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Is it possible to obtain the sequences from polyclonal antibody protein mixture via mass spec?
We have been using pAbs from an immunized goat for quite a few years but now the goat died. We only have the antigen affinity purified pAb proteins. Is it possible to obtain the sequences?
We have immunized several other goats, the resulting pAbs performed far worse than the one 'golden goat' produced. We are desperate ...
Thank you.

It appears that sequencing polyclonal antibody pools is a difficult thing to do de novo because of some technical limitations in terms of recovery of the specific high-affinity antibody/antibodies within the polyclonal pool that you are trying to find.
I'm no expert at all, but I did a simple search and came up with  the following paper for detecting polyclonal antibodies from SARS-CoV-2 vaccinated persons:

Le Bihan, T., Nunez de Villavicencio Diaz, T., Reitzel, C. et al. De novo protein sequencing of antibodies for identification of neutralizing antibodies in human plasma post SARS-CoV-2 vaccination. Nat Commun 15, 8790 (2024). https://doi.org/10.1038/s41467-024-53105-8

They looked at identification of antibodies and came to the conclusion that it was best and easiest to use B-cell sequencing along with protein sequencing. However, you don't have this opportunity because you only have purified IgG.
They identified 5 interesting papers (refs 20-24 in the reference section):

Frank A, Pevzner P. PepNovo: de novo peptide sequencing via probabilistic network modeling. Anal Chem. 2005 Feb 15;77(4):964-73. doi: 10.1021/ac048788h. PMID: 15858974.

Ma B, Zhang K, Hendrie C, Liang C, Li M, Doherty-Kirby A, Lajoie G. PEAKS: powerful software for peptide de novo sequencing by tandem mass spectrometry. Rapid Commun Mass Spectrom. 2003;17(20):2337-42. doi: 10.1002/rcm.1196. PMID: 14558135.

Liu K, Ye Y, Li S, Tang H. Accurate de novo peptide sequencing using fully convolutional neural networks. Nat Commun. 2023 Dec 2;14(1):7974. doi: 10.1038/s41467-023-43010-x. PMID: 38042873; PMCID: PMC10693636.

Eloff, K. et al. De novo peptide sequencing with InstaNovo: accurate, database-free peptide identification for large scale proteomics experiments. Preprint at bioRxiv https://doi.org/10.1101/2023.08.30.555055.

Yilmaz, M., Fondrie, W. E., Bittremieux, W., Oh, S. & Noble, W. S. De novo mass spectrometry peptide sequencing with a transformer model. 39th Int. Confer. Mach. Learn. 162, 25514–25522 (2022).

As you can see from the titles, most of these use some sort of machine learning/"AI" to help the sequencing identification. You would need to talk to your protein sequencing facility to see if they are capable of doing this, or perhaps get a grant to collaborate with a specialist group to do this work.
Reference 28 in the paper is also interesting:

Bondt, A. et al. Into the dark serum proteome: personalized features of IgG1 and IgA1 repertoires in severe COVID-19 patients. Mol. Cell Proteomics 23. https://doi.org/10.1016/j.mcpro.2023.100690 (2023).

A look at the "Cited By" section in the PubMed page for each article might be of use to you for more relevant references.
You might also have an advantage in having the lesser affinity goat sera, which you could potentially use for comparison of the antisera after sequencing to look for differences.
However, the high affinity ones might not also be high abundance, and I suspect that the work involved is a whole (potentially expensive) research project in itself for only one reagent, as you would need to generate each identified antibody and compare affinity to your protein target.

Thank you Bob! This is very helpful. The first paper you mentioned claims that they obtained some functional antibody sequences without using the RNA seq info, which could be useful in my situation. I will reach out to the group and see if they can help me! Thanks again for sharing this!

@JohnTran No problem. Looks like an interesting topic. At first glance I would have thought a trivial problem, so was surprised to find the complexity. Note how recent all those papers are, right at the cutting edge of technology at the moment it would seem.

I want to report back as I have reached out to the group behind this paper https://www.nature.com/articles/s41467-024-53105-8.
They said they have done similar projects in the past to convert goat pAbs to mAbs. This is a case study they shared with me. https://www.rapidnovor.com/sequencing-recombinant-goat-polyclonal-antibodies/. They offer this as a commercial service (huge surprise to me, most people including myself did not think this is possible). I will have to get the budget approved, but I feel hopeful.


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Why "Having chlorophyll without photosynthesis is actually very dangerous" and "like living with a bomb"?
The Phys.org article Scientists discover first organism with chlorophyll genes that doesn't photosynthesize says

"For the first time scientists have found an organism that can produce chlorophyll but does not engage in photosynthesis.

It is referring to the new paper in Nature A widespread coral-infecting apicomplexan with chlorophyll biosynthesis genes (paywalled).

"This is the second most abundant cohabitant of coral on the planet and it hasn't been seen until now," says Patrick Keeling, a University of British Columbia botanist and senior researcher overseeing the study published in Nature. "This organism poses completely new biochemical questions. It looks like a parasite, and it's definitely not photosynthetic. But it still makes chlorophyll."
[...]
Chlorophyll is the green pigment found in plants and algae that allows them to absorb energy from sunlight during photosynthesis.
"Having chlorophyll without photosynthesis is actually very dangerous because chlorophyll is very good at capturing energy, but without photosynthesis to release the energy slowly it is like living with a bomb in your cells," Keeling says.

Question: Why is it that "Having chlorophyll without photosynthesis is actually very dangerous" and "like living with a bomb"?

While I lack detailed knowledge of this organism's internal structure, it's plausible that since it is still carrying out photocapture and acid pump that the acid pump directly powers ATP synthesis like it would normally do in mitochondria. It would take a link between the plastids and the mitochondira to do, but that's not ridiciulously implausible.

It is important to note, at least from my understanding of the article, that the organism doesn't actually produce chlorophyll; it merely has the genes to do so, but they seem to be inactive.

They're referring to the fact that a bomb can release a lot of energy under the right circumstances.

Chlorophyll absorbs photons (light). The energy in the photon extracts an electron from a molecule of water. Electron transfer creates intermediate superoxide and hydroxyl radicals from the oxygen and hydrogen from the donor water molecule.
In normal photosynthesis, these radicals are quickly used to power the reduction of NADP to NADPH and the synthesis of ATP from ADP. NADPH and ATP in turn power the synthesis of sugars from carbon dioxide and water, via the Calvin cycle.
These radicals are highly reactive. If they hang around and don't get used properly in redox reactions, they will just as happily attack DNA, proteins, and structural lipids within the cell, and are therefore dangerous. In normal plant cells that get too much sun, for instance, free radicals can build up and cause cell damage.
My guess is that the author's "bomb" is made up of higher concentrations of these radicals within a cell with no apparent machinery to perform the downstream (photosynthetic) chemical reactions needed to consume them safely.
Edit
I skimmed the (sadly, paywalled) paper, and it sounds like my guess was right, that it is indeed these radicals that are the danger from having chlorophyll, with no light-independent (Calvin cycle) mediated reactions to safely consume the energy in them:

Chlorophyll itself has no natural biological function outside of
  photosynthesis, so if photosystems are indeed absent, corallicolids
  must have evolved a novel use for either chlorophyll or its closely
  related precursors or derivatives. However, these molecules generally
  function in light harvesting, which would be destructive to cellular
  integrity without the coupling of the resulting high-energy compounds
  to photosynthesis. Other possibilities are functions in light sensing,
  photo-quenching or the regulation of haem synthesis, but these too
  leave open the question of what the cell would do with the highenergy end products.

What's not clear to me is that the genes that help generate chlorophyll are expressed, but the cells are unpigmented. I don't see any explanation where the chlorophyll and associated proteins are localized in the cell — seems like a missing part of the paper, or I missed that part when skimming. Or perhaps the organism has evolved interesting and novel ways to manage the damage caused by these oxygen radicals, or has other mechanisms for consuming them, yet to be identified.
Should motivate further research, especially if these organisms share ancestry with malaria and toxoplasmosis — there might be something interesting to learn that would help with eliminating these diseases. I imagine a biochemical "radical bomb" could be very handy for destroying parasites, if there was a way to expose them to light or some other source of photons; perhaps some drug therapies could target the relevant genes and induce the parasite to destroy itself. Interesting paper.

I see what you mean, thanks! So maybe the "bomb" analogy isn't fitting, but this certainly sounds like the situation could be potentially dangerous.

It would be great if you could provide some references.

"It transfers the energy of a photon as an electron to a molecule of water". I believe that's the electron-transport chain you're thinking of. The end-product of photosynthesis is glucose AFAIK.

Chlorophyll (and more commonly porphyrins) are in fact used to kill cells by light exposure in photodynamic therapy (Song et al., 2014)

Is this the main reason why plants get 'burnt' by too much sun?

@elzell I would say that's usual dehydration/UV induced damage. Usually chlorophyll synthesis is regulated and there are anti-oxidants to prevent oxidative damage. Note that excessive sunlight also burns animals.

Well now this just leaves me wondering if these organisms are doing anything with this chlorophyll.  Are they just in some really weird evolutionary niche where they manage to produce chlorophyll they don't need, without it being a large enough burden to stop the species from surviving?

@JMac it seems unlikely to me that its doing literally nothing (especially given how other members of the family have lost the genes for chlorophyll), but biology seems to constantly find weird uses for things. Maybe the free radicals fend off bacteria/viruses or something...

@user1136 most microorganisms are nearly completely transparent to visible light. Deliberately absorbing light via chlorophyll seems unlikely to have a protective effect.

@user1136 Dunaliella is photosynthetic (using chlorophyll), and beta-carotene has a known role in preventing the generation of reaction oxygen from chlorophyll: ref I strongly suspect its that role which is protecting Dunaliella, and not because it is absorbing light. If you lack a photosynthetic system (like the organism in the OP), I struggle to see how absorbing more energy could ever be protective, compared to letting it pass through.

@user1136 see here for general information. Or to quote directly: "In oxygenic photosynthetic organisms, chlorophyll triplets are harmful excited states readily reacting with molecular oxygen to yield the reactive oxygen species (ROS) singlet oxygen. " ref. There is no electron involved, the triplet chlorophyll transfers energy and excites the oxygen, making it reactive and destructive to cells. Beta-carotene quenches excited chlorophyll before this happens and thus protects the cell.

@user1136 I am not sure what article you are referring to but the article I quoted in my last comment directly states "Carotenoids have a photoprotective role in photosynthetic membranes by
preventing photoxidative damage through quenching of chlorophyll singlets and triplets"

@AlexReynolds Your edits are great but I was hoping for a source that says that accumulation of chlorophyll without the other photosynthetic machinery actually increases the cell mortality by induction of ROS. Your theory is quite pertinent but suitable references would be perfect. Your answer is great so I don't want to add another one. Some papers on photodynamic therapy might have a good lead if specific papers on chlorophyll induced toxicity are not there.

Alex Reynolds has explained why “Having chlorophyll without photosynthesis is actually very dangerous”, but I think that the original sensational statement by Phys.org is unhelpful as it distracts from the real question. However that’s what you get with so-called ‘free’ journalism.
Obviously organisms don’t synthesize complex molecules without a reason. If the corals don’t perform photosynthesis, they use the high-energy electrons produced from the light photons for something else. To quote from the paper:

Chlorophyll itself has no natural biological function outside of photosynthesis, so if photosystems are indeed absent, corallicolids must have evolved a novel use for either chlorophyll or its closely related precursors or derivatives. However, these molecules generally function in light harvesting, which would be destructive to cellular integrity without the coupling of the resulting high-energy compounds to photosynthesis. Other possibilities are functions in light sensing, photo-quenching or the regulation of haem synthesis, but these too leave open the question of what the cell would do with the high- energy end products. Moreover, we detected corallicolids in sun coral (Tubastrea sp.) and black coral (order Antipatharia), both of which are considered to be non-photosynthetic corals, which further suggests that corallicolids deviate from classical modes of light harvesting.

The interesting question is what they use it for. Bombs are for writers that don’t do biochemistry.

You probably didn't notice but the article is directly quoting one of the authors. The reference to "bomb" is in quotation marks, with the author's name following immediately. Your bone to pick is with the author himself, not with Phys.org or "free journalism" (which it isn't, Phys.org has advertisements). I also felt it was strange that an author of the paper would use this wording, You may want to fix this glaring error in the beginning of your otherwise helpful answer. Thanks!

(-1) because first and final sentences are inaccurate and should be corrected. You're claiming that the author of the Nature paper doesn't do biochemistry. Yikes!

"Obviously organisms don’t synthesize complex molecules without a reason." I don't see this as obvious; vestigial structures are a counterexample. The reason could simply be random chance that hasn't been selected against.

@user1136 that's an interesting editorial. The paragraph immediately before the one to which you refer also has significance here with respect to this organism producing but not using chlorophyl; "...or indeed the very presence, of a protein may be very significant or totally irrelevant depending on whether it is following a ‘don’t care’ condition."

@Bob Certainly in general you are correct, but in this specific case the evidence is suggestive of selection.

Although you pose an interesting question ("what they use it for"), you don't really answer uhohs' question. And your spike remarks are redundant IMHO.

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

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

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

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

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

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Does drinking coffee have negative effects?
From what I collected, coffee is a magical potion that lets you feel energetic, and essentially not-sleepy. But are there any tradeoffs? I mean, if it was so beneficial, wouldn't the human body produce caffeine naturally?

First of all, the fact that a substance is beneficial does not mean that our body will, perforce, produce it naturally. Think of oxygen and water for example1.
As for the negative effects of coffee drinking, yes there are many although coffee has both a positive and a detrimental effect on human health. The main active ingredient in coffee is caffeine which can have the following negative effects:

Caffeine can increase blood pressure in non-habitual consumers.
High blood pressure is associated with an increase in strokes, and cerebral
vascular disease, which in turn increase the risk of multi-infarct dementia.
Caffeine may reduce control of fine motor movements (e.g., producing shaky hands)
Caffeine can stimulate urination.
Caffeine can increase cortisol secretion, some tolerance is developed.
Caffeine can contribute to increased insomnia and sleep latency.
Caffeine withdrawal produces headache, fatigue and decreased alertness.
Caffeine is addictive.
High doses of caffeine (300 mg or higher) can cause anxiety.
High caffeine consumption has been linked to an increase in the likelihood of experiencing auditory hallucinations. A study conducted by the La Trobe University School of Psychological Sciences revealed that as few as five cups of coffee a day could trigger the phenomenon.
High caffeine consumption accelerates bone loss at the spine in elderly postmenopausal women.

The list above comes from the very comprehensive wikipedia page on the health effects of caffeine. In fact, wikipedia is particularly good on this subject, see the following pages:
http://en.wikipedia.org/wiki/Caffeine
http://en.wikipedia.org/wiki/Health_effects_of_caffeine
http://en.wikipedia.org/wiki/Health_effects_of_coffee
1 Our bodies do produce both Oxygen and water as byproducts of various reactions but nowhere near enough to satisfy our need for these substances.

I understand the need of writing a generic answer but... it all depends on doses, frequency of assumption and the person who drinks the coffee. Caffeine has very different effects at the molecular level depending on its concentration, so it is very difficult to generalize. For instance, 300 mg of caffeine are ~4 cups of espresso, which you generally don't drink at the same time.

@nico, of course it does, everything is dosage dependent. However, the question was not about what the effect of a specific dose of coffee is, it was about coffee in general. All I said was that caffeine can produce the listed effects. if you can give an answer listing different effects of long term cofee consumption at different doses please do, considering how much of the stuff I drink, I would very much like to read it :).

As always, it depends.
To be more precise, let's presume you are asking about habitual coffee consumption. Thus, for people asking: "I really like to drink several cups of coffee per day, but I have heard this might be unhealthy. Should I be worried?"
Based on my reading of O'Keefe, J. H. et al. (2013), overarching results indicate you should not be overly worried (but exception cases will follow):

a growing body of data suggests that habitual coffee consumption is neutral to beneficial regarding the risks of a variety of adverse CV outcomes including coronary heart disease, congestive heart failure, arrhythmias, and stroke. Moreover, large epidemiological studies suggest that regular coffee drinkers have reduced risks of mortality, both CV and all-cause. The potential benefits also include protection against neurodegenerative diseases, improved asthma control, and lower risk of select gastrointestinal diseases. A daily intake of ∼2 to 3 cups of coffee appears to be safe and is associated with neutral to beneficial effects for most of the studied health outcomes.

However, you might want to be cautious in regards to:

... potential risks (which are mostly related to its high caffeine content) including anxiety, insomnia, tremulousness, and palpitations, as well as bone loss and possibly increased risk of fractures.

And ...

Those with dyslipidemia may consider brewed and filtered coffee as opposed to preparations made from boiling beans without filtering.

So if you have trouble sleeping, already have an overly anxious personality, are prone to fractures, or have dyslipidemia, you might want to consult your doctor about your coffee intake.
A systematic review and meta-analysis investigates the effects of coffee on blood pressure and cardiovascular disease (CVD) in hypertensive individuals (Mesas, A. E. et al., 2011) and concludes:

The results of this review have clinical implications for the control of hypertensive patients. On the one hand, the acute increase in BP may temporarily increase the risk of a cardiovascular event (10, 11). This is consistent with the increased risk of coronary disease and stroke in the hours after coffee consumption. Thus, hypertensive patients with uncontrolled BP should avoid consuming large doses of caffeine. ... However, we found no evidence to justify avoidance of habitual coffee consumption in well-controlled hypertensive patients; therefore, in these patients, medical recommendations should prioritize modification of other lifestyles, such as quitting smoking, controlling weight, and increasing physical activity.

O'Keefe, J. H., Bhatti, S. K., Patil, H. R., DiNicolantonio, J. J., Lucan, S. C., & Lavie, C. J. (2013). Effects of habitual coffee consumption on cardiometabolic disease, cardiovascular health, and all-cause mortality. Journal of the American College of Cardiology, 62(12), 1043-1051.
Mesas, A. E., Leon-Muñoz, L. M., Rodriguez-Artalejo, F., & Lopez-Garcia, E. (2011). The effect of coffee on blood pressure and cardiovascular disease in hypertensive individuals: a systematic review and meta-analysis. The American journal of clinical nutrition, 94(4), 1113-1126.

Likely another relevant recent meta-analysis (I haven't read it): Poole, R., Kennedy, O. J., Roderick, P., Fallowfield, J. A., Hayes, P. C., & Parkes, J. (2017). Coffee consumption and health: umbrella review of meta-analyses of multiple health outcomes. Bmj, 359, j5024.

There are copious studies on the health effects of coffee. The overall conclusion is that people who drink coffee have slightly less health issues than people that don't.
BMJ:
The umbrella review identified 201 meta-analyses of observational research with 67 unique health outcomes and 17 meta-analyses of interventional research with nine unique outcomes. Coffee consumption was more often associated with benefit than harm for a range of health outcomes across exposures including high versus low, any versus none, and one extra cup a day.
https://www.bmj.com/content/359/bmj.j5024
For adults consuming moderate amounts of coffee (3-4 cups/d providing 300-400 mg/d of caffeine), there is little evidence of health risks and some evidence of health benefits. https://www.ncbi.nlm.nih.gov/pubmed/16507475

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

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

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

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

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

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

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


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Are there any intersections between the biochemical pathways of uracil biosynthesis (or metabolism) and methionine degradation in eukaryotes?
Is there any way in which uracil biosynthesis or metabolism could help cell in degradation of toxic levels of methionine?

Uracil degradation doesnt produce aspartate, but beta alanin

No, I don't think there are any intersections, and I can't see how uracil metabolism would have any influence upon methionine degradation.
Methionine degradation is shown in Figure 1 below. The end product is succinyl CoA which is fed into the TCA cycle. The only obvious by-product is cysteine which doesn't have any connection with uracil biosynthesis.
Uracil biosynthesis (as UMP) is shown in Figure 2: it is built from CO2 and NH3. Uracil degradation produces CO2 NH3 and aspartate.
There are certainly no shared intermediates in these pathways, and I can't come up with any convincing indirect connections either.
Figure 1. Methionine degradation

Figure 2. Uracil biosynthesis

Theoretically, produced CO2 would buffer (minor) acidity from sulfate but that's both minor.


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Is there life on other planets and if so how frequent?
Some shed tears of joy as the news about the successful landing of the Mars Rover Curiosity came in. Then the most comprehensive 3D map of our observable universe was published. 2012 is literally an astronomical year.
As an layman I would like to know about scientists current understanding about the frequency models that life forms on other planets?
See also:

Drake equation

Although we are getting very encouraging signs, there is no indisputable evidence that life has been found other than earthly life.  I think Europa is probably more exciting than Mars, where giant reservoirs of water have been found and the temperatures are imaginably hospitable.  Too bad its so far away!

Giant reservoirs of water have not been found on Europa, although it is hypothesized that there may be a subsurface water ocean due to the way that the surface ice has deformed. However, I do agree that Europa is an exciting target. Enceladus also, which has been seen to have cryovolcanos spurting out water-ice. I suspect Mars is too dry and cold. We'll see.

It’s interesting to note that at least among leading astronomers there seems to be no question about this at all: the existence of extraterrestrial life is simply assumed. The only question is about when we find it, not whether (see e.g. some New Scientist issue from earlier this year).

@Konrad Rudolph Astrophysicist Max Tegmark believes that we are alone. Alone as in any other life being beyond the horizon of the visable universe (he's big on multiverses). It is a valid standpoint since we never have observed extraterrestrial life and we don't understand how life originates. He certainly seems to be in the minority, though.

Wrong forum. Try for astronomy.stackexchange.com. We can't even attempt to answer the bio half yet.

OK, so we know a couple of things about life in the universe. Note, however, that this is not really an answer and is also not very biological in nature.
So, we don't know how life began on the Earth. However, do know that:

The probability of life evolving on a planet in the universe is non-zero (since we exist) and,
So far, we have not found evidence for life elsewhere in the universe.

So this leaves us with two main possibilities:

Life is rare in the universe.
Life is common in the universe but for some reason we do not detect it.

This latter possibility is basically a restatement of the Fermi Paradox which says

"The universe is very big and there should be lots of alien life out
  there. Where is everybody?"

In the case that life is common, we can speculate extensively on why we have not detected  it so far. For example:

We haven't been looking long enough (SETI has been running for only a few decades)
We haven't been looking hard enough (the budget of SETI etc. is not large)
We haven't been looking in the right way. We are currently looking mainly in the radio regime, maybe aliens broadcast in X (where X is part of the E/M spectrum or something else entirely, e.g. gravity waves, tachyons)
Life is common, but intelligent life is rare (this would be my guess)
Life is common and intelligent, and doesn't want to answer (why? ask a xenopsychologist)

OK, so these are just some examples of "solutions" to the Fermi Paradox. There are many more which are much more exotic. My personal favourite of these is that we live in a simulated universe and the coders have not included additional alien life in the simulation. It would explain some strange "coincidences" about fundamental physical constants, but what simulation, no matter how good, would ever come up with cauliflower cheese for example?
However, until we actually detect life on another planet we will still be in the dark. The next generation of telescopes will be able to do this for nearby exoplanets if life is present on them and has affected the biosphere in a detectable way.
Edit - You mention "frequency models", but all we can currently say is that the probability of life on other planets is not zero - due to our existence - as I mentioned at the start
Some references:

A joint analysis of the Drake equation and the Fermi paradox, 2012, arXiv, Prantzos, N.
The Fermi Paradox, Self-Replicating Probes, and the Interstellar Transportation Bandwidth, 2011, arXiv, Wiley, K.B.
Interstellar colonization - A new parameter for the Drake equation, 1980, Icarus, vol. 41, 193, Walters, C., Hoover, R. A., Kotra, R. K.

"the probability of life on other planets is not zero" We can't even say that. The anthropic principle, you know. We cannot count ourselves as an observation, because our existance is necessary for making any observation. Our existance is perfectly consistent with us being alone. We have zero data.

Poshpaws, good answer.
As I understand we can only "look" into the past, since cosmologically speaking light is really slow. Light also disperses and becomes incoherent with long distances.
"Simple" cellular life seems to be an evolutionary prerequisite, and they are not in the habit of sending out powerful radiotransmissions into space (i.e. weak-point of the SETI Proj.).
There is also no reason why life should have terraformed a planet to the point of being spectroscopically detectable in the albedo.
A lower bound on the number of habitable planets in a galaxy like ours, would be great.

An amusing thing happens. We know that earth is already disappearing as a cosmic radio source. If you substitute 100 years for L in the drake equation, you get expected number of civilizations = 1. That must be us.

According to this, 1.2% of stars have planets that can support life. According to Google, there are 300,000,000,000 stars in the Milky Way. That means 3,600,000 stars can support life. Each of these stars  is estimated to have 1-2 planets that can support life. For the sake of simplicity, I'll use 1.5 to represent this, since it is the average of 1 and 2. 1.5×3,600,000=5,400,000 planets capable of supporting life. Looking around the web, there are wildly different estimates of the odds of life evolving on one of these planets (from 1%-100%), but 100% seems like the most common. This means that, statistically, the odds of extraterrestrial life existing are extremely high.

One thing is whether a planet is in a habitable zone - something we can begin to estimate with exoplanet observations - another is to know the probability of life evolving on the planet. Until we start to see evidence for extraterrestrial life (e.g. biosignatures) this is still a complete guess.

Uhh the number of possibly life-supporting planets per star is << 1 because most stars forming planets end up with hot jupiters.

Can we extend this to ask (excluding our own solar system), how far away we would have to look before we might reasonably expect to find some form of extra-terrestrial life? In other words, combine the likely number of life-supporting planets with the spatial distribution of stars in the galaxy to derive a mean distance between possibly/likely life-bearing star systems.


text:
Why do carrots spoil so fast?
The carrots we buy from a supermarkets spoil very fast, albeit giving many consumers a false sense of preservability due to their structural rigidity. The answer extends to many other vegetables many of us eat:

 Larsinio (2006)- wikimedia, public domain, DOR 27/09/2012
The question is, why do well aerated carrots spoil in the matter of days, at room temperature?
Things to consider: a tuberous rhizome with rough and segmented skin / oxygen levels / levels of aeration / relatively high sugar content / differences in immediate microbiome / lack of possible synergies which the earth provides...the majority of antibiotics is extracted from soil microorganisms {1},{2}....

Remember that tubers are designed for a relatively anaerobic environment. My guess is that what you are seeing is related to that. Oxidation perhaps? Aerobic bacteria gone wild?

I think carrot keeps long time in refrigerator. Why store it at room temp when optimal storing condition is refrigerator ?

@Andrei Initially I wanted to explain that in the post as well and include storage conditions. But I consider it best to just ask one question at a time. Regardless, did you have consistently success w. long-term fridge storage?

can you reference your declaration that carrots spoil fast please since I also think that it depends on a lot of factors like where it was grown, the kind of fertilizers used etc

Strange question...Carrots usually (>95% of the time) last for 1+ months for me in the fridge. I'd hardly say that's a quick rate of spoiling

First we will take a look at the lines of resistance of a carrot. There are three

The skin - The first line of resistance is the outer membrane or skin of the carrot and chemical compounds that are normally present
  there. Two antifungal polyacetylenes, falcarinol and falcarindiol, and
  an isocoumarin, 6-methoxymellein, are present in small amounts in a
  normal carrot and present the first barrier in undamaged carrots.
Post Harvest - If during harvest or post harvest handling this barrier is broken, the surface is punctured, scraped or sliced,
  microorganisms may begin to grow. The carrot at this point begins a
  wound healing process by accumulating suberin, a complex
  polysaccharide, at the wound site. Along with suberin, lignin is also
  accumulated. Suberisation is complete within 48 hours after wounding,
  and lignification is complete within 168 hours of wounding..
Phytoalexin barrier - The last and most important line of resistance is the phytoalexin barrier. Phytoalexins are chemicals
  produced by plants that impart disease resistance in response to
  mechanical injury, physiological stimuli or infection. Scopoletin, a
  coumarin,and para-hydroxy benzoic acid, a phenol, are apparently early
  arrivals on the scene but later disappear (reference).

There are three enemies of carrot storage: wilt, re-growth and rot.
Some reasons for carrots rotting faster:
Many fruits and vegetables start to produce ethylene gas when they start to ripen. Some foods are extremely sensitive to ethylene gas which makes them rot faster (reference). I am guessing that you keep different vegetables close together. Maybe if you stored carrots separately, it might make them last a bit longer.

Major post-harvest losses in carrots are due to Sclerotinia rot,
  Botrytis rot, Bacterial soft rot (Erwinia) and Sour rot (Geotrichum).
  Of these, Sclerotinia rot is the most prevalent.The Sclerotinia fungus
  infects the carrot roots in the field through the crown. During
  storage, the Sclerotinia fungus produces a white, cottony mycelium
  which covers the roots. Infected roots are usually soft and watery (reference).

There would definitely be more reasons but I am guessing that these are the major contributors to it rotting faster.


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How are blood vessels affected by UV and infrared radiation?
The lining of the blood vessel as an interface and boundary layer is of existential necessity to the life-support of mammals.
My question is:
How are major blood vessels and the blood vessel lining affected by sun-irradiation in humans, when exposed through equal or less than a millimeter of skin in total (including subcutaneous fatty tissue)?
Information regarding infrared exposure is welcome too.

Source: http://www.dermatology.ucsf.edu/skincancer/General/prevention/UV_Radiation.aspx
Thanks.

UV rays cause damage is by thinning the walls of surface blood vessels, leading to bruising, bleeding, and the appearance of blood vessels through the skin. Longwave UV radiation (UV-A) accounts for up to 95% of the UV radiation that reaches the earth's surface. Although UV-A is less intense than UV-B, it is more prevalent and can penetrate deeper into the skin layers, affecting the connective tissue and blood vessels, which results in premature aging - Photoaging.
At the same time UVB – is even more dangerous than UVA radiation and also causes skin damage and skin cancer. It affects the surface skin layer. The skin responds by releasing chemicals that dilate blood vessels. This causes fluid leakage and inflammation – better known as sunburn.
I am not quite sure what chemicals are generated by UV radiations beneath the skin surface. I guess it might be excess free radicals which accumulate and cause damage to blood vessels since they are delicate. There is one theory which talks about damages to skin due to Free Radical theory of aging
To give an example how UV radiation affects the blood vessel here:

In actinic purpura, UV radiation damages the structural collagen that supports the walls of the skin's tiny blood vessels. Particularly in older people, this collagen damage makes blood vessels more fragile and more likely to rupture following a slight impact.

Below figure to give an idea of how strong UV radiations are:


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Is this may-flowering grass an Echinochloa (barnyard grass)?
There's a grass growing in my thyme pot on my balcony, that's currently flowering (end of May, Paris region, France, southern exposure, windy conditions), and I'm wondering what species it is:

Here are a picture where details of the flower and leaves may be more visible:

I tried to search using my old determination key for French flora (G. Bonnier / G. De Layens), and after much hesitations, I guess it could be what is called "Oplismenus Grus-galli" in this book.
Internet tells me it is now called Echinochloa crus-galli. The base of the plant indeed has a similar way of growing, and the flowers are a bit similar.
Does this look plausible? Do you see a better match?
Can I use the seeds when they are ripe (for instance to put in home-made bread)?


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Is it firmly established, that mutations are sufficient for cancer?
It is evident for scientists, that all cancer cells have some mutated genes. Say mutations in general.
But this evidence means necessary condition.
But what about sufficient conditions?
Is it possible, that mutations are necessary but insufficient for cancer?
I.e. may be other factors exist, which are probably more important?

About what other factors are you thinking?

Does not matter, but I can imagine some.

Can you tell me the ones you have in mind?

For example, I speculate, that immune tolerance is controlled by suppressor cells, that are antigen specific. I.e. for each tissue, which is not causing immune response, there is a specific suppressor population. If extra suppressors appear, then immune system become tolerant for cancer. If mutation occurs after that, then cancer develops. Contrary: if kill specific suppressor population, cancer will regress.

@Chris, so what can you say?

Acquiring mutations (more than one) are the necessary (and sufficient) steps on the way to cancer. The current opinion is that cells need "multiple hits" to fully transform into a cancer cell. It is also called the Knudson hypothesis, the original paper is here.
For example melanocytes (the pigment cells in the body) which acquire the activating BRAF V600E mutation (which is an important step in getting a melanoma cell, this mutation is found in about 70% of all melanoma) is not enough to transform the cell. Other mutations are necessary to do this.
Among the things important for cells to become malignant are to escape the apoptosis mechanisms of the cells and also the immune system. Both are linked to the mutation, inactivation or epigenetic silencing of genes, so I would say genes are the key to cancer.
For further readings these two articles should be interesting:

Are oncogenes sufficient to cause human cancer?
Significance of multiple mutations in cancer

I was thinking of this, and have more questions...

See next question pls http://biology.stackexchange.com/questions/17208/why-cancer-mutations-do-accumulate-sequentially


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Reverse tomography to create 3D scalpel
Isn't it possible to reverse tomography methods to create means to deliver heat or radiation precisely in 3D? This would be "3D scalpel" i.e. device which would be able to eradicate tumor cells precisely in otherwise unreachable areas?

This is the idea behind http://en.wikipedia.org/wiki/Radiosurgery (a.k.a., "Gamma knife")

Some people are also studying that kind of things with ultrasounds using time reversal. For example against kidney stones. But ultrasounds have problems (mainly because of their wavelength) and are not that easy to use against tumours in unreachable areas. I think there are also studies about time reversal for electromagnetic waves, but that also yields some problems.

The principle of targeting cancers with high intensity radiation is already in use. For example:
http://www.mayoclinic.org/tests-procedures/gamma-knife-radiosurgery/basics/definition/prc-20014760


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Is process, opposite for growth, known for mammals?
Every animal born small, then grow larger and larger.
The same is true for parts of the animal bodies.
Is there any cases, when body or part of the body diminishes in size and mass, while staying healthy?

Do any example of structure existing in insect's larvaes but not in adults would answer your question? What about the thin skin that human baby have between their fingers and get lost later?

In humans at least (I'm not sure about other mammals), the thymus grown until puberty and then shrinks gradually, a process called involution. I'm not sure if this meets your criteria. The thymus remains "healthy," but it's function greatly diminishes over time.

Not a mammal, but the paradoxical frog (Pseudis paradoxa) starts life as a small tadpole that grows into a large tadpole and ends up as a much smaller frog. There are bound to be other examples of this phenomenon, but this is the one that immediately sprang to mind.


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How are different types of cells created from zygote?
In the process of mitosis that starts from zygote, how do different cells appear? What happens that some cells become one type and some another?
For example, is there a cell that divides into a blood cell and a skin cell?

The word you want to search for is "differentiation". http://en.wikipedia.org/wiki/Cellular_differentiation

differentiation starts

@Memmin Thanks for giving me the right term, thus the right direction. Sometimes not knowing the terminology is the whole problem.

The process of formation of different types of cells that differ in morphology and function is termed as cell differentiation. In multi-celled organism, each task of life is carried out by different types of  specialized cells say nerve cell for transmitting impulses, muscle cells for coordinating movement and these cells differ in their appearance and function, but originated from the same parental cell, the zygote. These specialized cells are formed by a process called differentiation.
Cell differentiation is the process by which genetically identical cells of an embryo become specialized.

From a fertilized egg, at least 250 distinct types of differentiated cells are present in adults.
Zygote->determination ->differentiation

Cell specialization involves the preferential synthesis of some specific proteins like antibodies in plasma cells or Hb in erythrocytes.
The genome is the same in all cells of our body, but only certain genes are turned on and other genes are switched off and this lead to specialization. That is, genes active in the neurons may not be active in muscle cells. For instance, genes for actin and myosin filaments are present in all animal cells, but these genes are active only in muscle cells.
http://www.biologyexams4u.com/2012/08/cell-differentiation.html

I'm not sure about the first developmental stages but, given you already have hundreds of cells with slightly different physiology, the next developmental stages like dev. of neural tube happen through excretion of translation factors and growth factors in several cells. Each of those cells that are in a region where more than one excretion overlaps get a higher dose than the others. This is the signal for the cell to differentiate into another type, by changing its physiology. Such factor excretions are important events, and the genes encoding for the factors are evolutionally highly conserved (so called homeobox proteins).
However, this has nothing to do with mitosis. The newly divided cell does not decide on its own but reacts to a stimulus, like skin cells develop into skin cells because they are on the outside of the cell ball. Excreted factors do the fine tuning.

I was looking for differentiation in the early development stages. But nonetheless, thanks for the info.


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Do memories have mass?
If it were possible to live forever, would our brains grow infinitely with the number of memories that we store? Or would we remove old memories as we create new ones?

there is a related discussion on CogSci.SE.

Does your computer get heavier, the more data you store on its hard drive?

You would need to live a long, long, long, long time for this to become remotely problematic.
Your question seems to suppose that a memory is "stored" by a neuron, and since neurons have mass, then the more memories we have the more our brains will weigh. Actually, neurogenesis is pretty rare in the adult brain--most of the cortex is fixed, and new neurons do not grow. (The hippocampus is the best known counterexample, but it's important to note that contrary to lore, the hippocampus doesn't store memories per sé, though it is involved in the formation and retrieval of memories).
Memories are represented in the brain as patterns of firing neurons. Let's say, for simplicity, that each neuron can either be on or off. Since there are 86 billion neurons in the brain, we can experience 2^86bn possible brain states. That's a lot.
Of course there are a lot of simplifications here--most notably, there is a lot of structure to the brain, and so i'm not suggesting you can store 2^86bn memories--but the logic is the same. Even with only 1,000 neurons, we can store a ridiculous amount of information (2^1000).
I would like to comment on MCM's answer as well, because I don't think it's true that we "remove" old memories. Or rather, the topic is still being debated in cognitive science today. For an old take on it, see renowned memory researcher Endel Tulving's (1974) article, in which he says:

When we forget something we once knew, it does not necessarily mean that the memory trace has been lost; it may only be inaccessible

The idea is that some memories are suppressed (no, not repressed), being rendered inaccessible. Robert Bjork and John Anderson have (separately) done some nice work in this area.
So before you worry about this becoming a problem, I suspect you need to work out the secret of immortality first.

Tulving, E. (1974). Cue-Dependent Forgetting: When we forget something
  we once knew, it does not necessarily mean that the memory trace has
  been lost; it may only be inaccessible. American Scientist, 74-82.

The expected number of atoms in the universe is around 2^{266}, very far from your figure.

whoops, you're right. math error, should've noticed it. i've rolled back to the previous edit.

Why are you assuming that 1000 neurons give 2^1000 possible states? A neuron can be connected to multiple neurons, and certain connections are stimulatory and certain inhibitory, it is wrong to compare biological neuronal network to computational neuronal network, because that is not how things work in the brain. On the other hand, having 86 billion neurons is very different than having 86 billion neurons involved in memory formation...

as i said, i oversimplify things quite a bit. my point here is simply to show that if memories are represented as patterns of neuronal firing, the combinatorics is such that the brain has a vast amount of 'storage', even if only a miniscule fraction of those patterns could represent memories. im happy to edit if you have suggestions to make this more clear, but i'm not trying to make any claims about hard numbers.

We already remove old ones and create new ones. I doubt you remember most of Geometry, for instance.
As for capacity, this article from Scientific American gives a good overview of what we can estimate with our current knowledge.

For comparison, if your brain worked like a digital video recorder in a television, 2.5 petabytes would be enough to hold three million hours of TV shows. You would have to leave the TV running continuously for more than 300 years to use up all that storage.
The brain’s exact storage capacity for memories is difficult to calculate. First, we do not know how to measure the size of a memory. Second, certain memories involve more details and thus take up more space; other memories are forgotten and thus free up space. Additionally, some information is just not worth remembering in the first place.

So, there is an upper limit. Where is it? Well, probably a bit longer than our reasonable lifespan at the moment.

You've struck upon an interesting point with your example, actually, someone who is a surveyor would probably remember a lot of geometry.  Our ability to do so depends on context and usage of the information.

Two downvotes without a comment? Jeez. People, I implore you, if you think my answer is inadequate - say as much. I will happily do further research if I have the time and willpower.

I have not downvoted (nor upvoted) the answer but personally I really don't like when journalists amuse themselves speaking of petabytes of information, as if the brain was a computer. It is not and the reality is that we currently do not know enough about memory formation to give any meaningful answer to this type of problems.

@nico - The author is a Professor of Psychology, not a journalist.

@MCM: even if he was a Nobel Prize I would maintain my point...

@nico - Sure, but at least you voice your point. ;)


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Are there any antigen electronic sensors?
Is it possible somehow to attach antibody to silicon or to other electronic component chemical, and have electronic detector of correspondent antigen?
Does such devices exist?

Try Googling "antibody biosensor" to get started.


text:
External tissues, connected to the body?
Some cancer tumors suppress themselves from spreading. When such tumors are removed by surgery, the metastasis process is accelerated.
Isn't it possible to put such tumors into external device like hemodialysis device and slow metastasis process this way?
Are there any experiments or clinical usages of own body tissues in such a devices? Not for cancer, but probably for some other reasons, in humans and animals?
Some sort of grafting for animals.
Such a tissue can interact with main body by blood and cause some effects.

I've actually wondered this myself from time to time, without ever bothering to look it up.  Well, it's actually happening.  That WSJ article says the following, which just blows my mind:

Researchers at the Rogosin Institute are taking tumor cells from mice, encapsulating them in beads made from a seaweed-derived sugar called agarose, and implanting them in the abdomen of cancer patients. There, cells in the beads secrete proteins researchers believe could signal a patient's cancer to stop growing, shrink or even die.
So far, at least 30 patients have been treated with the cancer beads in an initial human study, and a phase two or intermediate-stage trial has been launched—with the approval of the U.S. Food and Drug Administration—to test the technique in patients with advanced colon, pancreatic and prostate cancers.

You can find the info on the Phase II trial here; they are currently at the "recruiting participants" point.

[The treatment] consists of small beads that contain mouse cancer cells from a mouse kidney cancer cell line. The cells in the beads produce substances that have been shown to slow or stop the growth of tumors in experimental animals, veterinary patients, and 23 humans with different types of cancers in a Phase 1 safety trial.


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Plant identification - variegated ivy-like
What plant is this? It's in the UK, grown in a pot, and looks like a variegated ivy.
Leaves are about 2 cm in diameter, and the full plant about 50 cm.

Found an answer myself, so here it is.
This is Ceropegia linearis ssp. woodii, also known as hearts on a string or hearts entangled.
More information about the plant can be found at https://www.rhs.org.uk/plants/details?plantid=5862


text:
Is it possible to purify antigens from a vaccine and to separate them from the adjuvant?
I need to separate the antigens from several vaccines in order to use them for coating microplates to run an indirect ELISA. I at least need to remove the adjuvant from the vaccines. Is this possible to do and if yes, how do I go about it?

The major component of a vaccine is the adjuvant, and according to Wikipedia the most commonly used adjuvants in human vaccines are aluminium salts.
Here for example is the composition of Recombivax HB, a hepatitis B vaccine produced by Merck Frosst and used in Canada (source of information is a Canadian website)

RECOMBIVAX HB ® [hepatitis B vaccine (recombinant)] is a non-infectious subunit viral vaccine consisting of surface antigen (HBsAg or Australia antigen) of hepatitis B virus produced in yeast cells. A portion of the hepatitis B virus gene, coding for HBsAg, is cloned into yeast and the vaccine for hepatitis B is produced from cultures of this recombinant yeast strain according to methods developed in the Merck Research Laboratories.
  Two formulations are available:
   •  10 µg/1.0 mL formulation: each 1.0 mL dose contains 10 µg of hepatitis B surface antigen adsorbed onto approximately 0.5 mg of amorphous aluminum hydroxyphosphate;
   •  40 µg/1.0 mL formulation: each 1.0 mL dose contains 40 µg of hepatitis B surface antigen adsorbed onto approximately 0.5 mg of amorphous aluminum hydroxyphosphate;
  Thimerosal (mercury derivative) 1:20,000 (50 µg/mL) has been added only to the preservative-containing formulations. All preparations have been treated with formaldehyde prior to adsorption onto amorphous aluminum hydroxyphosphate. The vaccine is of the adw subtype.

As explained in   Exley, C. et al. (2010) The immunobiology of aluminium adjuvants: how do they really work? Trends in Immunology, 31:103-109:

The vaccine preparation is primarily micrometer-sized clusters of nano-sized primary particles of the aluminium salt with which the antigen is associated by adsorption and entrapment. The avidity with which the adjuvant associates with the antigen will depend upon multiple factors, including the form of aluminium salt (usually oxyhydroxide or hydroxyphosphate), the physico-chemical properties of the antigen (including its overall charge and molecular weight), the mode of preparation of the antigen-adjuvant complex (for example, ratio of adjuvant to antigen), and the final solution pH. The latter will usually be around neutral (pH 7.0 +/-0.5), and, along with the highly super-saturated state of the aluminium salt, this will ensure that the concentration of soluble aluminium in the vaccine preparation remains below ca 2 mM. Similarly, there will be a variable proportion of antigen, often <1% of the total antigen load, that is not associated directly with the adjuvant, and some of this ‘free’ antigen may also be in a complex with aluminium., what this means is that the protein antigen is not soluble in the vaccine, but rather is adsorbed and/or entrapped in the inorganic particulate material.

What this means is that the protein antigen is not soluble in the vaccine, but rather is adsorbed and/or entrapped in the inorganic particulate material. The antigen itself has of course already been extensively purified before being incorporated into the vaccine, so the task of purifying the antigen from the Recombivax vaccine is one of releasing it from the inorganic adjuvant. The obvious thing to try first would be to isolate the particulate material by centrifugation, and then attempt to release the antigen from this in a soluble form: things to try would be extremes of pH, high salt concentrations, and detergents. SDS-PAGE would be used to monitor how much was released by these treatments.
Now the example that I gave above (Recombivax HB) is fairly straightforward because it contains a single protein antigen. Compare this to Pentacel, given as first vaccination to babies in Canada (same source as before).

Act-HIB ® Reconstituted with QUADRACEL ®Haemophilus b Conjugate Vaccine (Tetanus Protein – Conjugate) Reconstituted with Component Pertussis Vaccine and Diphtheria and Tetanus Toxoids Adsorbed Combined with Inactivated Poliomyelitis Vaccine.
  Each single dose (approximately 0.5 mL) after reconstitution contains:
   •  purified polyribose ribitol phosphate capsular polysaccharide (PRP) of Haemophilus influenzae type b covalently bound to 20 µg of tetanus protein 10 µg
   •  pertussis toxoid (PT) 20 µg
   •  filamentous haemaglutinin (FHA) 20 µg
   •  fimbrial agglutinogens 2 + 3 (FIM) 5 µg
   •  pertactin (PRN) 3 µg
   •  diphtheria toxoid 15 Lf
   •  tetanus toxoid 5 Lf
   •  poliovirus type 1 (Mahoney) 40 D-antigen units
   •  poliovirus type 2 (MEF1) 8 D-antigen units
   •  poliovirus type 3 (Saukett) 32 D-antigen units
   •  aluminum phosphate 1.5 mg
   •  2-phenoxyethanol (not as a preservative) 0.6% v/v
   •  polysorbate 80 10 ppm (by calculation)
   •  bovine serum ≤50 ng
   •  trace amounts of formaldehyde
   •  trace amounts of polymyxin B and neomycin may be present from the cell growth medium

This vaccine is clearly much more complex, so in this case, once the desired antigen(s) were freed from the adjuvant there would be a need to use standard protein purification techniques to separate the various contaminants.
Finally it's worth pointing out that unless you have access to large amounts of vaccine, you are going to be starting with quite small amounts of antigen (see above) so it will probably be quite a challenging purification.


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What type of cell do you start with in Meiosis?
Okay, I was learning about mitosis and meiosis in school and had a question. I know in Mitosis you first start off with a Diploid (2N) cell and then end up with two daughter cells that are also Diploid. However, in Meiosis, I know you end up with four Haploid Cells (N), but what exactly do you start off with? Is it like a single egg makes four more eggs or something? Or does it start off with a Diploid Cell and then end up with the Haploids? If so, what exactly is the starting cell called?

Meiosis starts with a diploid cell and produces four haploid cells.  In animals, the starting diploid cell is usually called a germ cell and the surviving haploid cells become gametes (sperm and ova).  (In animals, the female mitotic sequence produces only one ovum; the other three haploid cells become "polar bodies".)
In other organisms such as plants, the starting diploid cell is typically not called a "germ cell" as it is not distinguished early in the organism's life.  Instead the starting cell can be any undifferentiated diploid cell that finds itself in the appropriate location (e.g. in a flower) at the appropriate time.

During mitosis a diploid cell (2n = two copies of each chromosome, one from each parent) replicates its DNA so that it now has four copies of each chromosome. Then it divides, each daughter cell receives two copies of each chromosome and is again 2n.
In meiosis a diploid cell (2n) replicates its DNA so that it now has four copies of each chromosome. Then it divides, each daughter cell receives two copies of each chromosome and is again 2n. Then each of these divides once more without replicating DNA so that there are now four cells each with one copy of each chromosome (1n).
You might be tempted to think of a diploid cell which has replicated its DNA as tetraploid, but this word is not normally used in this context, since this is a transient 4n state.
This is a very broad overview. Have a look at the Wikipedia entry for meiosis to get a more detailed view and extended terminology.
@mgkrebbs (in comments):
If we are considering the meiotic divisions that create gametes, then in spermatogenesis the cell which undergoes meiosis is a primary spermatocyte, and in oogenesis it is a primary oocyte. Primary spermatocytes and primary oocytes are both diploid cells which undergo DNA replication before entering meiosis I.

Unfortunately, this answer does not answer the main question, stated in the title as "What type of cell do you start with in Meiosis?" and in the last sentence of the question body as "what exactly is the starting cell called?".

Meiosis starts with a somatic (diploid) cell. To make a long story very, very short, this one cell undergoes cytokinesis twice. You end up with four haploid cells, called gametes or sex cells.

I just want to say that this I believe is incorrect. Meiosis indeed does start with a diploid cell, however, this is not a somatic one and is rather a gametocyte. I recommend that you refer to this website: https://www.azolifesciences.com/article/Differences-Between-Stem-Cells-and-Somatic-Cells.aspx# which explains this concept.


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How does tree resin capture arthropods?
In regards to a published paper of a spider about to make a meal out of a parasitic wasp (http://www.tandfonline.com/doi/abs/10.1080/08912963.2011.640399#.U1kSV14gVBU), it reminded me of a issue I've often contemplating for some time:
Isn't tree resin very slow moving, for instance maple sap has an extremely high viscosity and therefore how does the resin engulf both an arthropod, such as a spider, quick enough for it to not move away from the slowly moving amber?

I believe it is more of the fact that the organism gets stuck to the residual resin on the plant itself, and becomes encased and later fossilised in the amber.
From LiveScience.Com:

A host of bugs, fungus and other life forms have been found trapped in amber from the time of the dinosaurs.  Bugs can become encased in amber if, while alive, they get stuck in the resin.

Although plant resin is slow-moving, the bug stands to be encased in it if it is already stuck to the tree itself, as there is a large amount of resin on the surface of the plant.  If they are crawling over the plant, or land on the surface, they would become stuck and later encased. It would be similar with other organisms as well, as plants and other organisms have been discovered preserved in this way.

These fossils represent some of the earliest African fossil records for a variety of arthropods, including wasps, barklice, moths, beetles, a primitive ant, a rare insect called a zorapteran, and a sheet-web weaving spider. Parasitic fungi that lived on the resin-bearing trees were also found, as well as filaments of bacteria and the remains of flowering plants and ferns.


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What would kill you first water or cola?
After discussing this with some colleagues, I devised the theory that you could drink more coca-cola in a single sitting than you could water, without killing you.
Defining the volume it would take for one of the liquids to kill you as the 'x volume'.
Thus the hypothesis goes that the x volume for water would be lower than that of coke.
This is based on the notion that water would affect the body's water potential significantly more than the cola solution. For instance, the large volume of water would diffuse, via osmosis, into your blood and this would reduce the water potential of the blood, which would in turn diffuse into your cells which would in turn damage the micro environments and prevent proper enzymatic activity in all aspects of the cell cycle: which would have devastating affects on the brain function. Given enough water: something that can be read about here (water intoxication).
Coca-cola on the other hand which has an acidic pH -- though I'm not entirely sure of it's water potential -- would not have the same disturbance on somatic cells in the body due to the acids and sugars. However, although the large consumption of cola may have longer term effects: would the x volume of coca cola be higher than that of water?

What is the duration of a "single sitting"? There are many other additional factors. You may die of some other effects due to the cola consumption. Without additional details this question cannot be answered.

The LD 50 listed on the wikipedia page you link to is 90 mL/kg, which would be about 6 liters for a 68 kg (150 lb) person. This is consistent with at least one report, where someone died from drinking 7 liters of water in 1.5 hours.
The mechanism by which water kills people is by lowering the amount of ions (chiefly sodium) in the blood. A condition called hyponatremia.
Coke contains four relevant looking ingredients: Water, sugar, phosphoric acid, caffeine. Coke also has carbonic acid from the carbonation, but I'll assume we're either talking about uncarbonated Coke, or that the carbonation does not contribute to toxicity (perhaps a bad assumption).
Before worrying about whether the water will kill you, let's verify that the caffeine and sugar won't kill you first.
It seems unlikely that the caffeine in the coke would kill you before the hyponatremia. The concentration of caffeine in coke is about 0.1 mg/mL, and the LD50 is > 150 mg/kg, so for the same 68 kg person, it would take about 100 L of coke to get a lethal dose of caffeine.
The sugar in coke is more deadly, but still not as bad as pure water. There are about 0.11 g sugar per mL of coke. The LD50 of sucrose is apparently around 30 g/kg. So it would take about 2 kg of sucrose to kill our 68 kg person. That is about 18.5 L of Coke.
The concentration of phosphoric acid in Coke is about 5 mM which is about 0.5 mg/mL. The LD50 is about 1530 mg/kg. Which works out to about 212 L of Coke to kill by phosphoric acid.
Now that we've ruled out some other possibilities, lets get back to whether coke will kill you faster or slower via hyponatremia than pure water will.
Take another look at the the nutrition information for Coke. Notice that Coke actually contains some sodium, about 0.13 mg/mL in fact. A drink called "Powerade Isotonic"  which claims to have a proper electrolyte balance contains sodium at 0.28 mg/mL.
So given that (A) what kills you first from drinking too much water is hyponatremia. (B) Coca-cola contains a non-trivial (but still less than many electrolyte drinks) amount of sodium. and (C) other potentially toxic components of Coca-Cola, such as acid and caffeine, require much higher doses to be toxic. It seems reasonable to conclude that Coca-Cola has a lower acute toxicity than distilled water.
Caveats:
I did not consider osmolarity. There could be some effect here that I'm overlooking.
I did not consider the effects of carbonation (soluble carbonic acid).
For people with certain medical conditions, such as diabetes or caffeine sensitivity, Coca-Cola may be toxic at much lower doses than for other people.


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Studying changes in DNA for causes of cancer
First of all let me say that I'm not into Biology myself... but I have a question for those of you who are.
From what I've read, cancer is caused by 'faulty' DNA that behaves abnormally. Mutations can occur for various reasons, ranging from simple 'copying errors' to environmental factors.
I was just wondering whether current research has dealt with storing DNA of people or animals (e.g. rodents) and observing how it changed, especially for cases where it eventually resulted in cancer. Something along the lines of this, but I'd like to know what research has actually been done so far.

I tried to comment but what I wrote is too long, so here it is as an answer of sorts.
If I understand the question, you are asking: has anyone done a prospective study where they store the DNA of individuals and then later, when some of these individuals get cancer, have a look for mutations that are associated with that cancer. In fact this is done all of the time, but it isn't necessary to store any DNA because the cancer patients will have the normal sequence in all of their non cancerous tissues - only the cancer cells will have the relevant mutations. See here for a recent example of this type of study that made the news.
Your BBC link is to a story in which the genomes of people will be analysed to determine if there are genetic factors which predispose them to cancer (and other diseases), but these won't be the mutations that actually create the cancerous cells.

There is a tremendous amount of information relating to mutations of genes and how they produce cancer.  In fact, this is multi-billion area of research.
What is even more interesting, is the aneuploidy hypothesis of cancer, in which it is chromosomal abnormalities, rather than mutations in single genes, that lead to cancer.
I suggest reading about it, there was an article by Peter Deusberg in a 2007 Scientific American article.


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Melting point of a fatty acid?
What factors determine the melting point of a fatty acid?

Chain length
The number of methylene group
The ionized state of the fatty acid
Its degree of saponification
Its ability to alter the entropy of water

Are you looking for one answer of the 5, or are multiple answers possible? If it's the latter, then it's 1, 4, 5 from a quick recollection.

You'll want to wait for a full answer. All of the answers will affect the melting point to some degree, but whether it's a significant amount is another thing.

You might look at this question and answer which was posted to SE.Biology but moved to SE.Chemistry. Logically I would expect that your question will also be moved.

(1) Chain Length

Will definitely affect melting point, as this website explains pretty well:
"Melting point principle: as the molecular weight increases, the melting point increases."

(2) Number of Methylene groups.

This is another way of describing unsaturated from saturated fats. The more saturated a fat is, the straighter it is. Methylene groups cause kinks, which disrupts the Van der Waals forces along the rest of the carbon chain.
As such, from the link above again:
"On the other hand, the introduction of one or more double bonds in the hydrocarbon chain in unsaturated fatty acids results in one or more "bends" in the molecule. The geometry of the double bond is almost always a cis configuration in natural fatty acids. These molecules do not "stack" very well. The intermolecular interactions are much weaker than saturated molecules. As a result, the melting points are much lower for unsaturated fatty acids."

(3) Ionized state of the fatty acid.

This will have a very minor affect. The fatty acid generally has an unpaired ester (-ate at the end) which can have a negative charge. However, from the link above again:
"However, in fatty acids, the non-polar hydrocarbon chain gives the molecule a non- polar character."
So even if the ester had a charge, the negative character is miniscule compared to the intermolecular forces exerted by the non-polar tail. Particularly since the charge can distribute amongst the two oxygen molecules which are conjugated, reducing the reactivity further.

(4) Degree of saponification.

I'm not super-familiar with the degree of saponification, but from a quick overview of the process I'd say this wouldn't affect melting point - counter to my comment. The process of making soap involves only the acidic portion of the fatty-acid triglycerides. That portion of the macromolecule is going to be pretty much the same regardless of the fatty acid, so it will have nearly the same reactivity regardless of its chain length and conjugation.
What will not saponify are usually waxes - which are pretty much fully-saturated hydrocarbon chains with very few (if any) acidic sites. Parafin Wax, for instance, does not saponify, and has the formula ${C_{31}H_{64}}$.

(5) Ability to alter entropy of water.

Like the degree of saponification option above, the ability of a fatty acid to alter the entropy of water correlates to the number of reactive sites throughout the molecule. As-such, unsaturated fats (those with methylene groups) are going to be slightly more reactive as pi-bonds are more reactive than sigma bonds.
So, given that this answer relies on a previous option, it's probably better to go with the previous option.
Ultimately, if I were answering the question I'd choose 1, 2 since the rest either depend on those two or are miniscule. However, beware that it's your question to answer and not mine.


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Difference between "transcriptional activity" and "RNA expression"
I am working with a network object where the nodes are different events in molecular biology.
Specifically;
Catalytic activity of X,
RNA expression of X,
GTP-bound activity of X,
Kinase activity of X,
Oxidoreductase activity of X,
Phosphatase axtivity of X,
Transcriptional activity of X,
Phosphorylation at residue Y.
What is the difference between RNA expression and Transcriptional activity? And which is the one that an Affymetrix microarray is measuring?
eg.;
transcriptional activity of KLF2, transcriptional activity of ATF2 RNA expression of HSPA1A RNA, and expression of CYP1B1

I'm not familiar with what you're doing, but off the top of my head I'd say that the RNA Expression might be referring to everything post-nucleus in that the Introns are missing. The Transcriptase would show more activity because it would still Transcribe both Introns and Exons.

In your case, RNA expression and transcriptional activity probably differ in the stage of processing. Transcriptional activity refers to the binding and processive activity of RNA polymerase. There are different ways to measure this experimentally, but with a microarray you are measuring the amount of actual transcripts relative to the control array.
RNA expression usually refers to the amount of mature transcripts but is often used interchangeably with transcriptional activity. The distinction is made at the sample extraction stage and whether or not the RNA was selectively recovered using poly-A selection or other methods that isolate mature transcripts.
What your microarray will measure depends on the probe library constructed on the array and whether you are applying total RNA or selective RNA. Probes matching mature transcripts report for RNA expression. Probes matching immature or nascent transcripts can be used to measure transcriptional activity.
Careful probe design is required to distinguish between the different levels of processing.


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Gastro-intestinal physiology reference
I am a physicist but I have always wanted to understand how my digestion takes place in as much detail as possible. I have no idea about books or reference on the subject of Gastro-intestinal and digestive physiology. Can you help me?

are you asking about reference of some books based on it?

@agharehanabbas a reference :)

If you enjoy physics, Boron and Boulpaep text book of medical physiology is the book for you!

If you have no medical background at all, you will need a general text that teaches more than just digestive physiology. That is because you need to understand the function of other systems that have an influence over the digestive system (for example, the peripheral nervous system).
Here are a few good general references to get you started:

Physiology by Linda Costanzo, arguably the most synthetic. Extremely good, but I am unsure of its value for someone who has no medical background.
Vander's Human Physiology, arguably the simplest, used in first year of medical school.
Medical Physiology by  Walter F. Boron, arguably the most complex, I would not recommend it as a first try.

You can start by trying to read the digestive physiology chapters, and look up the knowledge you lack in other chapters.


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How many colors can colorblind people really see compared to normal color vision?
A person with normal vision, it seems, can see 7,000,000 colors.
How many can a colorblind person see?
I'm not as much interested in the exact number, or the technicalities that might exist due to different types of color blindness (let's just consider the most prevalent colorblindness, which is red-green I think) but I'm more interested in how low or what percentage would that number be w.r.t. to the normal vision? Is it like half, or only 10%, or much closer like 90%?
This is sort of a follow up of this question. If 3 cone cells can see between 7,000,000 colors, how many would 2 see?


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What would happen if you slowly crushed a live brain?
In a hypothetical scenario, if you cut open a person's skull to show the live brain, and then you slowly start to crush it..
At what point would the person loose consciousness?
What would the person be feeling all this time?
Would it cause pain?

I'm voting to close this question as off-topic because it is tasteless and stupid.

just watch a film studying TNT shrapnel inclusions of the brain, javelin skull perforations, and stories of the numerous suicides attempts involving a few nail gun shots to both sides of the head. In some scenarios people have survived with 8 nail gun perforations into their brains. The wording of your question is not at all scientific by the way. It is worded like a nazi experimentor or a horror movie script.

It depends on what part of the brain you are "crushing."
When we do brain surgery we often do exactly what you describe. That is, we open the skull and often remove part of the brain. However, in our case usually the part we are removing is diseased or malfunctioning to begin with.
There are areas of the brain that are known as eloquent and those that are considered "not eloquent." This is an overly simplistic but educationally instructive way to classify things. Eloquent brain regions are those regions that when disturbed will cause an obvious and devastating neurological injury. Examples are primary motor/sensory cortex, broca's area, wernicke's area etc. Noneloquent areas are those that can be damaged or resected and the sequelae are less obvious. For example, you can remove quite a bit of frontal lobe before you notice a problem. However, an appropriate and sensitive behavioral test/instrument may still pick up the deficit.
Damage to the brainstem and thalamus is more devastating and even small injury to this area can cause major deficits and changes in the level of consciousness. Injury to different levels of the brainstem produces different level of consciousness. Again, it really depends on the precise location and extent of injury and there is no single answer to your question.
As the brain itself has no pain receptors the patient would not really feel much pain even if you caused major deficits. However, again it depends on the location. You could theoretically irritate thalamic sensory regions and cause chronic pain syndromes but your lesion would have to be pretty precise.

It seems there's way too many variables here.  Crushing can occur in a number of ways, leading to different primary damage in different regions first and different people have a different level of system failure thresholds.
Technically, there are no pain sensors on the brain, so you wouldn't feel any pain in the classical sense.  However, it's hard to determine how you would affect the pain interpretation circuits (again, "crushing" can occur a number of different ways); you could inadvertently cause pain signals.
Losing consciousness would also depend on when what region of brian is crushed.  And how it's crushed.  Most of our higher processing regions associated with consciousness are on the very outer surface of our brain.  In one scenario, if it just gets compressed, and damage tend to accumulate in the center of the brain first, it would be a different outcome than if it was some kind of shear crushing force that damaged outer brian first.


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To what extent is eating and nutrition important in recovery from minor illness like viral fever?
I'm guessing it is important,  but just to be a little more precise,

What would be the maximum amount of calories above which it is just a waste (or even harmful)
How much does the metabolism raise during the illness?
More carbs or more proteins? (or less?)

During infection a body has to produce absolute masses of immune cells, raise your temperature via increased metabolism, repair tissue damage, migrate components of the immune system including proteins and cells, produce masses of antibodies and probably lot's more.
A lot of protein components need to be made which require protein synthesis and energy. Metabolism of fats and carbs goes up too. Also, importantly, vitamins are a key part of the immune system serving to migrate the immune system  such as vitamin D aids migration of cells to the skin. Vitamin C is required for collagen synthesis in repair. Minerals are required for the metalloenzymes. However your dependency on each component depends on the type of infection, your immune response, your natural state including your reserves of everything.
How important is it? Very. I've listed what the things are needed for which gives an indication of how important they are. If starved, the body will do the best it can by focussing its resources on the thing it deems most important.


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Difference between medicinal caffeine and regular caffeine
There are some OTC paracetamol tablets, some with caffeine. Is this caffeine the same as the regular caffeine (found in a coffee)? Does it perform better than it in any way?

From a pharmacology point of view, there is no difference between caffeine in caffeine pills and in a cup of coffee. It doesn't matter, how a chemical substance (in this case caffeine) is made, the effect of the substance is the same. What can make a difference is the presence of secondary plant ingredients.
For pure caffeine there are two possible sources: By chemical synthesis ("A Novel Method of Caffeine Synthesis from Uracil") and as a byproduct of the decaffeination process when producing decaffeinated coffee.
What is also different is the amount of caffeine. While pills contain standardized amounts of caffeine, the amount for caffeine in brewed coffee varies between different kinds of coffee beans as well as for different brewing methods. See this figure (from here):


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How do cells figure out the big-picture shape?
I'm wondering what makes cells to divide (and stop) in such a way that they make our hands the shape that our hands are...

with hands, there is cell division initially to give rise to a palm bud (fingers not separate). Subsequently, the cells between the fingers (digits) die by apoptosis to give hand its shape.

That is exactly what is studied in developmental biology, which is a huge field of research.

Hands are complicated and the genetic machinery behind their shape doubly so.
It's easier to figure out worm segments first, and then work up from there. An egg has head/tail information encoded in it even before fertilization: see here
You can imagine the first or second cell division would give a 'head' cell with higher concentration of head polarity transcription factors. These transcription factors switch on other regulatory genes, and the complexity works upwards from there. For more information about how worms and other segmented animals work out what goes where see Hox genes. The sad truth is that most of how this is done is unknown or not well understood.


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Is there a medical condition in which you can't cut your hair?
Just curious, does there exist a medical condition in which a patient is advised not to or simply cannot cut their (head) hair?

Hair is not alive, so there shouldn't be any problems with that.

Patients on blood thinners are advised to avoid cutting risks, which would suggest "no shaving", but presumably depilation by other means would not have that risk.

What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Alopecia and balding, these individual experience hair loss, thus nothing to cut


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A good textbook on Neuroscience
I want to start learning Neuroscience. Can someone give me an advice about a nice textbook for beginners? I'm particularly interested in the application of Neuroscience in programming and AI development. Thanks in advance.

This is too open-ended.  As an aside, it sounds more like you are interested in artificial neural networks, anyway.

Artificial and biological neural network share only the name... Understanding, say, how a neuron fires an action potential, would not really give you any advantage if you are just interested in AI. On the other hand, there are tons of interesting computational neuroscience problems, which instead require deep understanding of biological processes, but are not necessarily related to AI.

"Principles of Neural Science" by Kandel and Schwartz. That was my introductory textbook for neuroscience at Berkeley.

If you are interested in computational neuroscience, I recommend Dayan and Abbott's book: http://www.amazon.com/gp/aw/d/0262541858/ref=redir_mdp_mobile/181-1988504-8834745. This is not a book on neuroscience, not AI, although this particular book has more math than the other introductory neuroscience textbooks I've seen.


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Is there any documented case in which floating substances led to the introduction of a new species?
Floating substances in the marine or freshwater environment often carry hitch hiking organisms. It is argued that many species may use this dispersal vector to reach new habitats, however to my knowledge there is no hard evidence / no documented case. This may be because of the difficulty to associate an established species with a certain vector of introduction.
By floating substances I refer to natural floating substances such as detached algae, trees or pumice and those of anthropogenic origin such as litter items, detached buoys, etc. (in whatever aquatic environment: sea, lakes, rivers)
Any help to find a reference / documented case study is very welcome!

But not including actual sea-going vessels?

Right, no vessels. Their dispersal capacity, especially considering vessels with ballast tanks, is not readily comparable to other floating "substances" and IMHO better understood.

As far as I know, this is dicussed for the distribution of geckos through the pacific. They are common on quite a number of islands.

im pretty sure it happens all the time - geologically speaking.  @Chris could cite 'Voyage of the Beagle' for the galapagos chapters really

There is a number of reported cases of marine species reaching new locations through "hitchhiking" in recent times. However, it seems harder to find reports of species actually becoming established in a new location through this.
The following articles describe examples of species transported with ocean debris:
In an early study on the dispersal of plastic pellets (3), it was suggested that pellets encrusted with the bryozoan Membranipora tuberculata was transported to New Zealand across the Tasman Sea from Australia. Barring one exception, this was the first time the species was observed in New Zealand waters.
Appendix A of a later article by the same author (1) contains 13 examples of species transported by sea (not necessarily through debris, or invasive), including the previous example. Of it, the author writes that

Later, L. M. Stevens (1992, unpublished data) was to report that [Membranipora tuberculata]
  was abundant on both eastern and western shores around northernmost
  New Zealand.

Thus, this is possibly a case of a species transported on floating debris and subsequently becoming established in a new habitat.
Jose Derraik also deals with the topic in a review (4):

Plastics floating at sea may acquire a fauna of various encrusting
  organisms such as bacteria, diatoms, algae, barnacles, hydroids and
  tunicates (Carpenter et al., 1972; Carpenter and Smith, 1972; Minchin,
  1996; Clark, 1997). The bryozoan Membranipora tuberculata, for
  instance, is believed to have crossed the Tasman Sea, from Australia
  to New Zealand, encrusted on plastic pellets (Gregory, 1978). The same
  species together with another bryozoan (Electra tenella) were found on
  plastics washed ashore on the Florida coast, USA, and they seem to be
  increasingtheir abundance in the region by driftingon plastic debris
  from the Caribbean area (Winston, 1982; Winston et al., 1997). Minchin
  (1996) also describes barnacles that crossed the North Atlantic Ocean
  attached to plastic debris. Drift plastics can therefore increase the
  range of certain marine organisms or introduce species into an
  environment where they were previously absent (Winston, 1982).

Finally, the book Marine Pollution: New Research (2) contains the following passage which ends with the observation that conclusive proof is difficult to obtain:

Drift plastics are known to have introduced exotic marine species to
  several areas (Winston et al., 1997; Deraik, 2002). Winston et al.
  (1997) reported that the non-indegenous oyster Lopha cristagalli was
  fond on plastics wshed ashore in southern New Zealand, and that the
  exotic bryozoan Thalamoperella evelinae was found on plastics washed
  ashore in Florida. Barnes and Milnder (2005) fond the exotic barnacle
  Elminius modestus on plastic debris in the Shetland Islands (Atlantic
  Ocean). The bryozoaen Membranipora tuberculate is believed to have
  crossed the Tasman Sea from Australia to New Zealand rafting on
  plastic pellets (Gregory, 1978). M Tuberculate and the bryozan Electra
  tenella seem to be increasing their abundance on the Florida coast by
  drifting on plastic debris from the Caribbean sea (Winston, 1982
  Winston et al, 1997). Maso et al. (2003) (...) However, attributing a
  marine biological invasion to floating marine debris and not to other
  mechanisms is very difficult in most cases, and available data are
  generally insufficient.


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Vitamin and mineral contents of common fruits
I'm looking for nutritional data, mostly vitamin and mineral contents of common fruits, such as apples, bananas, oranges, kiwis etc.
Are there scientific (published and peer-reviewed) sources that list or compare those? I spent an hour on Google Scholar but most of the sources there discuss only a small aspect (e.g. vitamin C content) or compare different states of fruits (frozen, fresh, canned). I'm not well educated in human nutritional aspects so I may overlook this one keyword to search for.
I'm aware of tables on the Internet discussing these aspects but I need a solid scientific basis.

Found a source that seems somewhat reliable: http://ndb.nal.usda.gov/

Do you want to answer the question yourself (which is perfectly ok), or shall I do this?

I know two databases for such information: The "National Nutrient Database for Standard Reference" (reference 1) from the United States Department of Agriculture (which you list yourself) and the "Nutrition Data" (reference 2) Database. Both allow searching for specific foods and give the values back. I like the second more, since it gives you the complete output it has and you don't have to choose three single nutrients like for the USDA database.
References:

USDA National Nutrient Database for Standard Reference
Nutrition Data


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How well do Eppendorf cups seal?
I am considering to send some samples overseas in Eppendorf cups. They are the standard plastic cups of 1 to 2 mL capacity. Of course they may tip over during their journey and I'd like to know how well they seal or if there is any danger that anything leaks from inside the cup. The samples are fixed in alcohol if that is relevant.

Is this the proper StackExchange site to asks these questions?

Can you get some tubes with screw lids as these are used for freezing cells? They are tight.

@Stockfisch Why wouldn't questions about laboratory technique be welcome here? I'm not aware of a StackExchange designated for lab technique questions, though I often feel like one should exist. But that's a discussion for meta.

I have never had  problem with tubes leaking. However, if you are worried about them getting somehow popped open in transit, you might consider wrapping the lid in parafilm. Alternately, there are lid locks that you could use like these.
@Chris has a good point about screw-cap tubes, they could also work, and are probably a lot sturdier, in case of actual damage.

The screw cap vials would probably also benefit from parafilm. If you're extra paranoid, put each vial in a 50mL Falcon Tube to catch anything that leaks, then wrap the Falcon Tube in parafilm too.