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Are (baseline) high blood levels of melatonin associated with either circadian rhythm or mood disorders?
(Exogenous) melatonin is administered at night for treatment of circadian rhythm disorders, but melatonin taken during the day is linked with depression.
I would like to know if high blood levels of (endogenous) melatonin (at a steady state, throughout the day) might be linked with mood or sleep disorders (or have any effect at all), or if the body's response to melatonin adjusts accordingly.
I think the answer to this SE question is related, but I can't find the source using a reverse image search.

This question isn't fully answered - I found nothing on circadian rhythm disorders.

I found a recent PLoS article that said that none of hypochondriasis, depression, hysteria, psychopathic deviate, masculinity-femininity, psychasthenia, schizophrenia, or social intraversion (on the MMPI-2) "were associated with any melatonin parameter."
However, it does appear that "increases scores of Hypomania and Paranoia were associated with a shorter DLMO-DLMOff interval" (duration of melatonin production).
The only thing that concerns me are the significance and the effect size of the latter two results.  I can't tell whether they corrected for multiple comparisons or not.
Reference:  Burgess HJ, Fogg LF (2008) Individual Differences in the Amount and Timing of Salivary Melatonin Secretion. PLoS ONE 3(8): e3055. doi:10.1371/journal.pone.0003055


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What would cause E. coli to change from filamentous growth to normal growth?
In my lab we've observed a phenomenon in which a culture of E. coli is found to shift from normal rod growth to filamentous growth and then back to normal rod growth again several times over the course of 400 hours. This was shown by an OD600 graph which oscillates from high values (~5) to low (~0.5) (the culture was also viewed directly).
The shift to filamentous growth is usually associated with an SOS response in E. coli and this makes sense (the media is M9 supplemented with 0.2% casamino acid and 0.1mM thiamine hydrochloride), however we don't know why it switches back from filamentous to normal growth.
Has anyone observed a similar phenomenon? Does anyone have any suggestions why this might be happening?

How exactly is the culture maintained over the 400 h period? Are there any periodic events?

I have found that E.coli turns from single cells to filaments when stress by predators such as myxobacteria or amoeba. why in the same batch cells turn from filaments to single cells is not clear to me. Is it a fed bactch and do they keep growing?

Expression of sfiA (sulA) causes filamentation during the SOS response, so presumably sfiA is induced, as part of SOS, in response to some sort of DNA damage. Once the DNA damage is repaired the SOS genes, including sfiA, will be repressed again and normal growth will resume.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902570/
In addition to the other answer(s), E. coli has been shown to have filamentous spikes even under controlled conditions. This is not the same situation as it sounds like you have a non synchronized culture in which this happens, but it could be related.

I found that E. coli exposed to predators such as amoeba changes completely from normal form to filaments (on agar) that look wound up like spaghetti but are not only longer but significantly wider. In this form the predator can't attack E. coli and it lives among the amoeba for extended periods. It does not look like a simple point mutation to me, which merely disables cell from cell dissociation.
So I have now two types of E.coli, opaque whitish looking filmaentous colonies and the normal more translucent colonies. In one case the filamentous form turned back to the normal form after repeated transfers on predator free plates.
So the question here could be: which is the E. coli that lives in the real world out there in soil water and biofilms?
Ralf Cord-Ruwisch Aug 2014

When you add a citation, can you either provide a link to the PubMed (or the journal) or provide a complete citation including journal, volume, year, issue and page number. This makes it easier for people to actually find them.

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What is a simple protocol for staining cells in suspension?
I am an engineering student studying how electric fields affect cells, specifically the phenomena of electroporation in living cells.
I know that electroporation is widely used for introducing genes into cells, but running a full transfection experiment is not so feasible in the lab I am working in.
My question is:
If I want to demonstrate the principle of electroporation, i.e. that cells open up and intake substances from the environment, by using some kind of a dye which i can later visualize, what could be a good model for this type of experiment? Specifically - what dye, what cells could be used for this?

Are we talking about mammalian cells or bacteria?

That's probably part of his question ;)

You will get a lot of false-positives using the following method, and a real transfection of a fluorescent protein is always the way to go, because then you will prove that the transfection was really successful.
That said, you could try to use DAPI, followed by fluorescence microscopy or flow cytometry. DAPI is a very bright stain for DNA and cannot pass an intact cell membrane. If the cell membrane is disrupted, e. g. by necrosis, DAPI will enter the cell. I have never seen anyone trying to prove electroporation this way, but it will be worth a try. It could be that the time is too short for DAPI to enter the cell, so you'd need to tweak your setup.
I'd try the following: Prepare a cell solution with DAPI (something like 5 µM concentration should do). Split the solution into two electroporation cuvettes, perform the electroporation with one cuvette, leave the second one untouched as a control. After the electroporation, analyse the samples MOMENTARILY (means: within a few minutes) using a flow cytometer (if possible).
As for the cells, you could use anything. I suggest eukaryotic cells because they are more easy to visualize than bacteria. However, you would need a laminar flow hood for aseptic handling of cells. In theory you could also use bacteria, which are more easy to handle, but I'm not experienced with immunofluorescence in bacteria.

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Are ape communities more "anarchist" or "communist" in structure?
I am using these terms because we can imagine them quite good, I guess ;)
By "anarchist" I mean that the ape wants to live without the rule of others apes(same biological race or other) and he pursue his own goals (replication, getting food etc.)
By "communist" I mean working together in groups because of the "higher"purpose (better chance to protect themselves, getting food easier, other benefits)
I am particlarly interested in apes, excluding us, of course.

I edited your title heavily - sorry but hopefully this is what you meant?

Great apes live in social groups which definitely have rules.  They seem to be more like a clan or family because of the size.  So maybe if you were forced to choose you might say communist.

I think your definitions of 'anarchism' and 'communism' do not reflect the actual political ideas at all. I think you were looking for the terms "selfish" and "cooperative" or "altruistic".

Among the great apes, chimpanzees and gorillas live in very hierarchical, male-dominated clans that are often in violent conflict with other clans. Bonobos, on the other hand, lead very peaceful lives, and are female-dominated, using sexual contact as a manner of communication to reduce tension within and between groups. Orangutans are largely solitary animals, with heavy parental investment (7 years, longest among non-human primates), wherein the mother lives separately with her child during the early years of development. Among the lesser apes, gibbons and siamangs are also highly territorial and pair-bonded, though notably, polyandrous siamang groups have been shown to display higher degrees of cooperation.
Though Anarchism varies greatly between different definitions, the most popular form of contemporary Anarchism values non-hierarchical organization, centered around mutual aid, rather than the kind of isolated individualism that you seem to associate with the term. By this definition, bonobos would be more "Anarchist" than chimpanzees. By your definition, orangutans might be the most "Anarchist."
Your definition of "Communism" is closer to the contemporary definition of Anarchism above, due mainly to the historical trajectory of Communism, which in practice, did not work out so well, leaving contemporary utopian thinkers largely in the Anarchist camp. By your definition of "Communism," bonobos may be the most "Communist"; however, if you mean the state-based gulag Communism of popular culture (ie portrayals of the Soviet Union), then you might say that chimps were more Communist. This is because individual chimps sacrifice individual goal attainment for group ends under the coercion of the alpha male chimp. Of course, some people may call that Fascism.
You may want to take a look at primatologist Franz De Waal's research on bonobos vs. chimpanzees. As a pacifist, he has a bit of an agenda, in terms of trying to prove that female-dominated bonobo "societies" are inherently more cooperative and less hierarchical. Another primatologist that agrees with this view is Harvard primatologist Richard Wrangham, who looks at hierarchical organization and violent behaviors in chimpanzees.
Robert Sapolsky's research on baboons may also be of interest to you. He found a clan of baboons, in which all the alpha males had died from tuberculosis due to exposure to an infected meat found in a neighboring human village. He noted, then, that the remaining baboons lived much more peaceably and cooperatively than other observed clans, and furthermore, that this clan retained its "culture" and passed on its more cooperative ways of behaving to new members in the clan, therefore demonstrating that perhaps baboons (and other primates) are capable of having and passing on "culture." - Perhaps a more "Anarchist" culture than nature normally prescribes.
However, as a caveat, I must say: it is tenuous to make direct associations between ape behavior and human societies. Human culture, social intelligence, and symbolic reasoning facilitate human political systems. Though Sapolsky's work suggests primates may also be capable of some form of "culture," biological descriptions of ape social organization is insufficient to explain human behavior.


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Why can all animals swim in water without learning to swim but humans cannot?
I had a question since I was a child. I was always curious about the fact that all animals can swim in water. They don't need any training or to learn swimming. But humans need to learn to swim. Why ?
I am a technical person and not in biology after my 10th year in school. Can anybody please shed some light on this question?

Can you back up the assertion that all mammals can swim without being taught?

i think it's reasonable to say that a new born porpoise or otter needs very little instruction compared to a human baby to learn to swim.  Human learning is an unusual process, even though some animals have the capacity to learn it takes years and hardly ever goes past the abilities of 5 year old, say.

I found a website that claims "Most animals are good swimmers. In fact, they can swim from the time they’re born. But some animals have to be taught how to swim. This group includes people, gorillas and chimpanzees."

Wow .. Thank you all for the quick responses . I thought only humans cannot swim without learning. But some animals also have the same case.

possible duplicate of Can all mammals swim?

@fileunderwater Though the question is a duplicate, this post seems to have better answers or atleast offers a different perspective. I am not sure if it is right to close the post as a duplicate. I am nonetheless VTC this question because the other one is more detailed and better researched.

@WYSIWYG Maybe a candidate for merging by the moderators?

@fileunderwater can posts be merged?

@WYSIWYG I've read that it is possible, but I haven't seen it in practice at BioSE yet. See e.g. http://meta.stackexchange.com/questions/16437/when-merging-questions-leave-the-duplicate-one-as-a-placeholder and http://stackoverflow.com/questions/20674300/how-to-compare-%CE%BC-and-%C2%B5-in-c-sharp/20674425#20674425 (labelled as "merged" below the Q).

While I am not sure I buy your assertion that all mammals know how to swim, I would say that humans are at least as good as dogs when swimming. If you drop a human in water we will instinctively flap around and try too keep our head out of the water in about as elegant a way as a dog. The main problem for humans is panicking. Someone who does not know how to swim is likely to panic and not manage to keep their head out of the water. Remember that humans float in water, if you keep calm you should be able to keep your head above the water line easily enough.
Dogs can't swim as such, they simply do the same motions in the water as they do on land. There is no different action happening, they don't instinctively do a breast stroke.
In addition, human infants actually have a couple of instincts that make them "swim" (source):

The Diving Reflex
The diving reflex, or bradycardic response, means that infants whose heads are submerged in water will naturally hold their breath. Their heart rate will also slow down while they are underwater. This reflex disappears after about six months of age.
The Swimming Reflex
Newborns placed stomach-side down in water will move their arms and
legs in a repetitive "swimming" motion. This is known as the swimming
reflex. This reflex, too, begins to fade at about the six-month mark.

That is no better and no worse than any other non-aquatic mammal can do. Try dropping a cat in water* and telling me she is a graceful swimmer :).
* Don't, that's not nice.

I know cats hate water :)

It is almost funny to see a cat in the water though :) ...If you're lucky enough to see it before they come flying back out XD

Unlike Terdon I think that you are generally correct in your assertion that animals can swim whereas humans can't (although I'm sure there are exceptions). However, I think his answer contains the real answer:

Dogs can't swim as such, they simply do the same motions in the water as they do on land. There is no different action happening, they don't instinctively do a breast stroke.

Try making walking motions underwater, see how well they work for you. Whereas for a four legged animal their land based motions function as a passable swimming motion and the shape and weight distribution of their body means they can keep breathing simply by holding their heads up, humans need to learn a new skill in order to swim.
I'd note, however, that a human who has learnt to swim is much better at it than the natural swimming ability of a quadruped.


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RACE pcr product
I'm a molecular bio novice, and I'm trying to understand the differences between regular PCR and RACE PCR.  If it wanted to sequence my PCR product that might be hundreds, if not thousands of bps long, I should use RACE PCR correct?  My goal is to sequence the active site of some enzymes I'm interested in, but I'm not sure how to go about designing PCR primers for a specific site on my protein.  Additionally, the active site is over 100 amino acids long, which would imply that my PCR product has to be over 300 bps long.  Regular PCR amplicons have trouble amplifying long strands of DNA correct?  I was thnking about using RACE PCR to amplify my entire cDNA strand that is 4000 bps long and then just sequencing the RACE product.  Would RACE work for that many bps in my cDNA?

This is a lot of questions in one very compressed paragraph.  It would probably be best if you asked separate questions.

Judging by your post history, it seems like you may want to pick up an introductory book on molecular biology. This question is really asking a number of questions. I will attempt to answer the difference between PCR and RACE, and I would suggest asking the others as separate questions, as @dd3 has suggested.
Polymerase Chain Reaction (PCR) is the basic method of amplifying a small amount of DNA (the template) into an exponentially large amount of DNA. This method assumes the knowledge of the sequence of (at least) the regions of DNA flanking what you wish to amplify. Using these flanking sequences, two short oligonucleotides (e.g., 18-24 nucleotides), called primers, are ordered such that one primer matches the 5' strand at the start of the sequence, while the other primer matches the 3' strand at the end of the sequence. When these primers are mixed together with the template DNA, and a DNA polymerase enzyme, and subjected to specific temperature cycles, amplification occurs.
RACE PCR is a specific type of PCR. RACE (Rapid Amplification of cDNA Ends) PCR is used when the template strand to be amplified is a specific mRNA message. In other words, this form of PCR produces a DNA copy of cDNA from an mRNA starting product. The exact details of RACE depends on which type you wish to use and can be looked up elsewhere.


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How does LCR compare to Assembly PCR
The question pretty much explains itself. How do the two methods compare? I've always used Assembly PCR but the method is prone to mistakes and I'm curious how it compares to Ligase Chain Reaction (LCR).

I am looking at this myself for gene synthesis.  OpenWetWare has a link to discussing the two.

I have used both Gibson assembly (what you mean by assembly?) and LCR as replacements for blunt or sticky ended cloning. LCR has, for me, worked better in that a higher proportion of constructs that come out have been assembled correctly and I have noticed no mutations after LCR while I have seen them somewhat often with Gibson.

Welcome at Biology SE! Your answer is greatly appreciated, but on this site we prefer answers backed up with scientific references, Please provide objective references (if possible) to support your answer.

Thanks for the clarification Nandor. Also it would be much more helpful if you provide quantitative information when you are quoting your own data rather than 'higher proportion' - this would help viewers make their own judgements about which method they would want to use.

In any PCR reaction ( including  the assembly PCR ) the substrate of the reaction is a mix of mono nucleotides. Specific oligos serve as primer by annealing on the template and that are extended by a DNA polymerase. It is a polymerization reaction.
In the LCR there are no mono nucleotides instead you have many different oligos that anneal one after the other on the template and a DNA ligase is used to join them together to form a longer DNA molecule. It is a ligation reaction.
This two reactions have much in common. Firstly, they rely on the annealing of oligos on a template. Secondly, both the polymerase and the ligase need to be thermostable. In fact, both reactions leverage the thermostability of the enzymes to carry on cycles of annealing, reaction (polymerization or ligation) and melting. After each cycle the template DNA is copied so you end up with an exponential amplification of your template with both techniques.
Here a nice presentation that showing these concepts with some graphics.


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Improving Gel Extraction yields
How can I improve my Gel Extraction yields. We use the standard protocol from Qiagen, gel extraction, dissolve in QG buffer at 42C and purify via anion exchange columns. However, with 500 ng we ultimately get 100 ng for a 20% yield. I was curious what else has been tried for gel extraction.
We also add IPA and NaOAc to the dissolved mixture prior to the column purification.

When I optimized gel extraction in my hands, two factors turned out to be critical in maximizing gel extraction yield:
The pH of the eluting solution. I used to elute the final product with DEPC-treated water initially, but the yield would vary a lot as the pH of the water changed. Using buffer EB is better, since it maintains a stable pH 8.
Most importantly, *incubate the eluting solution with the column as long a possible (and also elute twice). * I incubate for about 10 min, which is longer than what they recommend but it works much better.

I also want to use this post to mention there are cheaper alternatives to the Qiagen kits, such as the ones here: http://www.mn-net.com/, that work just as well and sometimes better. Using those can save you a lot of money. This is not an ad: I or my lab are not in any way affiliated with the company or website I'm linking to. I'm just sharing customer experience.

Try dissolving at 50C.  In the Qiagen gel extraction kit, it says to dissolve at 50C or until completely dissolved.
The size of the gel is important too.  Make sure it is 1.5% or less, and the size of the gel needs to be less than 400 mg.
Also, pay attention to the first step.  If the liquid is not the same color as the color of the first QG buffer then there is a pH problem.

Elute from the column with Elution Buffer that has been preheated to 50-60 degrees. I stick mine in the incubator for the duration of the extraction so it is warm when I come to elute. It seems to help yield.


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What's the difference between a free chromosome fragment and an extrachromosomal array?
This is reference to a review on C. elegans mosaic analysis by Yochem and Herman, in which the authors make a distinction between free chromosome fragments and extrachromosomal arrays.
For the former, they reference Herman 1984.
For the latter, they reference Lackner et al 1994 and Miller et al 1996, but these are studies that use extrachromosomal arrays, not papers defining them as a technique, per se.
I am curious to know what the distinction is - I am under the impression that extrachromosomal arrays are fragments with many copies of the gene of interest + a marker.

I added an answer below, but please supply better answers if you have them!

I asked my professor, and the answer appears to be differences in both the generation and the final product.
Free chromosome fragments are created through irradiation/other damage of the germline in one animal.  Through a series of crosses, it is possible to introduce individual fragments (containing a duplication of your gene of interest, as well as a marker) into a mutant background.  The extrachromosomal fragment will be lost during mitosis at various points in development, and in a mosaic analysis, you can look for the loss of your marker (and therefore the loss of the wildtype allele), and see if yfg product is required in certain cell types for a wildtype phenotype.
Extrachromosomal arrays are created by cloning, and you typically have many copies of both the gene and marker.  It's the same principle as free chromosomal fragments in terms of mosaic analysis, but it's very powerful, as you can easily clone individual genes (versus irradiating and hoping to discover yfg on a fragment) and markers (and now you can use non-endogenous markers like GFP).
Even though extrachromosomal arrays are comparatively easier to generate, the problem is that you end up with many copies of the gene, which leads to non-endogenous dosage levels. Even if this doesn't cause a completely different mutant phenotype in the cells, it is possible that enough of these proteins could segregate at mitosis into the daughter cells, such that even if the fragment is lost, you could still have your gene product around in the daughter cells (if your marker protein didn't also segregate like this, you might draw erroneous conclusions about the necessity of yfg product in those particular cells).


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Does preservation in ethanol alter leaf litter mass?
I have benthic samples that were collected with an Ekman dredge from some small ponds.  The samples contain quite a bit of coarse particulate organic matter (CPOM, basically dead leaves).  I would like to quantify the amount of CPOM in the samples but they were preserved with 70% ethanol in the field.
Is there any evidence that ethanol preservation alters benthic CPOM mass?

How do you plan to separate the POM from the rest of the sample?

We run the samples through a 1 mm sieve to separate CPOM from the remaining sample.  The coarse fraction is then dried at 50 dC and ashed at 550 dC to determine LOI and % OM.

This sounds like something that would be straightforward to test empirically. As a bonus, any effect of EtOH on your samples (bias) could (possibly) be quantified and accounted for, especially if the effect is small. The questions you are asking will inform how best to do this. But I do suspect EtOH might dissolve some hydrophobic compounds in the coarse fraction. Maybe try evaporating it first and adding water. Not ideal, but likely more informative than throwing samples out!

This paper implies the EtOH extractable fraction in willow leaf litter is small ~2% http://download.springer.com/static/pdf/61/art%253A10.1007%252FBF00337374.pdf?auth66=1384973693_83a38241ac58aaa903579eadfcf550a8&ext=.pdf but this will vary by species (eg pine tar). Again, this effect can be measured on samples similar to yours.

@Abe Thanks for the paper, I look forward to reading it.  We are actually testing this now.  The initial tests with fairly old OM showed no effect but we are planning some tests with fresher OM to see if that makes a difference.

It's very likely that you should have at least minor changes in mass.

The reason is because ethanol can extract a number of substances from leaves (e.g. tannins, pigments, etc.).

However, you could still easily double check on your own.
You could still figure out the mass of the CPOM even without knowing the answer to this answer directly.

Drain and collect the EtOH.
Determine mass of separated CPOM.
Determine the excess mass present due to any leaching/dissolving from the CPOM by using density = mass / volume (or ρ=M/V) with your collected volume of ethanol.

EtOH has a density of 0.789 g/mL  at 20°C. 70% EtOH has a density of 0.885 g/ml at 20°C.
Determine the volume of the collected EtOH.
Determine the mass you'd expect of "pure" 70% EtOH given your volume (m = ρV )
Determine the mass of the collected EtOH
Subtract the expected mass from your calculated measured mass. The difference (if any) would represent mass leached/dissolved from the CPOM.

But consider that EtOH evaporates quite rapidly which could give you a false reading. Why not try with some leaves of a not-that-important-sample? Weight them before, put them in alcohol for some weeks and weight after (let the alcohol attached to the leaf litter evaporate before weighting).

Evaporation shouldn't matter  because  you  would  measure  densities.  Any CPOM mass  would remain in  the  fluid.  In fact,   with evaporation,  the concentration of remnant cpom would  increase  per ml,  and so would likely make  subtle density discrepencies  even more apparent

Ok, thanks for clarifying, I wasn't aware of that.

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Is there an optimal illumination level for human habitats/workplaces?
I know of melanopsin, a photo pigment in mammal eye that helps regulate circadian rhythms. It responds most strongly to blue spectrum light. There have been experiments that demonstrated that intensity of light is proportional to the impact on circadian rhythm regulation/ melatonin suppression.
This is why I'm interested if there is some optimal illumination intensity that has been demonstrated to result in better health/cognition in humans. I heard anecdotal reports of full spectrum lighting improving attention in classrooms, but is there some chart or figure which says how much is "too much light".

It seems there has been some work done on too much light affecting human health, but in regards to lack of darkness at night, rather than too much during the day. Without the appropriate amount of darkness at key times melatonin production and the major clock regulator or SCN can be disrupted and lose sync with the peripheral clocks. See here [1] for a comprehensive article with loads of information and other links to studies done on this topic.
This part in particular illustrates some of the problems associated with too much light:
"Overexposure to sun-mimicking light is also believed to play a role in the increase of insulin resistance, type 2 diabetes and obesity in developed countries (where round-the-clock illumination is more prevalent). Some research also shows that too much sun-mimicking light ups our craving for carbohydrates.
Before humans started cultivating grains, carbohydrate energy was available only from spring to fall. In response, our bodies evolved to stock up on carbohydrates during the growing season to prepare for winter, when no carbohydrates were available. In turn, we didn’t crave carbohydrates in the winter. All that changed with the light bulb, write T. S. Wiley and Bent Formby, PhD, in Lights Out: Sleep, Sugar and Survival (Atria, 2001)"
This might be a bit off topic but check out http://www.lightingdeluxe.com/workplace-lighting-ergonomics.html and the HSE has some info on what the required lighting conditons in the workplace should be [2]. They only mention lighting conditions with reference to reducing levels of stress in the workplace though.
Also not directly related but pretty cool; an article in Science from 1998 found that light shining on the back of the knees may be able to regulate circadian rhythms [3].
[1] http://experiencelife.com/article/light-rhythms/
[2] (scroll to the lighting section) http://www.hse.gov.uk/humanfactors/topics/lighting.htm#lighting
[3] Wright, K.P. Jr. & C.A. Czeisler. Absence of circadian phase resetting in response to bright light behind the knees. Science 297, 571 (July 26, 2002).
or if you don't have access http://www.genomenewsnetwork.org/articles/08_02/bright_knees.shtml


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Is there a way to measure the amount of bytes that are possible to encode in a DNA molecule?
When I saw a DNA molecule for the first time, it kinda reminded me of a hard drive. It consists of slots and there are some possible combinations for each slot; in the hard drive these possible combinations would be 0's and 1's. In DNA, these slots would be G's, A's, T's, C's.
So, is there a way to measure the amount of bytes that are encoded in a DNA molecule?
I've made this question before in another forum, but the answerer provided me only with Shannon's theorem, which is $K=L-\frac{(1-q^L)^n}{q^L}$ and told me a little about genetic redundancy. I could only search for the ammount of slots which are present in the DNA, but this genetic redundancy thing got me stuck.

I am not sure what your question is - there are indeed four nucleotide bases in DNA, and these correspond to the "slots" you mention. You may want to have a look here: http://bitesizebio.com/articles/how-much-information-is-stored-in-the-human-genome/

This is the answer. I was just confused to the real ammount of data - because of the genetic redundancy.

You might find this thread over at skeptics interesting.

Unfortunately the answer is highly dependent on what you mean. In the simplest terms, comparing it directly to how we measure data storage in digital media, the number of different states of a DNA string of length $n$ can have is simply $4^n$. A byte holds $2^8$ different states so the number of bytes in a DNA string of length $n$ is $\frac{n}{4}$. Of course, actually accessing this information would be more difficult than simply having it in a strand of DNA.
DNA in real organisms is not random, however, so sequences are not randomly distributed meaning that you could compress that information down into less bits than that, Shannon information style.
However, you can decently argue that this doesn't really tell us how much information is in real DNA because real DNA has structure that matters. It has exons and introns and promoter regions and so on. Meanwhile, the sequences in protein coding regions are a lot more important than sequences in non-coding regions for the most part. Large parts of the genome are functionally irrelevant but because of this they tend to be more random and thus have higher Shannon information.

And then there was ENCODE's definition of function...

You might also be interested in this paper from EMBL-EBI about storing data on DNA.
Towards practical, high-capacity, low-maintenance information storage in synthesized DNA
They show they can get 757,051 bytes or a Shannon information 10 of 5.2 × 106 bits onto 153,335 strings of DNA, each comprising 117 nucleotides (nt).
George Church had a similar paper recently as well - Science


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Do dolphins really sleep?
I have always wondered, if dolphins sleep with one eye opened, do they really sleep at all?
According to this article dolphins indeed shut down their brains.
I already googled it. No help from wikipedia or other articles and publications found.

Of course we should note that our brain does not "shut down" (whatever that means) when we sleep.

I'd say that unihemispheric sleep and adaptations like it really are sleep - the brain activity on one side of the brain gives a characteristic sleep pattern.  It certainly must satisfy the needs of an aquatic mammal like a dolphin or a whale since they have to be partially conscious to breathe by surfacing regularly.
It does seem to affect the brain physiology, but is there a reason you would not call it sleep?

I suppose that it depends on how sleep is defined. If we define it a a mechanism by which the brain repairs itself in an altered state, then, yes they do indeed sleep. Just not with all of their brain at once.


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Complexity in creating transgenic animals (e.g., mice)
Many papers I have seen describing transgenic rodent models (and presumably applicable to other model organisms) involve the knock-in, or modification to, a single gene, possibly two genes. With respect to recombineering techniques, what prevents targeting multiple genes in a single organism? For instance, if I wanted to simultaneously knock-in some genes and knock-out others within the same mouse, would I be forced to generate individually modified transgenic lines and then do some "fancy" breeding to generate the multiple-modified mice?

One reason is the low likelihood of success. Modifying a gene almost always involves a recombination event of plasmid DNA with a target site in the genome (and I say almost just because there may be some method that I don't know about, but all the ones I'm familiar with do). The likelihood of that decreases exponentially with the number of genes you're trying to modify. If you're trying to make several mutants of individual genes the likelihood of success decreases only linearly.
Another reason is having more knowledge and experimental power. You can learn little from a double mutant if you don't also have the individual mutants to compare. In fact, most reviewers would ask for individual mutant data if you've made a double mutant in your paper. This is especially true with flies and worms, as crosses take less time with them.
Also, the more mutant genes you have, the weaker the animal. Your mutants may not be viable at all with too many mutations.

Hmm...I forgot to mention the obvious problem with combinatorial effects that you brought up. I was assuming that the effects of single mutations were already known. These are interesting points you bring up.

If you have the individual mutants already, it's just much cheaper to set up crosses than to make a whole new transgenic.

You could introduce multiple transgenes into your embryonic cell line before injecting into the blastocyst. That way you don't have to do it individually one by one and then breed them all together, which can take a lot of resources. This is especially necessary when your genes are really close together (genetic linkage) and hence would not breed in a Mendelian ratio. Either way, each gene you try to modify usually takes at least a few months. I think CRISPR has made it faster, but still its a lot of gel blotting to make sure you generated the transgene.


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What kind of caterpillar type bug is this?
I've made a photo using the reversed 58 mm lens and my cropped DSLR:

Could you please help? I really don't know where this came from.
I found it in Russia.

Cannot help you but maybe it could be useful if you specified where you found it (inside, outside, which country, when, etc.?)

I found it in my kitchen on a clean plate from IKEA :) Country is Russia.

Likely to be a black carpet beetle larvae

http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn7436.html
For more facts try: http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn7436.html
Don't worry though, they live everywhere!
Wikipedia has some info on the family of beetles that they belong to (http://en.wikipedia.org/wiki/Dermestidae). I don't think they really cause any harm, except in natural history museums where they tend to munch the collections of animals...although this can also be a good thing:
'They are used in taxidermy and by natural history museums to clean animal skeletons' 1
1 VanClay, Mary. "Bitten By the Bug". www.johnsonstring.com. Retrieved November 10, 2012.

Definitely Dermestidae, but Dermestes lardarius (Larder beetle), Attagenus pellio (Fur beetle) and Anthrenus museorum (Museum beetle) are all common and likely. They can all be pest, also outside of museums, on e.g. fabrics, fur etc., but most that you find inside you house come from the outside. It might be worth the effort to check your clothes, other fabrics, stuffed animals or other suitable substrates if you find many of them.


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How does paracetamol interfere with immune system?
Paracetamol is used to reduce body temperature when it is to high. The high body temperature (fever) is known to be an indication that immune system fights against an infection.
In this context I have two related questions:

Is high body temperature one of the mechanisms of immune system to suppress an infection or it is just a side effect?
If it is just a side effect, does paracetamol remove it by decreasing the intensity with which immune system fights with an infection or not?

Your first question is a repeat of this one: http://biology.stackexchange.com/questions/7541/if-fever-is-a-natural-immune-defense-why-do-people-take-drugs-to-lower-it

First question: Yes. The immune system releases pyrogenic cytokines such as IL-1. Bacteria aren't typically used to 37C, they prefer working at under that temperature to function in the environment. Our body however can take a few degrees here or there however this severely compromises the bacterial enzyme activity. The same is true for other pathogen enzymes. The body also increases copper concentrations in the blood for similar reasons. Problem is of course if the body goes into overdrive and raises our temperature too much, this compromises our own ability to fight the infection so in that case antipyretics like paracetamol can reduce fever.
Second question. It isn't a side effect, however paracetamol works by blocking things like IL-1 that raise temperature. How IL-1 raises your temperature is quite interesting, it tells the hypothalamus (our thermostat) that it should be set higher. So we feel cold (so we try to keep ourselves warm) and the body thinks it's cold (so it increases the temperature by burning glucose mainly)


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What controls the size of breasts?
I am not a biology student, just a curious person. To be specific, I'm talking about female humans. I know that it might apply to other mammals.
What controls the size of breasts?
I have heard about progesterone hormone.

Is it just progesterone?

Are there any other factors?

I have seen a movie in which couple talks about breast size increases after sex. Is it true?

Can somebody give more info on this?

Prolactin may be a good candidate.

The known factors seem to be mainly oestrogen and genetic (although I haven't been able whatsoever to find detail on what genes):
Manning et al (1997): Breast asymmetry and phenotypic quality in women. Evolution and Human Behavior, 17 (2): 129–143.

Our data support the thesis that mammotropic hormones, particularly estrogen, are harmful because they suppress the immune system. Heavy women with high levels of body fat produce more estrogen and, therefore, bigger breasts. However, more estrogen leads to an increase in breast asymmetry. Women with “good genes” are able to produce symmetric breasts despite the presence of large quantities of estrogen. Large and symmetric breasts are therefore honest signals of high phenotypic quality in women.

The first signs of breast growth begin as a girl reaches her teens. The fat in the connective tissues starts to accumulate when the ovaries begin to secrete (express) estrogen. The breasts will then grow. Also, the duct system begins to grow. These breast changes often occur at the same time as pubic hair and armpit growth.
After menstruation and ovulation, maturing begins in the breasts with the formation of secretory glands near the milk ducts. With the development of many glands, lobules, and breasts that continue to mature and grow, the duct system and breasts also continue to develop. Each woman's breast growth rate is different.
In the end it's estrogen and the amount of fat that accumulate in the breast, that are largely responsible for the size of the breasts.

You've been busy! Unfortunately this doesn't seem to provide any new information and most of it is not actually answering the original question. Please focus on providing high quality answers rather than quantity.

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


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Can the kidneys utilize ketone bodies for energy?
Ketone bodies are water-soluble and should pose no problem to the kidneys because of solubility. If the kidneys are able to utilize ketone bodies for energy, then they must express the enzyme 3-ketoacyl-CoA transferase, correct?
Do the kidneys express the enzyme 3-ketoacyl-CoA transferase?
Can kidneys use ketone bodies as fuel?

This article's abstract says that 3-ketoacid-CoA transferase was found in the kidney: http://www.nature.com/pr/journal/v42/n4/abs/pr19972518a.html

Alexandria's answer:
This article's abstract says that 3-ketoacid-CoA transferase was found in the kidney: nature.com/pr/journal/v42/n4/abs/pr19972518a.html


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What metabolic activities are performed by a developing human fetus's liver?
I understand that organ function varies with the stages of development. Does a fetal liver EVER perform lipogenesis, gluconeogenesis, make bile, etc? Or does it only begin performing these actions postnatally?
I have heard that a fetus delivered between 24-26 weeks can potentially be "okay" with proper care and monitoring in a hospital. I would assume (please correct me if I'm wrong) that this implies the fetus's liver has developed at this time. So in the case of a fetus that was not delivered at 24-26 weeks, does it spend the remainder of the pregnancy in a fully functioning state? Or at least, which functions does it begin to perform?
I've been trying to find an answer on Google, but one walks a fine line when searching for human development information -- either the results are oversimplified "expecting mothers" websites, or journal articles speculating about the effect of X on the development of Y in the mouse/chick/zebrafish/giraffe/et cetera other nonhuman model.

It's old and I can't get access to this issue of the Annals of the New York Academy of Science, but it looks like it has some relevant information. Sifting through the abstracts it seems the vasculature of the fetal liver is completed at around 8 weeks although is still different to the adult vasculature because of the umbilical vein. The growth of the organ itself goes through different stages with each lobe growing different amounts:

They start the same size
12 weeks the left lobe is twice as large as the right
36 weeks the left is 10% larger than the right
at birth they are the same size
5days after birth the right is 10% larger
adults, they are the same size

And, studies have been conducted with dyes to look at liver function in both its capacity to concentrate the dyes and secrete it into the bile. The fetal liver can carry out bile acid synthesis, despite lacking digestive purposes, from very early on (Suchy et al. 1987). The fetus does however require help in removing the toxic cholephilic organic anions (COAs), which is done via the placenta. This review describes more.
There is also evidence to suggest the newborn's liver is not performing all the usual metabolic processes of children or adults (from looking at drug toxicity and delays in excretion/detoxification), as would be expected. More recent literature notes the fetal liver lobes (right and left) as having differnt biochemical capacities and independent function due to the right one getting less oxygen. Also, a layer of drug metabolising enzymes normally present in adults is missing in the fetal liver, although its capacity for drug metabolism is still better than that of rodents.

In the adult liver, there is a clear zonation of metabolism of carbohydrates, proteins, lipids, and bile salts. In the livers of fetal rats, mice, and humans, this heterogeneous distribution of enzymes and metabolic function does not exist initially. Towards the end of gestation, the adult pattern of heterogeneity for these processes begins to emerge, and after birth, the adult pattern is rapidly established (Ring et al. 1999)

There is in vitro evidence for the activity of glutathione S-transferase and sulfotransferases in the human fetal liver. Returning to the asymmetry of fetal liver function (albeit in sheep..) it was found that levels of malondialdehyde, an index of lipid peroxidation, oxygen consumption, and CYP levels (a family of oxidative enzymes), are higher in the left lobe than the right lobe of the fetal liver which evens out after birth.
So in conclusion, looks like a variety of metabolic enzymes are present in the human fetal liver from very early on after the organ is formed. We know a varitey of metabolic enzymes are present and the drug/dye metabolism studies show there is some fetal liver activity, albeit reduced from that of an adult or child. The limitation with many of the studies that have been done is that they have to use in vitro data and extrapolate to the in vivo situation, so I guess we still don't really know for sure how metabolically active it is. It is clear though that it remains inefficient and unable to carry out all the functions required of it during childhood/adulthood until after further development after birth when it has stopped growing and adapted to ex utero conditions.
References
Ring JA, Ghabrial H, Ching MS, Smallwood RA, Morgan DJ. Fetal hepatic drug elimination. Pharmacol Ther. 1999 Dec;84(3):429-45.
Suchy FJ, Bucuvalas JC, Novak DA. Determinants of bile formation during development: Ontogeny of hepatic bile acid metabolism and transport. Semin Liver Dis 1987; 7(2): 77-84

I found that a search through Google Books was helpful...
While without the excretion of feces, it might seem as if the liver would not be active, but the liver tissue is not only active in development and tissue generation but serves direct physiological function as well.
After initial phases of development, the liver produces fetal red blood cells which is normally a function carried out by specialized bone marrow hematopoietic cells.
Over the course of fetal development the liver develops its typical functions.  It breaks down old red blood cells and stores their iron, and pushes the waste bilins and other waste products to the umbilical cord to keep the fetus clean.  The liver also synthesizes and stores fats.

Thanks for the Google Books link ("develops its typical functions"). I was most curious about whether the fetal liver functions in response to nutrients obtained through the placenta, but this is the most informative source I've seen so far. Thank you!

The key thing to remember is that the liver cleans out the blood - esp chemical toxins and cells that are past their prime - that function can't be performed by the mother as the blood of the fetus does not mix with the mother's directly.


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Why human cannot stand still in one place?
When a human stands in one place, he cannot stand still but we can see the body slightly swings.
Is this due to the Earth rotation or it has something with biology and muscles relaxations?
I have not been able to find a concrete documents on this thing.

Is the human inebriated?

Is the human nervous? More seriously, the fields from the Earth - gravity plus centrifugal plus Coriolis and other forces - are almost exactly constant in time. So the human may either be able to deal with constant forces or not. If there are swings, the cause is clearly inside the human. Small changes of the tension in the muscles - due to small electric signals or variations of the concentration of sugars etc. - have observable impacts on the location of the bones etc. A way to answer is that the human muscles are surely much more volatile than the Earth's gravity+centrifugal fields.

I was in a big group of people and we listed for a talk standing. After some time I noticed that we all slightly swing. No one was drunk or nervous. they are really small swings, unnoticeable if you don't pay attention to them.

Slone, I agree with you, I am aware of such things, too. Even a perfectly non-drunk person is also unable to walk exactly along a straight path, the inevitable deviations are in centimeters etc. Humans aren't perfect and they're not dead. They swing although less than jellyfish.

Although at first sight this might seem to be biology rather than physics, maintenance of human posture is an example of control theory. Indeed a quick Google will find many publications on it - I found a good review here.
A standing human is a dynamical system that is not in equilibrium so it requires a (closed loop) feedback system to maintain it. This means sensors in your body detect deviations from your desired posture and muscles contract to return you to it. The problem is that there is a lower limit to the movements you can detect i.e. you body moves a certain distance before your muscles respond and move it back. The result is that even when we try to stand absolutely still we are actually continually moving then correcting that movement.
Some people are better at maintaining posture than others, so some people can stand stiller than others. Plus the ability declines with age, as I can testify from personal experience :-)


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One flybase gene number (FBgn), many Affymetrix Id's
I am trying to convert a set of Affymetrix ID's, like this one 143053_at_3745, to Flybase Gene Numbers (FBgn) like this one FBgn0000015. I have downloaded the Flybase file required to do so (as described here) but I have noticed that most of the FBgn's have more than one associated Affy id.
My question is, how do I know which to assign to my data? From the list of affy-ids that I have, how do I label each one with the appropriate FBgn? I am using data from the Ayroles et al 2009 (DGRP) which has a column of AffyID which look similar to the ones in the Flybase file but shorter (1638273_at). Perhaps I don't grasp why there would be more than one.
Some have one affy id which is repeated across 15 columns in the file, whereas some seem to have several affy id's associated with them.
Some questions this problem raises:
Why does a singular FBgn identifier have more than one associated affy identifier?
Why do some datasets, such as the dataset I have, have shorter versions of the affy identifier?
Where can I find an up to date and appropriate list matching these Affy id's the FBgn identifiers correctly?

perhaps @shigeta knows this...

Is it possible that there are multiple probes for the same gene? You've said that most of the FBgns have multiple Affy IDs associated with them, but you haven't said the converse.

I suspect that is the case, but I am not familiar with the technicalities of affymetrix chip design, and was confused as to why there would be some with the same - though further examination shows that the latter part (after the final underscore) changes within that subset.

I can answer this - I may not have time to dig though the file you are pointing to... but here's some explanation - lmk if you need more.
The shorter names (123456_at) are the original names for the probe sets that Affymetrix gave.  The file you area asking about has been extended for FlyBase's purpose and I'm only dimly aware of its existence. It looks like Flybase has tried to rename the probe set to a minimal gene list and create less ambiguous mappings.  I'm not familiar with it.  If I have time Ill try to look at it and put something here, but I'm fairly slammed this week.
In general you should know, there is a many to many relationship between probe sets from arrays and genes.
There are a few reasons for this.  The most common reasons:
More than one probe set per gene
1) More than one start sequence per gene. The IVT arrays such as you are looking at read only the 3' end of the gene.  If there are  more than one such terminii, you will have more than one probe set.
2) Duplicate genes.  If the 3' end of the gene has been duplicated recently, then a probe set may read more than one gene and not be able to distinguish them, so it will have both gene references in its annotation files.
3) Duplicate probe sets. For older arrays, this did happen where the probes in two probe sets will be mostly or entirely the same.
4) formerly separate genes are now joined into a single gene.  This is similar to (1) above, but with the added reason that two neighboring transcripts seen separately at the time of the array design are currently known to be part of the same transcript.  This is something we often don't think about, but the array may have been designed before your current gene of interest had a full length sequence.
In several cases the transcription behavior of the two probe sets will be quite different and you can decide which one to take based on how it behaves experimentally.  for example one of the probe sets may never respond while another one may register large changes with biological sample conditions.  Sorry I can't be of more help here. There are too many possible scenarios to consider to write about cogently.
More than one gene per probe set
1) a single stretch of DNA, even on the same strand, may simply be associated with more than one gene and the probe set will read both of them.
2) Even if they are not exactly the same, some genes resemble each other in nucleotide sequence that is impossible to choose probes which do not read both of them.
Since they have similar read length to a probe set, all this is also true to some extent for short read NGS sequencers in RNASeq data.
As you can hopefully see, ambiguity is something you have to expect to some extent when deciding to work with a biological system.  In many cases (~ 80%) you will have a single gene read per probe set, but with those odds you'll be looking at the genome browser for a half dozen of your favorite experimental results.

glad it sufficed - there's always more... lol

seemingly so...


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Why do some people find vegetables so repellent when evolutionarily they should find them an attractive and thus tasty food?
Why do certain people (especially kids) find vegetables so "repellent" when evolutionarily they should find them an attractive and thus tasty food?
I ask this question because if Darwin's theory of evolution is true then foods like vegetables that us human beings have been eating and attaining better health from eating for millions of years should have a taste that accordingly attracts us to them.

Your view of "so repellent" may be cultural or a result of growing up in the western world

I "tuned down" a little bit the question. Saying that "people find vegetables repellent" is a gross exaggeration. Some people may do, but I would not say that they are the majority (unless you have proof otherwise).

It would be nice to see some actual numbers (peer-reviewed papers anyone?) showing food preferences in different countries... that may tell a lot.

I tend to think this is a conditioned response, not entirely an evolved one.  People who don't eat meat habitually cannot stand it.  same is true for large amounts of sugar.

Evolution is not that simple. There is no selective pressure for a feature if it does not ultimately in some way benefit reproduction or the offspring. Vegetables are healthy for us now because we live much longer than we used to in an environment not dominated by us, and they contain many nutrients which help to sustain a healthy body beyond, say, 50.
However, if you imagine an average life span of around 30, it becomes clearer why evolution would favour foods high in energy over foods containing high amounts of micronutrients. Over such a time span, the long-term effects of a diet rich in fat and sugar do not develop significantly, but the energy supply is exactly what is needed to sustain bare life to the reproductive age.

A healthy diet is also more likely to result in us being more healthy and thus looking more attractive to potential mates so it still seems odd that the foods that are among the richest in said vitamins are so repugnant to us.

Attractiveness is a cultural value - it wasn't long ago (only a few hundred years) that the ideal figure was actually everything else than slim. Have a look at depictions of beautiful women and men in art throughout the centuries (e.g. in the antique god/esses of beauty, or paintings of literary figures which are supposed to be beautiful). Healthiness also depends on context. As I said, today what we consider healthy are things that sustain a healthy body for a long life. Not long ago, what was healthy were things that sustain life at all.

While I'm flattered that you accepted my answer already, I would suggest that you leave it open for a bit longer to encourage other people to give their answers. My answer was not a very good answer in the sense that it's only reasoning and not drawing upon any reliable sources :)

OK I appreciate your honesty, for that I will leave it open and unaccept your answer, but I will also upvote your answer.

There are presumably also availability factors.  If bland or slightly bitter foods are easily acquired relative to sweet and rich foods, then mere hunger might be sufficient motivation for consumption.  Overconsumption is perhaps the major danger of good-tasting foods; when they are rare/expensive this is less of a danger.  Also it takes time and selective pressure to deliver an evolutionary change; modern agriculture and commerce are somewhat new.  If health detriments are primarily quick death at post-reproductive age, the selective pressure against such might be relatively low.

@Armatus body fat is a special case, and not that related to micronutrient deficiencies. I do not believe there are any cultures anywhere in which rickets, pockmarked skin, missing teeth, and other signs of vitamin deficiency are valued.

@octern Thanks for your comment! Could you clarify how micronutrient deficiencies relate to the question, answer or my comment earlier?

In the comments, Brenton Horne said that a healthy diet increases attractiveness, and you responded that "attractiveness is a cultural value". I was pointing out that while preferences for body fatness have changed, most of the ways in which micronutrient-rich vegetables can contribute to appearance have been consistently favorable.

Let me also say that I am shocked, shocked that you did not immediately pick up the context for a two year old conversation that was abruptly resumed.

I must humbly apologise for this most intolerable shortcoming of mine, I shall endeavour to re-read every word I write on the internet at least every six months! [I actually did re-read the whole thread earlier, but failed to make the connection] On topic, I would expect overweight to be indeed related to micronutrient deficiencies - in that overconsumption of food (particularly the kinds of foods available in such cultures where overweight was considered attractive) would simultaneously at least prevent deficiency.

Though in retrospect, I'm not sure anything about attractiveness, i.e. sexual selection, is very relevant to evolution of taste - at the very least considering that overcoming our sense of taste is a pretty easy thing to do in order to increase attractiveness (which is very evident today).

Vegetables provide calories and don't kill you. For a hunter-gatherer, that's reason enough to eat them even if you don't like the flavor a lot. Finding nourishing foods "repellent" is a modern luxury.
Additionally, the bitter flavors in vegetables may be less noticeable to people who were not raised from infancy with hyperpalatable, sugar-sweetened food.

To a certain extent how much people like various foods is a relative thing. Vegetables are indeed more desirable as food over, say, rocks, but often less desirable than, say, cake. Our bodies get more energy from sugar than vegetable matter, so evolutionarily we prefer the taste of sugar.
This is complicated by the fact that our tastes are often learned/environmental. Like, I love clams but I know many people hate clams; there isn't some biological reason for this, it just comes down to I grew up near the coast and they grew up inland.

Can you please add some references?

I would suspect there are many reasons from behavioral to genetics to anthropological. I think the answer you are looking for (as you have posted it here) is sensitivity to phenylthiocarbamide or PTC. PTC is an organosulpher thiourea. It has a very bitter taste and the ability to taste PTC is determined by ones genetics. It I s a dominant trait and about 2/3 of the population can taste it. Although it is not found in food there is a large body of evidence linking the ability to taste other thiourea compounds with dietary habits. For example, smokers and coffee nuts are more likely able to taste PTC. They also more often dislike certain vegetables. If you ever want to find out if you have the ability to taste it you can try tasting test strips that contain PTC.


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Did the Swedish cod fishery expand in the past years?
The Marine Stewardship Council states that the cod fishery in the Eastern Baltic sea recovered well and issued it's MSC certificate to the Swedish cod fishery in 2011 for that region. (MSC 2011)
Data downloaded from EUROSTAT shows that Portugal, a main importer of codfish and -products, imported less and less from Norway (besides Iceland and UK the main supplier) (FAO 2006); dropping from around 20,000 tons (2001) to < 1,000 tons (2011) and more and more from Sweden; < 5,000 tons until 2003 versus > 30,000 in 2010 and 2011.
This trade data does not necessarily show the origin of a product but rather the country that is selling the fish. I wonder if either the Swedish cod fishery expanded in the past few (~ five) years; Portugal changed it's main supplier from Norway to Sweden for whatever reason; or Sweden buys cod from Norway and distributes it.
Depending on this the answer may not be so closely related to biology but I hope to get an idea here.

A "fisheries" tag would be useful in my opinion.

[ichthyology]+[ethnobiology]="fisheries", more or less.

If by 'fishery' you mean "amount of fish caught", the answer is a qualified no. Sweden's catch has been stable or perhaps slightly increasing since a low in 2005, but the catch is still much lower than a decade ago (Statistics Sweden). This is presumably due in large part to the quotas set on Total Allowable Catch for various sea regions.
If by 'fishery' you mean "amount of fish in the sea", the answer is a qualified yes. Most Swedish cod catch (>90%) comes from the Baltic, where stocks have been recovering since 2006 after steep declines in the eighties (ICES full report and executive summary for Eastern Baltic). Presumably, this recovery is also due in large part to the quotas set on Total Allowable Catch, i.e. to the reduction in cod mortality due to fishing.

Sweden's cod catch for all regions, and the ICES estimated Spawning Stock Biomass of cod in the Eastern Baltic. Both are in thousands of metric tons, but note that the scales differ by a factor of ten)

No idea how this is affecting import/export, although Statistics Sweden might have that data. One biology related possibility is that Eastern Baltic stocks (presumably accessed more by Sweden) are doing better than North Sea stocks (presumably accessed more by Norway), but that's just a guess, you'd have to check the data.

Thank you. I spoke to a large codfish producer in Portugal who stated that their cod still mainly originates from Norway (> 80%), i.e. is caught in Norwegian waters, with no relevant share of the Swedish cod fishery. I assume that the considered trade data is inconsistent and includes more complex trade relationships that may be hard to entangle.


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What could cause hairs to gray at the tips but not the roots?
I have noticed that some of my sporadic gray hairs are gray at the tip side but oddly, not near the roots.  Some are even only gray in the middle.  I find all of this very counter intuitive, and I assure you nobody is secretly dying my hair.
How does the graying process work, and how is it that this can be happening?

I have the same, I take it a good sign though - Benjamin Button kind of vibe. Not all, but quite a few grey hair are dark at the root. If I had to guess what could be causing it - I would say: stress, keto diet, lack of sleep (causing grey hair), and once those things are removed coloured hair start growing again. Though it's pure speculation on a sample of one.

When Googled, this question only comes up with this and one Quora post with the rest about how hairs grey starting at the roots. I'll submit what was in the Quora post to help someone find information: One person claimed swimming a lot in chlorinated water could bleach the tips of hair. Another person said exposure to sunlight might do this. A final person said it could be from damaged hair (split ends, etc.), meaning the fix is a trim to get rid of the damaged hairs. That last one matched my scenario best. I'll see if my hair becomes grey at the tips again after a trim.

After years of this, I am still wondering what the heck is going on. My informal observations are that for virtually all hairs that aren't entirely grey, the grey part is the part closer to the root, with typically a fairly distinct cutoff where it becomes grey. For what it's worth, these are chest hairs.

Interesting question, I am not sure if I have a definite answer, but at least some ideas:
The pigment in the hair is made by specialized cells, the melanocytes. The make the pigment (eumelanin=dark and pheomelanin=red/yellowish) which is then deposited into the growing hair. They are located at the bottom of hair bulb and usually die at the end of each hair cycle. To have the hair of the next hair cycle colored as well, this melanocyte population in the hair bulb needs to be replenished. This is done by melanocate stem cells, which live in the hair bulge and which start to reproduce and differentiate in melanocyte which then migrate down to the hair bulb. There is an excellent article following this process:

Mechanisms of hair graying: incomplete melanocyte stem cell
maintenance in the niche.

The hair later gets grey (low pigment) and white (no pigment) when these melanocytes are not, or not fulley replenished in later hair cycles. Why this happens, there are a few hypothesis.
First, its possible, that with age the melanocyte stem cell population (which not only need to replenish the melanocytes, but also need to maintain its own population) is getting smaller and disappears over time. This process would explain gradually graying over time. See this reference:

Melanocyte stem cell maintenance and hair graying.

Another possibility is the presence of reactive oxigen species (ROS) which occur naturally in melanocytes. Over time, the enzyme which intercepts this ROS (catalase) is getting less active or present in the cells and thus oxidative damage is getting bigger, damaging the melanocytes and their ability to make pigment. It would actually bleach itself...

Senile hair graying: H2O2-mediated oxidative stress affects human
hair color by blunting methionine sulfoxide repair

Melanin has also an important role in intercepting ROS, so in this process less and less pigment is made (as the damage accumulates) and this also leads to hair, which is less pigmented for exogeneous oxidative stress:

Towards a "free radical theory of graying": melanocyte apoptosis in
the aging human hair follicle is an indicator of oxidative stress
induced tissue damage.

It could be possible (and this is a wild guess) that the phenomenon of the tips graying first is situated by this. Hair less protected against exogeneous oxidative stress (smoke, UV etc.) so the melanin is "used up" during this until the hair greys at the tip, since its the oldest and most exposed part of the hair. This article by Tobin gives also a nice overview:

The cell biology of human hair follicle pigmentation

Your hair grows out from the roots, and typically as you age, the pigments (melanin) that would normally keep your hair a certain colour are not produced anymore because the pigment producing cells (melanocytes) start to die.
They're likely different colours in the middle because that will be the result of a gradual dying off of the melanocytes at the base of that strand. As a result the root (newest part of the hair) will typically be gray when they have mostly all died off, the middle will have a bit of melanin because it was produced when there were still some functional melanocytes, and the tip (the oldest part of the hair) will still be full of melanin from when it was produced when the melanocytes were alive.
As for why this happens it's not fully understood why the melanocytes die as we age, but the gene Bcl-2 has been found to be essential for the maintenance of melanocytes. Mutations in this gene could be responsible for premature graying [1]. There is some literature on the role of Bcl2 family genes as regulators of cell death [2][3] but how these things are connected seems largely still unknown.
[1] http://www.nbcnews.com/id/6750793/ns/health-cancer/t/research-yields-clues-why-hair-turns-gray/#.UVCu21dONvJ
[2] http://www.annualreviews.org/doi/abs/10.1146/annurev.immunol.16.1.395?journalCode=immunol
[3] http://genomics.senescence.info/genes/entry.php?hgnc=BCL2
There have been some reports of people indicating that a change in lifestyle and/or diet have led to a decrease in gray hairs, or even that the hair begins to regain its colour leaving a gray section at the tip or in the middle. I've only found one relevant article which makes reference to some research into the restoration of hair growth and colour in mice[4]. An American group are studying the role of the Wnt signaling protein in controlling the activity of melanocytes. I'm just speculating here, but it could be that fluctuations in Wnt protein production (possibly influenced by diet and lifestyle and overall health) may switch melanocyte melanin production on and off. I haven't been able to find any literature to back up this hypothesis though.
[4] http://inventors.about.com/od/gstartinventions/a/Cure-For-Grey-Hair.htm

Sorry, I realized I mis-typed what actually happens.  The counter intuitive aspect is seeing gray tips or middles, not roots, like one would expect.. editing.

I edited my question; if you could please update your answer to reflect my corrected question, that would be great.

The last link is at least questionable. TRP-2 (or usually called DCT) is of course also present in follicular melanocytes in the hair, otherwise there would be not eumelanin (dark) pigmentation. The observation that Wnt may play a role is pretty broad, since Wnt signalling is essential for the melanocyte to function. I can go through my library tomorrow and write some more about it if wanted (the topic is pretty old).

This is a consistent phenomenon with me and I don't live a stressful life and eat pretty consistently, so I'm skeptical that it's environmental.  About 20 to 30% of my graying hairs are like this (black at the roots, gray on the oldest half.)  @Chris I'd love to hear more.

@JeffAxelrod Done. Took a bit longer than anticipated.

I think this is not the best answer here to the question. Chris covers the topic better, I think, since he mentions H2O2 mediated oxidative stress, and ROS, too. All answers could cover Genetics more clearly. Nevertheless, I like the mentioning of Bcl2 here.


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More proteins from diet when common cold and flu?
My coach says that I need to eat 1.2 - 1.5 grams of proteins per kilogram when I have a common cold and flu.
I normally eat one gram of proteins per kilogram, while double it when doing my exercise training.
He explained that the reason why you need to get more good proteins when you are sick is that the body is building antibodies by the adaptive immune system and later for innate immunity.
I think he can be right based only on my own experiences getting better from common cold with low protein diet - it just takes a lot of time, while under high protein diet, you get better faster.
I also think his explanation makes complete sense to me, since antibodies and antigens are proteins.
Why do you need more proteins when you are sick?

Who says antigens must be proteins? Is this true? Many will be peptides of course but surely not all antigens are proteins. Anyway, you don't build antigens, whatever pathogen has infected you does.

no antigens don't have to be proteins, they can be a variety of things like pollen, chemicals, parts of a pathogen, or even endogenous components of cells (such as those which are targeted in autoimmune disease- so technically you can build antigens) and your body produces antibodies against them

Your body needs more energy when you are ill to facilitate the recovery process which includes the production of white blood cells to help fight the infection. This shouldn't be limited to proteins though, carbs are also very important as they are provide high amounts of energy. Basically just making sure you eat a varied and balanced diet is more important when you are ill to make sure your body receives the nutrients it needs to fight infection and heal itself. As it is having to work harder when you are ill it makes sense to eat more high energy foods. Micronutrients are also very important!

Minerals such as selenium and zinc work to keep the immune system strong. These minerals are found in protein rich foods such as beans, nuts, meat, and poultry. — Source

Although if your diet is varied you should be getting plenty of these anyway, without needing to take supplements.

Remember that your coach shouldn't give dietary advice unless he's trained as a dietician. Protein isn't as important as glucose really, that's the thing you burn the most. However you use everything: vitamins to tell the immune cells where to go, proteins to make antibodies, glucose to fuel millions and millions of neutrophils and other cells. Even fat stores may start to move in order to keep your glucose high but not too high. The excess protein is unlikely to do you harm, it'll just get urinated out typically. Minerals can be used by enzymes to make them active that are in charge of destroying bacteria.
So as a rough summary, eat healthily. Exactly how you should eat before getting ill to limit the duration or prevent symptoms in the first place. If you lack the minerals and vitamins during the time you're ill you probably lack them all the time round so don't change what you eat when you're ill, but change what you eat when you're well and then your body will have everything stocked up when you're ill and all you need to eat is glucose and drink plenty of fluids and if possible continue with the healthy stuff.


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What limits the size of fish compared to marine mammals?
The largest extant fish species is the whale shark (Rhincodon typus). With a length of 13 meters and a mass of about 20-30 metric tons, the whale shark is relatively small compared to the largest mammals, blue whales (Balaenoptera musculus, 180 tons) and fin whales (Balaenoptera physalus, 120 tons).
Is there a physical, physiological, or anatomical explanation why fish never reached the size of marine mammals?
Bigger isn't necessarily better, but I was wondering if there is a simple explanation why fish species are so much smaller than marine mammals.

I'd suggest that one factor could be the difficulties of breathing water - it is highly inefficient. The following is a summary of this response to a TREE article.
Fish spend 10-30% of their energy on breathing because it is so inefficient to use gills because diffusion rates are much slower and oxygen is less abundant. Gills grow in proportionate scales to body size, generally for every 100% increase in body size there is a 50-90% increase in gill size. Thus the larger fish species are working on a lesser body mass/gill size ratio so they can't take up oxygen very easily.
From this I'd suggest it is difficult for fish to grow gill systems much larger than those of a whale shark as it would become to inefficient for them thrive. By comparison whales are air breathers so, despite "breathing" (collecting fresh air) less frequently they can get much more oxygen from it.
I'm sure there is more to it but at least this is a starting idea. If anyone has more then feel free to add to/edit this answer, I merely suggest this as one possible theory and it is not my field.

That is very interesting and definitely a possible reason. I was not aware of the fact that extracting oxygen from water was such an energy drain for fish. This might mean that larger fish species did exist at some point when the atmosphere (and the oceans) had a higher oxygen level.

that is quite plausible: http://news.bbc.co.uk/2/hi/uk_news/scotland/glasgow_and_west/8522789.stm

But the metabolic rate of fish is a fraction that of mammals, so they don't necessarily require as efficient an oxygen delivery system.

Moreover mammals have four-chambered heart which makes the cardio-vascular system more organized and efficient. Basically the mixing of oxygenated and de-oxygenated blood is prevented.

A nice point @WYSIWYG


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Is stereo olfactory ability restricted to humans?
Most animals I see around seem to have two nostrils - humans, snakes, birds, fish .. and so on. From reading online I see that 2 nostrils provide a stereo olfactory effect. This stereo effect is caused by the difference in flow of air through the nostrils.
Does this stereo effect apply only to humans? Are there any animals that have a different number of nostrils? Say, more than 2, or less.

Moles and rats also smell in stereo (Catania 2013 and Rajan et al 2006), as do desert ants (link).  The latter is rather interesting, given that ants "smell" using their antennae, which suggests multiple sensory structures, not necessarily nostrils, are required for stereo olfactory ability.
EDIT: Hammerhead sharks have two nares and also stereo olfactory ability (here).  Dolphins have one spiracle, as do a number of other cetaceans.
It's actually not clear whether humans have stereo olfactory ability, (see edit below)  as the "stereo" aspect derives from having nostrils that are sampling from different spatial locations.  However, the research in the eastern mole suggests that this is not so far-fetched an idea, as their nostrils are not so far apart.
EDIT of EDIT: I take that back about humans: we do appear to have stereo olfaction.


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What causes humans to be sleepy?
Is there a hormone or group of hormones that regulates when we feel sleepy late at night, or in the morning?  Or is sleepiness caused by some other non-hormonal mechanism?  (e.g. pure psychological, or neuronal.)

The release of the hormone melatonin is responsible for the feeling of sleepiness. It is released by the pineal gland and production starts when the light fades, as it's production is inhibited by light stimulation of the retina, the onset of the production is called dim-light melatonin onset. Artificial supplementation can increase sleep quality and regularity related to some sleep disorders and is often administered as pills or patches.
Adenosine is an inhibitory neuromodulator, ie it inhibits neural activity. Neural activity can be either excitatory or inhibitory and adenosine more strongly inhibits the excitatory neural activity. Thus, increased adenosine levels should decrease excitatory effect of nervous stimuli and make you feel more relaxed & sleepy.
Other hormones & neural pathways may be involved (serotonin and the serotonergic neural pathways for example) as well as other stimuli like other people's behaviours (yawning, stretching etc.).
This page and the wiki entry on melatonin have much more information.
From sleepfoundation:

Melatonin is a natural hormone made by your body's pineal gland - a
  pea-sized gland located just above the middle of the brain. During the
  day the pineal is inactive. When the sun goes down and darkness
  occurs, the pineal is "turned on" and begins to actively produce
  melatonin, which is released into the blood. Usually, this occurs
  around 9 p.m. As a result, melatonin levels in the blood rise sharply
  and you begin to feel less alert. Sleep becomes more inviting.
  Melatonin levels in the blood stay elevated for about 12 hours - all
  through the night - before the light of a new day when they fall back
  to low daytime levels by about 9 a.m. Daytime levels of melatonin are
  barely detectable.

Thanks rg255.  Unfortunately the link "This page" in the last sentence is inaccessible.  Also,  during my own research today I found something on "adenosine" influencing sleepiness but found the article hard to understand.  Do you know what triggers adensine build up, which apparently causes sleepiness?

@chris did the first link work? ("release of the hormone...") if so, that is the same page

No the first one didn't either.  Even just vaxa.com gives the error "403 - Forbidden: Access is denied."

@Chris edited to include quote from Växa site and effects/action of adenosine

What about sleepiness during day time? How is that brought about?