text:
Ramifications and possibility of a diet consuming exclusively of human semen
Semen is a thick, nutritious liquid, rich in vitamins (such as C, B12), amino acids, lipids, monosaccharides (fructose), et cetera. Can semen's ability to fulfill the needs of human organism provide enough essential nutrients to keep the body alive and functional? And if so, would it be a healthy life?
Can a glass of ejaculate a day keep The Reaper/doctor away? If not, how long could a person survive on a "diet" like this?

Don't know why this one was down-voted. Up-voted to offset. This is a question concerning human biological processes, despite unsettling implications to some responders.

Right, I do realise that semen content varies, also, question that should have been asked is 'roughly, how long one can take that diet [I mean - is it more like 3 weeks or 3 months - or else] and what exactly is most likely to cause death'. I should be more specific. Thanks for help however, kind sir MCM - and, can't vitamin K be manufactured by intestinal flora?

@MCM it may concern human biological processes, but it's not relevant for anything. I don't see how this is any more valuable than any other "how long can I live eating only X" almost all of which are simply rhetorical "just curious" questions with nothing particularly useful about them.

I downvoted because the question as phrased is not suitable for this site. Asking "what is the nutritional content of human semen" would be more appropriate for a biology forum. In what possible context would you be confronted with a situation where you had to survive on male ejaculate?

I agree the question is not the best, but it is not a topic forbidden in the FAQ, and it is an answerable question that doesn't require an extended conversation or a book's worth of text. While it would have been nice to have the question phrased better, as Poshpaws suggested, not everyone will think in that manner - and I don't see why they should be excluded. Once a question like this has been asked and thoroughly answered, then it can serve as a reference for future questions.

The question is absurd on a number of levels, but also on the level of energetics. The expenditure of energy and number of individuals required to generate a sustainable amount would far outweigh any benefits provided and would only be the diet of the Emperor or the Pharaoh, i.e. only someone with dominion over a large numbers subjects. @MCM also left out a very obvious drawback, that seminal fluid is a vector for a host of pathogens, from HIV, Hepatitis, HPV, Gonorrhea, Chlamydia, etc.

No, you cannot live off of semen.
A source from Columbia.edu:

A typical ejaculation fills up about one teaspoon; the actual amount is determined by a man's age (younger men usually make more semen), when he last ejaculated, and how long he's aroused before ejaculating, among other factors. Contrary to what you've heard, semen is not loaded with calories. Each teaspoon of ejaculate has about 5 - 7 calories and some 200 - 500 million sperm. Since sperm make up only about 1 percent of semen, what accounts for the other 99 percent? Well, its other ingredients include:

Fructose sugar
Water
Ascorbic acid (a.k.a., vitamin C)
Citric acid
Enzymes
Protein
Phosphate and bicarbonate buffers (bases)
Zinc

Can swallowing semen enrich a protein poor diet? Unless you're gulping gallons of it each day, it's no substitute for real nutritious cuisine!

From a non-academic, but apparently well-informed source, semen contains:

Semen contains only 15 calories and boy does it have a lot of stuff in it. So let's have a look. Ejaculate contains ascorbic acid, blood-group antigens, calcium, chlorine, cholesterol, choline, citric acid, creatine, deoxyribonucleic acid (DNA), fructose, glutathione, hyaluronidase, inositol, lactic acid, magnesium, nitrogen, phosphorous, potassium, purine, pyrimidine, pyruvic acid, sodium, sorbitol, spermidine, spermine, urea, uric acid, vitamin B12, and zinc.

I've highlighted the nutritionally-relevant ingredients. You'll notice that there is some overlap - with the Columbia source. What you won't notice, though, are the rest of the Essential Vitamins and Minerals:
Vitamin A (retinol)
Vitamin B1 (thiamin)
Vitamin B2 (riboflavin, vitamin G)
Vitamin B3 (niacin, vitamin P, vitamin PP)
Vitamin B5 (pantothenic acid)
Vitamin B6 (pyridoxine, pyridoxamine, or pyridoxal)
Vitamin B7 (biotin, vitamin H)
Vitamin B9 (folic acid, folate, vitamin M)
Vitamin D (ergocalciferol, or cholecalciferol)
Vitamin E (tocopherol)
Vitamin K (naphthoquinoids)
Chloride (Cl−)
Chromium (Cr)[4]
Cobalt (Co) (as part of Vitamin B12)
Copper (Cu)
Iodine (I)
Iron (Fe)
Manganese (Mn)
Molybdenum (Mo)
Nickel (Ni)
Selenium (Se)
Sulfur (S) numerous roles[5]

I should also mention that the specific amounts of each ingredient will vary from person to person, as diet can play a major role in flavor resulting from the changed nutritional content (i.e. - higher fructose levels).
As perhaps the most reliable source I could find, there is a Wikipedia article with references concerning the makeup of human seminal fluid and has this information:

amino acids, citrate, enzymes, flavins, fructose (2–5 mg per mL semen,3 the main energy source of sperm cells, which rely entirely on sugars from the seminal plasma for energy), phosphorylcholine, prostaglandins (involved in suppressing an immune response by the female against the foreign semen), proteins, vitamin C
acid phosphatase, citric acid, fibrinolysin, prostate specific antigen, proteolytic enzymes, zinc

It echoes the other sources closely, and still yields insufficient evidence that a person could live off of semen exclusively.
As for how long you can live? From a Scientific American article concerning starvation there have been confirmed instances of hungers strikes lasting up to 40 days. Assuming you could consume enough semen to sustain your body's daily Caloric requirements, you would die of malnutrition eventually. Scurvy - the inadequate intake of Vitamin C (Ascorbic Acid) - would probably be the culprit, as deficiency becomes clinical in 1 to 3 months with the later stages of Scurvy being: "...more severe and life threatening; common manifestations include generalized edema, severe jaundice, hemolysis, acute spontaneous bleeding, neuropathy, fever, convulsions, and death."
Assuming that there is enough Vitamin C in semen, you would die of other deficiencies. Since Vitamin B1 (Thiamine) is water-soluble (is not stored in your fatty tissues), not found in semen at all, and the body only reserves about a month's worth, after 30 days you would start to experience Beriberi - which is only slightly less fun than Scurvy.

An impressive answer. However, that first constituent from the second source - "aboutonia". I can find no trace of a definition for this. All Google results seem to point back to this source, it isn't in my dictionary and it doesn't generate any hits at PubMed. Presumably it was originally "Ejaculate contains about [something].." but I can't come up with a candidate that explains the "onia"

Right, I do realise that semen content varies, also, question that should have been asked is 'roughly, how long one can take that diet [I mean - is it more like 3 weeks or 3 months - or else] and what exactly is most likely to cause death'. I should be more specific. Thanks for help however, kind sir MCM - and, can't vitamin K be manufactured by intestinal flora?

@Alan Boyd - I wouldn't be surprised if they meant albumen, or something similar. It's not the greatest source, but there weren't any "hard" sources for the nutritional content of semen like journal articles or studies. There's supposedly a 2004 study out of Sydney, but I couldn't find it.

@Arwil - Vitamin K can be manufactured by intestinal flora, yes, but not in the amounts necessary to sustain human life. My personal opinion is that you wouldn't live for much more than a month. There have been hunger strikes for as long as 40 days, but if the semen didn't contain enough Vitamin C then Scurvy would kill you in a few weeks.
Edit: Also removed "aboutonia" since it's not a real compound.

I see. So, summing up, consumption of significant amount of semen, sufficient to postpone suffering from malnutrition and scurvy, can probably lead to about 2 months of not so quality life, ending in agony of 'deficiency-based' diseases, such as beri-beri. Thanks a lot, you really did a tremendous job!


text:
on/off behavior of neural networks
What causes a group of disembodied neurons in a dish to fire after a silence? If there are no neurons providing a stimulus for more firing (as in a dish of disembodied rat neurons), then why don't they simply cease firing after the synchronized burst completes?

Are we talking of tissue slices or dissociated cell cultures?

The similar phenomena (spontaneous brain activity in rats after ~ 20 seconds of silence following decapitation) is studied in Zandt B-J, ten Haken B, van Dijk JG, van Putten MJAM. 2011. Neural dynamics during anoxia and the “wave of death” and is explained as a result of membrane depolarization. I don't know whether such reasoning could be applied to cell cultures though.

@aland: it mainly depends on the neuronal type. Not all neuron display bursting behaviour, and not all are synchronised. Certain (e.g. SCN) can be kept in vitro for days and continue with their "bursting life" with no problem. I am quite busy right now, when I have time I will try and give an answer.

There are a number of different wiring scenarios that could lead to this type of behavior, even in a dissociated neuronal cell culture.  The two major cases are neurons that are truly isolated from each other, and collections of neurons that connect together.  Since your question refers to firing and synchronized bursts, I'll restrict my discussion to the generation of spontaneous action potentials - but keep in mind that not all synaptic communication requires an action potential (the vast majority of internal connections within the retina, for example)
In the case of ensembles neurons in vitro, spontaneous activity is fairly typical.  One simple way to get this activity is for a subset of cells in the network to be inherently spontaneously active.  In the case of single, isolated neurons, this kind of individual cell spontaneous activity could also result in a single neuron firing spikes in a periodic fashion.  So for example purposes, let's explore how a single cell could produce this kind of activity.
Since action potentials are triggered by a sufficiently strong depolarization, we need to identify potential membrane polarizing sources.  When dealing with single cells, the major controllers of cell membrane voltage potential are the voltage gated ion channels.  When open these channels can cause, depending on their type and cellular/extracellular conditions, either a depolarization or hyperpolarization in the cell.  And, most interestingly, whether they are open or not depends on the cell membrane's polarization state.
That makes voltage gated channels excellent at feedback:

a depolarizing channel that is depolarization gated will further activate itself once activated, leading to yet more activation.  This is a positive feedback cycle.
a hyperpolarizing channel that is depolarization gated will, upon depolarization of the cell open and serve to hyperpolarize the cell until the initial depolarization has been removed.  In this way it would serve as a negative feedback source.

Physiologists have thoroughly characterized many of these cells, and they have many more states beyond an "open" and "closed", such as different levels of "inactivated".  But we don't need to know about those to answer your question.
The last piece we do need is brownian motion which is the movement of particles due to their bombardment by other particles.  This motion can with some frequency cause voltage gated channels to spontaneously open or close, which introduces noise into the system.
As you can imagine, if you have a positive feedback channel that is gated spontaneously, it will make it briefly more likely for other depolarization gated channels to be activated.  Positive feedback can quickly lead to a rapid depolarization of the cell, which could be observed as a burst of spikes.  If you include a set of slower reacting depolarization gated hyperpolarizing channels, then it's easy to construct a scenario where the cell would depolarize spontaneously with no apparent input, then have a quiescent period where a prolonged hyperpolarization makes it less likely to fire spontaneously.
Voila, bursting in an isolated neuron.  Place a set of those neurons in a network and you can get generate a lot of spontaneous activity.

Great response, and I'm sorry it took so long to get back to you! After a month or so of reading and coding, I've finally got a respectable Hodgin-Huxley network simulation running. I'll definitely look into coding up some noise inspired by brownian motion. Thanks!

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text:
Why is it sometimes difficult to resuspend E. coli in P1?
It's a curiosity question. When I'm doing minipreps after pelleting the bacteria sometimes it's very easy to resuspend them in P1 (Qiagen kit), but sometimes they form a rubbery clump that is very hard to break up with a pipette and I have to vortex the tubes. It interests me because it adds more time to my lab work and I wish I could avoid it.

how old/dead are the bacteria?  resuspending fresh pellets seems easier to me..?

Straight from 16h culture.

When I do giga preps, I have to weigh the pellets and put 7g of cells into a 1L pyrex bottle, then add the P1 and a small stir bar  that helps beat the pellet apart with vigorous mixing. Using more than 7g can overload the column with DNA and give a poor yield.

This is particularly an issue when you do maxipreps and the pellet is 200x the size of the pellet from a miniprep. The reasons why? Maybe you're pelleting at too high of a g-force (pure speculation). Alternatively, you could be growing the cells too long. I typically miniprep after a 12 hr culture. If you're seeing any darker colors in your pellet, you have a significant amount of dead cells. Those dead lysed cells will spill out their genomic DNA which is very viscous.
For maxipreps, you can't break up the pellet merely by pipetting up and down a few times and calling it a day. What you can do is swirl the side where the pellet is and breakup the clumps. Alternatively you can use a different pipet tip (for an extensive discussion on this very topic see Pipetting damage to cells). I change to a P200 for my minipreps and pipetting only the area around the pellet seems to do the trick for me. For maxipreps I use a P1000 which is better than using a 5mL syringe.

I don't think that the pellets are darker, but I've noticed that sometimes the shaker causes my tubes to screw themselves. Could it be because they don't get enough air?

@MaciejTrybilo, what is your final OD?

I'd have to measure next time. What would you consider excessive?

It depends on your cells and what media you're using. The OD is more to check about the aeration. A lower OD would indicate that. Too high? Maybe use more P1.

@MaciejTrybiło  more areation is better. If your tubes get lose maybe they get more shaking, therefore more areation and so faster growth. And the ratio surface for volume matters here. That's why I always use 50mL Falcon tubes even for 5mL cultures.

@carandraug I also use those. I leave the caps loose and I notice that sometimes the shaker causes them to screw on quite tightly. Even though they seem to grow well (the culture is very cloudy and I get a decent size pellet) I was wondering whether it made them switch completely to anaerobic respiration and cause this gummy pellet somehow. Just a thought.

@MaciejTrybiło nah! That shouldn't be a problem. I always close the tubes very tightly, afraid as hell that the tubes will open and I get contamination.

Are you pelleting using a swinging bucket centrifuge and the 50 mL falcons? If so, then the pellet should be squarely in bottom. That should make things easier.

What I do to avoid this is to ressuspend the cells by pipetting up and down the P1 (ressuspension) buffer on the side of the tube. This way, every time takes only a bit of cells every time and big clumps are avoided. The  only times I used to get big clumps hard to ressuspend were when I went poking at the pellets first.

Yes, I do that too. In the situations I'm talking about, rather than slowly breaking up into a cloud, the pellet will unstick as a whole from the bottom of the tube and clog the tip.

We routinely use E. coli preps from 16-18h overnight cultures. The cultures don't show any overt signs of lysis (sometimes you can see cellular debris if the culture has indeed overgrown). I have also noticed inconsistent times when resuspending the pellet. For my own use, centrifuging at too great a g-force or for too long can increase the likelihood of making a difficult pellet. For example, I will typically spin a miniprep culture aliquot on a refrigerated table top centrifuge for 3 min @ 5,000 g.
I always vortex my bacterial pellet to resuspend and I have had great success with this method, though I'm well aware others will pipette up and down. What I normally do to increase the ease of resuspension is to add the buffer, and let the tubes sit in the fridge for 5-10 minutes. For whatever reason, letting the pellet literally chill makes resuspension very easy relative to immediate resuspension.
EDIT: I have also observed strain-specific differences. JM109 seem a little stickier than DH5a and TOP10.

An interesting addendum, I can pellet my cells for 3 minutes @ 1,000 g.

@bobthejoe - is that so? I'll have to try it next time. I've always done it at exceedingly high g forces.

since we're going into specifics with experimental protocols, I might as well get a precise answer. The Qiagen manual suggests 6,000xg for 15 minutes for Maxipreps and 6,800xg for 3 minutes for minipreps. Sounds like the geometry of rotors may make a small difference but that shouldn't affect the sedimentation velocity.

Some things to consider. If you spinning too fast and too long, that is going to pack the pellet more. You can spin longer at a slower speed and you will notice your pellet is not as tightly packed. I always do 2000 rpm, 20 minutes, 4C if I'm doing a midi or maxi sized prep and harvesting bacteria in a 50ml conical.
If I'm doing a miniprep I will take the 1.5 micro centrifuge tube (with pellet and buffer p1) and scrape the bottom of the tube 1 or 2 times across all the holes in the rack. This vibrates the tube good loosening and breaking up the pellet. You can consistently perform this step across many samples, this does a good job of re suspending the bugs.
I have noticed that cultures that are overgrown, contaminated, or grown in incorrectly formulated lysogeny broth, will give the pellet some weird characteristic including color and the pellet 'texture.'

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Terminology question: the scope of an allele in an organism
Let us consider a gene FOO with novel type foo.
If I were discussing an organism that has inherited foo in every cell during classical zygote formation, then I would ordinarily just say that the organism has foo.
If I were discussing a SNP of FOO that gives rise to foo in a tumor cell of an organism, I wouldn't say that the organism has foo, but I might say that the tumor has it.
If I were discussing a chimeric or mosaic organism in which some fraction of the chimera had foo and the other fraction had FOO, I would have to say something like "in foo-containing cells ..."
But what if I wanted to particularly draw attention to the scope of applicability of the allele in question? That is, I want to talk about the scope explicitly, rather than implicitly. How could I directly refer to the scope of applicability of an allele? Is there a single adjective that captures the concept of "This organism has foo in every cell except in rare ones where a point mutation may have occurred; it's probably been inherited during normal meiosis" and is there a contrasting term for "The organism only has foo in a particular subset of its cells and there is some other genetic process necessary to explain that."?

I have never seen a term applied to that - although there was a question on here a few weeks ago about something similar. Can't find it now though!

I've also never heard of it.  Perhaps it's best to refer to it in the context of the chronology of development (e.g., "the foo mutation happened early in development and is thus prevalent in most cell lineages in the organism")?

If I were discussing a SNP of FOO that gives rise to foo in a tumor
  cell of an organism, I wouldn't say that the organism has foo, but I
  might say that the tumor has it.

You can call it a somatic mutation. See this paper. They report such mutations in cancer.
You can use the term like this:

Carcinoma tissue had a somatic mutation in XYZ oncogene, thereby making it constitutively active.

If I were discussing a chimeric or mosaic organism in which some
  fraction of the chimera had foo and the other fraction had FOO

In this case you can say:

The organism is chimeric for gene-X, expressing variants X1 and X2

From this article:

Effects of AngII-Infusion Into LDL Receptor−/− Mice That Were Chimeric
  for AT1a Receptors


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How does "inheritance of methylation" of DNA and/or histones work?
What are the current models/ideas describing the mechanisms explaining inheritance of methylation on DNA resp. histone level?
Is there evidance of this "setup" information being really duplicated/inherited during a cell division process?
Pointers? Articles? What is the current state of knowledge regarding this?

Jon Wilkins has a nice introduction to imprinting.  He does a nice job of introducing the idea methylation and how these patterns are maintained during development and cell division.  Further, he links to some interesting papers on the subject.


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Is cell senescence in culture comparable to that in vivo?
A cell is 'senescent' when is has permanently left the cell-cycle. This can be caused by stresses, or by reaching the 'Hayflick limit' (the cell has reached its replicative lifespan, as defined by its telomeres).
Cells cultured in vitro can be used as models to study senescence (or sometimes 'ageing', although the distinction there is not necessarily within scope of this question) by growing the same population of cells for a long time (many passages). A common method to identify a senescent cell population is to use beta-galactosidase staining.
I was wondering to what degree senescent cells in culture (identified by beta-gal staining) are actually comparable to those you might expect in vivo. I ask because it seems to me that a terminally senescent cell may not actually survive long in an organism, so what we refer to as senescent cells in vivo are actually pre-senescent cells? I haven't got any basis for this, just a feeling. (Very scientific I know).

maybe the term you are looking for is 'apoptosis'?

Senescence does not equal cell death, but is simply an arrested state in which the cell still remains viable (1). It has been shown throughout the literature that this state corresponds with an altered cell cycle profile different from contact inhibition or damage-induced arrest (2). This corresponds with an enlarged cell size, altered gene expression (3, 4), and the pH-dependent expression of β-galactosidase (5). This has been shown both in cultured cells and in animal models (6, 7).

Goldstein, S. (1990) Science 249, 1129-1133.
Sherwood, S. W. et al. (1988) Proc. Natl. Acad. Sci. , USA 85, 9086-9090.
Cristofalo, V. J. et al. (1998) Crit. Rev. Eukaryot Gene Expr. 8, 43-80.
Linskens, M. H. et al. (1995) Nucleic Acid Res. 23, 3244-3251.
Dimri, G. et al. (1995) Proc. Natl. Acad. Sci., USA 92, 9363-9367.
Swarbrick, A. et al. (2008) Proc. Natl. Acad. Sci., USA 105, 5402-7.
Efeyan, A. et al. (2009) PLoS One 4, e5475.

Hi - thanks for the info on senescent cells. So you are saying that cells senesced in culture are comparable to those in vivo? Or you are saying that they are not comparable, because senescent cells in vivo are not necessarily replicatively senesced cells?

Cells in culture are necessarily different than those in vivo, as they are (generally) lacking the 3D structure, extra-cellular matrix, and heterogeneity found in tissues, but fundamentally senescence is the same across all cells, regardless of where they happen to be living at the moment. It is characterized by the phenotypes I mentioned above, including cell cycle arrest and replication inhibition. "Replicatively senesced" is redundant :)

I wouldn't have said redundant, simply because that is what our in vivo experiment was designed to emulate - we have aged a culture of cells (human primary cell lines) by repeated passage until growth arrest (confirmed by β-galactosidase, morphological changes, and drastic slowing of doubling time). We are now using these as models of senescence in vitro. If I understand you correctly then this is a reasonable model because senescent cells tend to display quite a homogenous phenotype? So even though senescent cells in vitro may have arrived by a different route, this is still a good model?

I can't judge your model as a whole (appropriateness of cell lines used, method of culture, etc.), but this sounds pretty good. The senescent cell phenotype is fairly homogeneous, allowing for the fact that different cell types and different cell lines can have vastly different overall phenotypes in terms of gene expression, morphology, etc., and these may be affected by the route by which senescence was arrived. The model sounds good, but keep in mind it's only a model, and you need to judge your assumptions carefully when looking at your results.

Many thanks indeed for your input, and the links.

No problem at all. If you like the answer, would you mind marking it as such? Thanks!


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Is there an advantage to linear chromosomes?
The DNA copying enzymes have a hard time working to the end of a chromosome. For circular chromosomes this is not a problem, since there is not a sharp 'end'. However, for a linear chromosome, without extra mechanisms in place, a bit of DNA is lost off the end of the chromosome after each replication. Because of this, eukaryotes have a telomere to cap off their chromosomes.
In most cells of a mutli-cellular organism, this telomere is slowly worn away after each reproduction leading to apoptosis. Cells that need to reproduce indefinitely such as germ and stem cells have to invest in extra mechanisms to replenish the telomere. For multi-cellular eukaryotes I can see how this might be usefull (for instance as a cancer counter mechanism). However, multi-cellular organisms evolved from single-cell eukaryotes.
I cannot see a reason for wanting apoptosis in a single-cell organism. However, single cell eukaryotes (say yeast) still have linear chromosomes with telomere caps. What advantage did linear chromosomes provide single-cell eukaryotes to offset the extra investment in reparing the telomere?

Related questions

What is the advantage of circular DNA in bacteria?

Off the top of my head I would say storage. It would be incredibly difficult to wind a circular genome around histones and continue to condense it until you hit the necessary info-density. However, since I don't haven't done the proper legwork, I'll not "Answer" yet. :)

@MCM that was my first guess, too... especially with the other big difference between pro and euk being the tight space of nucleus. However, I couldn't think of why folding a very long circular genome would be fundamentally more difficult than a linear one (in fact it would make certain kinds of knots more difficult, avoiding potential damage). I also know a negative amount of biology so couldn't think of how to start the literature search myself :D.

I'm almost convinced it's simple Torque problem. Condensing a linear genome isn't hard on the actual DNA so much as it's simply wrapping around histones, and histones congregating. The Torque is taken care of because the two ends are free. In a closed-loop genome, the minute you start wrapping it around anything or condensing it the Torque is going to build and build. You might be able to disperse it among the entire genome, but soon you'll have a lot of stress to deal with. It might just be circular genomes break if they're condensed.

@MCM if you could work that into an answer, I think it would be a decent one and I would enjoy reading it in detail. I was hopping for a more subtle answers (maybe related to life-histories), but I am happy with this, too :D.

Linking number? I think this goes with @MCM's torque issue.

It is possible to isolate yeast strains in which chromosome III forms a ring. Circularisation is driven by the components of the heterothallic mating-type switch mechanism. The sequences that are involved in the recombination event that causes circularisation lie near the telomeres, and no essential genes are lost during ring formation. Since haploid strains bearing this form of chromosome III are viable, I deduce that the corresponding chromatin structure is not messed up enough to interfere with growth. I have searched for actual data on this, but have drawn a blank.

Would it allow better recombination and/or better share of genetic material? When Conjugation occur in bacteria the sequence which is copied and transmitted is linear (even when only the F+ plasmid is transmitted if I'm not mistaken). If you recombine 2 lines you get 2 lines, if you recombine 2 circles you get a möbius strip!

I don't think the problem is torque. mainly because at the DNA level, water is very viscous. And DNA of a chromosomes being a very long molecule (tens centimeters long), a linear molecule would behave like a circular one, removing torque would be very difficult. My guess, is that organism with linear chromosome tend to be ones which under go meiosis. Chromosomes pairup, form chiasmata and exchange chromosome segments. On a linear chromosome, both odd and even exchange events resolve fine. In circular chromosomes, odd exchange lead to chromosome fusion. Even chiasmata resolve to two chromosomes

I think it is the wrong question. You assume that eukaryotes developed from a single-cell organism with circular DNA. Then, clearly, there must have been an advantage of (newly) developing a linear genome. But eukaryotes could have developed from an organism with linear DNA, too. There are still a few bacterial species with linear chromosomes, so this is not unlikely. We don't know, however.
On the other hand, if linearisation developed independently, you can learn from bacteria why it might have occurred:
J. N. Volff, J. Altenbuchner: A new beginning with new ends: linearisation of circular chromosomes during bacterial evolution. In: FEMS microbiology letters. 186, 2, May 2000, 143–150, PMID 10802162. (Review).
Abstract:

Bacterial circular chromosomes have sporadically become linearised
  during prokaryote evolution. Unrelated bacteria, including the
  spirochete Borrelia burgdorferi and the actinomycete Streptomyces,
  have linear chromosomes. Linear chromosomes may have been formed
  through integration of linear plasmids. Linear chromosomes use linear
  plasmid strategies to resolve the 'end-of-replication problem', but
  they have generally retained from their circular ancestors a central
  origin of replication. Streptomyces linear chromosomes are very
  unstable and at high frequency undergo amplifications and large
  deletions, often removing the telomeres. At least in Streptomyces,
  chromosome linearity is reversible: circular chromosomes arise
  spontaneously as products of genetic instability or can be generated
  artificially by targeted recombination. Streptomyces circularised
  chromosomes are very unstable as well, indicating that genetic
  instability is not confined to the linearised chromosomes. Bacterial
  linear chromosomes may contain telomere-linked regions of enhanced
  genomic plasticity, which undergo more frequent genetic exchanges and
  rearrangements and allow differential evolution of genes, depending on
  their chromosomal location.

I think its related to structure, like the noncoding (junk) DNA contributes to structure my guess would be that the Linear genome "just happend" and there was no way of going back.
That could have been because of Phage/Viral predation radical changes in genome structure will make it certainly very hard for viruses to adept. So in the early days of the eukaryotes the different genome would have provided a very strong protection against viral predation and thus would have allowed those organisms to reproduce nearly inhindered from the selective pressure of viruses. Which allowed for evolution to take place structures developed that make a step back impossible.
but yeah those are just WILD guesses

An interesting theory! Could you expand with sources?


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Mutation-immunity in Luria-Delbruck experiment
If experiments like those of Luria and Delbruck on E. coli and T1 phage are the main source of our confidence in the mutation-immunity model, is it then highly unlikely that there are other types of bacteria for which an encounter with a phage is the mutagenic (or immunity-conferring) event?
Are the two possibilities in principle mutually exclusive?

No. There was a recent surprising paper on a bacterial adaptive immune system. I cannot find it, unfortunately.

No. Surprisingly, there is an adaptive immune system in prokaryotes. This is still widely unknown. The newest review is
S. Al-Attar, E. R. Westra et al: Clustered regularly interspaced short palindromic repeats (CRISPRs): the hallmark of an ingenious antiviral defense mechanism in prokaryotes. In: Biological chemistry. 392, 4, April 2011, 277–289. doi:10.1515/BC.2011.042. PMID 21294681. (Review).
Cited from abstract:

Many prokaryotes contain the recently discovered defense system
  against mobile genetic elements. This defense system contains a unique
  type of repetitive DNA stretches, termed Clustered Regularly
  Interspaced Short Palindromic Repeats (CRISPRs). CRISPRs consist of
  identical repeated DNA sequences (repeats), interspaced by highly
  variable sequences referred to as spacers. The spacers originate from
  either phages or plasmids and comprise the prokaryotes' 'immunological
  memory'. CRISPR-associated (cas) genes encode conserved proteins that
  together with CRISPRs make-up the CRISPR/Cas system, responsible for
  defending the prokaryotic cell against invaders.

and

An application of the CRISPR/Cas system is the immunization of
  industry-relevant prokaryotes (or eukaryotes) against mobile-genetic
  invasion. In addition, the high variability of the CRISPR spacer
  content can be exploited for phylogenetic and evolutionary studies.
  Despite impressive progress during the last couple of years, the
  elucidation of several fundamental details will be a major challenge
  in future research.


text:
Is breathing in deodorant fumes dangerous for my brain?
I noticed that I sometimes get dizzy when I accidentaly breathe in too much Axe. Also, I find the smell of alchohol rich deodorants quite unpleasant. But, I was wondering, is it actually dangerous? Can some chemical (alchohol) pass the blood-brain barrier and hurt my brain? Can it hurt other organs? It might be that I'm just dizzy because of the lack of oxygen...

I think there is no doubt alcohol passes the BBB, that is how you get intoxicated when you drink it.

But can such miniscule (assumption, correct me if I'm wrong) amounts of alchohol a) actually pass, and b) hurt me in a significant way?

I don't know, I was just saying that alcohol (specifically ethanol) has no problem passing the BBB, I am not sure about doses etc. in deodorants, sorry.

You can definitely absorb alcohols by breathing them in.  But doing do is far less efficient than drinking alcohol, so you don't have anything to worry about on that front.
To address your concern we have to answer two questions: how much alcohol is transfered per unit time and is there a local dosing effect due to proximity to the blood brain barrier.
It is probably pretty obvious that while alcohol evaporates rapidly compared to water, it still takes quite awhile. Imagine trying to inhale a glass of whiskey. You would get a serious headache but 30 minutes in you would still have an almost full glass of whiskey and no alcohol buzz. For an amusing anecdote relating how hard it is to get drunk off of inhaling even from a machine designed for it, see here
As to the second point - Fortunately, the blood brain barrier is a two way street for alcohol, which means that you can't get drunk in your brain if you don't have high levels of alcohol in your bloodstream. The two would dialyze into a reasonably balanced equilibrium.


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What distinguishes "coding" from "noncoding" DNA?
I've been reading a bit about "junk DNA" and how much of our genome consists of this "non coding DNA" in comparison to "coding DNA".
I'm just an interested layperson but I thought all combinations of three base pairs encoded one amino acid, with some amino acids being encoded by more than one combination of base pairs.
But if that were true then all of our DNA would encode something.
Or if only a tiny percentage of our DNA is "coding" that would mean that the vast majority of possible combinations of three base pairs don't represent any amino acid.
Or it could mean that there are a small number of "meaningless" combinations of three base pairs, but that those combinations are vastly overrepresented in our genome.
Which is correct? What am I missing?

Would anyone like to add junk-dna and/or noncoding-dna (or should that be non-coding-dna tags? I barely have enough rep here to breathe (-:

Wikipedia has a well-written page on the genetic code with tables and pictures showing all the possible triplets and their meaning!

@Hippietrail To the meta!!!!

You are correct in thinking that any sequence of bases corresponds, via the genetic code, to a sequence of amino acids. However not all stretches of DNA are actually transcribed into mRNA for translation into proteins. For this to happen the stretch of DNA requires (DNA-encoded) elements to promote and regulate the transcription and translation processes, and this, very broadly, is what defines a gene: a segment of DNA which has the required components to direct the synthesis of a protein (or in some cases an RNA that will not be translated into a protein). The segments of DNA that correspond to mRNA for proteins and to other RNA molecules are referred to as coding sequences.
Now, I've omitted lots of details here: some genes encode RNA molecules, such as ribosomal RNAs, which are not translated into proteins; eukaryotic genes include stretches of sequence (called introns) that are spliced out of the transcript before the mRNA>protein step. The original definition (if there ever was a definition) of "junk" DNA included these introns, as well as regions of DNA lying outside the coding sequences. We now know that there is useful information stored in much of this DNA, even though it doesn't code for anything directly via the genetic code.

Hmm @DanielStandage 's answer got more votes but AlanBoyd your answer here answers my actual question. Both answers are full of interesting stuff but this is the one I'm accepting.

What "useful information" it could be?

You bring up a good point. "Coding" is a term that obviously carries some historical baggage that is gradually becoming less and less relevant. "Coding DNA" has typically been used to refer to DNA that encodes one or more functional protein products, which are constructed from an mRNA intermediate. As we've been learning over the last several years (and as was confirmed by the recent release of 30+ coordinated, high-profile publications from the ENCODE project), DNA that is not "coding DNA" is not "junk" or "meaningless"--it simply does not, to our knowledge, encode a protein. There is still a lot to learn about what precisely the function and purpose of this DNA is, but we do know that a lot of it is transcribed into RNA and that a lot of it has been associated with human disease.

Yes I put "junk" in scare quotes precisely because it's not really junk. So while I knew it wasn't junk I wanted to know a bit more deeply what non-coding DNA is. It seems that the terms "coding" etc are ambiguous if my understanding is right.

@hippietrail Agreed. A lot of what is sometimes called "non-coding DNA" indeed encodes something...just not a protein! We're definitely going to have to revisit our terminology as a community, but that is a slooooow process. Case in point: "junk DNA" is still commonly used. :-/

Coding is a term with a clear meaning in relation to DNA. It implies that that DNA encodes a protein (via mRNA). This is not historical "baggage", it is historical usage. Non-coding does not imply non-functional, nor did it historically, when all that was known was the genomes of bacteria. Promoters? Origins of replication? A misleading answer.

DNA regions coding for proteins and RNA's comprise a rather small portion  of total eucaryotic DNA.They are associated with special upstream signal sequences
(promoters,enchancers,"boxes"etc) translation initiation triplets  and translation termination  signals ,which all together establish a reading frame
provide information for  the formation of the translation complex and the regulation of the whole translation process.
Non coding DNA is by no means junk just because  we do not understand it well enough yet.However it is known to play important roles in the formation of chromatin structure and its transformations which are crucial for exposing /hiding  genes and their regulatory sequences to the proteins and cofactors
working on them.They are characterized by large amounts of repetitive sequences and may also contain silenced ancient genes .

It is better to add a citations to further cement your claims in your answer.


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Why is the frog genome so much larger than a fish's?
As we have heard in the summaries of the human ENCODE project, 80 per cent of junk DNA appears to have an essential function. Many fish have a genome with only one tenth the size of a usual vertebrate genome. Why can fish have 1/10th of junk DNA and be still fully functional? What has a frog more than a fish has? I'm especially interested if we can see the difference somewhere, complexity of physiology or anatomy, or such.
Jap. puffer fish genome: 390 Megabases, 47,800-49,000 genes (UniProt)
Medaka genome: 690 Megabases, 24,600 genes
Clawed frog: 1,500 Megabases, 23,500 genes

I think this question, like at least a few others, is based on a misunderstanding of ENCODE’s use of the word “function”. Maybe we should have a kind of FAQ for that. (Disclaimer: I agree with their usage of the word. Others, e.g. Larry Moran, disagree – vehemently.)

I also read in Wikipedia's article about ENCODE that their method of detecting "functional" DNA is prone to false positives, as it emphasizes sensitivity over specificity.

Genome size is a poor indicator of an organism's complexity (already an ill-defined term). We cannot assume by any means that a larger genome corresponds to a more "complex" organism. There are some plants whose genomes are larger than most mammals, and indeed the largest eukaryotic genome (at least as of 2010) is the plant Paris japonica, weighing in at 1C = 152.23 pg (compared to Homo sapiens at 1C = 3 pg). Anecdotally, in my previous research lab I discussed with a colleague a fungal species whose genome size differed by orders of magnitude between different individuals of that species.
It should never surprise you to see an organism with a larger genome size than what you may consider to be a more complex organism.

Just saw this on Twitter, and wanted to point it out. https://twitter.com/DanGraur/status/372712933525946368

See here for an ENCODE author's reflections on their use of the word "functional". (I don't think anyone is using the word "essential".)
It is clear from this that, for them, one class of functional DNA is intronic DNA: i.e. introns are defined by ENCODE as functional DNA. It is well known that puffer fish have reduced genomes and that this is largely due to the presence of much smaller introns, although the number and positioning of these introns is broadly similar to what is seen in other vertebrates. One classic example of this is the huntingtin gene which is 7.5 times shorter in pufferfish than in humans even though both genes have 67 introns. In fact the average fish genome size is 5-6 times bigger than that for pufferfish (zebrafish is around this average value).
Although ENCODE are defining intronic DNA as functional I don't think that they are claiming a specific function for each and every intron, let alone each base in those introns. So there is still  a lot of scope for the observed differences in genome size.

I think the last paragraph nails it (and, incidentally, the controversy about ENCODE’s 80% figure) – although intronic DNA is just a small part, much more is in repeat elements.

That's a good read!


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Does retinal detachment happen more frequently at night?
My understanding and experience is that during the night photoreceptors are less tightly coupled to the retinal pigment epithelium.  Does this make it more likely for a retinal detachment to happen at night?

In case of normal, healthy person, no, I don't think so. In fact, retinal detachment could happen at anytime of the day. Main causes are diseases and illness, such as AIDS, diabetic retinopathy, cancer, or trauma such as post-cataract surgery and being hit/kicked hard on the eyes.


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How to learn DNA Origami
Can you tell me is there any good softwares and tutorials which can be used to learn DNA Origami. I am new to this and want to learn from basics.
Advance thanks for your help
edited: INSILICO

I am assuming you want to do it in silico, right?

you can also do a little origami DNA... http://www.youtube.com/watch?v=0jOapfqVZlo

@nico yes, my current idea is to do it in insilico..but may be in future i will try to do it in invitro also..it will be helpful if any one can explained both procedure

Try this.

cadnano simplifies and enhances the process of designing three-dimensional DNA origami nanostructures. Through its user-friendly 2D and 3D interfaces it accelerates the creation of arbitrary designs. The embedded rules within cadnano paired with the finite element analysis performed by cando, provide relative certainty of the stability of the structures.

I would try to read everything from Shawn Douglas's body of work. cadnano is definitely the best start.

According to Rothemund, the original algorithm in the DNA origami paper is the same and much improved in caDNAno.


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What is the species of these mushrooms?
The mushrooms are gilled with a light-brown cap. The stem is widened to the base.
What species is it? Is it considered edible?
They are found in mixed forest in Moscow, Russia. They grow in the ground quite separated from each other.

Looks like Boletus edulis. If that is the case is not only edible but extremely yummy. However, please do not trust me too much on this, I am no mushroom expert.

@nico it cannot be boletus because it is gilled, while boletus is pored.

Please, describe where have you found them (geographic location, type of habitat). This kind of information is very useful for species identification.

@Anixx: told you not to trust me on that :P

@Marta Cz-C done

This is Clitocybe Nebularis, an edible species.

I had a quick look in my books (for the British Isles and Europe) but although I found a couple of candidates I don't feel confident in either identification.
I suggest that you have a look at Roger Phillips' online identification guide  - this will suggest a few identification criteria that you haven't considered in your question.

"No results found. We were unable to find a match for your search."

For the record, my two candidates were False Death Cap (immature specimens) and St. George's Mushroom (but this is a spring fruiting species). These were based on the general colour and swollen stem base only.

@Alan Boyd the cap is smooth and there is no veil at the basement. Also there is no skirt. Very far from False Death Cap.

@Alan Boyd My candidates are species of Cortinarius genus (Cortinarius glaucopus http://for-grib.ru/IMAGES/pautinnik-sizonozhkovyjj-cortinarius-glaucopus-lllo5b.jpeg Cortinarius praestans http://www.aranzadi-zientziak.org/fileadmin/images/micologia/Eskaneatuak/09_digital/cortinarius_praestans_paa_091103.jpg Cortinarius esculentus http://infofishing.ru/uploads/posts/2011-12/1322998170_pautinnik.jpg ), Tricholoma portentosum http://www.dipbot.unict.it/funghi_etna/photogallery/Tricholoma%20portentosum.jpg Clytocybe nebularis http://nepoganki.narod.ru/Photos/074_photo.jpg

http://farm6.staticflickr.com/5190/5602239343_08378ce877_m.jpg

Or Clitocybe clavipes http://mycoweb.narod.ru/fungi/Submitted/SJG2/Clitocybe_clavipes_JS20040829_med.jpg

It turned out to be young Clitocybe Nebularis, an edible and tasty mushroom.


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Is there any documented evidence for suicide among vertebrates other than humans?
Is there any documented evidence for suicide among vertebrates other than humans? Lemmings not accepted !

Does whales beaching themselves count as suicide? Wikipedia defines suicide as "the act of intentionally causing one's own death", but, in my opinion, it's hard to determine intentions of non-human creatures.

Supposedly Tarsiers will commit suicide when in captivity by banging their heads against a wall.  But I think it is difficult to distinguish between "that animal went crazy and lost its sense of self preservation" from "that animal committed suicide".

Hmm... Lemmings? :)

He said the L- word ...

I heard of a boar species where one boar will face the attacker and fight a losing battle, buying time so that the group can safely evacuate the area.

@aland That's the problem isn't it? How do we know thatt whales are really intentionally beaching themselves?

I would be curious to check if unicellular organisms commit apoptosis.

Here's a short piece about animal suicide from Time: http://www.time.com/time/health/article/0,8599,1973486,00.html

From Wikipedia: "It is not a mass suicide, but the result of their migratory behavior. Driven by strong biological urges, some species of lemmings may migrate in large groups when population density becomes too great. Lemmings can swim and may choose to cross a body of water in search of a new habitat. In such cases, many may drown if the body of water is so wide as to stretch their physical capability to the limit. This fact, combined with the unexplained fluctuations in the population of Norwegian lemmings, gave rise to the misconception." Misconception.

Well, there are certain behaviors that may qualify. The clearest example I know of would be sexual cannibalism, and more specifically (source):

The redback spider is one of only two animals to date where the male
  has been found to actively assist the female in sexual cannibalism. In
  the process of mating, the much smaller male somersaults to place his
  abdomen over the female's mouthparts. In about two of three cases, the
  female fully consumes the male while mating continues. Males which are
  not eaten die of their injuries soon after mating.

That sounds pretty suicidal to me...
A less flagrant but commoner example is that of mothers dying to nourish their offspring. Again often seen in spiders, the best example I know of is the giant pacific octopus (Enteroctopus dofleini). The female will chose a den and lay her eggs. She will then spend her last weeks tending her young, never leaving the lair to hunt. Eventually she dies of hunger and her body nourishes her young. My source here is the wonderful BBC life documentary series.
Neither of these are vertebrates of course but still, I thought the suicidal little spider was interesting.

is right - basically animals care less about their lives when they have reproduced or when there are lots of near relative (like a bee hive, an ant colony or a clutch of cockaroaches or guppies).  They may not overtly be committing suicide, but they will defend their nests to the death or take what would seem to be tremendous risks just for some food.

@shigeta, yes this question got me thinking about social insects. I would have mentioned it but for the fact that the question asks for vertebrates (and I already mentioned two invertebrates :) ) and that, for hive insects, it might be more correct to see the hive as the individual. That raises other questions of course...

I did say vertebrates since that was the original discussion I had, but evidence for "suicide" in any organism is interesting..

Ostensibly, its the conditions of selection that cause this not as much the branch of the family tree you come from.  On the other hand there are fewer animals whose lives are cheaper than insects. Lizards will eat their own eggs... that's not suicide tho.

There's a cool new paper that documents for the first time a male spider (dark fishing spider) whose physiology causes death upon mating.  its a one time deal for these boys. http://rsbl.royalsocietypublishing.org/content/9/4/20130113

@shigeta, ouch!

The problem is that committing suicide, using the commonplace definition of it, would require an understanding of death. I am sure that an animal can have a basic understanding of the death of others, so far as they realise the difference between a living companion and it's dead body. But if they understand that this lifeless body will never go "back to normal" again and that there is also future death for themselves, I am not convinced.
So, without the understanding of the own, irreversible death, there is (following the definition) no suicide.

Totally not an answer. He's asking for evidence, not philosophical stuff.

The problem is, he did not ask if there is evidence for other vertebrates killing themselves. (As I would guess by the "Lemmings not accepted.") There is. So, the question is really can we classify any of these occurrences of them killing themselves as suicide.

According to this article whales could kill themselves by swimming to the beach and even when pushed back to the water, they return or dogs can drown in the water when suffer a lot.

Answer: Yes.
As Zoobiquity points out, gorillas sometimes die from self neglect (starvation) caused by clinical depression. These, besides humans, are likely the only animals to do so through self-neglect.
Then again, one could call scrapie (a prion disease in sheep) or tail-plucking disorder (in parrots and other birds) and other self-mutilative disorders as a form of suicide, but the actual wounds themselves aren't liable to kill the animal.


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Is DNA mutation locally energetically stabilizing the DNA molecule
I am no biologist, but as a physicist, a spontaneous mutation (seen as a chemical transformation) should lower the energy of the system, at least locally. So I wonder if any research has been done along these lines for the DNA.

Not all reactions lower the chemical potential energy of all of their products - consider any endothermic reaction, in which heat energy becomes chemical potential energy. Reactions actually happen to increase the entropy of the universe, not the stability of it - looking at potentials is an approximation only.

Even if you just want to approximate the truth by considering energy potentials, why shouldn't your understanding equally predispose you to the expectation that the other reaction product would become lower energy?

@Mason: Physical systems always spontaneously evolve to lower energy state.

@hanuman, I'm with Masonk. DNA mutations are more a result of entropy than any enthalpic driving force. Plus, what system are we talking about, DNA? Cell? Life?

I am a physicist: thermodynamics entropy is a macroscopic parameter (as T) which is only defined for systems made of a large number of particles like a gas. There is no thermodynamics for a single molecule...You just have QM, energy and momemtum conservation for a single molecule.

@Hanuman, from a stat thermo point of view, the polymer isn't merely a single molecule but rather beads on a string. From what I understand, you should be able to quantify entropy by comparing the number of states W. Furthermore, in the problem that you are providing, you are not looking at a single DNA molecule but external factors like mutagens and enzymes. Those molecules will act in concert to increase the entropy of the system.

a spontaneous mutation (seen as a chemical transformation) should lower the energy of the system

Why do you think that? Because it’s an endothermic reaction?
Consider that mutations don’t happen “just like that” (at least to my knowledge) –they are triggered by external energy influx from things like reactive oxygen species or ionising radiation. So yes, they cost energy but that energy doesn’t come energetically unstable chemical bonds; it is supplemented from external sources.
So it’s not necessarily true that mutations produce lower-energy chemical bonds.

I'm going to attempt an answer to this at the level of undergraduate biochemistry: apologies in advance if this is not sufficiently sophisticated.
The most frequent spontaneous mutation is deamination of cytosine to uracil (hydrolysis with loss of ammonia). Strictly in terms of the double helical structure of the DNA molecule this, it seems to me, would be destabilizing because of the change from a GC base pair (3 hydrogen bonds) to a GU base pair (2 hydrogen bonds).

Thanks for your answer. If the DNA molecule is locally destabilized by a spontaneous mutation, the odds for an other spontaneous mutation to restore the stability locally are greater and that should slow evolution to a standstill if only spontaneous mutation were to be considered.

The reaction kinetics of DNA mutations are complicated by the fact that the DNA doesn't exist in isolation, and in fact is actively processed and maintained by the cellular machinery.
For example, as Alan Boyd notes, the most common spontaneous mutation is the deamination of cytosine to uracil: Cyt + H2O → NH3 + Ura.  On its own, the reverse of this reaction, i.e. spontaneous amination of uracil to cytosine, would be very unlikely, if only because the low concentration of ammonia compared to water in cellular fluid.
However, in a living cell, there are DNA repair enzymes that actively look for uracil in DNA and remove it, allowing other enzymes to come along and replace it with the original cytosine.  This keeps the effective Cyt → Ura mutation rate far below what it would be in the absence of active repair.


text:
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.

I've seen in a documentary that inuit, eating only seals for a longer period of time are some of the most healthy people on the planet.
However I can't seem to find that documentary anymore.
I did found a wiki article about this subject:
Inuit diet Article

The only thing I can find in your Wikipedia link is a mention of larger livers in Inuit people. The part about bring healthy because of this is not clear - it could be that this seal diet just happens to be better in terms of baseline nutrition, nothing to do with absorption.


text:
What is the relationship between Homocysteine and Norepinephrine metabolic cycles?
I've been researching neuromodulators and have taken a look at the Norepinephrine/Noradrenaline  system.
The diagram of biosynthesis of Norepinephrine is presented in the wikipedia article:
Catecholamines_biosynthesis
The diagram appears to state that Dopamine gets converted to Norepinephrine , which gets converted to Epinephrine, and as a side effect, Homocysteine cycle gets advanced too (or is it involved?).
This article describes the homocysteine biosynthesis
I would like to understand what this means when two biosynthesis cycles are related like that. If I envision two cycles as connected gears, then turning one would turn the other, and if one is malfunctioning, so will the other. Is this a correct analogy?
What are the implications of the Homocysteine and Norepinephrine cycles touching each other? As far as I understand, Epinephrine(Adrenaline) is a stress related hormone, does this mean that stress also results in elevating the levels of Homocysteine ?
Thank you for your clarification!

Norepinephrine is converted to epinephrine by phenylethanolamine N-methyltransferase (PNMT). In mammals PNMT is just one member of a large family of methyltransferases which use S-adenosylmethionine (AdoMet) as a cofactor to provide a methyl group. These methyltransferases are involved in a very diverse set of pathways including the synthesis of nucleic acids and of certain phospholipids, as well as the methylation of DNA and histones.
As you point out, these reactions generate homocysteine via S-adenosylhomocysteine. However, because AdoMet is such a critically important cofactor it is thought that cellular levels are tightly regulated. As part of this regulation, homocysteine is re-methylated to methionine via two different routes requiring either methionine synthase or betaine-homocysteine methyltransferase. Methionine synthase obtains the required methyl group from 5-methyltetrahydrofolate in a vitamin B12 (actually methylcobalamin)-dependent reaction. This latter reaction links the AdoMet-based methyl transfer system to the other part of the cellular one-carbon economy, the folate pool. This is why vitamin B12 deficiency leads to hyperhomocysteinemia.

This Figure is reproduced from Luka et al. (2009) Glycine N-methyltransferase and regulation of S-adenosylmethionine levels. J. Biol. Chem. 284:22507–22511. I show it here just to illustrate the point that there are, in fact, many gears interacting in this system. The minireview is interesting and I recommend it to you.
In conclusion, my answer to your question is that it is unlikely that stress leads to elevated levels of homocysteine as long as all of the relevant regulatory machinery is functioning correctly. If there is a problem with homocysteine recycling then yes, homocysteine levels would rise, but given that there so many AdoMet-dependent methylation reactions it is unclear how big a contribution PNMT would make to the overall homocysteine load.


text:
Phenotypic Variation of cattle - looking for academic sources
Can someone please point me in the direction of a good academic article on the following:
What are possible sources of phenotypic variation of different 400 day weights of cattle?
Furthermore how much variation is likely to be due to each contributing source?
I have tried the following searches in google scholar:

Phenotypic, genetic, environmental cattle weight
Phenotypic variation cattle weight
Phenotypic variation
Phenotypic variation, genetic
genetic variation, dam, sire

this is a subject that has been well understood by cattle breeders but is not an academic research topic I think.  This is not my field, but this article might point you in the right direction http://www.theatlantic.com/technology/archive/2012/05/the-perfect-milk-machine-how-big-data-transformed-the-dairy-industry/256423/

Online Mendelian Inheritance in Animals (OMIA) is a database of genes, inherited disorders and traits in more than 135 animal species (other than human and mouse). At the moment, it has about 400 entries for Bos taurus, mostly disease phenotypes. This is probably the only attempt to exhaustively list such phenotypes.


text:
Can a person become addicted to tea?
Can one become addicted to tea like coffee addicts or smokers? I heard there are some common substances in tea and coffee, do they cause addiction?

Note that there's physiological/psychological addiction. Two very different things.

Yes, both tea (black tea at least, English speakers usually mean black tea when they say tea anyway) and coffee have caffeine which is addictive.
Apparently, being able to correctly reply to this question involves defining the word "addiction". My guess is that the negative connotation of the word "addiction" will cause some pressure to not use it.
Here's a recent review on caffeine addiction that says that caffeine is not addictive. I do not agree with their arguments but I'll leave it to the reader to judge.

Here's a decent link affirming different articles I've read before: http://www.medicinenet.com/caffeine/page2.htm     Basically, carandraug is correct. Caffeine is addictive, though not to the entire population, and the withdrawal symptoms (which are basically lack of energy and headaches) rarely last more than a few days. It is NOT a narcotic that acts as a neurotransmitter (like nicotine), thus its addictive capacity and withdrawal symptoms aren't comparable.

Doesn't green tea have caffeine, too?

@rwst yes, green tea does have caffeine as well (I said black tea at least, other teas may have caffeine. But I'm sure this days, one can buy even green tea without caffeine)

@rwst: green tea and black tea are the same plant (the tea plant, Camelia sinensis). carandraug: I will gladly upvote this answer if you link to some study or review showing that caffeine is addictive (should not be difficult to find).

@nico I did the opposite. I added a review that says it's not addictive and invite the reader to be critic of what they read.

I think I've heard that green tea (and white tea) have less caffeine than black.


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How exactly are game theoretical evolutionary models described during implementation for computer simulations?
When a biologist or a layman tries to reason the evolutionary explanation for something, they would simply use English with some math thrown in (for a random example, pick any explanation out of "The Selfish Gene" -- for example, the reasoning why "discriminate in favor of one's own eggs" strategy is employed by Guillemots, in "Genesmanship" chapter, page 103. I won't quote it in full since it's a page worth of text).
Another example of such a wall of English is (Dawkins-inspired) Bio.SE question: " Why is 'Grudger' an evolutionary stable strategy? "
When a biologist tries to actually model evolutionary development to see which traits would win, they would need to somehow teach the computer to implement that model: what the environmental factors are, what the genotype involved is, how exactly it's expressed in different phenotypal and extended phenotypal traits, and how environment would affect an individual with that phenotype.
My question is: is there some sort of standard way to build such a model? A domain specific language (in computer science terminology) that is used by many different biologists or some standard modeling packages/software? E.g. some sort of special XML format, etc...
Or is it always just hand-built custom implementation by individual researchers for their current model?

Just to clarify:

I'm NOT asking what the models look like theoretically. I'm asking what language/format (if any standard one exists) is used to encode them to run simulations.
If there are discrepancies between the type/purposes of models, the ones I'm most interested in are game theoretical ones.

The impetus of this question is, if I'm curious to see how a specific model would behave, would I have to code the entire thing - mode, language, and simulator - from scratch (likely incorrectly, being a layman); or there are some standard packages that do it for you as long as you use some proper language to describe your model.

Unfortunately the guillemot example is a bad one - Dawkins was wrong about it (and very obviously so). He forgets to account for the fact that if a bird lays twice as many eggs as any other in the colony, his eggs are twice as likely to be excluded from care.

@RichardSmith - Seems counterintuitive to me. If the only eggs being excluded are the ones that no bird claims; you lay 2x eggs, and there's 5% of you with that specific strategy, then (assuming you have a colony of 100, with 1 egg clutch for normals), you have 105 eggs total, so 5 will be excluded. Each egg has ~1% chance of being excluded, so for BOTH of your eggs to be excluded, the chances are 1%x1%=0.01%. Nearly 100 times better than a single-egg bird.

It's not the chance of both eggs being excluded that Dawkins talks about, he talks about the chance of having an egg excluded. It's still true that it would be worth cheating for the first few birds. The wider point about the trait not being an ESS might be true, but his specific explanation is not. In your specific example, if there are 105 eggs and 5 are excluded, each egg has a ~5% (more precisely, 4.76%), not ~1%, chance of being excluded. In any case, your question was interesting so I'm writing a model of the Guillemot situation. I'll report back when done :)

The field most closely associated with game theoretic models in biology is evolutionary game theory. If modeling is required, then the typical paradigm is agent-based modeling, and a good introductory book is:

Yoav Shoham and Kevin Leyton-Brown
  [2009], "Multiagent systems:
  algorithmic, game-theoretic, and
  logical foundations", Cambridge
  University press.

As for actually building the model, and what to describe/how, I will take you through my usual procedure since this is a field I specialize in:

Define what type of strategies you think are relevant to the interactions you are modeling. Select what you expect the payoff of those strategies to be. For instance, if you are studying the evolution of cooperation, you might select 'Cooperate' and 'Defect' as your strategies and the Prisoner's dilemma as your pay-off matrix, but maybe you will pick something more general. Unfortunately, in most of EGT a clear distinction between genotype and phenotype is not drawn, and they are usually equated. At the end of this step you have a game matrix G. Sometimes when mutation or innovation are explicitly necessary even in the inviscid model, further analytic approaches are taken at this stage. I recommend Hofbauer & Sigmund (2003) for a broad treatment of step 1.
Now you need a basic intuition of what the 'default' behavior in this interaction is, so solve the replicator dynamics of G.
The main interest in EGT right now is structured populations. This is where computational modeling is typically used. However, before I turn to simulation, I first try the best analytic approach I know. I use the Ohtsuki-Nowak transform on G to analytically solve the interaction for random graphs (Ohtsuki & Nowak, 2006).
If I am still interested in the question, and steps 2 and 3 didn't capture all the subtlety of the system I want to study, then I start building a multi-agent computational model. I make sure that my model has some way to scale to the completely inviscid case of replicatory dynamics, and the simply-structured case of ON-transform. If my computational model disagrees with the analytic approach in these regimes, then I become worried. Otherwise, I continue with standard agent-based modeling techniques. Personally, I code in Matlab. I have never seen a modern EGT simulation that required the performance of C/Fortran. As suggested in another answer, if you don't have a programming background then you can use NetLogo. However, my experience is that the models are typically simple enough to implement from scratch, and NetLogo models typically hide from you some very important subtleties (like which reproduction rule to use: death-birth, birth-death, immitation?) and usually lead to weaker papers.

Note the broad theme. These models are typically described as differential equations, and this approach is preferred to agent-based models. However, if a clean differential equations approach does not capture all the subtleties of what you are studying, then an ABM paradigm is adopted.

The particular language a bioligist uses depends on the trade-offs between speed and ease of programming.  Many models are written in C or Fortran if speed is paramount.  On the other hand people will write models in higher level languages if speed is less important.  These would be Python, R, MatLab, etc...  In my models, which are written mostly in Python, I write all the classes from scratch and then all the simulation components by hand as well.  Since almost all models are mathematical in nature, the language is inconsequential.  Algorithms should behave similarly across platforms.  If you're looking for examples of easy ways to code up game theoretic models, consider NetLogo, they have some nice examples using game theory.

This. I would say most people use the language they know best, so for non-programmer scientists that's python or perl, for mathematicians it's matlab, mathematica, or berkeley madonna, and for programmers it's c or some descendant.

No generally used DSLs? Is that because it's too hard to develop, or just nobody needs it?

Probably both. Berkeley Madonna is specifically for modelling, but it's horrible, so it's not that widely used.

I'd say that as far as DSLs go, Logo is a DSL for individual based models, but most biologists can program in another language that's more flexible.  Also both python (in scipy) and R have ODE solving capabilities so you don't have to use Madonna.

There is no single way to build such a model.  They can vary from a simple mathematical statement like Hamilton's rule (rB>C) to the chemical diffusion models used to describe the patterns in animal skin coloring (like zebra stripes, leopard spots and the like).
There are efforts to build molecular models of entire cells like this model of mycobacterium genitalium dividing, which integrates nearly 30 different mathematical models to describe different aspects of the organism.  There are efforts to build such a model of an entire brain as well.
Another common sort of model for evolutionary biology is the use of game theory, where different strategies can be posed one against another as in the prisoner's dilemma competition Dawkins describes in the Selfish Gene.
It goes on and on.  Basically biological modeling is driven by the sorts of mathematical models that we know.   New models will reveal new paradigms of how biology works.  They can be highly mathematical, but their relative importance and when they apply and what they mean are more analogy than proof.
For instance in the prisoner's dilemma, the first contests showed that Tit for Tat was the strongest model - generally assisting others, but betraying when there is a history of betrayal.  The ideas at the time moved towards general cooperation in populations.  More recent replays have shown that if there is a team of entrants that make extraordinary gifts to each other (allow betrayal without retribution), then they can compete against other models quite well.
One can never prove that a selfish model for the prisoner's dilemma will not show up, though biological systems to seem to be highly cooperative.  That is a model, not a proof.

My question was mostly aimed at game theoretical ones

Please see updates to the question. I'm not asking how the models are tested. I'm asking what language (if a standard one exists) is used to communicate the model parameters to the simulation.

I think the answer would be no - R could be a standard in the coming years, but i've seen several languages touted in various courses including Excel.

Let's hope R doesn't become standard for anything other than stats - it's the ugliest programming language since J.


text:
Is there a physiological difference between love and infatuation?
I find that people generally distinguish between love and infatuation. Is there a physiological difference between the two? Or are they biologically identical, and the difference is circumstantial?

Could you elaborate on what you feel the distinction between the 2 is? Infatuation could just mean obsession, whereas love could imply a more physical attraction?

I don't really know the difference. It's kind of what I'm asking.

My point was simply that the interpretation of the words is quite subjective, unless you define them in the question. E.g. dictionary.com definition #1 for infatuation is [to inspire or possess with a foolish or unreasoning passion, as of love], and love as [a profoundly tender, passionate affection for another person]. Is this how you interpret them? Or would you say they feelings are more divergent? In my opinion you could probably use either definition for each word, depending on the context.

I'm sure I don't know. I'm essentially asking about the biological definitions of those words, if there are any.

The distinction (if there even is one) is likely to be at the psychological level, rather than biological... but that's just my gut feeling - I've not read that anywhere!

Assuming that our emotions are the psychological manifestations of chemical changes in our bodies (an assumption I have no trouble with but one that others may take umbrage at), any emotion will be different.
If your brain can distinguish between two emotions, then the underlying chemistry through which these emotions are expressed will be different.
This is not to say that we, as scientists, can quantify this. Definitely not today at any rate. Simply that there will almost certainly be a physiological difference between any emotional state that can be differentiated by your brain. Otherwise the brain would not register different emotions.

UPDATE:
Human language has different words for different feelings. There is often a type of feeling "continuum" with different words representing different ranges on this scale. For example:
Adoration--->Love-->Infatuation-->Affection-->Indifference-->Dislike-->Hate
How you decide to qualify an emotion you are feeling is more a question of semantics than biology. The point I am making here is that each point on that scale (and every point in between that we haven't explicitly assigned a word to) will represent a slightly different mix of various chemical signals in your body.
If your question is more about the English language words love and infatuation, their definition and distinguishing between them, try posting on English.SE.

Okay, but I don't even know if the brain can differentiate between infatuation and love.

If  you can differentiate, your brain can.

I don't know that I can differentiate between the two.

@Avi, see my updated answer.

That answers my question (that answer being "no").

Using the Triarchic Theory of Love proposed by Robert Sternberg, love is divided into three components:

Intimacy
Passion
Commitment

Using the theory's particular Infatuation is just the passion portion of love which is lacking in intimacy and commitment required for Consummate Love or True Love.
Physiologically speaking, this is when a certain sense of dependency comes in and as we know from years of addiction research, there is a physiological difference between liking sex physically and liking sex with a particular person for non-physical reasons.

Psychologically infatuation is associated with a projection - attributing to a person the qualities of an idealized person. This is not the only example of projection - similar explanation is given to irrational hate or immediate dislike, which are usually based on projecting a certain stereotype, attributed to a person due to their physical characteristics, superficial elements of their behavior, social status, etc. This is how people come to immediately think of a black person as a criminal, beautiful woman as promiscuous, a bearded guy as a terrorist, rich as callous, poor as lazy, etc.
Being based on superficial characteristics, such projections disappear when we get to know the person better, which is why infatuation passes after a few weeks or months - one learns that the object of one's infatuation differs from the idealized image. Then love, as opposed to infatuation, is a lasting feeling of the attachment to a person, when one is no more ignorant of their faults.

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


text:
Microbiome Data
How is it possible to access microbiome data like that found here? I'd like to perform analyses on similar type of data, but cannot find OTU data like that at the Human Biome Project. Thanks for any leads.

Purely computational questions are better suited for http://biostars.org

This .csv files (comma-separated value) can be imported into Galaxy (usegalaxy.org)
I recommend that you take a look at that web app, it has many build in applications for analysis.
Also this site has a lot of quick video tutorials.

Thanks for the link. I'll check it out. My goal was to get OTU prevalence data (like at the exploredata.net site) and not just the Human Biome Data (regardless of format [e.g., csv, FASTA,etc.]) on what constitutes a particular OTU.

The data that you are pointing to are files in .csv (comma-separated value) format. They can be opened, after downloading, by any standard spreadsheet programme, including Excel, as well as programmatically (e.g. in Python using the csv module)
Apologies if you understood this and were asking for something more.


text:
Pharmacologically, can tricyclic antidepressants have a side-effect profile similar to neuroleptics?
Torticollis (wryneck, cervical dystonia) is a neurologic movement disorder causing involuntary muscle spasms in the neck. Often, neuroleptics can cause such a side effect.  I'm wondering if this condition could also be part of the side-effect profile of  tricyclic antidepressants, like amitriptyline.
Some potential indications:

Often the basal ganglia are associated with neurological conditions such as movement disorders. -> Do amitriptylines effect the basal ganglia?
Dressler and Benecke claim that "Of all patients treated with neuroleptics approximately 2 to 3% develop acute dystonic reactions within days of therapy initiation .When highly potent neuroleptics are used this rate may increase to over 50 %.Young men are at a particularly high risk. Cranial, pharyngeal, cervical and axial muscles are most commonly affected causing oculogyric crisis, grimacing, fixation of the jaw, retrocollis, torticollis or even opisthotonic posturing." -> Do tricyclic antidepressants operate similar to neuroleptics?
Geyer and Bressman claim that dystonia can be caused by certain drugs: "In addition to inherited forms of secondary dystonia (dystonia-plus syndromes and neurodegenerative diseases), a variety of acquired insults can cause secondary dystonia in previously unaffected individuals. Many cases are iatrogenic, resulting from drugs that block dopamine receptors; antipsychotic and antiemetic drugs are the most common culprits." -> even though amitriptyline doesn't seem to block dopamine, maybe there is some kind of connection?
Tricyclic antidepressants sometimes seem to be used to treat torticollis, so is the reverse effect of causing the condition also thinkable?

I'm not sure your question is allowed, and if it is, I'm not positive you'll get an answer. This sounds dangerously close to medical advice regarding possible side-effects, which only a trained physician or medical professional should give you. If you're curious about a specific mechanism of amitriptylines, then please specify. Otherwise, I suggest you take it up with your local M.D./D.O.

I can assure you that this I'm not seeking for medical advice by posting this question. I'm not sure either if I will get an answer here, but I didn't know a better place to ask for now. I have considered emailing the authors of the cited papers, but I think I'll try that a bit later.

Btw. if someone upvoted the question once more I could fix the links (only two links are allowed under 10 reputation).

I fixed the links for you and tried to rework the question a bit to make it more objective rather than advice-seeking.  See if it still carries the original meaning.

Torticollis can occur for several reasons, one of which is a side effect of certain drugs. Rather than highlight one specific drug it is perhaps better to talk about the mechanism of action by which this occurs.
Torticollis in a drug induced form is classed as an extrapyramidial side effect. Classically results from some medications which have anti-dopaminergic effects. The neurotransmitter dopamine is important for the regulation of movement. Different medications have different degrees of anti-dopaminergic effect. To complicate things further there are several different types of dopamine receptors and different drugs have different effects depending on their action on these receptors.
Classically drugs that have been associated with extrapyramidial side effects are some of the antipsychotics but there are case reports of this with trycyclics http://www.ncbi.nlm.nih.gov/pmc/articles/PMC489096/ however this appears to be a very rare, see http://www.sciencedirect.com/science/article/pii/S0924977X97004057.
The paradoxical treatment of torticollis might be dependent on the cause of the condition.  Tricyclic anti-depressants have anti-cholinergic effects, i.e. they block the effects of the neurotransmitter acetylcholine. This neurotransmitter works in opposition to dopamine in the basal ganglia (part of the brain responsible for movement control) as such might be used when the dystonia is as a result of doperminergic disregulation.
If you are at all concerned that you may be suffering side effects of any medication, then I highly recommend that you go and discuss this matter with your doctor. The above  is a simplified explanation of some of the reasons why these side effects may occur. It is not intended as information for the purposes of self diagnosis and treatment.


text:
Why are some berries poisonous?
In my understanding, the evolutional function of berries is to be eaten and pood out somewhere else, so that the seeds of the plant spread. Is this so? Then why are some berries poisonous?

A berry may be poisonous for one species, but not for others. See also: http://ask.metafilter.com/131461/Dont-they-want-to-be-eaten

I have no clue whether or not it is true but maybe it is for the same reason why pathogenic bacteria are pathogenic. The berries are poisonous so that they can kill the host and that in turn is the mechanism of plant spread.

A great explanation, and gorgeous pictures, on the Kew blog this week: Why Fruits Are Poisonous

While poison affects not every organism equally, plants did develop some poisons to avoid being eaten. However, if you look at the great multitude of so-called secondary metabolites, most of them are poisonous to either viruses, bacteria, fungi or other microorganisms, or insects, or even other plants. Plant evolution just hasn't had time to adapt to humans.
So, if some substance from plants is a poison to us, it's accidentally so, and the target was another organism. Examples: nicotine is first and foremost an insecticide, nematistat, and herbicide; aconitine, atropine, caffeine are insecticides; many essential oils (causing allergies in human) are antimicrobial and so on.
This has also to do with the fact that nerve cell physiology has not much changed since they developed in the first multi-celled animals, and poisons for insect nerves have at least some effect on human nerves.

All along I thought that the lack of poison and the presence in other berries is due to co-evolution between berry eaters that don't digest the seed wall(advantageous to the plant) and berry eaters that can digest the seed wall(not advantageous to the plant).

While an interesting answer, the examples you gave were not berries.  Fruits and berries are especially of interest, because the function of fruit and berries is to be eaten.


text:
Is consuming sugar with food as beneficial as consuming glucose (~half of the amount of sugar)?
A few years back I heard at biology class that sugar's molecule consists of half the number of elements of a glucose molecule. So not counting the energy needed to transform two sugar molecules in one glucose molecule, isn't it almost the same (eating N amount of sugar) as eating N/2 of glucose?

You have it backwards. One sugar molecule is equivalent to two glucose molecules, though the actual structure of sugar (Sucrose) is a Glucose + Fructose combination.
While Glucose is metabolized via Glycolysis into two molecules of Pyruvate (which are then used in the Citric Acid Cycle), Fructose enters the Glycolysis metabolism at a later stage as shown here:

The GA-3-P is then turned into 2-Phosphoglycerate and then into 2x Pyruvate.
The end result is that a single Sucrose molecule (Glucose + Fructose) [aka - Sugar] is equivalent to 4x Pyruvate, whereas Glucose alone is equivalent to 2x Pyruvate. Or, if you prefer, a single Glucose molecule results in about 32-36 ATP produced, whereas Sucrose will result in 64-72 ATP produced - with ATP being the primary energy carrier of the cell.

Is consuming sugar with food as beneficial as consuming glucose (~half of the amount of sugar)?
What is referred to in everyday language as "sugar" is sucrose. Each sucrose molecule consists of one glucose molecule and one fructose molecule linked by a chemical bond. These two, glucose and fructose are, in terms of energy value, identical.
Whether they are equally beneficial, or indeed beneficial at all (from a nutritional point of view), is a very big question.
P.S. (in response to MCM):
But... fructose metabolism is largely carried out by the liver. If you are consuming sucrose then the glucose component will raise insulin levels and the liver will be in anabolic mode. The fructose will be converted to liver glycogen via glucose-6-phosphate (as shown in your diagram) and also to triglyceride for export to adipose tissue where it is stored as fat. So the energy yield from fructose will be deferred, whereas the glucose will be used by all tissues immediately.
Later on, as insulin levels fall (and glucagon levels rise) the liver glycogen will be mobilised as glucose for export to other tissues. Some of the triglyceride will be mobilised from the adipose tissue for use as fuel too, but it is widely believed that with a typical Western diet there is a net movement from fructose>fat which contributes to the rise in levels of obesity. Indeed some scientists believe that fructose is the main culprit.

Yes, fatty-acid anabolism is certainly one potential pathway for Fructose. However, the original question was not about typical diets or insulin levels. The original question was directly comparing the potential enegy between Sucrose and Glucose. As you point out, even in fatty-acid anabolism the energy from Fructose is only deferred - not eliminated. Sucrose is equivalent to two Glucose molecules in terms of energy obtained, and I thought the Fructokinase pathway was the easiest way to demonstrate that. :-)