect of increased calorie intake on sex hormones and chosen mating strategy in humans.
I'm aware that humans have a dual mating strategy - somewhere between pair bond and casual mating. There are a number of physical measures to indicate this - such as sexual dismorphism between male and female, sperm counts and tested size, as well as age of puberty of females.
I've recently listened to a podcast that suggested that long term increased calorie intake causes differences between two mating strategies in case of apes. An example given was that gibbon ape filled their ecological niche and has no predators. Their population size is controlled by food supply. This makes food scarce and gibbons are more monogamous with more paternal investment (to teach offspring to forage)
At the same time another kind of savanna dwelling ape has natural predators limiting population and thus having more food supply. This ape has more offspring and less paternal investment and more promiscuity. It is as if they are more sexually active.
I'm interested if there is any truth to this and if this is also applicable to humans. Does increased calorie intake long term increases libido, while caloric restrictions reduce it?

The podcast sounds interesting. Could you supply the source?

@James I believe this is the podcast in question:  https://www.youtube.com/watch?v=D9isrAUsQjA


text:
DNA content in plant seeds vs. fruit flesh
Is there a publication comparing DNA yield and/or PCR-amplifiability after extraction from fruit flesh (like apples, oranges, cherries etc) in comparison to seeds of the same fruits?
I would prefer a reference, but your unpublished experience is also interesting to me.

A quick guess is that it will be easier to extract DNA (without inhibitors) from fresh material, since the seeds are made to survive. This can cause problems in the preparation.

Cell walls are a major problem for (sequencing length) DNA extraction. You will normally have more usable yield from the fruit flesh than from hard seeds. Another problem might be essential oil in the fruit flesh, though.

It depends on the seed and fruit you're talking about.
The amount of DNA in your crushed up sample of plant matter depends on only one thing--how many cells are in your sample. Look at this diagram of a kernel of corn (U of Indiana):

There are different cell densities in each area--in the endosperm, the cells can be huge (and therefore have a lower density of DNA when compared with the embryo).
Let's look at a stained mustard seed (U of London):

As you can see, the cells here are very dense. More dense means more DNA per unit sample.
As far as fruit is concerned, the same rule of thumb applies. Verner, 1938 shows some cool apple tissue histology that might give you an idea of cell density in fruit tissue (again, it will be different in different fruits--search for "fruitname histology" if you're interested).
However, now that we've talked about density, we need to actually think about getting the DNA out. The extraction process is actually much more important in terms of your final yield.
Many plant seeds contain polyphenolics, which can cause DNA degradation. This protocol (Cornell U) details many of the possible shortcomings:

These compounds have also been reported to cause difficulty in DNA purification in other plant species; polysaccharides (Murray and Thompson, 1980; Fang et al., 1992); polyphenolic compounds (Katterman and Shattuck, 1983; Couch and Fritz, 1990; Howland et al. 1991; Collins and Symons, 1992); and sticky and resinous materials (Webb and Knapp, 1990).

These contaminants can degrade DNA, but also render it unusable in PCR amplification and endonuclease digestion (Kim et al. 1997, Cornell U, EPICENTRE Biotechnologies).
Overall, there are definitely species-specific differences in fruit/seed plant DNA content. Practically, however, the most important factor in DNA yield and viability for future experimentation is sample purity and contamination. Specific fruits and seeds may contain one or more of the above contaminants, so the answer to "Seeds or fruits?" definitely depends on the species of plant you're working with.


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What class of histone deacetylase (HDAC) inhibitor is sodium valproate (VPA)?
VPA is a known HDAC inhibitor. But I cannot find what class it is.
What class is it?
And is there any method of finding an answer better than floundering with Google?

This is explained at the WP page for HDAC. There are five classes:

hydroxamic acids (or hydroxamates), such as trichostatin A
cyclic tetrapeptides (such as trapoxin B), and the depsipeptides
benzamides
electrophilic ketones
the aliphatic acid compounds such as phenylbutyrate and valproic acid

and valproate is in the final class, aliphatic acids.


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Which are mobile and immobile elements in plants?
I am confused with this element or nutrient classification in the plants, since some authors set elements like $\ce{S}$ and $\ce{Ni}$ as mobile and other as immobile elements (Citation 1, 2, 3, 4, 5). Then, I would like to know if there is a fixed and official classification.
I found a classification only for those elements:
Mobile: $\ce{N}$, $\ce{Mg}$, $\ce{P}$, $\ce{S}$, $\ce{K}$, $\ce{Ni}$
Immobile: $\ce{B}$, $\ce{Ca}$, $\ce{Mn}$, $\ce{Fe}$, $\ce{Co}$, $\ce{Cu}$, $\ce{Zn}$.
And what about the rest of elements like $\ce{Sr}$, $\ce{Mo}$, $\ce{Ba}$, $\ce{Pb}$, etc?

Can you cite a source for the classification you provided?

Here the citations, I couldn't put those in my question because at the moment my profile doesn't accept more than two links.
[1]: http://www.gettextbooks.com/isbn/9780824759049
[2]: http://msue.anr.msu.edu/news/knowing_nutrient_mobility_is_helpful_in_diagnosing_plant_nutrient_deficienc
[3]: http://broome.soil.ncsu.edu/ssc012/Lecture/topic17.html
[4]: http://lee.ifas.ufl.edu/Hort/Videos_and_Powerpoints/Presentation2013.pdf
[5]: http://nrcca.cals.cornell.edu/soilFertilityCA/CA1/CA1_print.html

What does it mean for an element to be mobile or immobile in plants?
Generally speaking, mobile elements are those that can be moved from older to newer tissue in the plant, while immobile ones cannot be.  For example, calcium is incorporated into the cell wall, so it is immobile; it cannot be relocated later.
Plants with a deficiency of mobile elements (e.g. nitrogen) will exhibit damage to older tissues as the nutrients are moved to new growth.  Conversely, plants lacking immobile elements (e.g. calcium) will exhibit stunted new growth while the older tissues stay healthy.  Some elements (e.g. sulphur) fall somewhere between these two extremes.
To illustrate this concept, here is a plant with nitrogen deficiency (source).  Notice how the older leaves are dying while the newer leaves are relatively normal.

Is there an official list of mobile and immobile elements?
No.  You will probably have to survey the literature yourself to come up with such a list.
Why are some elements not mentioned in the sources?
Elements like Pb or Sr do not appear in either list because plants generally do not use these elements at all.  Only a few elements are present in any appreciable quantity in plants.  The main elements used are C, H, O, P, K, N, S, Ca, Fe, and Mg. Additionally, some other elements such as Cu, Mo, Al, and Cl are used in trace amounts as enzymatic cofactors.  Si is used for structural purposes in some plants.
However, even for "useless" elements, it is possible to study how these elements are absorbed transported through a given plant.  For instance, Rediske and Selders (1953) studied the absorption of strontium by bean plants using radioactive labeling, and concluded that the element was not relocated once absorbed by the plant.  This would make it an immobile element.
References

Feldman, Lewis J. (23 February 2015). Water Relations, Mineral Nutrition, Fruit Development (YouTube). Biology 1B. UC Berkeley. At 32:20.
Lewis, Helen (9 January 2012). "Mobile vs Immobile Nutrients". Mastering Horticulture.
Rediske, J. H. and Selders, A. A. (October 1953). "The Absorption and Translocation of Strontium by Plants". Plant Physiology 28 (4): 594–605. PMC 540423.


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Hair loss in a nuclear submarine?
Biologically, how prevalent is hair loss on a nuclear submarine? How can prolonged exposure to radiation levels typically present on a nuclear sub affect a person, say over a year or even more?

http://nnsa.energy.gov/sites/default/files/nnsa/02-12-multiplefiles/NT-11-2%20FINAL.pdf

@canadianer Actually that is one of the links that I have mentioned in the answer I put up.

I did check your post to see if you had included it but apparently I missed it!

Nice question but wonder if better served In Physics stack?

The question is not clear. Can you improve it by providing more context and writing out what you are asking? Specifically, are you talking about nuclear submarines?

I knew a man in one of my chemistry classes who served on a nuclear submarine and worked with the reactor. He not only still had a full head of hair but told me that his radiation exposure tag picked up more radiation in a day on the beach than in 6 months next to the reactor. Obviously it's an anecdote, but I generally think people are too afraid of radiation.

Just read the pdf @canadianer linked, and it says average exposure per person per year is 0.022REM, wikipedia says people should be exposed to less than 100mREM per year, which is about 5 times more than what the naval personnel are exposed too. I may have missed something, I only spent 90 seconds to find these numbers.

If the question is related to exposure to radiation in a Nuclear submarine then the answer is valid for radiation exposure irrespective of the place.
As you are aware there are many effects of radiation. Some of them are.

Nausea and vomiting
Diarrhea
Skin burns (skin reddening)
Weakness
Lethargy and fatigue
Loss of appetite (anorexia)
Fainting
Dehydration
Inflammation of tissues (swelling, redness or tenderness)
Hemorrhages under the skin
Bleeding from your nose, gums or mouth
Anemia
Hair loss (usually from just the scalp)
Decrease in platelets (reference)

Of course there is no safe quantity of radiation that has been quantified (reference) and there are personal anecdotes by submarine officers about first hand problems they faced due to radiation (reference). However, since this is a career you chose, you can be happy that the amount of radiation that you would be exposed to has decreased over the years (reference). Since you are interested in the biological aspect of what happens in your body due to radiation, I quote

When cells -- and what lies within them -- get exposed to radiation,
  components of DNA and critical proteins within the cell get all jazzed
  up (ionized), meaning that the electrons with our atoms get kicked
  out, causing the DNA strands to break and the proteins to cramp up
  (denature).
Ionizing Radiation:

Leads to the production of free radicals
Breaks critical chemical bonds
Leads to changes in cellular structure within irradiated cells
Damages vital molecules, such as DNA, RNA, and other regulatory
  proteins

Because our cells are mostly water, this ionizing radiation breaking
  H$_2$0 down is harmful to free radicals (H$^+$ and OH$^-$). While cells are
  damaged by free radicals all the time, they normally repair
  themselves, keeping the body healthy. However, high doses of radiation
  can damage the cell's ability to repair itself, and then all hell
  breaks loose.
This shakes things up all over the body.
Let's do a head-to-toe walk-through to investigate how high doses of
  radiation can damage the human body.
BRAIN: Nerve cells (neurons) and brain blood vessels can die, leading to seizures.
EYES: Radiation exposure increases the risk of cataracts.
THYROID: When a nuclear reactor malfunctions, radioactive iodine (I-131) can be released into the atmosphere (this is one of the
  particles that hangs out in a "radioactive plume"). The thyroid is
  very sensitive to the effects of I-131 (in fact, I-131's affinity for
  the thyroid is used therapeutically to specifically attract radiation
  to the thyroid in order to treat thyroid cancer and overactive
  thyroid). When a healthy thyroid is exposed to I-131, it can lead to
  decreased thyroid function and, over time, thyroid cancer.
LUNGS: When you breathe in invisible nuclear fallout particles, it can lead to lung cancer down the road.
HEART: High doses of radiation can damage the cells in the blood vessels that feed the heart, reducing cardiac function.
GI TRACT: Sensitive cells in the intestinal lining can be damaged, leading to nausea, bloody vomiting, and bloody diarrhea.
REPRODUCTIVE ORGANS: Rapidly dividing cells (eggs and sperm) in the ovaries and testes can die, leading to sterility.
SKIN: Rapidly dividing skin cells can be damaged, leading to skin lesions and burn.
LYMPHATIC SYSTEM: Rapidly dividing lymphatic cells die and damaged bone marrow may have trouble replenishing these immune-boosting cells,
  increasing the risk of infection (reference).

Many jobs have occupational diseases connected with it so I would say don't worry about it too much, enjoy your job and keep your fingers off the firing mechanism.

Nice answer. While the effects of a given are arguably kinda unknown, it would still be interesting to have some measurements (in Bequerel/Curries, in Greys or even more useful in Sievert/rems) or radioactivity in submarine.

@Remi.b Don't recall finding any but could exist.


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Influence of eating at late night on sleep
I have often heard the saying that one shouldn't eat a mountain of food because blood will go to the stomach and it'll be difficult to sleep well because the stomach can't rest at night.
I see that the blood goes to the stomach when you eat something to digest the food. Have any studies been done on whether it does actually affect the quality of sleeping?

Who exactly is the 'you' here?  I do (though I don't eat a mountain of food at any time); other people may or may not.  Depends on the individual.

I do not have any scientific information about your question but, I want to share my experience, last night I ate a cup of soup an hour before I slept and I had several nightmares during night and when I woke up, I did not felt good

According to Crispim et al 2011, caloric intake late at night is correlated negatively with sleep quality:

We conclude that food intake during the nocturnal period is correlated with negative effects on the sleep quality of healthy individuals. Indeed, food intake near the sleeping period (dinner and late night snack) was negatively associated with sleep quality variables.

The paper is an interesting read. Here's their figure 1 which shows the correlation between sleep latency (how long it takes to fall asleep) and nocturnal caloric intake:

Thick line: men
Thin line: women
Basically, it shows that people who eat more at night take longer to fall asleep, and other results show that it's also correlated negatively with other sleep quality indicators.

Really interesting, I would never have expected that huge difference between men and women


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How scientists can be confident that human embryo tail is really a tail?
From Wikipedia:

Human embryos have a tail that measures about one-sixth of the size of the embryo itself. As the embryo develops into a fetus, the tail is absorbed by the growing body.

How are we sure that it is a real tail and is not a superficial resemblance of something else?
I ask this because some creationist guy challenged me in this regard.

I just want to ask one thing: what else could it (tail-like thing) be, another hand or another leg?

It is an extension of the vertebrae. Isn't that a good reason?

@user40602 If you consider your question has been answered, you can check your favourite answer.

We can be sure it's a tail because it is an extension of the vertebrae, and we define "tail" as an extension of the vertebrae, among other things.

tail
tāl/
noun: tail; plural noun: tails

the hindmost part of an animal, especially when prolonged beyond the rest of the body, such as the flexible extension of the backbone in a vertebrate, the feathers at the hind end of a bird, or a terminal appendage in an insect.

Emphasis mine. Source: www.oxforddictionaries.com

Some mention of the identical embryology would make this better, the human tail is not just a tail because of its location. not all tails are the same.  the human tail is homologous with other vertebrate tails.

Well, what would you call it? Have a look at the images below (source):

If you would call what other species have tails, then the human one should also be called so. After all, they are extremely similar (the last image, k, is human):

a Echidna or spiny anteater (Tachyglossus aculeatus).
  Because of the extreme rarity of monotreme material we
  were only able to obtain this embryo, which is younger than the
  tailbud stage. b Brush-tailed possum (Trichosurus vulpecula). c
  Eastern Australian native “cat” (Dasyurus quoll). d Domestic cat*
  (Felis catus). e Domestic dog (Canis familiaris). f Domestic sheep
  (Ovis aries). g Scaly anteater (Manis javanica). h Rat (Rattus norvegicus).
  i Rabbit (Oryctolagus cuniculus). j Hedgehog (Erinaceus
  europaeus). k Human (Homo sapiens).

The above image was taken from M.K. RIchardson et. al.,Anat Embryol (1997) 196:91–106 (a PDF can be found here)

FUN FACT
Let's start with a fun fact!
In some rare cases, humans can get born with a tail. These tails can then be removed by surgical procedure. Such procedure are quite simple and are a relatively old procedure (see Speigelmann et al. 1985).
What is a tail?

The tail is the section at the rear end of an animal's body [..]. It is the part of the body that corresponds roughly to the sacrum and coccyx in mammals, reptiles, and birds

Source: Wikipedia
Sacrum and Coccyx are the last parts of the vertebral column. A tail is therefore, just an extension of the vertebral column.
How does it look like in humans?

Is it really a tail that we see?
Yes! Human embryo have been dissected and histologic analyses were performed. There are no doubt, it is a tail!
See Dao and Netski (1984), Belzberg et al. (1991) and Fallon and Simandi (2005) for further description and evidence.


text:
Does copper exacerbate wounds?
There is a three edged stiletto (weapon, not shoe) with a triangular cross-section that is often touted as being "extra dangerous" because of the triangular puncture it makes, and its copper construction. The claim is that the copper inclusion causes something colloquially referred to as "blood poisoning."
Is there any basis to the idea that a copper blade would cause some kind of secondary toxic effect?

Can you post a link either to the weapon itself or to some other source discussing its "extra dangerousness"? I've found some triple-edged stilettos, but nothing made of copper.

That's the trouble, it's all been anecdotal. I've seen these copper stilettos sold at fairs and whatnot, some of which even by otherwise reputable vendors, but I can't find any info online.

Copper is a micronutrient and is essential for human body. See here

Meaning it is toxic only at levels the body can't handle and its deficiency can cause some health issues

Ironically, copper and copper-containing alloys are also known to have antimicrobial properties (https://en.wikipedia.org/wiki/Antimicrobial_properties_of_copper), meaning that it's conceivable that you'd be less likely to get blood poisoning from a copper blade.

Excess copper in the body can be toxic but I'm not sure a copper blade would be especially toxic unless it was coated with something else or it remained in the wound. Copper can be acutely toxic when ingested, or chronically over a long period of exposure (like lead), but is more often associated with a failure in copper excretion. Since the body has ways of dealing with excess copper, I just don't see much merit in the super-toxic copper blade, unless it is designed to break off in the target.

I also think, that the copper is much less of a problem than a deep wound by such a weapon.


text:
What is the word for being inured to loss of biological diversity?
In the title.  The word has been coined relatively recently for the phenomenon of getting used to loss of diversity because of the gradual rate it happens at.  For example, not finding it strange that there are far fewer invertebrates around now than there were 30 years ago - car windscreens in the summer were covered in dead insects, whereas now that rarely happens.  Both time points are noticeably distinct in biological richness, but we quickly get used to the state of things now.  I can't find it on Google!

biocide conditioning/acculturation/habituation. Naturacidal ambivalence.

I'm voting to close this question as off-topic because it is a language question, rather than a question about a problem in biology.

@David It's a question about terminology within ecology. I'd say that fits in Biology

Actually this is a question about the word used to describe a psychological response to a biological phenomenon.  I have to agree that this doesn't seem to belong here — maybe Psychology & Neuroscience? —— Please take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Does stronger reaction to vaccine (fever, days of nausea) mean that an immune system would have reacted the same to the virus?
I have heard that the real danger of Covid-19 is the strong immune response. Is it more likely that a person's immune system would have reacted dangerously to the virus?

Please give a source for the claim rather than ‘I have heard’. Thank you.

These studies suggest that young people have stronger reactions to the vaccines than older people. So your hypothesis is contradictory to the studies that we have for the moment:
img 1
img 2


text:
Does minimizing hunger maximize weight gain?
Due to the "obesity epidemic," there is a lot of focus on the causes of weight gain. We typically talk about strategies to cause weight loss, but what about strategies to minimize/maximize hunger?
Is there a way that hunger can be cured by eating a certain distribution of calories as a function of time? For example, if I have 2000 calories of food and I can eat it at any time, how should I spread out eating it over a day to maximize/minimize weight gain?  What would be the physical differences for me if I ate a small snack every minute of the day versus eating all 2000 calories at once?
Likewise what about weight gain? Would it be easier to gain weight if someone waits until they are very hungry and overeats during that hunger window, or if they eat over a wider window?

No, there are hunger free "diets" that you will safely lose weight on. An analogy might be that minimizing spending does not get you out of poverty.

What I mean is, given you will eat the same amount of food in a day, how will eating it in different time-frames affect your weight loss/gain

The digestive system absorbs food 24/7, time of day of consumption has little effect on absorption,   the main difference is day and night. your body is super efficient at absorbing calories, they go straight into the blood, . The excess sugar also is stored as fat efficiently at all times that your blood is flowing, day/night cycles are the main variant, except that night time is only a pause, you can't circumvent digestion based on times consumed.

Part of the obesity problem is that people eat recreationally, rather than just when they're hungry.  Or from cultural expectations: do you (if mainstream American) really stop eating Thanksgiving dinner when you stop being hungry?

Regarding the question in your title: minimizing hunger could be synonymous with leptin responsiveness. For example, leptin deficient or leptin resistant mice are known to become extremely obese - this is because leptin, the 'satiety' hormone, not only signals for you to stop eating, it also elevates the body's energy expenditure and stimulates thermogenesis.
An interesting strategy I've heard, though I don't know how effective it is, is increasing leptin sensitivity through the composition of your diet.
Another interesting element is that hunger, which is mediated by hormones such as ghrelin, decrease energy expenditure by multiple metabolic methods. So being hungry isn't always conducive to losing weight.
I believe most of the answer to your questions relies in these concepts. If you're talking about food distribution throughout your day, schedule it so that you're not very hungry for prolonged periods. Same with food type, eat foods that satiate for longer periods of time, unlike foods such as white rice.
If you want to read up a bit more, I suggest looking into AMPK, and the role these hormones and food composition has on it. AMPK reading


text:
E.O. Wilson on sociobiology and the origin of morality
Somewhere in E.O Wilson's writing, he discusses how human values are rooted in our nature as a specific kind of animal. He argues that we have an identifiable optimal living place -- a grove at the top of a hill, with surrounding grassland give an area of clear view, overlooking a body of water. He then goes on to further make this case by imagining that naked mole rats have risen to intelligence. He pens a speech that such a being might give on some patriotic holiday. And boy howdy, it sure does not sound like any epideictic speech you could imagine a human giving. The use of shit as a metaphor for sustenance alone is sufficiently jarring, but there were a bunch more, all firmly anchored in aspects of mole rat biology and social structure that differ from ours.
I would like to cite and quote this passage. I thought this was either in Biophilia or Consilience, but I have not been able to find it in either book, or in a bunch of other searches via google scholar, and through my own books and ebooks of his.
Does this sound familiar to anyone? Can you point me toward where I would find it?

@com.prehensible If andrewH could quote the section verbatim, I'm sure it would be easy for him to find the relevant text.
To andrewH: I have not actually read any of EO Wilson's work, although I'm familiar with it from secondary sources. Have you looked in 'Sociobiology: The New Synthesis' or 'On Human Nature'?

It could also be from 'The Biophilia Hypothesis.' But I don't know at all for sure.

If human values are rooted in our nature, why don't we all have the same values?

@Eff it would be good to state the source of the information and the logic of the metaphor, not confuse readers with garden-fence English: we can't hear the vocal tone of the theatrically phrased question, without confusion. Indian, Australian and 2nd language english people don't understand Boy Howdy and epideictic! most of us have to fetch a dictionary. E O Wilson doesn't start his written phrases with And! E O Wilson is kind and if you address him a written request, he will respond to you in writing through is secretary or by mail / email. My friend wrote to him and had a signed letter.

@com.prehensible That's fair. And I think it's a good idea to email EO Wilson.

1930's professors are happy with handwritten mail, they may be diligent with email, it's hit and miss.

I think its from "Genesis, the deep origin of societies"

@jamesqf Humans are a complicated mix of instinct and reflection.  Wilson isn't trying to claim that everything you think and believe is rooted solely in your evolutionary history.  What he states in this arena is actually rather non-controversial, that human values are founded on evolutionary contingencies that would differ if we had emerged via a different natural history.  Let's take, for example, a taboo against killing small children.  You could claim that certain societies do kill small children but they always have to justify the act, implying that this is something that naturally makes

@jamesqf Humans uncomfortable.  This would not necessarily be the case in a society of intelligent pelicans, who always lay more eggs than they support and kill at least one child from almost every litter.  Such a society might consider it natural to have a minimum age to be worthy of moral consideration, whereas we would find such a thing abhorrent.  While our beliefs and social structures are heavily culturally influenced, even those cultural influences are ultimately contingent on our biology.

@Jeremiah: "...whereas we would find such a thing abhorrent." But not all humans do, or have historically.  E.g. the classical practice of exposing unwanted infants, or Victorian foundling homes.  And at the other extreme, we have the "pro-life" types who want to push that minimum age to before birth, even to conception, and others who find that abhorrent.

@jamesqf the thing about that is that we are aware of these practice because of justifications put in writing by the cultures that did these things because they were aware of the need for justification. This is something that is a moral hazard for us at all points in history. Things that have no moral dimension need no justification. What we even decide to pay attention to in the first place is driven by evolutionary contingencies. Human birth rates and reproductive strategies prime us to raise the killing of offspring as a moral issue in the first place.

@Jeremiah: Granted, I'm not an expert in the writings of ancient cultures (or even of Victorian England), but I don't know of them because of attempts to justify them, but simply because they were mentioned in passing as ordinary aspects of the culture.  I could also, given room enough and time, cite many more examples of things considered moral by one group, highly immoral by another.  For a current example, consider marijuana use in the US today.

@jamesfq but it wasn’t just a normal and accepted part of these societies. In Ancient Greece and Rome the practice of infanticide was seen as evil and barbarous, which is why they did it through exposure, to allay their own guilt by “putting it in the hands of the gods”. The same reason was behind infanticide by exposure in the Christian Middle Ages. In Victorian England infanticide was an unfortunate consequence of support being torn away from poor women, forcing them to do what they had to to survive but women were put on trial for this and could only escape litigation by claiming insanity.

@Jeremiah: Nope, not in Genesis.


text:
Identify bone found on beach in Scotland
Found on a beach in Scotland, it's about 10cm long, any ideas what it is?

You should add the size too. it's a piece of skull. what's on the other side?

I cannot seem to add another picture but is is the same but 2 reccess on both sides. Is around 4 inches

It’s been suggested that it is A seal skull?

without scale this impossible to answer.

@karen you can upload 2-3 images, perhaps try a screenshot of thw image if the phone camera is too many mp for the site.


text:
Identifying an insect in Cambridge UK
I have come across an insect in Cambridge UK that I could not identify.
I tried to find this in various catalogues of local insects without success. The insect was about 1-2cm in length and didn't move at all until it was disturbed. I found it around 11am. We are currently experiencing high temperature variations (8C-20C).
Could someone please help identify it and point me at any useful resources I can use in the future?

It's a greater bee fly, Bombylius major, a nectar feeder and generalist floral pollinator which pollinates hundreds of species of flowers. It lays eggs near real bee nests and it's larvae feed from the bee larvae.
https://en.wikipedia.org/wiki/Bombylius_major

Thank you!! What a fascinating creature, can't belive I have never come across it before.


text:
What is the common diet of food-related IBS patients? Besides most patients being lactose intolerant, what other intolerances do they face?
I am currently writing a paper on irritable bowel syndrome, and I was wondering what the common diet of a patient with food-related IBS consists of. I've already begun discussing the pathogenesis of the disorder, but I want to start making a connection between food and IBS. I understand that most patients tend to be lactose intolerant, but I am also interested to see if there are any other common intolerances associated with IBS.

IBS stands for Irritable Bowel Syndrome. The IBS symptoms include belly pain, diarrhea, bloating and constipation. Different persons have an intolerance to different food items. You can know what's causing trouble in you by taking a test at http://intolerancelab.co.uk/intolerance-2.
The most common diets that you can prefer to get rid of IBS symptoms are:

High Fiber Diets can help prevent constipation.
For some people, high fiber diet is intolerant. They should switch to a low fiber diet.
You should prefer a gluten-free diet.
Have a low-fat diet and get rid of a number of health problems.

Some food items that can cause food intolerance are:

Dairy products
Soy products
Fructose
Wheat
Gluten

Fermentable carbohydrates may cause problems in some IBS patients. Recent work suggests that restricting these foods may improve the symptoms in some patients.
http://www.nature.com/nrgastro/journal/v11/n4/abs/nrgastro.2013.259.html
More information can be found by looking for the FODMAP diet.

This is from a recent abstract relating to FODMAPS:  Food intolerance in irritable bowel syndrome (IBS) is increasingly being recognized, with patients convinced that diet plays a role in symptom induction. Evidence is building to implicate fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) in the onset of abdominal pain, bloating, wind and altered bowel habit through their fermentation and osmotic effects. Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3388522/

The question was originally about food tolerance, but was meant to question intolerance to the food, hence the comment. I think the OP essentially worded the question incorrectly, which has now been corrected. Hence I shall remove the comment shortly.


text:
Definition of "Effective population size"
Could you explain to me, what is the meaning of "Effective population size ($N_e$)"?
I would appreciate an example as well.

This is potentially a good question, but too vague in its current form. You should say what context you mean so that a better explanation can be given. What formula did it occur in?

I'll add an informal answer to complement @Remi.b's excellent answer. In a very simple sense, you can think of the effective population size as the number of reproducing (breeding) individuals in a population. Nature Education has a very good (and free) Scitable article on Genetic Drift and Effective Population Size. The article makes four points, which I've annotated below.

The population has an equal number of males and females. All
individuals are able to reproduce.

Populations of many species contain individuals that have not yet reached sexual maturity, have passed an age of reproductive capability, or might have a genetic condition that prevents reproduction.  All of these individuals count towards the census population size (actual number of individuals present) but not count towards effective population size because they can't reproduce.

All individuals in the population are equally likely to reproduce.
Mating is random.

Not all indivduals (assuming individuals that meet assumption #1 above) are equally likely to reproduce. For example, the process of sexual selection means that some individuals are much more likely to reproduce than other individuals. Sexual selection is not random, and lowers effective population size.

The number of breeding individuals is constant from one generation to
the next.

Population sizes for some species can fluctuate over many generations. For example, freshwater mussels have declined rapidly in population size due to habitat loss and other factors. Nearly 72% of the species in the United State and Canada are endangered, threatened or of conservation concern (Williams et al. 1993). The population sizes for the majority of mussels species are but a fraction of what they once were. This is the case for many endangered species. This too lowers effective population size.
Here's a simple mathematical treatment to highlight points 1-3. Consider a population of zebras. Zebras like the Plains Zebra (Equus quagga) form harems where one male mates with several females. He prevents other males from mating with the females in his harem. Let's make the following assumptions: 1) the population has 250 males and 250 females, all capable of breeding and 2) each male that is able to form a harem gets five females. If so, then only 50 males will actually get to reproduce. The census size is 500 individuals but the effective population size, as shown in Remi.b's answer, is calculate by
$$N_e = \frac{4N_m N_f}{N_m+N_F}$$
where, $N_e$ is the effective population size, $N_m$ is the number of breeding males and $N_f$ is the number of breeding females. Given assumptions 1 and 2 above, $N_m$ is 50 and $N_f$ is 250 (50 males $\times$ 5 females each). Therefore,
$$N_e = \frac{4\times 50 \times 250}{50 + 250} = 166.67$$
Clearly, the effective population size is much smaller than the census population size.

Short answer: The effective population size of a population is the corresponding population size of a idealized (fisherian) population that would function in the same way with respect to genetic drift and inbreeding as the focal population under interest.

Long answer, below.
Definitions:
Heterogenity: the probability that two randomly sampled alleles in the population are identical (identical by descent).
Census Population Size: The census population size ($N$) is the number of individuals in the population.
Fisherian population
A fisherian population is an idealized population of size $N$, where all individuals mate at random, there is no selection, there is no population structure, there is no mutation and generations are non-overlapping. There probably are no perfectly fisherian populations in nature!
Genetic drift causes a decrease in heterogeneity. As the genetic drift is a function of the population size (see this post) this decrease of heterogeneity is a function of the population size. The heterogeneity at time $t$ is:
$$ H_t = H_{0}\left( 1-\frac{1}{2N} \right)^t$$
, where $H_0$ is the heterogeneity at $t=0$. You can verify by yourself that as $t$ increase , $H_t$ decreases. Also, as $N$ decreases, $H_t$ decreases. In other words, the longer you observe, the more heterogeneity gets lost and the smaller is the population, the higher is the loss of heterogeneity.
Effective Population Size
Let Pop_A be a real population. The effective population size ($Ne$) of Pop_A is the size of an idealized fisherian population that would have the same loss of heterogeneity than Pop_A.
You can read the above sentence twice to make sure you understand it. It basically is the definition of the concept of effective population size.
In other words: Let $N$ be the population size of Pop_A. If Pop_A is a perfect fisherian population, then its loss of heterozygosity through time is given by:
$$ H_t = H_{0}\left( 1-\frac{1}{2N} \right)^t$$
If Pop_A is not a perfect fisherian population, then it's decrease in heterozygosity is greater than the one given by the above formula. The decrease in heterozygosity of Pop_A corresponds to the decrease of heterozygosity of an idealize fisherian population of a different size. This size is called the effective population size $Ne$. So, we can rewrite the loss of heterogosity through time of Pop_A as:
$$ H_t = H_{0}\left( 1-\frac{1}{2Ne} \right)^t$$
(Note $N$ has been replaced by $Ne$)
, where $Ne$ is the effective population size of Pop_A.
Usually $Ne < N$, meaning that a real population undergoes more genetic drift than does a fisherian population of the same census size. There are many reasons that may yield a real population to have a higher drift than it would be expected with the same census size but respecting the assumptions of the fisherian population. Below I discuss three reasons:
Examples
Unequal sex-ratio
Think as a first example of a population where the sex-ratio is extremely biased to the point of having one male for 99 females. In such population, half of the alleles of a given locus at the next generation will come directly from the father. In such situations, the genetic drift is much higher than what would be expected from a fisherian population of size 100. Therefore $Ne<N=100$. To calculate $Ne$ when the sex-ratio in unequal you can use this formula:
$$Ne=\frac{4N_mN_f}{N_m+N_f}$$
, where $N_m$ and $N_f$ are the census populatino size of males and females respectively. You can verify that when $N_f = N_m$, then $N_f + N_m = N = Ne$.
Variation in population size through time
If your population size varies throughout a given time (a year for example) and that at time $t=3$ (a given period of the year) the census population size is given by $N_i$, then the effective population size is:
$$Ne = \frac{1}{\frac{1}{t}\sum_{i=1}^t\frac{1}{N_i}}$$
This is particularly relevant for insects for example which population size varies a lot between seasons.
Selection
Think now of a population where there is a great variance in fitness (there is selection). In such population, maybe all offspring will be produced by only a tenth of the current population. As a result the effective population is ten times smaller than the census population size.

You can probably find all these informations from wikipedia: http://en.wikipedia.org/wiki/Effective_population_size
Let me know if the concept of the effective population makes more sense to you now.

I hope you are ok with my edit suggestions.


text:
Is the Klein's bottle a good analogy to the relation between T-tubule and sarcolemma?
I am not quite seeing how the T-tubule and sarcolemma is connected. It says that the T-tubule is an "invagination" of the sarcolemma, which is sarcolemma folded from the inside to form a T-tubule
Can someone verify whether the following picture is a good presentation of this relationship?

Klien bottle has zero volume. It is not distantly related to the t-tubules or other such structures.

Can you provide a citation stating the relationship between the two structures?

So he's just trying to find an analogy for how the sarcolemma folds into the t-tubule, and if this is anything like how a klein bottle works.

If we're looking at diagrams for the t-tubule with respect to the sarcolemma, we see the two are actually fused:

The function therein is to allow depolarization to penetrate the interior of the cell quickly. The surface isn't transected anywhere, it simply folds inward. You can visualize this by sort of pushing a hole through some putty with a finger, and making a hole to the other side. Really no need to upvote me here, just easier to paste images in answers.


text:
Why do smaller mammals move intermittently?

I was watching a nice little video on youtube but couldn't help but notice how snappy smaller animals such as rats and chipmunks move. By snappy I mean how the animal moves in almost discrete states pausing between each movement.
Is this a trivial observation or something inherent in the neuro-synapse or muscular make-up of these animals?

Not just mammals. Insects and reptiles do this too.

Human soldiers do it, too. And many animals live in what amounts to a war zone.

Are they actually pausing more than larger animals? I mean, if I speed up videos of elephants they look snappy with intermittent movements (or e.g. some of the people in this time lapse), and if I slow down videos of chipmunks they look smooth and continuous like larger animals (sort of like this). I think it's just a relative time thing?

Just to add an interesting (but exceptional) example, tiger beetles move so fast that they are essentially blind during movement; they dash in short straight lines, then must stop to locate their prey and make another dash. Not the case for most animals, but a fun one.

Short answer
Intermittent locomotion can increase the detection of prey by predators (e.g.  rats), while it may lead to reduced attack rates in prey animals (e.g., rats and chipmunks). It may also increase physical endurance.
Background
Rather than moving continuously through the environment, many animals interrupt their locomotion with frequent brief pauses. Pauses increase the time required to travel a given distance and add costs of acceleration and deceleration to the
energetic cost of locomotion. From an adaptation perspective, pausing should provide benefits that outweigh these costs (Adam & kramer, 1998).
One potential benefit of pausing is increased detection of prey by predators. Slower movement speeds likely improve prey detection by providing more time to
scan a given visual field.
A second plausible benefit is reduced attack rate by predators. Many predators are more likely to attack moving prey, perhaps because such prey is more easily detected or recognized. Indeed, motionlessness (‘freezing’) is a widespread
response by prey that detect a predator.
A third benefit may be increased endurance. For animals moving faster than their aerobically sustainable speeds, the maximum distance run can be increased by taking pauses. These pauses allow the clearance of lactate from the muscles through aerobic mechanisms.
PS: If you mean with 'snappy' not only that small animals move intermittently, but also 'fast', then Remi.b's answers nicely covers the story why small critters are quick. Basically, it comes down to Newton's second law, namely acceleration is inversely proportional to mass (a = F/m), but the size of muscle power is not. Hence, bigger animals have more mass and need a lot more force to build up to accelerate at the same speed. That build up of force needs time (ever witnessed the vertical lift-off of a space shuttle?) Hence, small critters accelerate quicker and allow them to move 'snappy'.
Reference
- Adam & kramer, Anim Behav (1998); 55: 109–117

I have no evidence for this, but I would also wager that stopping will improve your ability to scan your environment for predators.

Motion not only greatly increases your chances of being seen by something that wants to eat you (or something you want to eat), but it also increases your chances of being heard (or vibrationally detected), and/or smelled.

Well, this was pretty obvious answer. But why does this only apply to tiny creatures like mice and insects?

@TomášZato - I've never said it did. However, I agree a PS might be in place. What about the postscriptum add-on? Does that satisfy your critiques? (Why do I hate downvotes so much :-)

@TomášZato it doesn't, it is just that for larger animals the time between pauses is long enough people tend not to notice, many prey animals pause and scan for predators. also in larger animals movement between food sources is less common since they are both more energy efficient and tend to have different feeding mechanisms, so pauses are harder to notice.  https://royalsocietypublishing.org/doi/pdf/10.1098/rspb.2000.1388

In addition to @AliceD's excellent answer, I would like to add that a simple mechanistic relationship between body size and "snappiness" may explain the observed pattern.
Basics of biophysics
Difference in snappiness may result from a difference in the ability to accelerate your movement.
An increase in body size over one dimension (=body length) $x$ scales with an increase in volume and mass of the order of $x^3$. Muscle strength is dependent on the cross-sectional area of the muscle and therefore by a linear increase of $x$, strength increases by $x^2$.
Digging back to high school physics lectures, $F=Ma \left(\text{or } a=\frac{F}{M}\right)$ , where $F$ is a force, $M$ a mass and $a$ an acceleration. With an increase $x$ of the individual size (over one dimension, the length of the individual if you prefer), the force increases by $x^2$ and the mass increases by $x^3$, therefore the acceleration gets multiplied by $\frac{x^2}{x^3} = \frac{1}{x}$. Of course, nature is not all that easy, but if we assume it is, then the relation between the acceleration of movements and body size (=body length) should look like this:

An animal that is 4 times as big should make accelerate its arms and legs 4 times less.
Contrasting to @AliceD's answer
@AliceD listed plausible hypotheses for why there might have a selection for snappy movement in small animals but simpler explanation based on the physical properties of bodies might be enough to explain the observed pattern. It would be interesting to know exactly what the relationship between body size (=body length) and "snappiness" look like in nature to further this discussion.

Fun Facts
The mantis shrimp (see below picture) is able to accelerate its claws up to 10,400g (reference). More information about g (unit of acceleration) here. In short, a typical human can support up to 5g. 10,400g is absolutely insane! To offer some comparison: a baseball gets an acceleration that is only about a third of that of the mantis shrimp's claws. Mantis shrimps use their claws to break open clams. Here is a video. According to wikipedia, due to the friction of the claws against the water, small bubbles are formed and the temperature at the edge of those bubbles can go up to several thousands of °C.

Apparently, a jellyfish stinger can go up to 5,400,000g (reference) which appears to be about 30 times more than a bullet. You will find a list of examples of things that undergo various levels of acceleration on this wikipedia list.

I think the question is not on why they are fast, or accelerate quickly, but why they move intermittently.

I think this rather explains why larger animals do not make snappy movements: because all that accellerating and decellerating consumes too much power.

Difference in snappiness may result from difference in the ability to accelerate your movements. Larger animals do not make snappy movement because they can't while smaller animals can. It is true it doesn't explain why they would not slow down their movement. I would tend to think that it is simply generally beneficial to move fast.

@AliceD Maybe it's related? I mean, watching the OP's linked video, at least, it seems like being able to do things more quickly (interpreted as "snappy") leaves more time to do nothing in between. I know it's different, but if I could move 10x faster than I could now, I'd probably spend a bit more time not moving at all, since I already accomplished the intended movement and wouldn't fill time with unnecessary movements for no reason. I totally am pulling this comment out of my butt, though, so I dunno.

(Do bigger animals pause a lot too but on a slower scale? Like, if something makes a noise, I turn my head to look. Then I pause. Then I resume what I was doing. Does that count as intermittent but slower, same thing but not "snappy" ["snappy" just meaning relatively fast compared to the observer, really]?)

I very much agree @JasonC. I have a hard time to formulate the concept though.

Layman's hypothesis, but... It seems an animal using intermittent movement alternates between a hard-to-see state and a hard-to-catch state, with some degree of safety in both. Operating at a slower, sustained pace offers neither of these benefits and significantly less safety.
Wondering if "small mammals" is the right descriptor. The obvious examples seem to be rodents. Also vague: cats are small relative to horses, but they're not intermittent.
Maybe another way to look at this is "When/why does an animal uses their maximum speed?" Rodents seem to do it as a matter of routine locomotion, most mammals do it only when actively fleeing or pursuing.
Small lizards seem more akin to rodents in this regard than not-quite-as-small mammals.


text:
Highest Pressure Human Body Can Survive In?
One design for underwater human inhabited environments is to have equal pressure between the surrounding water and the submerged habitat, thus allowing a section of the floor to be open to the water and removing the necessity for strong plating to protect it.  This requires the air pressure within the environment to be greater than atmospheric pressure so that it can withstand the pressure of both the atmosphere and the pressure from the overlying water.
So how much pressure can the human body survive in without need for special suits and breathing apparatuses (as this would place a limit on how deep you could build such an environment without special accommodation)?
Edit: So far i've found an article about a man trapped in a sunken boat who survived for days in an air pocket trapped in the bathroom 100 feet down.  He couldn't resurface without the use of a diving bell and gradual decompression; but this case provides a lower bound for how high the highest pressure can be.
Calculations:  14.7 psi (atm pressure) + 1200 inches*0.037 psi/in^3 = 60 psi for the underwater pocket (roughly 4 times atmospheric pressure).
http://news.nationalgeographic.com/news/2013/12/131204-nigerian-air-bubble-survival-shipwreck-viral-video-science/

Without breathing apparatuses, the pressure isn't the limiting factor for survival. The lack of oxygen is...

Plants might refresh the air or might not; but supposing you had a means to freshen the air, and using whatever composition of the gas would maximize the highest pressure at which humans could breathe.  Or if that is too difficult, just plug in condensed atmospheric air.

oh... athmospheric pressure. I though you would be completely submersed, somehow, sorry. In this scenario, you would actually fare pretty well, AFAICT.

http://en.wikipedia.org/wiki/Deep_diving

do you consider a diving bell a diving apparatus?

I was just going to ask "How deep a diving bell can a human breathe in?" and saw this Q. Hoping to find an answer here..

It's common for saturation divers to live under pressure for weeks if not months at a time beyond a pressure of 1000 feet of seawater, but typically not more than 1500 feet. I believe the limitations are more economical rather than physiological. 1000 FSW requires special mixed gas controls to prevent the narcotic effects of nitrogen that occuer under pressure. That's why helium is added. But then helium steals the diver's heat, so special warming systems are required. Decompressing after these long periods takes days.

According to Israel Ramirez on Quora, the practical maximum is about 70 atmospheres of pressure. Any higher than that and people won't be able to breathe.

The deepest recorded simulated dive is still the on-shore French Hydra 10 experiment at 701 msw (meters salt water); at a pressure of 71 atm. Since breathing a mixture containing helium is required at such depths (to avoid the extreme narcosis produced by nitrogen at such depths), the new problem helium causes is

High-pressure nervous syndrome (HPNS). HPNS, brought on by breathing helium under extreme pressure causes tremors, myoclonic jerking, somnolence, EEG changes, visual disturbance, nausea, dizziness, and decreased mental performance. Symptoms of HPNS are exacerbated by rapid compression, a feature common to ultra-deep "bounce" dives.

Actually that Wikipedia description is a bit misleading, the problem is caused by any gas mixture, not just helium, but other gasses like nitrogen or hydrogen have a narcotic effect that counteracts HPNS. HPNS sets in at about 120m:

The high pressure
  neurological syndrome (HPNS) begins to show signs at about 1.3 MPa (120 m) and its effects intensify at greater depths.
  HPNS starts with tremor at the distal extremities, nausea, or moderate psychomotor and cognitive disturbances. More severe
  consequences are proximal tremor, vomit, hyperreflexia, sleepiness, and psychomotor or cognitive compromise. Fasciculations
  and myoclonia may occur during severe HPNS. Extreme cases may show psychosis bouts, and focalized or generalized
  convulsive seizures. Electrophysiological studies during HPNS display an EEG characterized by reduction of high frequency
  activity (alpha and beta waves) and increased slow activity, modification of evoked potentials of various modalities (auditory,
  visual, somatosensory), reduced nerve conduction velocity and changes in latency. Studies using experimental animals have
  shown that these signs and symptoms are progressive and directly dependent on the pressure. HPNS features at neuronal and
  network levels are depression of synaptic transmission and paradoxical hyperexcitability.

The problem with extreme helim pressure was partially alleviated in the Hydra experiments by mixing/replacing some of it with hydrogen, in the so-called Hydreliox mixture.

For the Hydra VIII mission at 50 atmospheres of ambient pressure, the mixture used was 49% hydrogen, 50.2% helium, and 0.8% oxygen.

The French did this based on prior experiments which found that the narcotic effect of hydrogen reduces HPNS (or even completely eliminates it at lower depths):

A H2-He-O2 mixture with 54 to 56% hydrogen was studied with 6 subjects (professional divers) during 2 dives to 450 m. The 38-h compression was the same as that used with other types of breathing mixtures (He-O2 and He-N2-O2). The results obtained during compression and during the stay at 450 m in H2-He-O2 show that the EEG changes (increase of theta activities in the anterior regions of the skull, decrease of alpha activities) are similar to those found with other respiratory mixtures. On the other hand, the other symptoms of high pressure neurologic syndrome (HPNS) were clearly improved for the same depths. Thus, neurologic symptoms (tremor, dysmetria, myoclonia, drowsiness) are nonexistent, and the performances during psychometric tests remain similar to those of the surface. Hydrogen, with its narcotic potency, suppresses some symptoms of HPNS and seems to open new perspectives for deep diving.

Of course, having hydrogen (in such large proportion) and oxygen in a gas mixture poses dangers of fire, explosion etc. This is avoided by decreasing the oxygen concentration; alas this cannot be a one-step process (for diving):

The major problem with hydrogen-oxygen mixtures is the potential for explosion. Although the concentration of oxygen needed for combustion of oxygen-hydrogen mixes varies a bit with pressure, a general rule of thumb is that hydrogen-oxygen mixes above 5 %  O2 are at-risk.. So, to avoid nasty fires and explosions, hydrogen is only considered as a breathing gas component at pressures where a less-than 5% oxygen concentration in the breathing gas mix gives a partial pressure of oxygen great enough to sustain life. Perhaps the most common example of a hydrogen-fire related disaster is the destruction of the Hindenburg dirigible. [...]
In 1944 Arne Zetterstrom discovered a way to breach the transition between compressed air and Hydrox without risking explosion. The technique was to descend to 100 feet and switch to a 4% oxygen / 96 % nitrogen mixture. After breathing this mix for sufficient time to allow the oxygen concentration in the lungs to drop below the "explosion threshold," the diver switched to Hydrox and continued descent. On ascent, the diver again used the Nitrox (4% O2 / 96% N2) as a transition between Hydrox and air. Using this technique, he descended to 363 feet. At that depth, the alteration in voice characteristics, coupled with excitement, made communication impossible and additional dives used a telegraph key.  [...]
During the mid 1960's research into the use of hydrogen in breathing gases resumed with animals breathing Hydrox for up to 24 hours at 70 Ata. One interesting aspect of the animal research was the suggestion that hydrogen reduced the HPNS (high pressure nervous syndrome) often observed with helium based gas mixes on deep dives. Ultimately animals would be taken to 3500 feet on hydrox.
In 1983 COMEX, the French deep diving concern (perhaps more famous in the US as the company providing the submersible used in the recovery of artifacts from the Titanic) began a series of dives to investigate the narcotic potential of hydrogen. Divers including H.G. DeLauze, President of COMEX, descended in open sea to approximately 300 feet for five minutes. The divers could not perceive a difference between Hydox and Heliox at that depth.  Chamber dives to 300 m (984 ft) demonstrated that hydrogen possessed a narcotic effect different from nitrogen. Hydrogen narcosis (the "hydrogen effect") had a tendency to be more psychotropic, i.e. more like LSD, while nitrogen narcosis had an effect similar to alcohol. This deeper work suggested that Hydrox as a binary gas mix would not be too useful at depths below about 500 feet.

Based on that COMEX developed a protocol of switching from heliox to hydreliox at 250msw.
A more recent (1994) COMEX paper reported that at 500m (on hydreliox), manual dexterity was about 80% of the surface one, while the arithmetic ability decreased to 60%. So not dying and being able to function as on the surface, aren't the same thing.
Also these experiments are time consuming and costly. In Hydra VIII, the whole thing took one month, of which only 10 days or so were spent at maximum depth. And in case "something bad happens" interventions aren't easy in such settings.
A 1984 American experiment with trimix at 650m was aborted after one of the three subjects (despite negative previous neuropsychiatric screening, as well having substantial commercial diving experience and successfully taking part in the previous experiments of the series) developed hallucinations and then full blown mania at 625-650m.

The Atlantis IV dive was designed to test the ability of 5%
  N2 trimix breathing mixture (5% N2, 0.5 atmosphere
  oxygen, with the balance helium) to counteract the
  [high pressure nervous] syndrome without nitrogen narcosis. [...]
The dive began with an initial compression rate of
  30 m/hour to 300 m (1000 ft) sea water equivalent
  pressure. By day 3 of the dive, at about 470 m, subject
  C had developed significant insomnia. On day 4 (540
  m), this subject became stressed and complained of
  mild auditory illusions of music and visual distortions
  consisting of a “halo effect” around the chamber’s
  apparatus. On day 5 (625 m) of the dive, the subject’s
  irritability, insomnia, and agitation worsened. He was medicated with temazepam, 60 mg, and achieved
  substantial relief of these symptoms after 15 hours’
  sleep. However, with further compression to 650 m,
  subject C experienced a recrudescence of auditory and
  visual illusions and developed rapid speech, racing
  thoughts, shortened attention span, and difficulty in
  focusing on tasks. Ankle clonus, marked hyperreflexia,
  and myoclonic jerking were documented, and he complained of nausea and weakness. In contrast, the other
  two subjects performed normally in almost all respects.
  On day 9 (650 m), the subject stated he felt “paranoid”
  and that he felt like “I’m going insane.” He
  began to carry a mirror to look at himself to “remind
  myself that I’m not a raving maniac.” He stated that
  colors were enhanced and vivid and he could see
  “unusual” mosaic patterns on the metalwork within
  the chamber. He was unable to comply with instructions
  to enable cognitive function to be tested because
  of extreme agitation and distractibility.[...]
Early on day 9 (650 m), the decision was made to
  halt the dive, but decompression from 650 m is still
  experimental and could not be accelerated. Because the
  decompression process was expected to last as long as 30 days, it was necessary to consider medicating the
  subject more intensively. Since lithium had been shown
  to exacerbate symptoms of the high pressure nervous
  syndrome in animals and the effects of phenothiazines
  at such high pressures were virtually unknown,
  the decision was made to control the diver’s agitation
  with benzodiazepines. Accordingly, diazepam was used in doses up to 120 mg/day. This treatment only
  mildly sedated the subject and provided no real control
  of his behavior.
  The subject’s agitation persisted over the next 14
  days and was marked by decrements in his cognitive
  function and bursts of aggressive paranoia, grandiosity,
  and irritability. By day 24 of the dive (383 m), the
  subject’s irritable and aggressive behavior was becoming
  potentially dangerous and led to the decision to
  medicate with chlorpromazine, up to 300 mg/day.
  Within 48 hours of the beginning of chlorpromazine
  treatment there was dramatic improvement in the
  subject’s behavior. He became relatively calm and
  better organized. He denied having illusions or hallucinations. [...]
Ten days after exiting the chamber, the subject again
  exhibited signs of hypomania including hyperactivity,
  insomnia, and irritability. Lithium carbonate therapy
  lessened these symptoms and was continued prophylactically
  for 6 months. It was then discontinued
  without any recurrence of symptoms.