text:
Are there known downsides to removing UV mutation hotspots to prevent some skin cancers (Genetic sunblock)?
Khavari et al. recently demonstrated that a significant fraction of  one of the major forms of skin cancer (cutaneous squamous cell carcinomas) are associated with a mutated KNSTRN gene (a protein associated with the kinetochore). They identify a specific region of the gene as being a hotspot for UV induced mutation and suggest that these mutations may be an early event in the development of this type of skin cancer.(1)
Abstract from their nature paper (paywalled):

Here we report the discovery of recurrent mutations concentrated at an ultraviolet signature hotspot in KNSTRN, which encodes a kinetochore protein, in 19% of cutaneous squamous cell carcinomas (SCCs). Cancer-associated KNSTRN mutations, most notably those encoding p.Ser24Phe, disrupt chromatid cohesion in normal cells, occur in SCC precursors, correlate with increased aneuploidy in primary tumors and enhance tumorigenesis in vivo. These findings suggest a role for KNSTRN mutagenesis in SCC development.(2)

My question:
Scientists could theoretically alter the nucleotide sequence of the KNSTRN gene to remove the mutation hotspot, potentially lowering the incidence of this type of skin cancer. But are there any downsides to doing so? Are there any cases where a UV mutatable hotspot has shown to have some useful function in a cell or organism?
Thanks!

http://www.sciencedaily.com/releases/2014/09/140907181722.htm
http://www.nature.com/ng/journal/vaop/ncurrent/full/ng.3091.html

Short-wave UV light (UVB and UVC) causes transition mutations at dipyrmidine sequences (ref.). In the work presented on KNSTRN quoted by the OP the authors report that 19 from a panel of 100 squamous cell carcinomas (SCC) contained a mutation in KNSTRN (and furthermore three of these contained no other mutation across the six genes that were analysed (Fig. 1b)). Normalising for ORF length this makes it the 3rd most recurrent mutated gene. It would seem therefore that it a fairly important mutagenic target. In a broadened set of SCCs they found a total of 29 KSTRN mutations, and of these 13 were Ser24Phe (TCC>TTC) mutations, which they refer to as a 'hotspot'.
Accepting the arguments in the answer from @Chris it is still interesting to consider how one might remove such a hotspot. The normal amino acid at this position is a serine. Here is the human codon useage for ser, obtained from here:

TCT 14.6%
TCC 22.0%
TCA 15.0%
TCG  6.0%
AGT 11.9%
AGC 19.4%

It would seem therefore that it would be theoretically possible to edit the Ser24 codon from the UV-sensitive TCC to AGC, essentially eliminating this 'hotspot'.
This, of course, doesn't answer the question - are there downsides to this? I already selected a synonymous codon with a similar frequency of useage so that shouldn't be a problem. However here is an example of a synonymous codon substitution which has an effect upon splicing of the LMNA gene resulting in muscular dystrophy, and the paper cites several other examples of this. (I haven't actually checked to see where the Ser24 codon lies in relation the exon-intron boundaries in the KNSTRN gene.) No doubt there are other mechanisms by which my proposed edit could have unwanted effects. It would have to be tested carefully, and so we come back around to a cost-benefit analysis - would it be worth developing this editing idea (even if it were feasible as a therapy) given that there are clearly many paths to SCC not involving this specific mutation.

This is a good point. In addition to maintaining the same amino acid and taking care to avoid splice site junctions, you'd have to consider if there were any protein, DNA or RNA interacting sequences encoded in the region of interest. If the region were in a non-coding transcript it could also be problematic. Anything else?

The region can also contain regulatory regions (also when this inside a gene) which you probably mess up with.

This is actually a bad idea for severeal reasons: First it is not a good idea to tamper with genes, especially not with ones which are involved in the regulation of mitosis and the correct segregation of sister chromatids. Remember that a one amino acid exchange because of a C to T transition causes the problems with SCC? Into what do you want to change the sequence anyway?
Then this is not the only mutation linked to SCC - mutations in TP53 and CDKN2A are more important here. And even if you manage to change the sequences here which are the causative reason for SCC there are other mutations that will then occur. Simply by chance. It is probably a good idea to target the mutant KNSTRN protein with a treatment as this is already done for other proteins (although these are usually enzymes), but changing it will most likely not only not work but cause other problems as well.
Another problem (even when you use a synonymous codon which does not lead to an amino acid exchange) is that you can disrupt genetic regulatory regions. Not all of these regions are located in the promoters of genes, quite a number of them are found inside of genes. Here even a single nucleotide exchange can prevent a transcription factor from binding to its recognition site. A prominent example for the is the HERC2/OCA2 polymorphism where a single nucleotide polymorphism in HERC2 alters a transcription factor binding site and thus alters the expression of OCA2.
The solution here is pretty easy: Avoid prolonged exposure to UV light whenever possible.

This is generally true, but for the specific regions in question, transgenic mice could be used to test these hypotheses, assuming the same effect held in mice.

The problem with mice is that they usually don't develop skin cancers. You need to use mice with other defects as well and this makes the model much weaker.

sure, though I think its far from saying that this is not a testable hypothesis, and that they will try to do so.

The problem with mutations is that this will cause severe problems when we change the code like this. So you have to think about cell type specific knock-ins (probably inducable) and then see what the outcome is. This is surely interesting in terms of basic research, but I don't see any practic use for it (which is no reason to not analyze this).

fair enough, @Chris!

@Chris I can see you're point but my question assumes a bit of technical knowledge - obviously one would want to avoid amino-acid changes. I realize other mutation will continue to occur elsewhere and that the engineered site may itself ocasionaly mutate - the point is to lower the mutation rate at this specific site. I think preventative genetic intervention could be vastly superior to antibodies, small molecules or other protein targeting methods but the technologies aren't quite there yet.


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Is it possible to elicit transient gene silencing by using virus induced gene silencing (VIGS) in plants?
I am looking for a molecular tech' which could result in transient gene silencing in plants. The objective is to not make transgenic plant, but to use these tech' to silence a gene of interest for a short time. From my limited knowledge, I found that virus induced gene silencing (VIGS) may be an option, I wonder how easy and how long such silencing last? Is there any alternative method?
I don't have any candidate gene to be silenced at this moment, but the tissue will be flower. so it would be nice if the protocol works for flower.
Thank you in advance

I haven't worked on alpha viruses since my first rotation in grad-school, but an important question that needs to be answered is when are you infecting the plant? If try to infect fully formed flowers you might have a hard time getting effective silencing across the whole tissue.

Virus induced gene silencing (VIGS) is definitely an option.
The ease of using VIGS depends on a lot of factors. Current VIGS vectors have limited host ranges. Depending on the species of plant that you are working with, there may or may not be suitable, pre-made VIGS vectors available and published techniques for using them. Many of the VIGS vectors that are available may be limited in terms of which tissues they can infect. Working with the vectors themselves requires that you have some way to propagate them and some way of getting them into your target plants (for example Biolistics, Agrobacterium or direct application of infectious virus).
There have been a number of VIGS vectors developed over the years, capable of infecting a diversity of plant species. Modified Tobacco mosaic virus (TMV) and Tobacco rattle virus (TRV) are two common VIGS vectors used for silencing in a variety of plants. TRV in particular is known to have a very wide host range. If your species doesn't fall within or even near the documented host range of available vectors it may be worth just trying a few different ones. Or, you could always isolate a virus specific to your target plant and build you're own. What fun!
The length of time that silencing will last is difficult to predict. In my experience, it will typically last a few weeks. But this may vary depending on a number of host factors and the VIGS vector used.
One potential alternative would be to just use Agrobacterium. It could be combined with a recombinase system to satisfy your condition of transience. To build such a system you could insert you're silencing construct into a binary vector. By including an inducible recombinase sequence adjacent to your silencing construct sequence and by flanking both of these with the recombinases recognition sequences, you would be able to remove inserted DNA at some point down the road after transforming the plant.
Again, depending on which species and variety of plant you're working on, this could require some trial and error as there may not be published techniques for Agro mediated transformation of you're target plant.
While Agro mediated transformation may not quite be what you're looking for in terms of transient silencing, it may be sufficient for a proof of concept.

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Do adult humans exchange beneficial bacteria? If so, how?
Recently there has been increasing interest and research into symbiotic bacteria present in humans and human gut. I'm aware of two new discoveries:

humans are surrounded by a unique cloud of bacteria, similar to fingerprint, useful in forensics
human brain and cognition could be influenced by gut bacteria that produces up to 90% of serotonin and dopamine in the human body (not sure how, vagus nerve is implicated)

I've also heard that mothers pass a lot of beneficial bacteria to children during childbirth to jump start intestinal flora. Apparently this happens as the baby travels through the birth canal.
This makes me ask - do adult humans share/ pass along symbiotic or beneficial bacteria or other micro organisms?
I'm aware of viruses and diseases that can be passed via blood or be transmitted sexually, but does anything beneficial get transmitted this way?

It comes down to a question of whether or not they are able to colonize the surfaces, skin, lungs, gut epithelium, not if they are exchanged. A large majority of gut microbiota are anaerobes and their ability to be passed in any medium other than direct contact with feces (how baby's born vaginally get their sampling of most of the maternal gut microbiome) is limited.

Also as an adult your own microbiome is part of your innate immune defenses and they keep out other organisms by taking up space on the exposed surfaces of the body. Pathogens have an advantage over commensals as they have virulence factors to let them gain the upper hand.

Nonpathological bacteria Staphylococcus epidermidis on the human skin are part of normal bacterial flora that help to protect against pathogenic bacteria, such as Staphylococcus aureus. You can get "infected" by Staphylococcus epidermidis the same way as by other skin bacteria and you get a potential benefit from them.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807625/
You can get beneficial effects from pathological bacteria passed from someone, if you you develop antibodies to them, so you can become more or less resistant to them. For example, if you are from US or Europe and travel to South Asia, you at high risk to get food poisoning from either bacteria or viruses, bot local people are at much lower risk, because they have "shared" microbes one from another.
You can get beneficial effects from probiotic supplements (live nonpathological bacteria), which prevent overgrowth of pathological bacteria in your large intestine. The bacteria in probiotics are similar than those in the human gut.

You forgot to add the most important bacteria when the baby passes through the birth canal.

@Muze, the question is strictly about adults.

Every human has it owns unique bacterial biome, and they acquire it the day they are born. Another interesting thing is that the bacteria that each individual acquires gets much of it from there family/parents. An analogy would be portions of bacterial biomes are passed down from generation to generation although each person does generally acquire a unique set of bacteria.
Bacteria is passed throughout the population all the time generally though you only hear about the negative transfers i.e pathogens. It is hard to track what gets transferred though as most bacteria is not culturable.
The Human Biome Project has been uncovering the variety of bacterial biomes among the human population in different demographics, etc. You would probably have a fun time looking through there and uncovering some cool information.
Here's the link: The Human Biome Project

Most exchanges, aside from neo-natal transfer, are fecal-oral. Some exchanges are pneumonic, but the study of those has been limited to pathogens. I am not aware of any studies of direct epithelial contact.
In humans, the preponderance of exchanges happen early in life (neo-natal). The current school of thought is that the microbiome is established by passing through the birth canal and through breast feeding. Only Archae and bacteria have been studied up to this point, and the study of the constellation of viruses is currently being proposed.

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text:
Is there a mechanism by which mammals lose interest in a partner after mating?
I'm reading the book called "Cupid's poison arrow", which revolves around a rather simple assumption: most mammals, including humans have a genetic program that is responsible for ever increasing dissatisfaction with a mate after intercourse with orgasm.
The book proceeds to give a number of examples, here's what I remember:

Coolidge effect, where libido is revived upon exposure to a novel, receptive partner.
Male rate copulating on average 8 times with a receptive female before losing interest
Sexual satiety setting off a 14-15 day hormonal cycle where [a male rat] would lose all interest in a partner

The book contains a large amount of anecdotal evidence of humans experiencing negative outlook on their partner after orgasmic intercourse, with more intense intercourse producing more intense dissatisfaction.
The author proceeds to formulate a hypothesis that humans and other mammals have a genetic program that fosters sepratation between mates and seeking of a novel mate as a mechanism to promote more genetic diversity in offspring (as opposed to monogamy)
Is there a scientific basis for such claims -  do mammals have a mechanism that draws them apart after intercourse or sexual satiety is achieved?

Looking for scientific justification? :-)

Scientific is the best kind of justification :P  But seriously, that hypothesis sounds really solid and like it has a lot of evidence. I want to know if it is valid.

Why should something like this be a genetic program specifically for this one thing, rather than just the expression of a general taste for diversity?  E.g. most people have favorite foods, but we'd regard an adult person who ate only one particular food as decidedly weird, and their diet would almost certainly be unhealthy.

Well from what I have been taught, and have studied, is that multiple partners for men does not equal more of their DNA persisting, because they are needed to provide for the offspring. So if they impregnate 10 different females and don't stick around, that really doesn't help them pass on their DNA because most would die. So having a family with the same partner does ensure more offspring survive. Humans are picky selecting their mate for the reason of wanting to get the best genetic combination possible to have the most offspring survive. A human child takes a lot of effort to raise to reproductive age, we aren't like some animals who are off and running. So our bodies invest a lot in making sure that happens, being flooded with bonding hormones after sex, women's bodies changing to nurse (and then not being able to hunt/gather/protect themselves) etc. So there is a hormonal cascade that happens to ensure you are going to stick around after mating.
I am really talking about our ancestors, but obviously some of their behavior has carried to us.
However having multiple partners DOES benefit the female. Males can't tell they are the father to a child until much later, after they have supported the pregnant mother, etc. Females can then have their DNA pass on in multiple combinations to ensure survival of more children. Pubic hair in women is thought to have evolved to hide any physical evidence of a recent mating with different males outside of the family. And if current statistics say anything - just as many women cheat on their spouse as men. And when cheated on women want to go after the other woman, because that's our competition and they may be taking the mate we worked so hard to get.
Humans are hard to compare to other animals because we can manipulate so much of what happens to us. But if the ultimate goal is to ensure the passing of DNA then that hypothesis (to me) doesn't fit with humans.
But then again, I am a woman and therefore could be biased haha. If you read an animal behavior textbook it will go into this in in detail, and state it much better than I can, and with supporting scientific evidence. As a biologist the term "anecdotal evidence" makes me cringe :)

Hi Whitney - Welcome to BiologySE! Thanks for your answer - generally we value references to back up the claims in individual answers. I know that some of this may be common knowledge to you (as much of what my answers are), but please try to include some citations of published works that support your answer. Feel free to edit the current answer and add to it - thanks for your contirbution

Thanks for an answer. From my knowledge of evoutionary psychology, your statement is incorrect. An attractive "bad boy" casanova can leave 50 children with single mothers and would outperform a pure pair bond partner.


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Is there any biological support for the concept of "chakras"?
Is there any support in modern biology for the ancient concept of "Chakras"?
I've seen the concept of 7 chakras linked to the major endocrine glands in the human body (pineal,thyroid, adrenal, testes, etc). This makes some sense, however, I've seen other numbering start to talk about 14, 21, etc number of chakras, which makes me skeptical.  Are chakras real?

I think the question should be migrated to skeptics.SE. In the same time, it will be very important to very accurately defined what is meant by "support for the concept of chakra". Does it mean "Is it true that there is more energy flowing at key points on our body" or does it mean "does medicine such as  effective?". Does it means something else?

If you agree, I think you can flag your own question to ask for migration. Again, I think (might be wrong) that the question will need some remodelling to make sense of "support for the concept of chakra".

I think no matter what definition of chakra you use, it's not suitable for a science based site.

I'm voting to close this question as off-topic because this question would be better suited on Skeptics.SE. Also I would suggest to clearly define what you would call a "support for the concept of chakras".

@canadianer I'm afraid I must disagree with you there. The chakra is, like many things, a guess, a "theory" if you will, developed through someone's observations to explain a concept that they do not understand. This is human nature, to wonder about something and attempt to explain it. Is this not science? Wonder is at the very heart of science and an attempt to explain an observation comes soon after.

Whether this theory is right or not is obviously arguable (not only for this theory, but for many, many others as well), however I do not think it should be closed. I think it would most likely fit in a little better over in Skeptics SE. though.

@CDB If you think it belongs at skeptics SE, then it sounds like you actually agree with me ;)

@cdb a guess is not a theory.

@canadianer It definitely belongs on a science based website, otherwise you would get some pretty scientifically unsound answers. I just don't think this should be it. Than again, this is a website specifically created to answer questions regarding biology, so perhaps it should be answered here?

@dustin Good point, I should have said hypothesis. My apologies.

As is the question is fit for neither sites. You need to define better, not just by referencing to an other page, what is the concept of chakras you reference to. Then if you can formulate a "common claim" Skeptics is a good place to ask if this claim is right (see the closest to a guideline for skeptics at http://meta.skeptics.stackexchange.com/a/2512 ) otherwise you can move it to the beta Health site  http://area51.stackexchange.com/proposals/66048/health but I think here is not a bad place to ask.


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Does anxiety about weight or eating cause people to become overweight?
A while ago I saw this TED talk about the futility of dieting. The speaker suggests that a body maintains a homeostatic weight point and returns to that weight after dieting has stopped:

Turns out the brain is an incredibly efficient regulator of body
  weight. Isn’t weight loss about how much you eat versus how much
  energy you burn? Nope, it’s not that simple an equation: it turns out
  that hunger and energy use are controlled by the brain, mostly behind
  the scenes, and this unconscious force is stronger than mere
  willpower. The brain has its own sense of what your body should weigh
  — no matter what you believe — called the set point, which has a range
  of about 15 pounds. While lifestyle changes can shift your weight
  within this range, it’s much harder to move outside of it.

The speaker suggests that once she gave up dieting, she actually lost weight. Since then I've seen a number of other anecdotal reports of people losing weight once they let go of the need to diet and started to "eat anything they wanted".
This makes me ask - does anxiety about weight and attempts to control one's eating cause people to put on weight? In other words, if there's some unresolved anxiety issue in one's life, does it cause the human body to start preparing for hard times by storing extra fat?

yes, anxiety can changes hormonal state of our body,which may reduce catabolic enzyme that leads to grow more fat. So, anxiety may be a cause of over weight


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Decreasing Solubility as Solvent Moves Higher in Paper Chromatography
In paper chromatography, as the mobile phase (I used 1:9 acetone/petroleum ether) climbs higher and higher, will the solubility of the solutes decrease as the solvent moves higher? I speak mostly about the beginning, when the solvent just begins to climb up the paper. Will the solutes travel right at the solvent front at the beginning, and then start to lag behind (and separate) as the solvent front moves higher?

The solubility of the solutes is the same at all points in the chromatography process. The solutes are clustered together at the beginning (at the solvent front) because none of them has moved very far yet. The reason for the separation of the solutes isn't that they become less soluble, it's that the solutes are moving at different speeds, like cars in an auto race:
  _______
 /____/SF\___
 |_,._____,._)
---`'-----`'--
  _______
 /____/S1\___
 |_,._____,._)
---`'-----`'--
  _______
 /____/S2\___
 |_,._____,._)
---`'-----`'--

At the beginning, both cars (solutes) S1 and S2 are even with the solute front car (SF) because the race (chromatography) has just begun. However, over time, the SF car outpaces S1 and S2 because it is moving faster.
                     _______
                    /____/SF\___
                    |_,._____,._)
                   ---`'-----`'--
         _______
        /____/S1\___
        |_,._____,._)
       ---`'-----`'--
              _______
             /____/S2\___
             |_,._____,._)
             ---`'-----`'--

And at the end, you get great separation:
                                                                _______
                                                               /____/SF\___
                                                               |_,._____,._)
                                                              ---`'-----`'--
                        _______
                       /____/S1\___
                       |_,._____,._)
                      ---`'-----`'--
                                           _______
                                          /____/S2\___
                                          |_,._____,._)
                                         ---`'-----`'--

(Thanks to retrojunkies.com for the ASCII car)

Great analogy to explain the answer! +1

Another helpful concept is RF, which is the distance traveled by the solute divided by the distance traveled by the solvent front. A very soluble compound may have an RF close to 1, so you'd only be able to see a difference between it and the solvent front after a significant distance.


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How does the body avoid making an immune response to self-antigens?
The body contains antigen-detecting and presenting cells (APCs) including leukocytes and cytokines each having their characteristic HLA genes consisting of different recognition sites that detect the foreign molecules. Although the immune system can respond to a huge amount of different proteins or other antigens, self-antigens are not attacked by the immune system. Why not?

Check the terminology you're using, like "antigen", and see that you are using it properly. As-is, I think someone can guess at what you are writing here but the way it's actually written is nonsensical. For example, do antigens "attack"?

related, but not quite duplicate: https://biology.stackexchange.com/questions/64897/autoimmunity-negative-selection-of-t-cells-apc. https://biology.stackexchange.com/questions/14067/autoimmunity-and-central-tolerance. Not sure if there's a good duplicate on self-tolerance that I missed though

@hali--the phenomenon you're asking about is "immune tolerance", or more specifically, "self immune tolerance". Those are helpful terms to google

Cytokines are not cells, they are proteins.

short answer, because your thymus tests every antigen binding protein against all your bodies antigens , helpful video, https://www.youtube.com/watch?v=LmpuerlbJu0

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Can Monsanto's (in)famous hybrid seed crops be cloned/grafted? If not, is there a technical or legal reason?
I understand that the seeds of a crop made from modern-day super hybrids will not, usually, produce the same quality plants in the next generation. Therefore, farmers have to buy new hybrid seeds each year (or season) from the original company. But, what if a farmer tried to clone his extremely productive plants?
Is there a scientific reason why modern hybrid varieties cannot be 'grafted', to create next season's high-quality crop, or is it due to a contract agreement signed by the farmers with their seed company? I am very curious as to why modern 'hybrid' crops cannot be propagated in this way.

Yes, it's stipulated very clearly in the contracts that any such efforts are strictly prohibited. Besides, would you want to graft an entire corn field?

I last worked on maize a mumble decades ago, but as far as I know grafting in grain producing grasses isn't practical. Please look for evidence that this is possible or if you meant some other type of plant please be specific. ——— Also note that the legal aspects of your question are off-topic for this site.

One needs to take into account how much work and research would go in cloning these productive plants - this is a task that Monsanto could handle, but probably not a single farmer. Also note the underlying misconception about how the capitalism works: if there was a way to to make these crops more productive, Monsanto would have already done  so and would charge a higher price for them. And if they tried to hide this knowledge in order to keep selling more lower quality crops, they would be quickly bypassed by their competitors or the farmers cloning the crops illegally.

You’re not even allowed to replant the seeds from the crop you harvested the year before.

@canadianer If the crop was a hybrid, there's not much point to replanting with the seeds, as they will all be different genetically.

My understanding is that at least some of it is due to F1 genetics, the F(n) generations will be different


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Any examples of an organism's life cycle where the reproductive stage occur before the 'adult' stage?
Most life cycles we knew of consist of a juvenile stage (e.g. larval for insects, sporozoite for some intracellular parasites), a reproductive stage and an adult stage. Usually the reproductive stage occur when the organism reached the adult stage.
But are their examples of organisms where its natural life cycle involve reproduction at an early stage, and then the parent then went through more distinctive stages after the reproductive stage and then dies off? For example:

The closest thing I can think of is the life cycle of mayflies, which dies a short period after the mating stage. But mayflies has only one adult stage thus it is does not really answer the question

I would guess not, since reproduction is really life's endgame

Yeast cells go around the cell cycle in both haploid and duploid states.

There are two important points here:

The adult phase is defined as the phase during which reproduction occurs. It is therefore impossible for reproduction not to occur during the adult phase as you would immediately call this phase the adult phase. Because of this purely semantic issue (nothing to do with biology) the answer to your question is necessarily "no".
Only kin selection/group selection/lineage selection makes life after the reproductive age possible. It is therefore a pretty rare phenomenon. If this is unclear, you may want to read things about the evolution of ageing such as this post for example.

Maybe a question that would be of higher interest would be something along the lines of: "Can you list species that have non/reproductive phases in between a reproductive phase and death?" or "Are there any species that undergo different reproductive phases during their lives such as being first a sneaker and then territorial (yes) or such reproducing asexually at first and then sexually (probably but can't think of any examples)?".


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Is there evidence to suggest that nutrients in vitamin capsules are not as readily absorbed as the same nutrients in whole foods?
I recently fell ill with a cold, and began to take a vitamin C capsule each day to help my immune system. When I noticed no change in my condition, I began to incorporate an abundance of citrus into my diet instead of taking the capsules. When I ate the citrus my condition began to improve markedly.
The ingredients listed by the vitamin manufacturer are:

Ascorbic Cellulose Gel
Hydroxypropyl Cellulose
Croscarmellose Sodium
Stearic Acid
Magnesium Stearate
Silicon Dioxide

Not excluding the possibility of coincidence, I was was intrigued. Has evidence been published to suggest that nutrients in whole foods like vitamin C in citrus fruits are more readily utilized in the body than nutrients in vitamin capsules?

That's a coincidence. If you had eaten the fruits first and the pills then, you would probably see it the other way round. The body does not decide between vitamins coming from fruit or pills.

I concluded that that was most likely, though the hypothesis occurred to me that whole foods contain secondary nutrients that encourage uptake or utility of primary nutrients. I'm not making any assumptions, just asking if anyone has tested that hypothesis.

Colds generally last a limited amount of time so your recovery probably has more to do with your body's natural response than any vitamins, synthetic or food-based.

Like the question,  but,  as you and others have already pointed out, your sickness scenario is likely due to coincidence.

Vitamin C bioavailability
According to the review Synthetic or Food-Derived Vitamin C—Are They Equally Bioavailable? (Nutrients, 2013), the bioavailability of vitamin C from foods and supplements is similar:

...all steady state comparative bioavailability studies in humans have
  shown no differences between synthetic and natural vitamin C,
  regardless of the subject population, study design or intervention
  used.

and, according to Institute of Medicine (in the US):

The type of food consumed has not been shown to have a significant
  effect on absorption of either intrinsic or supplemental vitamin C.

Vitamin C supplements as prevention for common cold
Vitamin C supplements, even in doses 200+ mg/day (more than 3 x recommended dietary allowance - RDA) do not likely help in common cold:

This review is restricted to placebo‐controlled trials testing 0.2 g
  per day or more of vitamin C.
  Twenty‐nine trial comparisons involving 11,306 participants
  contributed to the meta‐analysis on the risk ratio (RR) of developing
  a cold whilst taking prophylactic vitamin C.
  The failure of vitamin C supplementation to reduce the incidence of
  colds in the general population indicates that routine prophylaxis is
  not justified. Vitamin C could be useful for people exposed to brief
  periods of severe physical exercise. (Cochrane, 2007)

To get 200+ mg vitamin C from citruses, you would need to eat at least 3 oranges or 7 lemons.
Considering the above evidence, the improvement of cold symptoms was likely a natural process.
Bioavailability of other nutrients from foods/supplements
There is no general rule to say that nutrients from foods or supplements are absorbed better or worse; it can depend on a specific food and a specific supplement formulation.
Iron:

In our in vitro model, naturally iron-rich mineral waters and
  synthetic liquid iron formulations have equivalent or better
  bioavailability compared with ferrous iron sulphate tablets. (European Journal of Nutrition)

Iron-fortified foods:

Bioavailability of fortification iron varies widely with the iron
  compound used (56), and foods sensitive to color and flavor changes
  are usually fortified with water-insoluble iron compounds of low
  bioavailability. Iron compounds recommended for food fortification by
  the World Health Organization (WHO) (56) include ferrous sulfate,
  ferrous fumarate, ferric pyrophosphate, and electrolytic iron powder.
  Many cereal foods, however, are fortified with low-cost elemental iron
  powders, which are not recommended by WHO (57) and these have even
  lower bioavailability (AJCN, 2010).

Magnesium:

The results of serum and urine analysis indicated that Mg
  bioavailability was comparable for mineral waters with different
  mineralization levels, bread, and a dietary supplement. (Tandofline,
  2017)

Mg supplements comparison:

Studies on the bioavailability of different magnesium salts
  consistently demonstrate that organic salts of magnesium (e.g., Mg
  citrate) have a higher bioavailability than inorganic salts (e.g., Mg
  oxide) (Nutrients, 2019)

Potassium:

The bioavailability of potassium is as high from potatoes as from
  potassium gluconate supplements. (AJCN, 2016)

In conclusion, even if most studies mentioned in this answer suggest that nutrients from foods and supplements are equally bioavailable, you need to check specific supplement formulations, for example, iron from many fortified foods and magnesium oxide can have poor bioavailability. Anyway, the studies show that most people with normal blood nutrient levels do not need dietary supplements (Int J. Prev. Med., 2012 ; Annals of Internal Medicine, 2014).

The answer probably varies for different nutrients.  An informal article by ConsumerLab.com indicates that many vitamins are better absorbed from natural sources, but a few are actually more readily absorbed from supplements.
Looking at Vitamin C specifically, a 2013 review article by Carr and Vissers concluded as follows (emphasis mine):

Overall, a majority of animal studies have shown differences in the comparative bioavailability of synthetic versus food-derived vitamin C, or vitamin C in the presence of isolated bioflavonoids, although the results varied depending on the animal model, study design and body compartments measured. In contrast, all steady state comparative bioavailability studies in humans have shown no differences between synthetic and natural vitamin C, regardless of the subject population, study design or intervention used. Some pharmacokinetic studies in humans have shown transient and small comparative differences between synthetic and natural vitamin C, although these differences are likely to have minimal physiological impact.

In other words, with vitamin C natural and synthetic sources appear to be equally bioavailable for humans.  The authors do note that "Although synthetic and food-derived vitamin C appear to be equally bioavailable in humans, ingesting vitamin C as part of a whole food is considered preferable because of the concomitant consumption of numerous other macro- and micronutrients and phytochemicals, which will confer additional health benefits."
References:

Carr, Anitra C.; Vissers, Margreet C. M. (2013). "Synthetic or food-derived vitamin C—Are they equally bioavailable?". Nutrients 11 (5). pp. 4284–4304. doi:10.3390/nu5114284. PMC 3847730.

This is not a coincidence.  Food-sourced vitamins are prized because of being in bio-available form, soluble and absorbable.  The only way to make a vitamin more absorbable is to deliver it elementally, with no digestion required at all.
The best absorption rates are through sublingual administration of elemental sprays, no additives,no fillers, nothing except what your body needs for maintenance and repairs. There is a 2011 review of research here:
http://www.ijplsjournal.com/issues%20PDF%20files/nov2011/10.pdf

I don't think IJPLS is a real peer-reviewed journal, they are published by a sketchy open-access publisher and they list a fake impact factor on their website.


text:
Why does mint oil feel cold on the skin?
When putting (japanese) mintoil on the skin it produces a cool feeling.
You can experience this, when adding it to your bath or using a spray with mint oil on your skin. The cool feeling occures even if the actual temperature of the spray or bath is quite warm.
Where does this sensoric impression come from?

Anything related to mint usually contains menthol. What does it do? It triggers the TRPM8 ion channels, causing your skin's cold receptor to become sensitive, and causing it to overfire.
This causes the brain (receiving cold signals from skin) to feel cold, and that's why you feel cold.
I have summarised it in a few sentences, but as with any scientific discovery, it took quite a few years to fully understand what was going on. NCBI have summarised this quite nicely over here (http://www.ncbi.nlm.nih.gov/books/NBK5238/)


text:
What are the sources of energy that alcohol provides?
Milk contains sugar and proteins which give energy. What compounds in alcoholic beverages (edited) give energy? Are they more likely to turn into fat (as in beer belly) than blood glucose?

alcohol is not a mixture, it is one defined molecule, ethanol (assuming the colloquial definition of alcohol, it can also mean a class of molecules).

@MadScientist My bad, I meant alcoholic beverages like beer, wine, rum and whiskey.

Ethanol is converted into AcKoA, which can be "burned" in the Krebs cycle or can be used to build fatty acids.

By chronic alcohol consumption there is another pathway involving MEOS which converts ethanol to AcKoA as well.

Are they more likely to turn into fat (as in beer belly) than blood
  glucose?

It won't turn into glucose, just into fat.
Note:
It is suspected that in extreme cases, like low glucose diets and starvation there is an AcKoA -> glucose pathway.

2011 - In Silico Evidence for Gluconeogenesis from Fatty Acids in Humans

So in theory it is possible to convert ethanol to glucose, but there is not enough evidence of that yet. Normally this conversion (if it exists) does not happen, or it has a very low rate...

What compounds in alcoholic beverages (edited) give energy?

Mostly ethanol and sugar. E.g. sweet wine contains a lot of sugar, not just ethanol...

Is AcKoA more likely to be deposited as under-skin fat, like the myth of beer makes your belly especially fatter? Sorry I was vague about "turn into fat"

Liver does not produce fat normally, it just mediates the fat transport after eating by creating lipoproteins. I don't know the details of the process, but alcohol can cause fatty liver, so I think the fat is more likely deposited in the liver and in visceral fat depos, than by eating fatty foods. So the myth can be true, but you need more googling to find evidence. http://scholar.google.com

Regarding energy:
Going off the assumption that you are using 'alcohol' in the sense of 'alcoholic beverage', it really depends on what kind of beverage we're talking about, but all that information is on the label of the bottle, can or box.
As for ethanol itself, some energy is freed by the metabolising of ethanol into ethanal and further into ethanoic acid, before finally being decomposed to carbon dioxide and water.
Finally, energy is energy: The source of the energy doesn't really affect where the energy ends up, that depends mostly on external factors.

Regarding beer:
Ethanol gives roughly 7 kcal/g, compared to carbohydrates which give roughly 4 kcal/g.
100 ml of beer contains (about) 4 grams of ethanol, beyond which the carbohydrate content varies according to the beer in question, but usually hovers around 3 g.
At a rough estimate the caloric contribution from ethanol is about 0.28 kcal/ml, and carbohydrates about 0.12 kcal/ml. When accounting for the traces of proteins, this gives roughly 0.4 kcal/ml, roughly the same as your common or garden variety soda.

So what compound provides most of the energy in, say a beer?

@aitchnyu: Updating answer with this information now.

Right, ethanol can be oxidized.

Carbohydrates, as in leftover fruit sugars from the source?

@aitchnyu: In addition to additives and adulterants, yes.


text:
Is scratching in humans vestigal?
Scratching and biting helps furred animals dispose parasite insects from their surface. Is it a productive action for humans who have less fur, have hands that can pinch off parasites and can help each other out?
If evolution were perfect, humans would never scratch, and to resort to pinching off any actual parasites - scratching and biting could break skin and expose it to germs.

What? Humans keep scratching not as vestigial reaction but as environmental response.

Scratching is a response to itching.  Pinching an itch doesn't work nearly as well to relieve the itch.  And at least in much of the technically-advanced world, itching is not caused by parasites.  (Not limited to humans: both my dogs and horses like being scratched, despite no obvious signs of parasites.)

Humans usually scratch to stop itches. Because scratches are a more high-priority sensation than the itch, the nerves stop transmitting the itch signals to your brain for a while.


text:
What is this stinging/biting insect?
The missus was bitten/stung in the palm by this (we think) in NE Scotland this morning. Pain was immediate, described as like getting a pin stuck in her hand. Apparently her first attempt to flick it away failed, and it took her second attempt to remove it. Afterwards, a short black stinger appear to remain embedded and had to be removed with tweezers.
She got fairly immediate swelling (white circle around the site, and red swelling further out). Even 20 minutes later, the swelling and pain remain.
This may or may not be the entirety of the insect.

Location: NE Scotland (indoors)

Time of Year: Early October
Size: Very small. Few mm long at most

So, we just found a dead wasp nearby. Could this just be it's stinger?

@Charles I didn't notice it having a stinger, but it's rear segment appeared intact. I'm no expert though, so it sounds like mystery solved. ;)

The stinger that got stuck in your partner's skin isn't completely black. Its coloration shifts from dark brown near the abdomen to black to dark brown again at the tip of the stinger.
This identifies the stinger as one belonging to Vespula vulgaris, the common wasp as the stinger of the other most common stinging insect in Scotland (Apis mellifera or European honey bee) is honey brown to brown.
Once in a while a wasp can happen to get its stinger torn of when it's flicked away during its sting. Obviously it dies afterwards as also part of its intestines are torn.
Pictures of both stingers can be found below.

Thanks. Strangely, the item I pulled from her hand was more like a small black hair (we found the stinger on the bed afterwards).


text:
Altering the human genome
I recently had a conversation with a rather unusual gentleman who was, let's say, more than a little partial to conspiracy theories. He has this idea that governments are lowering "nanowires" from drones, to inject people with chemicals that modify their genetics in order to reduce their lifespan dramatically, or change their opinions and thoughts.
Clearly this man was a fruitcake, and the complexities of his psychology probably warrant a whole separate debate, but he did get me thinking about the theoretical side of how such a thing might be done.
So, as such, I have a few questions on the matter:

Is it even theoretically possible to alter human genetics using only an injected substance? I'd imagine trying to get a single DNA change to propogate through the entire body without being killed off by the immune system would be near impossible.
Since we are aware of genetic markers that are related to predispositions to certain medical conditions (e.g. heart problems, cancers, high blood pressure, strokes, etc), is it possible to modify human DNA to create these issues in a living person?
Has much research gone into how genetics affects thought and opinion, or the way we perceive and react to situations at an emotional level? If so, is it theoretically possible to alter this at a biological level?

I'm certainly not advocating any of this, and I apologise for the unusual nature of the question, but it's something I certainly find interesting to think about!

First of all it is important to note that, within certain limits, human DNA is not much different than, say, a mouse DNA: it has the same structure, it is constituted by the same bases etc etc. Therefore it is teorethically possible (leaving aside ethical issues, of course) to selectively modify it as you would do for a mouse. There are, however, some technical issues and obviously many ethical ones.
To answer specifically to your questions

Is it even theoretically possible to alter human genetics using only an injected substance?

Yes it is. Aside from the good example of radioactive substances given by Alexander, another good one (and probably one that is more common) is that of chemical mutagens.
It is important to understand that the mutation caused by these substances are random, or only partially selective.
For instance, certain substances, called intercalating agents can interpose themselves in between the bases of the DNA, interfering and possibly giving rise to mutations during DNA replication.
Other substances such as alkilating agents are a bit more specific, although still not gene- or locus- specific.
For instance ethylnitrosourea (ENU) favours A->T base transversions and AT->GC transitions.

I'd imagine trying to get a single DNA change to propogate through the entire body without being killed off by the immune system would be near impossible.

The immune system would not necessarily kill cells with mutations. Think of what happens during cancer developement.
Also, an extremely important point: mutating a somatic cell (i.e. not a sperm or an egg) can induce a mutant phenotype in the individual but it will not be transmitted to his/her progeny.

Since we are aware of genetic markers that are related to predispositions to certain medical conditions (e.g. heart problems, cancers, high blood pressure, strokes, etc), is it possible to modify human DNA to create these issues in a living person?

As Alexander says, there is much research in this field.
Some attempts of gene therapy have indeed been made, and some have a big potential. We are, however, still far away for gene therapy to become a routine treatment.
Also, remember that:

not all diseases are genetic diseases
not all genetic diseases are monogenic: some derive from a complex interplay of different factors and hence curing them is not as simple as providing the correct version of the mutated gene.

Has much research gone into how genetics affects thought and opinion, or the way we perceive and react to situations at an emotional level? If so, is it theoretically possible to alter this at a biological level?

Yes, but I would say that we are very very far away from a complete understanding of how thought and emotions are coded in our brain. The very difficult point is that one needs to study these events at multiple scales. We can study a big region of the brain and say that it is involved in fear coding, for instance. But then if you want to go deeper and study what happens at the single cell level you need to look at a lot of different cells to see how they interact between each other.
From the other side of the "size scale", it is possible to study biochemical processes in the single neuron, but then again it is difficult to study how these processes are integrated in big networks of cells, especially in vivo.

Thank you very much for the detailed answer. I'll certainly have to read into behavioral genetics!

Concerning the first question, it is very well possible to alter human genetics by injecting a highly radio-active substance that will eventually cause mutations almost all cells. The lifespan will be dramatically reduced, however and the condition is known as "radiation sickness"(link to Wikipedia).
But the person probably means so-called "directed mutations" (link to Wikipedia), when the changes of genetic information is not random, but rather at a certain place and towards a certain function.
Second point, this is the area of extensive research: if we could specifically cure a gene than many diseases that are incurable now (like cystic fibrosis) could be effectively treated.  The complete nanotechnology (link to Wikipedia) is all about it.
As to the third point, this is also a very old discussion about the role of nature (=genetics) and nurture (environment). Answering this question in the scope of other questions I can suggest that (genetic) knocking-out some inhibiting receptor systems in brain can lead to certain malfunctions and deceases, including the lymbic system that is responsible for emotions and perception.

Thanks for the answer. I hadn't considered nanotechnology as a possible injection payload - certainly very interesting stuff! I'll read through those wiki articles for more information.

Small point; if you're thinking about genome-altering nanotech, perhaps you're thinking of one of many viruses.

Is it even theoretically possible to alter human genetics using only
  an injected substance? I'd imagine trying to get a single DNA change
  to propogate through the entire body without being killed off by the
  immune system would be near impossible.

Yes, it is possible to alter human genetics through injectable carrier. You are also correct that it is currently impossible to make a DNA change to the entire body. It is possible to transform a a few percent of cells in a single tissue.

Since we are aware of genetic markers that are related to predispositions to certain medical conditions (e.g. heart problems,

cancers, high blood pressure, strokes, etc), is it possible to modify
  human DNA to create these issues in a living person?
  Yes, in theory. You genetically alter a human embryo... let said embryo grow up to a person. Then harvest that tissue from said living person. Similar to what is done in mice... just on humans. As you can imagine nobody is doing this right now. Breeding human for scientific experiments is very unethical (can slow... who want to wait 9months) and will unlikely to get public funding.

And also no, as in not in the way you are thinking The tech is no there yet.

Has much research gone into how genetics affects thought and
  opinion, or the way we perceive and react to situations at an
  emotional level? If so, is it theoretically possible to alter this at
  a biological level?

Yes there is. https://en.wikipedia.org/wiki/Human_behaviour_genetics
But as you can imagine, genetics affect behavior in broad strokes. Genetics does not affect if you are prefer to buy Airbus stock vs Boeing stock. It does affect board things like how much anxiety you can tolerate. How short a temper you have. How much preference do you have to novel experiences.
And upon this broad stock that genetics gives you, you as a person will write if you like challenging jobs, going places, new places, etc.


text:
Is there a strong reason to be sceptical about the "cured HIV patient" being reported by mainstream media?
There's a story going round the news about a baby that was, apparently, cured of HIV using a cocktail of drugs at an early age. The story piqued my interest, but details seem scarce. One of the main things I've seen being refuted about it is the difficulty in proving that (a) the child actually had HIV in the first place, and (b) that the child is really fully cured.
I've seen the following arguments:

Western Blot tests on young children are practically useless, since they test for antibodies. The child will likely have antibodies passed down by the HIV+ mother, regardless of whether the child has HIV. The test will show the antibodies, which may be mistaken for an active immune response from the child. As such, there will be a high false-positive rate on such tests.
Using PCR to attempt to identify a lack of HIV is flawed, since it may lay dormant in a small colony of T-cells until a secondary immune response is triggered, causing a new outbreak. As such, it is very difficult to show that a patient is "cured".

Are these arguments valid? Are there any other reasons to be sceptical about the claims? Any other information that might be useful in understanding the case?

Western Blot tests on young children are practically useless, since they test for antibodies. The child will likely have antibodies passed down by the HIV+ mother, regardless of whether the child has HIV. The test will show the antibodies, which may be mistaken for an active immune response from the child. As such, there will be a high false-positive rate on such tests.

The mother's T-cells are in the fetus anyways (15/18 Fetal lymph nodes contained T-reg cells). If the mother is infected and left untreated (as was the case with the Mississippi child), then the viral load is going to be high. The chances of it passing to the fetus are going to be high as a result.

Using PCR to attempt to identify a lack of HIV is flawed, since it may lay dormant in a small colony of T-cells until a secondary immune response is triggered, causing a new outbreak. As such, it is very difficult to show that a patient is "cured".

"Flawed" is the wrong word. The argument is built into the tests. The child was functionally cured - which means below detectable levels instead of "completely nonexistent within the body." Yes, it's entirely possible that the HIV is hiding somewhere in the body and could make a reappearance, but at the moment it's not showing any significant titer in the blood.
I don't think there's been a test developed that can assess the entire body to find the lone viral capsid left.
However - that isn't to say that the "cure" has been found. So far it's a single person cured this way. One. That makes it a case study, not a therapy, treatment, vaccine, or even reasonable assessment that it's possible to do again.

The one that actually makes me skeptical of the use of this is that this "cure" was primarily a massive dose of antiretrovirals used as catchup therapy because the infant's mother didn't have access to prophylactic treatments while she was pregnant and delivering.
Basically, it's a cure that requires you to have access to antivirals very, very near the beginning of infection, and is largely a solution to a problem that is "solved" in the developed world (maternal transmission of HIV is very rare).
It's not a cure that can be extended to the settings where a cure is most desperately needed. So while an excellent proof-of-concept, and a safety net for when someone is poorly served by the medical system? Sure, this is amazing. As some watershed moment in HIV research? Less convinced.


text:
What are the known energy capturing processes in biological systems?
I am not a biologist. I am aware that photosynthesis is the main process for capturing electromagnetic energy from the Sun. Also, I am aware that some bacteria can capture energy from boiling water and others from certain chemicals.

What are the known energy capturing processes in biological systems other than photosynthesis? I am looking for references or a good survey of all known mechanisms.
Is there an explanation for the ingenuity of evolution in solving the energy capturing (transforming) problem via multitude of mechanisms?

Apart from phototrophy, there is only chemotrophy (obtaining energy from redox reactions of chemical substances) and radiotrophy (obtaining energy from ionizing radiation such as gamma rays). However, radiotrophy as of now is only known to be a supplemental mode of energy and not a primary one.
Diversity is a central theme of evolution. It would be interesting if there was a single common mechanism for all modes of energy-nutrition which is perhaps true for the case of the chemiosmotic energy generating mechanism (ATP-synthase like systems which generate energy from chemical gradients). Otherwise, diversity is expected as the organisms evolve to survive in different environments.

Nice answer. Can you provide an example organism for each mechanism under chemotrophy and raditrophy?

@MohammadAl-Turkistany The link to the article gives the example of radiotrophic fungi. You can also check the other linked post. There are several chemotrophic bacteria. See the wikipedia link.

1:
The only two sources of energy that I could find (not that there aren't any others that I couldn't find or that haven't been discovered) are from light (plants) and "abiological compounds" (some bacteria).
Reference
http://link.springer.com/chapter/10.1007%2F10825622_4#page-1
It seems you have to buy this book, but the website does provide a preview containing the answer to your question (in the first paragraph).
2:
The likely explanation for having a multitude of ways of capturing energy is adaptive radiation. Having a different method of gathering energy would place the organism in a different ecological niche, which would have been otherwise unoccupied. This allows the organism to flourish. For example, heterotrophs evolved to metabolize a variety of compounds. Some digest mainly glucose, while others evolve to break down cellulose, amylose, protein, etc.
Further Reading
http://www.jstor.org/stable/2463047?seq=1#page_scan_tab_contents
https://en.wikipedia.org/wiki/Adaptive_radiation


text:
What are the psychedelic effects of (star) anise and how many people are affected?
Backstory:
My girlfriend reacts heavily to chocolate and drinks containing stellar anise, in a way that seems comparable to psychedelic drugs.
After consuming it, it takes approximately five minutes for the reaction to become apparent.
Observed Effects:
Due to the heavy reaction, she tends to avoid these foods, however, we could observe the following effects:

Heavy giggling, occasional outbursts of loud laughter;
Much less frequent: Crying (just kind of starts from the giggling and subsequently fades back into giggling);
Minor hallucinations (Sparkling hair, glowing faces);
Loss of motor skills, especially balance;
Feeling time pass much faster (to her, a 15 minute episode felt like 1-2 minutes, an hour like 5-10 minutes);
Some memory loss (probably related to the time perception?);
Unfocused mind;

Her speech remains clear and articulate.
Observations are anecdotal, as I only observed two episodes, and we realized what happened only after the first.
Googling Results:
Apparently, around 1-3% of humans react in some way. However I couldn't find any detailed explanations of the hows and whys, nor any actual research.
I am very curious about this. Is it dangerous? Are there any related effects (genetic disorders, maybe?). All explanations, and hints how to google better, are welcome.

This is interesting, but terrifying. Have you considered the possibility that there may be Japanese Star Anise (Illicium anisatum) adulterating what your girlfriend thinks is edible star anise (Illicium verum)? [Note, using the latin names may help your google searches as well, pointing them towards scientific literature]

No, the episodes we observed didn't happen with any homemade food. The first one happened with regular store brand chocolate (after that, she realized that she always behaved odd after eating this particular chocolate) and with Sambuca, of which we all drank some.
But thank you for the hint!

This is the correct SE site. PS: what is stellar anice? Don't you simply mean star anice?

Interesting question! As this post has been sitting around for a while I am going for some speculations. First you talk chocolate, which essentially contains the alkaloid theobromine. Anise contains the propenylbenzene (E)-anethole (Idle, 2005). Theobromine is a caffeine-derivative and basically produces alertness, but also restlessness and perhaps anxiety when administered in large amounts (wiki). In extremely high doses there can be LSD-like effects (anecdotal report). Perhaps (speculative) your girlfriend is especially sensitive. Then (E)-anethole: the late Alexander Shulgin, Godfather of MDMA, has made the etheric oils (in)famous as precursors for amphetamine synthesis. In themselves the propenylbenzenes like (E)-anethole are quite harmless, as they do not contain an amine group (a prerequisite for being called an alkaloid). However, heating (E)-anethole in the presence of ammonia may lead to the production of PMA, a compound structurally and neuropsychopharmacologically related to MDMA (Idle, 2005). Although a bit of chocolate and a sip of Sambuca do not meet any of these conditions, both chocolate and Sambuca do contain certain psychoactive compounds, or their immediate precursors.


text:
Medium for Pseudomonas?
What is a good minimal medium for Pseudomonas bacteria? Do I need different media for different Pseudomonas species?

Pseudomonas bacteria are generally not difficult to grow:

Rugged and opportunistic, Pseudomonas use a wide range of nutritional sources, even very simple nutritional environments without any organic compounds. - Sigma

For specific species, you'll want to use a selection medium. Sigma-Aldrich has a number of  commercial products for selection and I'm sure you can find a recipe that suits your species with a Google search.

Related reading:
Medium for the Selective Isolation of Members of the Genus Pseudomonas from Natural Habitats (Grant and Holt, 1977)
Evaluation of various selective media for the detection of Pseudomonas species in pasteurized milk (Van Tassell et al., 2012)


text:
Is the activity of enzymes in the human body affected by the outer temperature?
I have to do a research about the enzymes in the human body and the things that affect them. I know that the body temperature affects the activity of enzyemes but I'd like to know if the outer temperature of the air affects them, too?
When the temperature goes to 47°C or more we get tired and exhausted. Is this because the activity of enzymes decrease or is something else?!

Is this a homework question? What are your ideas for solving the question?

@Chris no i do a research and this's a part on it but i can't find the answer

Enzymes usualy have a relative narrow temperature optimum, for those of our body this is usually around 37°C. It is around 37,2°C in the morning and goes slightly up to 37,7°C in the evening (see reference 1 for details). The temparature optimum for most enzymes looks somewhat like displayed in the figure (from here, interesting to read):

Enzymes are relatively tolerant to lower temperatures (although their reaction rate is much lower), but generally they work. If you go too high with the temperature, the activity will soon be reduced to zero, as the enzymes are denaturated and are not able to catalyze any reaction.
The human body does quite a lot to control its temperature and to keep it within a pretty small limit. It does either excessive sweating (when it's hot) or shivering (when it's cold) to maintain its temperature within or at least near the optimum. For further details on the themorgulation have a look on the Wikipedia article on this topic or reference 2 and 3.
Although our enzymes work at slightly lower reaction rates when the body temperature is higher (think of fever), this is not a major issue. Slightly higher temperatures can thus be tolerated, although you don't feel very nice.
The effect of to hot temperatures is different, though. It is mostly due to not consuming enough water, so that the body has not the possibility to control its temperature via sweating. This condition will ultmatively lead to a heatstroke, see here for more details. Before you reach the temperature in which your enzymes reaction rate will go down drastically, you have long collapsed.

References:

A critical appraisal of 98.6 degrees F, the upper limit of the
normal body temperature, and other legacies of Carl Reinhold August
Wunderlich.
Skin blood flow in adult human thermoregulation: how it works, when
it does not, and why.
Thermoregulation: some concepts have changed. Functional
architecture of the thermoregulatory system

"Although our enzymes work at slightly lower reaction rates when the body temperature is higher (think of fever)..." I'm very puzzled by this statement. Do you have support for it? Without reading, I would posit that the body is metabolizing more quickly, thus generating additional heat.

He is doing more metabolism, not necessarily faster.

Sorry to repeat the request, but do you have support for that?

@anongoodnurse Have a look at this and this articles. They both show the activity of enzymes depending on the temperature. And both show a sharp decline in activity above 37°C. The first is acid phosphatase, the second pancreatic lipase.

Good grief! The first reference is about two enzymes, one from Pseudomonas and one from wheat! Since neither of these organisms are thermoregulatory, they do not even apply to warm blooded animals.


text:
How do kidney cells excrete their own wastes?
The kidney is composed of tissues, and those tissues are made up of numerous cells - so how do these cells excrete their wastes?
Lastly, are there any wastes in the venous blood (renal vein), what makes the renal artery and vein different? - what substances do they each carry?

Then there should be some selective resorption of water compared to urea somewhere along the Loop of Henle. That's how the kidney does all the amazing stuff it does. Read about the Loop of Henle and you'll have your answer to this and other great functions of the kidney, the autoregulatory functions, etc. It's amazing!

I checked my anatomy notes and online figures about the kidney. There is no mention about dedicated arteries for feeding kidney cells. So it does not work the same way as the heart does, where there is a dedicated coronary artery. The kidneys use the same blood vessels for filtering and for nutrition/waste transport purposes too.

Figure 1 - kidney anatomy - source

Figure 2 - nephron anatomy - source

The urea is created from NH4+ and HCO3- in the liver (mostly) and the kidney because of blood pH regulation purposes. It neutralizes the HCO3- created by the lungs from CO2 and OH-.

The urea cycle (also known as the Ornithine cycle) is a cycle of
  biochemical reactions occurring in many animals that produces urea
  ((NH2)2CO) from ammonia (NH3). This cycle was the first metabolic
  cycle discovered (Hans Krebs and Kurt Henseleit, 1932), five years
  before the discovery of the TCA cycle. In mammals, the urea cycle
  takes place primarily in the liver, and to a lesser extent in the
  kidney.
In chemical terms, urea synthesis is an irreversible, energy driven
  neutralization of the strong base HCO3- by the weak acid NH4+, and the
  average daily excretion of 30 g of urea is equivalent to the disposal
  of about 1 mol of HCO3- per day. Thus, a major function of hepatic
  urea synthesis is to effect this neutralization, without which the
  body would otherwise be confronted by a major load of alkali.
Urea is excreted by the kidney, and is normally present in plasma and
  body fluids at a concentration of 3.0–6.5 mmol/L.

wikipedia - Ornithine cycle
Textbook of Hepatology - Ammonia, urea production and pH regulation - Dieter Häussinger
1984 - The role of ureagenesis in pH homeostasis

The kidney reabsorbs urea in order to concentrate the urine:

Figure 3 - nephron with material transports - urea resorption at the end of the urine creation process - source

About 40% of the urea filtered is normally found in the final
  urine, since there is more reabsorption than secretion along the
  nephron.

wikipedia - Renal urea handling:
2007 - Critical Role of Urea in the Urine-Concentrating Mechanism

The kidney secretes the urea to the urine, but it absorbs more by the reabsorption than it secreted.

The kidney freely filters urea at the glomerulus, and then it both
  reabsorbs and secretes it. Because the tubules reabsorb more urea than
  they secrete, the amount of urea excreted in the urine is less than
  the quantity filtered. In the example shown in Figure 36-1A (i.e.,
  average urine flow), the kidneys excrete ∼40% of the filtered urea.
  The primary sites for urea reabsorption are the proximal tubule and
  the medullary collecting duct, whereas the primary sites for secretion
  are the thin limbs of the loop of Henle.

Medical Physiology by Walter F. Boron and Emile L.

So if we are talking about urea, then it is secreted to the urine. If we are talking about other waste products, then e.g. CO2 is certainly handled by the veins.

The kidneys keep the composition, or makeup, of the blood stable, which lets the body function.
Each kidney is made up of about a million filtering units called nephrons. The nephron includes a filter, called the glomerulus, and a tubule.
The nephrons work through a two-step process. The glomerulus lets fluid and waste products pass through it; however, it prevents blood cells and large molecules, mostly proteins, from passing. The filtered fluid then passes through the tubule, which sends needed minerals back to the bloodstream and removes wastes.

Could you describe "if you talking about the areas were the actual waste is dumped" a bit more precisely.  This is quite unclear as to what you mean.

This is not an answer to the question


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Aquarium snail identification
Many of these little snails suddenly appeared in our aquarium from nowhere.  I suspect that some snail eggs hitched a ride with some recently purchased plants.
Can anyone identify the species?  I am not having any luck with googling.
The photos show a baby snail of about 2-3 mm in size.  The shell is asymmetric, with one side looking completely flat (or concave).
These  are not pond snails.  We also have (uninvited) pond snails, but pond snails look different even when as small as these.  This new species has a lighter colour than pond snails, a more transparent shell of a different shape, and moves slower.

@Jestep Yes, all of these have the exact same shape, and they all have the exact same size, which is why I think that they hatched from eggs at the same time. The ramshorn photos I found appear to show a more symmetric shell.  I think that the reason why I cannot find anything that looks like this online is that they will change in appearance as they grow up.

I would post the images in some of the aquatic forums. These close ups are great by the way. http://www.aquaticplantcentral.com/ is a good one, there are some others as well.

These are a kind of ramshorn snail, as Jestep correctly guessed.  Now they are grown up and they are clearly identifiable as ramshorn.
I will post photos of adults when I get the opportunity.

Yes but Ramshorn is not an identification. What's the Latin scientific name?

Can you please pray the photos of the adults you mentioned? Thanks.


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Does tremor frequency generally increase as Parkinson's disease progresses?
I've been trying to research this question, but most if not all the on-line journals require costly subscription, and the studies that are posted look at tremor frequency with regards to other factors.
My question has to do with the tremor frequency, starting at early onset to later stages of Parkinson's disease - over the course of the disease, and without drug treatment (such as L-dopa), does the tremor frequency generally increase?

are you looking for frequency of tremor episodes (once a day, once an hour etc) or frequency of tremor as oscillatory motion (1Hz, 0.3Hz etc)?

Sorry I wasn't clear. I'm interested in the frequency of the neuromuscular oscillations.

The question is still unclear, there are multiple parameters related to tremor. Please, look at this article and decide if you need subsequent changes in the question http://www.mdpi.com/1660-4601/8/5/1478/htm

Mean frequency  (Cf) most likely expresses what I'm looking for.

Frequency of tremor typically remains constant for the person. Levadopa (sinemet) does not change the frequency.
Typically the tremor frequency will be in the range from 3Hz to 7Hz.  There is a common phrase when dealing with PWP (Person With Parkinson's Disease). If you have seen one PWP, you have seen one PWP.
Currently I am part of a study by the Micheal J Fox Foundation using Pebble Watches and Smart phones to monitor PD.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1014720/
Hughes AJ, Daniel SE, Kilford L, Lees AJ (1992) Accuracy of clinical diagnosis of Parkinson’s disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatry 55: 181-184.
https://blog.getpebble.com/2014/08/25/mjff-intel-parkinsons/


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How do we know that ammonites are a kind of cephalopod rather than another type of mollusc?
On a recent fossil hunting trip, I found a small fossil that an expert identified for me as an ammonite beak. He told me such fossils are not uncommon, but are not normally found with their parent shell due to the decay of the soft tissues holding the beak in place.
I know that under some unusual conditions, (i.e. the Burgess Shale) the soft tissues of animals can be preserved. And a quick google search reveals that there are rare belemnite fossils with their tentacles in place.
However I can find no reference to any ammonite fossils, nor any of the orthocone clades, with soft part preservation.
Shells of similar shape and structure are not unknown in other groups of mollusic (i.e gastropods). So: what characteristics of the shell make taxonomists sure that ammonites and orthocones are cephalopods rather than some other kind of mollusc?

Probably the presence of chambered shells with siphuncles, like present-day nautiloids.

I can find no reference to any ammonite fossils, nor any of the orthocone clades, with soft part preservation.
Soft–part preservation in heteromorph ammonites from the Cenomanian–Turonian Boundary Event (OAE 2) in north–west Germany
Soft-tissue preservation in the Middle Jurassic ammonite Cadoceras from Central Russia
And references therein for the handful of other ammonite soft part preservations

It really is mostly the siphuncle as @augurar mentioned. The siphuncle is present in modern ammonites, cuttlefish, and Spirula(a deep-sea squid with an internal chambered shell). It links shelled cephalopods neatly with other cephalopods(both extant and extinct) and distinguishes them from other shelled things like snails.

I am proud that I can answer your very, very good question!
You are right that the soft tissue of ammonites is very, very rare. But along with beaks (I believe you meant aptychi) you can find something with similar function called radula, which is (at least for devonian ammonoids) both in morphology and in number of elements identical to recent coleoids! Ammonites belong to ammonoids and this puts them closer to Coleoids than to Nautiloids. Nautiloids have very, very similar external shell, but with siphuncle going differently and many other details - one would expect them to be closely related.
It is now well known fact that ammonites are ammonoids. And that both ammonoids and coleoids evolved from bactrites.
For more info see:
Kröger, B., Vinther, J. & Fuchs, D. (2011): Cephalopod origin and evolution: A congruent picture emerging from fossils, development and molecules. ― Bioessays, 33, 602–613.


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What determines the colors and patterns of a clam shell?
Earlier this week I was looking at some bivalve shells that had ornate patterns which ranged in color from a light orange-pink to a deep orange-red. Here is an image I found online that seems to be of the same type of shell:

The friend who was with me said, "I wonder where the color comes from." We were trying to look for two shells with similar colors, patterns, and approximately equal sizes, and it was hard, even though we were looking through a large collection of similar shells.
What determines this ornate pigmentation? Is it influenced by environmental factors such as the minerals in the water? Does it have anything to do with the age or health of the organism? Or is it purely genetic? Is this determined by the same basic biological principle that determines the color of human hair, or is there something different at work in shells?

http://www.conchologistsofamerica.org/articles/1997/why-do-shells-have-their-colors.html

This post is pretty well written and seems to say that the evolutionary forces that produce shell color like this is not known.  There are suggestions that the color is camoflage or the result of metabolic byproducts or that the pigments serve to strengthen the shell.  Its hard to believe some of these theories given that some shells do fine without coloring (at least that humans can see).
Structurally, shells are living things.  [They consist of many layers of thin irregular calcium carbonate hexagonal plates that make the mineral portion of the shell. The plates are held together by a protein glue and renewed by cellular action][3].  Whatever their evolutionary motivations, the colors are biomolecules which are in the biomatrix binding the plates together. This is a reason that shells that are left out to dry in the sun can become bleached and brittle.
I wish I had some better references about the shell structure, but I'm remembering a lot of this from a one afternoon book report given in a class, not from any intensive study on my part.
This has influenced some ideas about things like tank armor, by the way.  At least there is funding for biomaterials research by agencies interested in tank armor.  Lamellar armor made of segmented plates can withstand tremendous impacts at a single point like a shell being dropped from a great height by a seabird or a shell hitting a tank. Plates just a few microns wide and a fraction of a micron deep shaped like irregular hexagons are hard to make if you aren't a mollusc so far though.

We were wondering the same thing after a day at the seaside.  It's apparently pretty complicated.  Here are a couple of articles I found about it.
https://academic.oup.com/mollus/article/72/2/157/1256402
"Mollusc shells have vivid colours and intricate patterns, but the pigments are practically unknown."
"The same colour in different taxa may be due to different pigments; different colours in the same taxon are due to different pigments; different colour saturation is due to different concentration of the same pigment."
"All the... coloured parts of the shells can be satisfactorily explained as due to polyenes and aragonite. Polyenes can be pigments, coloured compounds, as found in parrots' feathers..."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4930200/
"... the extraction and identification of pigments is extremely difficult. For example, in one recent study, more than 30 kg of shells of Haliotis discus hannai were required to obtain only 2.7 mg of purified pigment"
"Pheomelanins are macromolecules that contribute to the colour of human red hair, and although most commonly known in mammals and birds they have recently been identified as the screening pigment in the shell-eyes of chitons [77]. Pheomelanins may be brown, yellow or red in colour."
"There was no resolvable pattern of association between trace elements and pigmentation due to either porphyrins or eumelanin."

I would think that the minerals that are in the immediate environment have quite a bit to do with the color that is manifested in each shell.

This an opinion rather than an answer. If you want to invest time to write a proper answer (it can be rewarding!!!) please read this page https://biology.stackexchange.com/help/how-to-answer


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What happened to this seashell?
We found this seashell on a Mediterranean beach in the south of France. While most of the shells we found were quite intact, this one caught our attention.
It is light and littered with tiny holes, and thicker than other shells we found.
Is this due to erosion in the water? How did the shell look like before the ocean changed it? Was the shell simply exposed to the water for a longer time?

I'd say that the holes were made by animals. I know some mollusks can make holes on rocks, for instance https://en.wikipedia.org/wiki/Pholadidae
But in the case of this shell, the animals must be much smaller.

The holes are probably caused by one of a family of parasitic sponges.  The holes, as you'd expect, kill the oyster, and the sponge then takes up residence in the shell. A number of species of this family live in the Mediterranean, with Cliona apparently being the most common genus (e.g. Cliona celata and C. viridis).  Images of oyster shells after a Cliona infestation can be seen here and here; these images are more dramatic than the one you found, but show the same general pattern.

Very fascinating, thank you very much for explaining!


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Found an unknown species, whom should I contact?
My father has found a very queer looking insect. He'd been watching it for over half a year on the tree right next to our house  and in all this time hasn't been able to find anything like it on the internet. Yesterday it died, and we found it on our porch, dad's put it in an air-isolated box for identification, please let me know if you are interested. We can send a picture of it for you via email or any other provided way, or please let us know what we should do it and whom we should contact. We live in Sydney.
Thank you, best of luck in everything!

Welcome to Biology Stack Exchange. Species ID questions are quite common on this site - try uploading some photos of the insect and adding them to your question, and there is a very good chance that someone here can ID it for you. Make sure you also add the species-id tag. For insects I would advise adding details of the weather when it was seen.

And just a side note. Don't be afraid to actually post the picture. It isn't easy for someone to just steal it and claim it as his own. Plus it would be very easy to prove that you were the original poster. So I would recommend to just post it here. You will get more feedback that way.

To extend on Ria's point, even if someone stole the image, they can't steal the insect's corpse over the internet. If it really is a new species, that corpse will be more important evidence than any photograph.

As above, please upload a picture of the specie you've found to confirm your recent findings. It would be a good idea to contact a professor at a university in Sydney that works in the relevant field as he would be known as a reliable source for further referrals

It is kind of assumed that if you know enough t actually identify something as new you will know what to do about it. Searching the internet is not a great way to identify an organism.

Has it been identified yet?


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Age of shells on beach
As a child I watched tiny fiddler crabs living in conical shells, and many years later I find that people study fossil turritellids. So now I wonder: how old are shells, typically, that you see on beaches? Do they wear out after a year of sand abrasion? 100 years, a million? Is it known?

Might be able to do carbon-14 dating on the shells to determine the average age of shells on a beach. I do not know if this has ever been done, but it probably has. No clue where to look for this data.

Apparently it's tricky to radiodate seashells that have stayed in the sea. There's exchange with carbonate from the seawater, etc etc. There are a lot of worn out seashells that you can find on beaches. Conceivably you could do some kind of statistical analysis based on the amount of filled versus empty seashells and the age of the filled ones. (If seashells take one critter-lifetime to decay, you should see roughly equal numbers of live and dead shells) Most seashells are only a couple years old, using the dating method below.

Mollusk shells found on typical east coast (US) beaches can range from days old (the animal that made the shell died recently) to thousands of years old.  Some shells in our state, North Carolina, have been dated as 40,000 years old.  A high number of "seashells" found on east coast beaches are from mollusks that lived in the marsh on the back side of the island.   The presence of these shells on ocean beaches provides evidence of island migration - the island has moved landward over the marsh until what was once the marsh is now the ocean shore.  Once buried in the sand, the shell is well preserved until erosion uncovers it.  Occasionally, fossilized shells are washed up on beaches after having been dislodged from offshore limestone deposits - these shells can be millions of years old.
-Richard -
Carolina Ocean Studies

Ages of shell as a piece can be checked or counted.

Procedure:
1) Examine the shell's ridges with a magnifying glass.
2) Tabulate the number of ridges. You can approximate by number of cell per unit length.
3) Divide the total number of ridges by 365. Each day the little mollusk
 earns a new ridge, thus total will give you its age.
But, that is age of one shell. If you are asking the age of all of them in a beach, my guess would be as old as the beach.
Read more : http://www.ehow.com/how_6331956_tell-age-seashell.html

that is interesting but I wonder about the shell, not the animal. If the animal lived ten centuries ago, is it possible that the shell still exists? I call that shell 1000 years old.

@BobTerrell: Then surely the shell would be as old as the beach. Moreover, carbon dating would the last resort.

The shells you find on the beach are from molluscs (mostly bivalves and gastropods) not insects, which are arthropods.


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Genetic effects on personality
It is said that genes are partly responsible for the choices we make in our life; our genes help to create our environment, and then that environment can influence our personality. So, beside genes, what else is responsible for the other choices? Is there something else at work?

The answer to the question is in the sentence immediately before the question: “the environment can influence our personality.” With that in mind, what’s the real question?

Many genetic studies in this area have found that variation in serotonin receptors associates with differences in a number of personality traits. That one gene, or a very small number, turns up time and time again for something so complex as human personality makes me a bit suspicious.
Other factors at play:
Family dynamics
Culture and cultural norms
Society and societal norms (these could clash with the above two)
Exposures - drugs, toxins, diet, and many others
Traumatic events

The problem you are looking for is called the "Nature vs nurture" debate. Lots of scientists have written lots of books and papers and done lots of studies on the subject. As you can see, the title of the debate already includes the two main concerning factors: nature (genes) and nurture (environment).
These of course each include a variety of ways in which they influence personality. Genes provide the biological basis for your personality, they determine how everything in your body works1. At the same time, these genes build a system that has a life of its own - your brain.
It consists of neurons, and nobody knows how personalitites comes about from them exactly but somehow they do. Neurons reshape all the time in ways that no other cells do. The connections between them, synapses, are formed, destroyed, reinforced or weakened all the time - in response to things that take effect on them, for example the things that you see and hear, smell, taste and feel. A very interesting subject in this field is the study of neuronal networks, giving some insight into how memory and learning may work.
But while this may seem like external factors must then be more important for personality, it depends on the setup provided by your genes how your neurons respond to certain influences - what concentrations of neurotransmitters they produce and secrete etc.
As you can see, the only thing that is really safe to say is that it is not "either or", both definitely play a role.
1But even the biological development of the body has non-genetic influences - at the moment I can think of epigenetic inheritance though this seems to be disputed (see comments). Apart from that as far as I know there are uterine influences on embryonic development. And then there are the more or less obvious external influences such as cutting things off before they develop.

Interesting post! Do you know of any good review papers on the subject of neural networks, and modeling the neuronal reshaping? Or even any citations really!

I recently read "Wetware" by Dennis Bray, which is generally on the topic of intelligence and consciousness. I don't know how well-respected that is but I found it quite an interesting read, even if some of his claims are a bit off in my opinion. I can't offer any papers unfortunately though.

“epigenetic inheritance” in humans is still unproven and has considerable problems (germline–soma distinction, i.e. Weismann barrier, and reprogramming) so I wouldn’t put too much weight on that.

Is this better? :)

Furthermore the genotype of the individual does not represent the phenotype, it is about the expression profile of the genes rather than just their presence.


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Mechanics of going from DNA sequence to metabolic network
My apologies for possibly a naive question. I'm a statistics type and have been asked to assist with analysis of metabolic pathways (and networks). However, I would like to have at least a layman's understanding of how metabolic pathways/networks relate to DNA sequences. Been doing the Google for a few days and, given the results, it's clear I am not formulating the query correctly since nothing seems to be clicking.
Something that helps me understand the mechanics behind going from a string of T,A,G, and C's to a network of substrates,enzymes, and products.
Thanks in advance for your patience.

Welcome to Biology.SE, I fear this question might be too broad to be reasonably answered here. You might want to just start by reading an entry-level molecular genetics textbook. Any chance you can make your question about specific things you have a problem understanding?

Yeah, I was afraid of that. I was looking for a very introductory level bit of material(s) and was hoping that someone had put something together.  I'll understand if you close the question.

Do you mean the connection as it occurs in the cell, or how to model it (like, how to predict a function for a particular gene)?

The long Question is how to predict a function. To try to be more specific, I've tracked down the paper by A. M. Feist, M. J. Herrgård, I. Thiele, J. L. Reed, and B. Ø. Palsson, “Reconstruction of biochemical networks in microorganisms,” Nat Rev Micro, Feb. 2009. I'm trying to dig into Figure 1.

The question is not too broad, just involves a fair bit of work to both do the research and compose a response. I'll do the latter, but in brief.
The strings of the four nucleotides encode genes. Sometimes these genes are broken into protein-coding portions (exons) and sometimes intervening, non-coding regions (introns). Bacteria, for example do not have introns within genes while most human genes do. The nucleotides in the protein-coding portion of the gene do just that - give instructions on how to synthesize the protein by directing which tRNAs the ribosome uses to translate the genetic code into a protein chain.
A useful phrase is protein sequence dictates protein structure and that structure dictates function. So, the proteins do things and many act as enzymes or modulators of enzyme activity. An enzyme catalyzes a biochemical reaction, lowering the activation energy to go from reactant(s) to product(s). One enzyme can be thought of as one unit within a metabolic network. A modulator might activate or deactivate an existing enzyme. A protein kinase is a good example of a modulator.
Next, string some of those enzymes together to build a pathway. A common example is glycolysis. Think of this as a chain where the output or product of enzyme A serves as input to enzyme B, whose product is the input to enzyme C, and so on. These pathways are two-way, but it is exceedingly difficult to travel from the final product all the way up such a pathway to the initial input within the confines of a biological system. Thus, the pathways in practical terms are thought of as one-way.
However, the pathways do not function in isolation. The final product may serve as input to one, two or more other pathways. Your pathway of choice may begin with the output of another process. Furthermore, pathways can branch: Glycolysis can proceed to glyceraldehyde 3-phosphate and pyruvate, or directly after glucose 6-phosphate formation can be shunted to the pentose phosphate pathway to yield reducing power and 5-carbon sugars (to be used in ATP, CoA, FAD, NAD+, DNA and RNA). Now, pathways leading to other pathways and branches and such make a network.
You and your colleagues might want to know if genes within a metabolic network are over- or under-represented in a test compared to control. Or, genes for a given network are not present in one species compared to several others. Or, one could estimate the flux through such a network given a set of measures.
Peruse examples at both KEGG and Reactome, expecially at KEGG where you can view pathways pertinent to your organism(s) of choice.

Many thanks for getting this started. I understand (or least have an intuition about) everything after "... and that structure dictates function"; and I've wandered through the KEGG database.  So maybe the question is better phrased: How is the protein structure determined/predicted from the protein-coding portion?  (I think this is the 'reconstruction' part?)
Thanks again for you patience.  (I should add that I'm not immune to doing my own digging; a few pointers in the right direction would be appreciated.)

In general, assignments of function are based on sequence similarity (tools like BLAST) - comparing protein sequences to those with known or demonstrated function - or identification of functional motifs as in the Pfam, SMART, INTERPRO and others (http://ca.expasy.org/tools/).

Still a few open questions, but I think that gives me enough to start doing more focused background work.  Thanks!


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Which functional annotations could be useful?
Analyzing a genome, for a generic gene, which functional annotations (e.g from Gene Ontology) can help understanding its meaning/function or, at least, provide helpful informations?

Annotations of that gene
Annotations of orthologous genes (?)
Annotations of paralogous genes (?)
Co-expressed genes (given a biological condition) (?)
What else?

Thank you.

I'd add genetic effects of the gene and its orthologs in that own
host. Knockouts and overexpression are powerful in uncovering
function.
In terms of baseline or normal expression, I would add    tissue,
developmental or differentiation time points, and conditions which stimulate or repress expression.