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Are descriptive statistics sometimes more useful than tests of significance?
How does the biology community currently feel with regards to publishing descriptive and effect size statistics rather than significance stats?  Almost every journal article I read in the cell biology field almost always reports things like P values and stats tests to report statistical significance, but should effect sizes be more important to a biologist?  Do we even care if something is statistically significant if the effect size is negligible?  Rather than crunch for significance, could one get away with showing things like confidence intervals, eta^2, Cohen's d, and r values instead over P values?  P values tell you the odds that if you assume the null hypothesis is true, then the observation you're making are only 5%(assuming of course P<0.05).  However, this can lead to the logical fallacy as noted by Aristotle--theory A predicts that changing X will cause Y.  An experimenter thus performs experiments to manipulate X and sees changes in Y, therefore he/she concludes theory A is supported, which is however completely wrong.  Theories B, C, D, E....... could all also predict that X changes Y and may even be better at it.  Even if you conclude that your findings "support" theory A, it's still weak because you haven't ruled out all of the other possibilities.
So in order to avoid statistical significance relative to null hypothesis that has all sorts of pitfalls, can one just use descriptive and effect size statistics just as effectively, if not more so?

I wonder how much of this is because biologists have been taught statistical significance and haven't been taught to use effect size. In my introductory stats class in college, we never got beyond linear regression (yes, it was sad, but at least I learned R), and that was more stats than most people knew. I learned about effect size simply because of a well-informed PI whose background was not in biology. I, personally, would favor the use of descriptive and effect size statistics in combination with significance statistics, i.e. these are significantly different, by this much.

Agree with @dd3. You can try and talk about effect size and such, but then when the infamous third reviewer whines about p values you gotta play the game... To be honest most biologists I know (many of whom are very good at biology, nothing to say there) only have a very basic -and often slightly wrong- understanding of statistics. I can tell you I always have a hard time convincing people to use things like generalized mixed models or such. Most people will just say: I'll do a t-test or an ANOVA instead...

@nico: Agreed on all points. I would also agree that I am one of those people...which is why I visit Cross Validated.

On a related note: http://xkcd.com/882/

@GPI For a better answer this should really be on http://stats.stackexchange.com/ - you are asking biologists  when you could be asking statisticians, generally they know more about stats than us biologists! Personally I think each case is different so this question is also a bit difficult to answer, but my approach tends to be: do the stats, report the statistical significance and some descriptive statistics, but discuss the scientific significance - stat & sci significance are not perfectly correlated (p>0.005) ;)

(just because I feel it is better suited to cross validated it does not mean I would close this question - as I said biologists would probably ask this question a lot themselves - but could you place it on cross validated and put the link on here so we can find it?) @GPI

@dd3: well, but that just means that you DO want to understand what is the correct way of applying statistics to biological problems. I do not understand when people want to stay stuck with their t-test because "the rest is too difficult I won't understand it anyway". I am not a statistician either, but if I use a tool I want to know exactly what it gives me and how to use it correctly.

@Alan Boyd: even better http://www.wired.com/wiredscience/2009/09/fmrisalmon/

I think this is a valid question to as Biology because the standards of publication are different between fields of study. I'm sure any statistician will have problems with biological literature. You may have found an important, and biological effect which you can describe qualitatively. When it comes time to publish, if you cannot show the different quantitatively (and likely with a stats test), you limit yourself to publishing in a lower-tier journal.

I'm not a statistician, but I think the comments have got it right.  There is never a reason to omit P values, statistical power or some other measure that you have done something that is not a random outcome.
For the sake of reference lets define the terms you reference:
Eta squared is a ratio of the variances of two sets of measurements
Cohen's d is a measure of the difference between two means.
R value or Pearson Correlation describes the linearity of two numbers, usually one of them being a measurement and the second being an experimental variable.
These numbers as you say are descriptive, but they could be created by throwing coins and writing them up.  With small numbers of measurements, and a large enough range of possibilities, its possible to get terribly large numbers here.
Biology, medicine, social science and economics are really susceptible to this.  You go into the field and measure butterfly wings or do surveys of people's opinions, or try to guess who is going to win the election and its quite expensive to do more measurements.
If you are measuring something hard to determine because accuracy is important such as a close election race or that is really complicated such as which genes convey a susceptibility to type 2 diabetes (a problem which remains unsolved because so many genes play a role) you need large numbers of responses.  Yet each study that comes out gets some answer, but if you want to believe it these numbers should convince no one in most cases.
Microarray data and RNASeq data analysis for instance often suffer from this problem.  The measurements are all statistically significant but each one costs hundreds or even thousands of dollars.  Most experiments do a minimal three measurements to understand the variance in each measurement and then do 2 to 8 actual measurements.  That's not going to so revealing when working with a system with thousands of genes in it. one bad sample with slightly different culture conditions can ruin the experiment.
Our butterfly biologist may measure 100 butterflies and stop when the P values are 0.05 or 0.001 - its a lot of work camping out and setting nets.  The truth is that 5% is a number that can happen at random a lot.  Even a 0.1% error will happen in one in ten such experiments.  In thousands of experiments published that means that 10% of them have a mistake.  Not so great.
It gets worse though - not only significance, but bias needs consideration.  Because biologists and most other scientists don't understand statistics, the assumptions that we use when we calculate a P value are often inappropriate and don't give honest estimates of the chance that this is a random phenomenon.
If good looking result is chosen specifically to show to prove the point or some data are thrown out because they simply don't look good, or if a hypothesis is chosen in a biased way simply to fit an unreliable set of data.
Or the statistical assumptions of the calculation might simply be so inappropriate that to really cite them is an out and out lie. An everyday example of this is to do a BLAST search.  The E-value calculations, if read as a P value would be wrong, even though they are mathematically correct - two strings that show a 10% identity will have a small E value - 10^-8 for instance, but this is only the chance two strings of these lengths will have so many letters in common.  Anyone who plays with BLAST will quickly throw out anything that has less than 30% identity unless they are desperate, even though the E-values are infinitesimal.
John Ioannidis has made this subject his focus and has published widely on this topic.  A good place to start is his commentary "Why Most Published Research Findings Are False".

There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias. In this essay, I discuss the implications of these problems for the conduct and interpretation of research.

Very interesting response thank you.  Does anyone in the community use Bayesian statistics rather than classical statistics as well to analyze their data?  My understanding is that a Bayesian analysis will actually tell you the probability that YOUR hypothesis is correct based on data.  Are journals accepting of Bayesian stats?  It seems like a Bayesian analysis would also address the questions of false positives/negatives quite effectively.

There is lots of bioinformatics work with bayesian statistics. Use of Bayes rule by itself is not free us from the need to estimate statistical power of the probabilities used in the analysis though...

Of course reading BLAST e-values as p-values is wrong. e-values give the number of hits of this quality you would expect to find by chance, given the size of the hit and the size of the database (and the composition of the sequences in question, low complexity etc). They do not give the probability of finding such a hit. They are not even similar to p-values and should never be confused.

so you are saying they are never confused?  they are probabilities even though they are not p values. I'm open to other examples that can be used, but couldn't come up with one while writing.


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What determines the perceived pitch (frequency) of tinnitus?
I noticed that every time I suffer temporary tinnitus after going to a very loud concert, the frequency I perceive is identical. I'd put it somewhere around 17 kHz, but it's difficult to pin down with any real accuracy due to the dulling effect it has on external sound sources.
Is this frequency constant across all humans? If not, what determines the frequency? Note that I'm only interested in tinnitus caused by exposure to loud sounds, not other types of tinnitus such as idiopathic tinnitus or tinnitus caused as a side-effect of medication.

This question has been asked (and answered) on CogSci.SE as well: What's the Frequency of the ringing in my ear?

@Jeff Interesting, but rather indigestible and verbose. Would be nice to get an answer that explains things in simpler terms.

Is this frequency constant across all humans? No. If not what determines the frequency? In part, experience. You may consider leafing through some of the references if you find the answer insufficient.

Short answer
Perceived tinnitus pitch tends to resemble the frequency content of the loud sound that induced the tinnitus.
Background
Solid, laboratory-controlled studies to the perceived pitch of temporary, noise-induced tinnitus ("ringing in the ears") are ethically questionable, because researchers have to deliberately expose study subjects to potentially damaging loud sounds. Therefore, data on temporary noise-induced tinnitus are scarce and confined to a small handful of studies done in the 1960's (Henry & Meikle, 2000).
In one of these studies (Atherly et al., 1968) the authors exposed the study subjects to loud acoustic stimuli of various pure tones. The subjects reported to experience tinnitus pitched within a certain frequency band around the tonal stimuli received. The stimulus frequency and perceived pitch approached a 1:1 relationship, such that the tinnitus pitch was e.g. 4 kHz when the noise frequency was 4 kHz. Between-subject variability was, however, considerable. For example, at a stimulus of 6 kHz, the range of perceived pitch was 4-9 kHz.
The other study I found based on the review by Henry & Meikle (2000) showed that the perceived tinnitus pitch increased when the frequency of the loud tonal stimulus or frequency content of broadband noise increased (Loeb & Smith, 1967). Basically this confirms the data from Atherly et al. (1968). However, the perceived pitch did not coincide with the stimulus frequencies, and there was considerable variability between subjects. For example, some subjects reported multiple frequencies in their tinnitus, some reported a hissing tinnitus, while others did not develop any tinnitus at all (Loeb & Smith, 1967).
In all, your suggested perceived tinnitus pitch of 17 kHz is unexpected, given that noise-induced hearing loss (by loud music exposure etc.) typically results in a 4-kHz notch in the audiogram where hearing loss is greatest. Hence, tinnitus would be expected to occur around this frequency as well. But again, variability is very high and it may well be possible it is higher pitched in your case. Also note that 17 kHz is very high and near the upper audible frequency limit for humans (e.g., the sound an old CRT screen makes, i.e., hardly perceivable for many adults).
Most research on tinnitus has been done regarding patients with chronic tinnitus complaints that suffer from sensorineural hearing loss (i.e., damage to the hair cells in the cochlea). Typically, the perceived tinnitus pitch in this group is associated with their hearing loss. In other words, the pitch of the tinnitus generally matches a frequency range within the region of frequency loss (Eggermont & Roberts, 2004).
References
- Atherly et al., JASA 1968;44:1503-6
- Eggermont & Roberts, Trends Neurosci 2004;27:676-82
- Henry & Meikle, J Am Acad Audiol 2000;11:138-55
- Loeb & Smith, JASA 1967;42:453-5
Further reading
- What's the Frequency of the ringing in my ear?
- Can humans perceive sounds above 20 kHz?

Fantastic answer. Well sourced, too. I had all but forgotten about this question, so I'm glad you happened upon it. Regarding the 17kHz figure, I just ran a few pure tones (sine, saw) through my headphones and would say 14-15kHz is a more accurate ballpark.

@Polynomial - I never expected this late answer to be accepted :D Thanks :) 14-15 kHz sounds more plausible, but still very high. But possible, given the variability. It is a high pitched peep?

Given your comment as to why you asked this question - I am a bit afraid it is even more verbose than the related one at CogSci :) But I hope the 'Short answer' solved this somewhat

It's much more readable as prose, in my opinion. The other answer just seemed to be some snippets without context. And yes, the sound is very high, like a high-pitch squeal. I'm lucky enough to have retained my auditory sensitivity up to about 18kHz, despite the damage I've no doubt done at concerts, which may explain why I experience a higher pitch squeak.

Sounds all very reasonable, although noise-induced hearing loss typically results in a 4-kHz notch, well below the high frequencies. http://www.aafp.org/afp/2000/0501/p2749.html

I added these considerations in the answer - thanks for the addition :)

Good point. I hadn't considered that the hearing loss range was independent of the perceived frequency of the tinnitus squeal.

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Why do sneezes come in pairs or more?
I very rarely sneeze just once, usually there's two coming in a row, and I've noticed the same thing in other people and even in animals.  Is there any reason for this?

The very simple answer is that the causal factor or trigger hasn't disappeared after the first sneeze. Sneezing is a reflex, partially autonomous, to clear the nasal cavity of particles that don't belong there. As long as the trigger is not removed, the reflex is repeated.
This is also one of the reasons that allergies that cause sneezing, such as hay fever, continue as long as the factor causing the allergy is present.

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Current state of direct RNA sequencing
I had a colleague ask me recently whether mRNAs could be sequenced directly. I found this Nature paper[1] published by Helicos in 2009, in which they describe their developments in the area. It's been several years since this was published, and yet RNAseq and most other transcriptomic analysis is still done by first reverse transcribing RNA into complementary DNA.
What is the current state of RNA sequencing? Has Helicos failed to deliver on their technology? Have any other platforms risen to the challenge (or attempted to do so)? Or is the technology successfully in production and still simply overshadowed by the wide adoption of traditional cDNA-based sequencing methods?

Ozsolak F, Platt AR, Jones DR, Reifenberger JG, Sass LE, McInerney P, Thompson JF,  Bowers J, Jarosz M, Milos PM. 2009. Direct RNA sequencing. Nature, 461, 814-818, doi:10.1038/nature08390.

Helicos stopped shipping reagents around 2010-2011, as they couldn't compete with Illumina. For now it seems that reverse transcription -> Illumina-sequenced cDNA is so much cheaper than any other option, that's the method that is dominant.
Oxford Nanopore has discussed direct RNA profiling, but unfortunately their first product still hasn't shipped (for DNA or otherwise), and they haven't even released data, it may be a little while longer.

There was a paper that just came out about in situ RNA seq, but at the moment the limit of the sequence obtained is an underwhelming 4 bp. Still, its a cool technique and if it is advanced it could be useful in single cell RNA-seq, without the need of amplification or library prep
http://www.ncbi.nlm.nih.gov/pubmed/23852452


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Recombination-based vs. Sequence-based genetic mapping
Now that sequencing is becoming increasingly cheap, what is the value of recombination-based genetic mapping against the sequence-based genetic mapping?
I think that in the past recombination-based genetic maps were used as blueprints for sequencing projects. But since now the entire genome can be sequenced pretty cheaply both in time and money, what is the unique value of recombination-based genetic mapping?
One thing that comes to mind but I am not very sure. It might be suitable for mapping novel phenotypic markers e.g., unmapped diseases.

A couple of months ago I listened to a plant physiologist who strongly recommended recombination-based mapping over sequencing based mapping. The main reason he gave was the error-rate of 2nd generation sequencing. The error rate on Illumina platforms are about 1 % if I recall. In a small genome like that of Arabidopsis thaliana (157 Mbp) that accounts for over 1 million sequencing errors. That can of course be reduced having a proper sequencing depth and using the consensus sequence. But it can still cause problems if you're tracking a phenotype caused by an SNV. In plants like A. thaliana where back crossing can be used to create homozygous plants, recombination-based techniques can be particularily effective.
But he was talking from a plant physiologist's view when working with A. thaliana as a model organism. When working with humans which always are heterozygous, can't be back-crossed, don't have a generation time of six weeks and where samples sizes will probably be small I imagine that the situation is different. The classic geneticists' working with human diseases that I have talked have expressed fear that their work will soon be obsolete due to falling sequencing prices and growing sequence data collections.


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Is Hypericum Perforatum (St. John's wort) a C3 or C4 plant?
I've been curious as to which photosynthetic cycle St. John's wort uses to synthesise glucose and more complex carbohydrates. I know it probably won't be the crassulacean acid metabolism (CAM) cycle seeing how that applies mostly to plants that require a limited amount of water as opposed to St. John's wort which tends to prefer moisture. I suspect the answer to my question will be C3 seeing how they dominate in the plant kingdom and I know that St. John's wort requires relatively cool climates to grow successfully -- a trait characteristic of C3 plants seeing how high temperatures tend to cause excessive and wasteful photorespiration.

It's C3, according to the Illinois plant information network.  (See CO₂ fixation on this page.) This is the best I could find.


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What part of the cactus photosynthesizes?
In general, plants photosynthesize through their leaves and, to a much lesser extent, through their stems. Cacti, however, have no visible leaves, but instead spines. In what part of the cactus does the photosynthesis take place?

Since photosynthesis is correlated with chlorophyll, I'm guessing the green part.

In wiki there is a good answer for your question http://en.wikipedia.org/wiki/Cactus#Leaves
In plants photosynthesis takes place in chloroplasts. Chloroplasts may be in the cells of fruits, stems, but most of all in leaves. In some succulents (such as cacti), the main photosynthetic activity is associated with a stem.


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Is there an animal which, when eaten by other animal, poisons the predator and gets out of it's stomach?
It was a question in one competition, but it remained unanswered and i am curious about an answer.
There was a hint: American bullfrog
but i can not find any example of this behaviour on the web.

Close is the hagfish which turns the water around it into a choking slime when it gets attacked. In this video there are a bunch of predators that almost swallow the hagfish, and then spit them out.

The closest I can think of with that hint is a Middle Eastern beetle that hunts frogs and other amphibians:

In almost 400 face-offs, the amphibians only managed to get the larvae in their mouths seven times. Even then, they soon spat out the larvae, which quickly turned on them (first video below). One toad even managed to swallow a larva, which moved inside its stomach for two hours. For some reason, the toad eventually regurgitated its catch, and the larva, apparently unharmed, killed and ate the animal that had just eaten it (second video below).

However, it's only a pseudo-fit to the clue. The beetle doesn't hunt American bullfrogs, but ones native to its area of the world.

I think your clue probably leads to this video, which shows a rough-skinned newt (Taricha granulosa) consumed by a bullfrog (Rana catesbeiana). The frog then dies and the newt exhumes itself.
This is probably less likely in most settings since selection would quickly strike a balance between the prey's defensive toxin and the predator's immunity (for instance).  This is probably more likely to occur in invasion scenarios wherein the predator is naive to the prey defense (for example).

YES:
The rough skinned newt is very poisonous and can kill frogs and climb out of them. using a cocktail of heart stopping, paralyzing toxins, it can kill a human too.
http://video.nationalgeographic.com/video/weirdest-newt
Some frogs can make their predator vomit without killing them:
http://www.cairnspost.com.au/free-from-the-jaws-of-death-frog-escapes-snakes-stomach-after-being-regurgitated/news-story/861879b553964ec75866dd6ae354a5bd
And the Epomis Larvea make a frog attack them and then bite  it on the head, poison it and eat it, probably alive. https://www.youtube.com/watch?v=0y1FPm5WNVc
Some beetles can literally chew their way out of a venus fly trap using their mandibles, although perhaps that's less common in the wild. https://i.stack.imgur.com/lpY63.jpg ... other pages on that topic http://www.flytrapcare.com/phpBB3/holes-in-my-plants-t28144.html http://www.flytrapcare.com/phpBB3/earwigs-giving-my-plants-problems-t6041.html
this is the beetle that i confusedly watch eat its way completely out of the plant. they don't do that on tv! it took 2 days to escape.
http://www.naturespot.org.uk/species/common-red-soldier-beetle

I hadn't thought about this situation in plant carnivores, but that is an interesting consideration. Can you please add references for your last two statements?

ok i added some references.

Thanks @comprehensible That toad video is pretty incredible! I don't mean to be pedantic, but the photo of the fly trap isn't really evidence of your claim. Is there a reference that shows this happens and that it only happens outside the plant's natural range?

It's possible that a venus fly trap can get chewed by a beetle/ant within it's original habitat. What i meant to say is that... when i was a kid I had a venus fly trap once and gave it a common small beetle from the garden, because it had to eat something. it was a small beetle and the beetle completely ate a hole in the plant and managed to escape. It was a common red soldier beetle. ill add the references. I just thought it was fun info about the venus fly trap, difficult to know for sure about behaviour in the wild. thanks


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Zombie Ant Fungus?
Ophiocordyceps unilateralis is a parasitoidal fungus that alters the behavior of the infected.
Source: Wiki page.
How is the fungus able to alter the behavior of the infected to such specfic commands?
Does the fungus tap into the electrical signals of the brain directly or does it release some kind of hormone to alter the behavior?

Cool side note from the wiki page: "O. unilateralis has been known to destroy entire ant colonies. In response, ants have evolved the ability to sense that a member of the colony is infected; healthy ants will carry the dying one far away from the colony in order to avoid fungal spore exposure."

The fungus releases toxins, but how exactly this alters behavior is unclear.
You can read more here.  Pathogen manipulation of host behavior appears to have evolved a long time ago, and cordyceps is not the only pathogen that acts like this.

yup - its more likely to be mediated entirely by biochemical/chemical signals in the ant's body, possibly targeted to the brain, but possibly not.  this is one of the most interesting questions in biology today that is not cracked.  Anyone read "Parasite Rex?"


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Cereal Alpha and Beta Amylase temperature range and reaction rate
This question is motivated by a practical application in bread making.
While it is well known which are the optimal (highest reaction rate) temperatures for both alpha and beta amylase, I am not able to find any precise information concerning reaction rate as a function of temperature.

How does alpha and beta amylase activity change when temperature decreases?
At which temperatures does their activity stop?


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What is the minimum population size that Hardy-Weinberg calculations can be applied to?
I'm trying to find out if a particular allele is in Hardy-Weinberg disequilibrium, but the data is poor. What's the minimum population number that you can use to get any sort of respectable conclusion?
I've heard it's 5 individuals minimum for each genotype but can't find a source on that.

You can use power analysis to work out answers depending on the specifics of your data. The things you need to consider are:

The power of the test. This is the probability that the test will
fail to reject the null hypothesis even if in truth it is false
(Type II error). If the population is not in equilibrium, what is
the probability that the test will fail to detect this? This will largely depend on the costs of a Type II error. If the experiment is expensive in terms of time/money/animals used etc. you would want to make sure it will give a sold answer at the end.
The significance level. 0.05 is commonly used. The probability that
the null hypothesis is rejected even though it is true (Type I
error). If the population is in equilibrium, what is the probability
that the test will erroneously say it is in disequilibrium.
The degrees of freedom. The number of alleles.
The effect size. This is how far away from equilibrium you expect
your samples to be. The largest effect size would be extinction of
one allele. However, if two alleles are in a ratio of 100:101 across
the full population, this is a small effect size.

For the Pearson's Chi-squared test we can use (in R)
library(pwr)
pwr.chisq.test(w = 0.3, N = 40, df = 4, sig.level = 0.05 )

A rough guide for effect size (w) is 0.1, 0.3, and 0.5 for small, medium, and large effect sizes. There is more detail here. N is the total number of data points, df is the number of alleles. This function will give us a value for 1 minus the power of our test. A value of 0.9 means there is a 10% chance of failing to detect an effect that truly exists.
If we want to work out a suitable number of data points to collect we must decide what power we want. Say we decide that a 0.01 chance of doing the test, but failing to detect disequilibrium if it exists is acceptable.
pwr.chisq.test(w = 0.3, df = 4, sig.level = 0.05, power=0.99 )

tells us that 280 data points are needed.
Without estimates of effect size or a number of genotypes it is hard to give a straight answer to your question, but 5 per genotype seems very small.
If you have only two genotypes, you might choose to use the Fisher Exact Test in which case you can use power.fisher.test() in the statmod package. The definitions of effect size and degrees of freedom are slightly different but the idea is the same.

+1: nice to see power analysis mentioned every once in a while... too often biologists tend to skip on these things.

Thanks, whilst I asked this a long time ago and it's not very relevant to me now I'm sure this will help people in the future!

Yes I was aware it was old. But as you say hopefully useful for others. Having got information from stackexchange a million times but never asked a question, I know that it's potentially true.


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Long term liquid food diet by blending/grinding all quality foods one would normaly eat, not any weight loss or prepared drinks
I want to know what are the effects of not using your teeth to grind foods but preparing it before eating with blending and grinding them into a liquid.
Here I am not talking about any weight loss or fitness industry prepared drinks. I mean the ordinary raw and cooked foods like meat, vegetables, cereals, and fruits that one would normally eat in classic meals.
Would this decrease of work done by teeth and digestion system have positive or negative health effects?

I would definitely have a negative effect on mood. Why would you deprive yourself from the pleasure of eating a proper meal?

Don't get me wrong I love eating proper meals, however I don't see pleasure in eating to be my essential need. I could only regard it as an addiction if I needed it to improve my mood. I am only concerned about health effects when helping my body to process food.

It would probably only be a positive thing -- ultimately, you're increasing surface area of the food particles, which is what our digestive systems try to do anyway in order to absorb the most nutrients.

@Alexandria: any proof of that? Eating is not merely digesting food for sustainement, it is a much more complex event. What would happen to the secretion of food-related hormones for instance? Would satiety be obtained at the same point? Would you tend to eat less because of the lack of "aesthetic" appeal of liquid food? What would be the effect on the dopaminergic reward systems in the brain? What would be the effect on intestinal microbiota?

there is a pop nutritional concept of micronutrients, that yes the nutrients would be absorbed into your system more efficiently.  Its a reasonable argument to me.  Still if you are grinding up cheetos and lucky charms you're going to get faster sugar absorption into your system and it should increase the chance of diabetes.  if its broccoli kale and carrots it might help.  if its fewer calories with no meat, even better I think.

This New Yorker piece on "Soylent" is not peer-reviewed research, but goes into a lot of good, well written detail on the topic, including quotes from nutrition scientists, and anecdotes from users. It might make a good starting point. +1 for a good exploration of the cultural, as well as nutritional issues. http://www.newyorker.com/magazine/2014/05/12/the-end-of-food?currentPage=all

I was in a car accident age 19. Jaw was wired shut, food access was limited to one broken front tooth. It was liquid diet or nothing.
 So, I drank a lot of foods in liquid form, ( soups, etc. ) and a lot of Gerber's baby foods, and just about anything that could be pulverized in a blender.
 I gained weight like crazy. About 15 pounds in 2 months.
 The body takes advantage of having the harder work of digestion done for it. One of the advantages of cooking food is it's easier to digest. It is believed by some that such benefits to our life are the reason humans became the dominant force on this planet.

Well, the only logical explanation for your weight gain is too many calories. The weight gain is not relevant to me because I would control the amount of calories as I do with normal food.


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When does weak selection produce qualitatively different results from strong selection?
In evolutionary game theory, it is typical to model organisms as having a base fitness that is modified slightly by the game interaction. The ratio of the game effect versus the base fitness determines the strength of selection, with weak selection meaning the game modifies overall fitness only slightly, and strong selection meaning that the game payoff is a big part of the overall fitness of the organism.
Most analytic models like to assume weak selection because it allows the authors to Taylor expand the selection function and linearize it by dropping terms that are higher order in the stength of selection. However, it is unclear that results derived for weak selection would necessarily hold under strong selection. Are there mathematical (or computational) models where weak and strong selection produce qualitatively different results? If not, is there an argument as to why weak and strong selection should produce the same results?
I've also seen this discussion come up outside of evolutionary game theory, in a more general biological setting. In particular, with respect to inclusive fitness. The take away message I got was that in the regime of weak selection relatedness means what you expect it to mean, but for strong selection the concept becomes very slippery and counter-intuitive. What does inclusive fitness theory tell us about going from weak to strong selection? Again, I prefer arguments supported by clean mathematical or computational models over ones based on intuition and words alone.

I haven't had time to look closely at it, but you might find this paper interesting: Wu et al. 2010. Universality of weak selection. ArXiv. It seems like they try to bend the rules and study differences between models.

@fileunderwater thanks, I found that paper shortly after I asked the question and it is extremely relevant, I've been meaning to give a self-answer based on it but have been too busy with other things.

It has been shown that predictions based on weak selection can be different from that on strong selection.
In fact, for rare mutations, each strategy has stationary distribution at the mutation selection equilibrium. The rank of the component depicts the relative prevalence of the available strategies. Yet the rank of the components of this distribution can change with the selection intensity. Thus results obtained under weak selection can not generally carry over to strong selection.
For more details, please refer to Fig. 1 in [1] and Fig. 2 in the supplementary information of [2].
1 Julián García and Arne Traulsen, (2012), Journal of Theoretical Biology, Leaving the loners alone: Evolution of cooperation in the presence of antisocial punishment
2 Christoph Hauert, Arne Traulsen, Hannelore Brandt, Martin A. Nowak and Karl Sigmund, (2007), Science, Via freedom to coercion: the emergence of costly punishment


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Might a previously administered MPSV4 vaccine react with a newly administered MCV-4 vaccine?
This is a hypothetical situation.
Meningococcal polysaccharide vaccine (MPSV4) is a vaccine against Neisseria meningitidis.
MCV4 is a conjugate vaccine.
I would like to know if the polysaccharide base could interact with the conjugate base.
I think they would not act like booster doses and that the efficacy of the conjugate vaccine would be decreased, due to the lifelong effects of MPSV4.
Might MPSV4's polysaccharide base interact with MCV4's conjugate base, and if so, what might be the mechanism?


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Can cirrhosis be caused by physical compression of the body?
On a random forum, a member speculated that their cirrhosis was caused by wearing tight-fitting clothing such as a girdle or corset.  This leads me to the following question:

Question: Can cirrhosis be caused by physical compression of the body?

The list of causes on Wikipedia does not include this.  However, this may just be because the list is incomplete.  Alternatively, it may be because physical compression is unlikely to contribute to cirrhosis.
A plausible mechanism that springs to my mind is that physical compression leads to the constriction of hepatic veins, arteries and/or their tributaries.  But I suspect the rib cage would provide significant protection against this (see below).

There is the term “corset liver”. It describes changes (“grooves”) on the liver’s surface following external compression and subsequent local atrophy, e.g. from wearing a corset for a long time. (see Dancygier: Clinical Hepatology)
A paper from the 1980s describes some abnormality in the histological findings of liver tissue of dogs after chronic abdominal compression but without providing any details in the abstract (I don’t have access to the full version). They measured an increased pressure in the Vena cava and the portal vein. (Ueyoshi, Shima: Studies on spinal braces. With special reference to the effects of increased abdominal pressure. PMID 4093227.)
A (chronic) Budd–Chiari syndrome can also cause liver necrosis and consequently cirrhosis and can be the result of venous compression from e.g. tumors.
I doubt that a comparable chronic compression is possible from wearing clothing. Corsets are still used in orthopedic conditions. I have never heard about long-term side effects on liver tissue. The explanation for cirrhosis seems unlikely to me.

Thanks for that.  I think you're right... my suspicion is it's likely that any link with cirrhosis would have been discovered along with "corset liver" etc., and would be reasonably easy to find in the literature.


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Sequencing rtPCR product
So I have a validated set of primers for rtPCR from Biorad that contains SYBR green.  If I do rtPCR, can I use the rtPCR product after purifying it with a Qiagen PCR purification kit?  Also, I'm under the impression that the sequencing company needs primers to do sequencing, do I just use the PCR primer or one of the "universal" primers the company has?

Theoretically, you will still end up with a specific PCR amplicon, so you can sequence it with the same primers used for rt-PCR. By the way, do you mean real-time or reverse transcriptase PCR?

You can use the PCR purification kit for cleaning up the DNA.
You can use the primers that you used for RTPCR for sequencing. The universal primers would work only if the sequence complementary to it is there in the 3' end of your amplicon.


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How much can be said about behaviour (future) based on bloodgroup?
My bloodgroup for example is A+. How much information is knowing my bloodgroup? How much information can be known from a blood sample? I expect you to be able to clone if known a complete DNA sequence but how much would I recognize myself from a clone you make from my DNA e.g. behaviour?

There are quite a few questions in this post, in future you might want to split them up to receive better responses.

If I know you are A+ I know that you express a certain protein and not another one on your red blood cells. That's it. Note that there are thousands of different proteins in our body. I can probably know much more about your behaviour by Googling your name.

I'm not sure if you talk about personal matters or actual body behviour now. I meant for instance the behaviour of a leg or an arm or my physiology (and not so much online consumer behaviour or profiles)

The neurological basis of behavior is still unclear, and the genetic basis of behavior is even less clear.  What can be said is that genetics may predispose you to certain behaviors, but what the predisposing factors are, and how much they determine your behavior (and how much is due to environmental factors), is unclear.  And this varies for different behaviors -- if you want to read more about a particular behavior, you can try looking up the genetics of addiction.
If we want to examine the genetic basis of behavior, I don't think anyone would be looking at blood group, which is due to some physical characteristic that is not obviously linked with behavior (versus a differently structured neurotransmitter receptor, which is possibly more related). It's like using your height to explain your behavior.
EDIT: On cloning:
I should also mention that human reproductive cloning has not been successfully attempted, and if it were, you wouldn't get an exact copy of the donor of the genetic material (by the current technologies).  The most famous example of reproductive cloning, Dolly the sheep, required more than just nuclear DNA:

Dolly or any other animal created using nuclear transfer technology is
  not truly an identical clone of the donor animal. Only the clone's
  chromosomal or nuclear DNA is the same as the donor. Some of the
  clone's genetic materials come from the mitochondria in the cytoplasm
  of the enucleated egg. Mitochondria, which are organelles that serve
  as power sources to the cell, contain their own short segments of DNA.
  Acquired mutations in mitochondrial DNA are believed to play an
  important role in the aging process.

The source also has more information about cloning: http://www.ornl.gov/sci/techresources/Human_Genome/elsi/cloning.shtml


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If fever is a natural immune defense, why do people take drugs to lower it?
If fever is a natural defense against pathogens, why do sick people take NSAIDs to reduce the fever?

Personal comfort is the primary answer. Quite a bit of research has gone into fevers, and the current consensus is that Fevers less than 105F (40.5C) shouldn't necessarily be treated.
The primary reason the body raises its temperature (via the Hypothalamus in this case) is that bacteria and viruses tend to optimally thrive at 98.6F, which is also your body's optimal operating temperature. By raising the body's temperature, the bacteria/viruses become less efficient, allowing your body to "catch up" since the body's immune response takes time to ramp up before it reaches its peak (which is a bit after peak viral/bacterial load). Here's an example for Hepatitis (HBxAg = the virus, Anti-HBx = antibodies against the virus):

Along with the Fever, joint inflammation (part of the Innate Immune system's primary response) is also a coinciding symptom. So when your body begins to fight an infection you get a fever (which can make the environment uncomfortably hot/cold) and the tissues around your joints swell (which makes movement and relaxation uncomfortable). NSAIDs like Ibuprofen reduce those symptoms, making the duration of the infection more bearable. They do not reduce the length of the infection by any measure (and might increase it, though the research is not particularly conclusive), but can make the day go by better if you've used up all your sick days or have a child to take care of.
Basically, people take NSAIDs to reduce fevers for the same reason most take any over-the-counter pain medications. To make life a little easier in the meantime.


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If a receptor is inhibited throughout embryogenesis, could there be observable phenotypic differences in the adult?
So I read a journal article entitled "Maternal hypoxia and caffeine exposure depress fetal CV function during primary organogenesis" (Momoi, et al., 2012) and in essence the article speaks of the period of time in embryological development when the cardiovascular system is developing as being the time when the fetus is most susceptible to epigenetic events, and how adenosine and its A2 receptor have a role in dilating coronary arteries in hypoxic conditions. It later goes on to say that since caffeine is an adenosine A2 receptor antagonist, mothers who consume caffeine regularly create a suboptimal environment for the fetus - this is referred to in the article as IUGR (intrauterine growth restriction).
My question is: Are there any effects (or do you believe there could be effects) of this inhibition occurring during development that affect the fetus later in life? As in, do you think there would be adult phenotypic changes of any kind due to the regular inhibition of a receptor during development?
I thought about this for a while and all that was apparent to me is that if the mother was both consuming caffeine and hypoxic, then the fetus could experience myocardial damage because its coronary arteries wouldn't be receiving the signal to dilate and the heart might be "starved" of the proper oxygenation. But even so, the receptor would still be present in the adult. Do you think there could be a decrease in transcription of a receptor that is continuously blocked (you don't need to address this in your answer -- notice that I'm asking for an opinion, which you can choose to give or withhold)?
FYI: I'm writing a review on how maternal prenatal health contributes to the epigenetic profile of offspring and I'm actually focusing more on the epigenetic contributions to the adult hypertensive phenotype. I stumbled upon the CV/adenosine article and was curious about whether there could be any long-term changes, so I asked all you wise folk. It has been observed that mothers fed a low-protein diet give birth to children with reduced nephron count and glomerular hypertrophy -- my goal is to understand what the current state of knowledge of this mechanism is. So if you have any ideas about anything here, or you've got an awesome resource related to this material, I'd really appreciate hearing about it.


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What is the biological mechanism underlying caffeine intolerance? (CYP1A2 or other?)
As far as I can tell, caffeine metabolism occurs primarily via the CYP1A2 enzyme. I am curious as to whether mutations in the CYP1A2 gene are associated with caffeine intolerance.  Some site that is not necessarily reputable suggested that caffeine intolerance is due to absence of the enzyme to metabolize caffeine. I am having difficulty finding evidence either supporting or contradicting this claim.
Does anyone know if there is evidence that suggests mutations in CYP1A2 (and therefore inability to properly metabolize caffeine) are associated with caffeine intolerance, or if there is another proposed mechanism for caffeine intolerance?

Yesterday I learned about this cool database linker site called biograph.be, where you can type in a gene and suspected "disease" or condition and it will generate a map showing how they've been associated in literature. Here's a start: http://biograph.be/concept/graph/C0006644/C1332826

Unfortunately, neither 'caffeine allergy' nor 'caffeine intolerance' are recognized search terms. But that is a cool site. Thanks for the link.

Yes, that links to the association between caffeine and CYP2A1 - but all of the papers that come up seem to be related to pharmacological inhibition of the enzyme, which I already know is important for caffeine metabolism...I'm interested in mutations in the gene.

I have found that caffeine is mostly metabolized over CYP1A2 (as we know), but also over CYP1A1, CYP2E1 and CYP3A4. The question is how much the individual can cope with this alternate pathways if he is a CYP1A2 poor metabolizer. [1]
Secondly I found in my pharmaceutics textbook that CYP2A1 activity determination is indicated due to undesirable side effects to caffeine and theophyllin.[2]
UPDATE: 19.03.2013 12:30 GMT+1
@dd3: To clarify the second statement: I used the approach that theophyllin and caffeine are similar xanthin derivates. Since theophyllin is used as therapeutic drug in respiratory diseases (COPD etc.), I thought that scientific interest would be greater. And yes CYP1A2 plays an important role in both theophyllin tolerance and intollerance.
I found some new sources:
At first a study with CYP1A2 knock-out mice, which shows that the elimination of theophyllin takes 4-times longer in CYP1A2(-/-)mice. And they also assume that the same behaviour is also applicable to caffeine. [3]
Also there are two clinical studies by Japanese and Turkish scientists. The Japanese conclude, that theophyllin should be used with care in CYP1A2 poor metabolizer (even in haplotype poor metabolizer), since theophyllin has a narrow therapeutic range.[4] But the Turkish scientist assume that according to their findings, theophyllin is also metabolized over alternative pathways such as CYP2A13, CYP1A1, CYP2E1, CYP2D6 and CYP3A4. And according to this the genetic status of CYP1A2 is not as important as expected. [5]
Conclusion:
Assuming that theophyllin and caffeine are metabolized similarly, you can conclude that a mutation in CYP1A2 would lead to caffeine intolerance. In my experience people with caffeine intolerance describe severe nervousness after drinking a cup of coffee. Fatal cases I know were due to high consumption of energy drinks in children without or at least not known caffeine intolerance.

Sources

[1] http://informahealthcare.com/doi/abs/10.1081/DMR-120001392
[2] german source: http://www.medizinische-genetik.de/index.php?id=2642
[3] Derkenne S, Theophylline pharmacokinetics in mice: http://www.ncbi.nlm.nih.gov/pubmed/15970798
[4] Obase Y, Polymorphisms in the CYP1A2 gene and theophylline metabolism in patients with asthma. http://www.ncbi.nlm.nih.gov/pubmed/12732846
[5] Ahmet U, The effect of CYP1A2 gene polymorphisms on Theophylline metabolism and chronic obstructive pulmonary disease in Turkish patients http://www.jbmb.or.kr

Further Reading:

Xanthines as therapeutic drugs: http://web.carteret.edu/keoughp/LFreshwater/PHARM/NOTES/Xanthines.htm

Could you clarify your second statement? I'm not sure what you mean.  Google translate of the second page seems to indicate that mutations of CYP1A2 are associated with both caffeine tolerance and intolerance -- is this correct?


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Are there any viruses or bacteria which have evolved to withstand higher temperatures due to fever
My question was raised after receiving this information:

The primary reason the body raises its temperature (via the Hypothalamus in this case) is that bacteria and viruses tend to optimally thrive at 98.6F, which is also your body's optimal operating temperature.

I am just wondering if there are any viruses or bacteria that have gained the ability to prosper under fever temperatures through evolution? If not, why not?  Is there any biological restriction stopping such viral evolution?
Update:
I will try to explain my question.  As far as I know, evolution helps species to adapt to their environment.  For example, when people started using antibiotics we got new bacteria resistant to those antibiotics.
If fever is part of the innate immune reaction to viruses and bacteria, why hasn't this resulted in selection for fever-resistant variants? Why has evolution apparently stopped in this case?

There are bacteria that live in hotsprings, for them 100c is comfortable.

Are you asking if there are pathogenic bacteria that thrive at higher body temperatures?

I have updated my question and tryied to explain it.

Does anyone else cringe whenever stumbling upon 98.6°F?

Fever is just one of the many ways of the body's defense mechanism work. Under infection, human body can raise body temperature, release cytokins and activate white blood cells etc. Sometimes the bacteria can evade immune suppression or immune complement fixation so that they can stay inside a "fever-ish" body like they just don't care. Example: Pseudomonas aeruginosa. They can grow in 42 degree Celsius which surpass the normal fever temperature.
My answer may not be the best for your question. All I'm trying to say is that fever acts as a supportive role during an infection. Human body relies on heavy artilleries such as white blood cells and cytokin to clear the infection. That's why it will be more beneficial for the bacteria to evolve abilities to evade immune suppression and immune complement fixation. And bacteria know how to do those.


text:
How do animals decide what to eat and what not?
I want to know this in particular about animals that no longer eat what they used to eat. The best example in my opinion are chickens. Chickens are often held to eat all kinds of food we would otherwise throw away. Most of this, they would never find in nature.
Chickens almost eat everything, but there are things they don't. Also, they often have a clear preference for some food.
How can they differentiate this food? Do they use smell? Looks? How can they know smells of food they never had before?

To answer with a question: How do you decide what to eat (if you don't know whether something is edible)?
All animals have evolved taste and smell (and I'm sure even prior to eyesight). The purpose of taste and smell in terms of nutrition is to determine if something is edible. If something tastes bitter or extremely sour, this is mostly a warning sign for toxins or advanced microbial degradation. The same accounts for smell: If you let raw meat foul, the smell is unbearable. Why? Because our brain is telling us not to eat this.

Probably a lot of external and internal factors combined. But the most important would be the smell, eye sight and taste.
Smell can be, I would say 60-70%. When some particles arrive to the smell receptors, htne on the cellular level the receptor gives a "report" to other parts of the bady, especially brain etc. E.g. some seabirds, like storm petrels, recognize the odor of a compound emitted by krill, their main fare.
Almost all birds have great eyes, so this is a great long-distance food check.
But to be honest the taste is also a big issue and I think that all birds go through a phase when they eat everything and after learning what tastes good and bad (with combination of how it look like before they eat it and how it smelled, the infomrmation is stored in the brain.
Even though the birds have problems with complicated thought processes in their brain, I think that they are more than capable of storing and reusing this "good-bad-food" information from their brain.
There could be other factors like e.g. some birds are allergic to some food (yes, animals can be allergic too, even though their immune system is much stronger then ours) and the body will store in the brain to not eat that in the future.


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In humans what is the last metabolic process to cease after death?
After death which of our body's metabolic processes will continue functioning for the longest?

Slightly related to this question

I will wait for a better answer because I'm curious too. But here is my answer, you may be surprised because I think the last metabolic process to cease after death is not fancy at all, it can simply be cellular respiration. When oxygen is depleted, cellular respiration stop and it can't do any thing. Just like sleeping, your body is basically stop doing a lot of things except cellular respiration. Here is some info you may be interested. http://www.scientificamerican.com/article.cfm?id=experts-cell-metabolism-after-death

My answer isn't researched; it is speculative.
I interpret metabolic processes as anabolic or catabolic processes. I assert that only anaerobic processes can continue for a long time after vegetative death (the epithelia could house a counter-example of a post-mortem process, but I can't think of one), and I speculate that only catabolic processes are likely to have sufficient pools of reactants to continue after death. So we're looking for a catabolic process with a large reactant pool. Therefore I think that the action of digestive proteases will continue for the longest time, because these enzymes are very stable and could have a lot of substrate around (including, at a very slow rate, cleaving each other.) The neutralization of stomach pH would inactivate this process...I don't know how long that takes.
If something like blood clotting is considered a metabolic process, then probably that continues the longest. The binding of CO₂ by hemaglobin is probably faster than blood clotting. Again, I don't really consider those processes to be metabolic.

I can imagine your digestive proteases cleaving their way through the stomach lining ever so slowly after your death, before eventually the pH is neutralized. Not what I would have thought of. Good answer.


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Why do neurons die so fast without oxygen and nutrients?
Some human tissue can survive without oxygen a couple of minutes, even hours.
Why are the neurons are so "weak" and depends so much on oxygen and other nutrients and cannot live without them for more than a few seconds or 1 or 2 minutes?
Are they missing some parts of their cells which can store nutrients for worse times in favor of their function or what is the case?

Maybe because as soon as the hardware stops, the "software" is no more? (half-joking answer)

This has been addressed on quora: http://www.quora.com/Neuroscience-1/Why-do-neurons-die-so-quickly-when-deprived-of-oxygen

So, it is not the lack of stored stuff(oxygen, nutrients) in neurons? Does that mean that they could in fact survive if they want to, but actually the way how they respond to the lack of oxygen makes them die so quicky? So, ste structure/organelas in them could in fact support them for a longer time, but the "dead" signals they are receiving (chemically) turn them off and they die?

Well, it's not really a "dead" signal - excitation is part of normal neuronal activity. Excitotoxicity is when there is too much excitation and it kills the neuron: http://en.wikipedia.org/wiki/Excitotoxicity

Neurons use lot of energy to maintain their polarized state, this is not required to other cells [1,2].
When O2 or blood flow (which is carrying the nutrients) is reduced, the neuronal ATP levels breaks down very fast, with 90% ATP depleted in less than 5 minutes. Without ATP, the neuron can not maintain the correct ion flux, so depolarization occurs causing glutamate excitotoxicity, cell swelling and finally cell death.
1] http://www.acnp.org/g4/gn401000064/ch064.html
2] http://www.scientificamerican.com/article.cfm?id=why-does-the-brain-need-s

There are many factors contributing to neurons dying much faster than other cell types.
This website does not provide original references (for this question, it does for the rest of the article) but sounds trustworthy: http://neuropathology-web.org/chapter2/chapter2aHIE.html
Some factors extracted from here are:

Aside from small amounts in astrocytes, there is no glycogen storage in the brain.
Fatty acids cannot cross the blood-brain barrier.
Lack of a backup energy sources such as creatine phosphate in muscle cells.

Which leave the brain crucially dependent on oxydative phosphorylation, i.e. glucose and oxygen. Additionally of course, neurons are metabolically highly active and use up the small amounts of stored nutrients available at a faster rate than most cells. This is because they need to maintain strong ion gradients across their entire membrane, which spans a larger area than most other cell types due to extensive axonic and dendritic trees; not to mention constantly exocytosing neurotransmitters from the axon's numerous terminals.
Coupled with excitotoxicity as the actual mechanism inducing cell death as explained in the Quora answer linked above (http://www.quora.com/Neuroscience-1/Why-do-neurons-die-so-quickly-when-deprived-of-oxygen), this seems to be a sufficient explanation.

The short answer is: neurons do NOT always die quickly when deprived of nutrients.  The longer answer is the following:
I am a professional researcher in brain ischemia (ischemia = no blood flow), which is the topic of the question. Armatus' answer was correct insofar as neurons have very limited energy reserves and therefore loose ATP very quickly. Gianpaolo R gave the correct time course for ATP loss.  However, Gianpaolo R's explanation of cell death applies only if the ischemia lasts for about 20-30 minutes.  In this case, the cells swell and lyse by a process called necrosis.
However, if the duration without blood flow (which is the duration with no oxygen and nutrients) is less than 20 - 30 minutes, then the cells do not die by necrosis.  It is less well-known to lay people, but well-known to neurologists that the neurons will die days or weeks after the ischemia in a process called "delayed neuronal death".
What is also less known to lay people is that if the duration of ischemia is less than about 7 minutes (this depends on the species, e.g. human, rat mouse, etc), no neurons die, and in fact, they are protected for a short while from a similar insult.  This is a phenomenon known as "ischemic preconditioning".
The explanation of necrosis is uncontroversial.  However, no one knows what causes delayed neuronal death or preconditioning responses.  The excitotoxicity mentioned by Armatus is a popular theory in the field, that has been largely discredited for a variety of reasons I will not go into here.  It is also popular to believe the delayed neuronal death is due to a process called apoptosis, but this also has fallen out of favor in recent years.
Hence, right now, there are many competing ideas as to why the neurons die in a delayed fashion, and the simple fact is, no one knows for sure why they die in this way.
As you may imagine, being a worker in this field, I have a theory that I think is the most feasible of all.  But it is a mathematical theory that applies to any injured cell, not just neurons deprived of blood flow.  The theory is very simple conceptually.  It says that when a cell is injured it gets damaged (call it D), but also activates genetic responses to protect itself (call this S).  If the genetic protective responses are greater than the damage, that is, if S > D, then the cell recovers and lives.  If the damage is greater than the stress responses (D > S), the cell dies.  The rate at which the cell recovers or dies is inversely proportional to |D - S| after D and S have run their course interacting with each other.
This last statement precisely answers your questions. Neurons will die quickly when |D-S| is a large number.  They will die slowly when |D-S| is a small number.
Now, this is just a qualitative description. The theory actually consists of mathematical equations that predict many things. You will note it is a true theory and does not rely on the biological specifics of the system under study. I am currently measuring the theory in my lab.  I am confident it will be a very useful theory not only for explaining brain ischemia, but many other forms of cell injury.
The original article detailing this theory can be obtained at this link.

AFAIK permanent brain damage occurs after ~7 minutes of ischemia.  So what is going on between the ~7 minutes during which "no neurons die," and the up to ~30 minutes during which "the cells do not die by necrosis?"


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Agony, Hydrophobia and viruses in the light of evolutionary principles
I'm undergraduate physics student, but I've always been interested in biology. So I have a couple of questions about an application of the evolutionary principles to practice.

Agony as the last stage of dying.
Hydrophobia as symptom during Rabies.

Now I'm going to clarify what exactly I do not understand. In the first case it's not clear for me how this mechanism helps to survive, how it can help at all? In the second case it's not obvious why this virus causes such a symptom. As I think virus always create favorable environment for himselve (for reproduction). But how could water prevent it?

These might be better posed as separate questions.

I'm with Kevin. These seem like separate questions. To give you an idea of the first - Evolution via Natural Selection doesn't really 'care' how you die, as long as you've passed on your genes (reproduced) beforehand.

Agony is not always associated with the last stage of death, many pass peacefully - and the agony when it does occur is likely to be caused by the cause of death (ie a symptom) and possible exacerbated by the fact the person knows they are dying... And viruses/disease can have weird side effects on neural pathways which could be why we suffer from unusual neural episodes/behaviors

Maybe you mean fear of death?  I don't see that agony always accompanies death. Could you cite some reference or example?

Viruses and bacteria have a tendency to care mainly about eating and/or dividing. If the host dies, it's often a biproduct of toxin or foreign body accumulation. Agony in death, however, can be either physical or psychological and I'd count that as either too broad, or inaccurate (not everyone agonizes, as in painful symptoms). I wouldn't count the first question as having to do with biology/evolution.

The hydrophobia symptom is most likely a bi-product of the effects the virus has on the brain and not an evolutionarily derived strategy to create an appropriate environment to reproduce in. Just the same as other symptoms the infection causes, like fever for example, is a reaction the body has to the presence of the virus and not something the virus is doing on purpose to set up a better environment.
A bit old, but check out [1]: "Hydrophobia may represent an exaggerated respiratory tract irritant reflex with associated arousal potentiated by the selective destruction of brain stem inhibitory systmes."
So basically the virus is indirectly causing a fear of water. The destruction of brain cells and inflammation caused by the presence of the virus in the central nervous system cause a reflex in the respiratory tract which manifests as muscle spasms and renders the patient, who is already pretty out of it at this stage, unable and very unwilling to drink any fluids [2].
[1] http://europepmc.org/abstract/MED/982512 (Warrell DA, Transactions of the Royal Society of Tropical Medicine and Hygiene [1976, 70(3):188-195])
[2] http://publichealth.lacounty.gov/vet/rabiesmanual/clinical.htm

It's not actually a fear of water. It's that they have spasms on swallowing. Rabid animals will not swallow their saliva either. Hence the frothy mouth.

@anongoodnurse Because the brain prepares the body for swallowing before it occurs, thinking about swallowing may trigger the same reaction, which may appear as a conscious fear of water.

The fact that hydrophobia is a biproduct of the virus's effects on the brain doesn't necessarily mean that it is not evolutionarily selected for.  Rabies is transmitted via saliva in bites, so difficulty swallowing could very well have been selected for by evolutionary pressure (along with other behavioral effects such as increased aggression and hypersalivation).  In effect, the host's altered behavior can be considered part of the "extended phenotype" of the virus!

If your first question means: why is later-life ageing usually a long and painful process of degradation (rather than why do we have existential agony) with diseases of ageing like osteoporosis, heart disease, dementia - then I can offer one answer.
There is an absence (almost) of any selection pressure after reproductive age. Once individuals are past reproductive age, any such diseases, unless they place a great survival burden on the immediate (related) community/family, do not influence fitness of the population.
In other words, perhaps evolution has nothing to say about diseases of ageing, and no 'imperative' to purge our species of these afflictions.


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Where can I find historical data on world-wide ecology parameters?
I hope this is the right StackExchange forum for such a question.
I'm looking for large data sets on world-wide ecology parameters, such as annual temperatures by latitude, annual rainfall, CO₂ and O₂ concentration in the atmosphere and in the oceans, data about the insect population, plants, algae, and so on.
Is there any research institute or NGO collecting such data and making it available to the public?

What time interval are you interested in? NASA collects a whole lot of information about abiotic parameters with their satellites on a global scale. They can be explored here: http://earthdata.nasa.gov/ and here http://oceancolor.gsfc.nasa.gov/ (for the oceans).

That's a great resource, I didn't even know NASA did that.

These examples are good

Adding some additional database sources:
-- Climate --
Prism
The PRISM Climate Group gathers climate observations from a wide range of monitoring networks, applies sophisticated quality control measures, and develops spatial climate datasets to reveal short- and long-term climate patterns.
WorldClim
WorldClim is a set of global climate layers (climate grids) with a spatial resolution of about 1 square kilometer. The data can be used for mapping and spatial modeling in a GIS or with other computer programs.
NOAA's NCEI
NOAA's National Centers for Environmental Information (NCEI) are responsible for hosting and providing public access to one of the most significant archives for environmental data on Earth with over 20 petabytes of comprehensive atmospheric, coastal, oceanic, and geophysical data. See NCDC (climate), NODC (Oceans), NGDC (Geophysics), and NCDDC (Coasts).

NCEI has a HUGE repository of datasets. Sometimes you have to dig (e.g., here).

TROPICAL STORM TRACKS DATABASE
The storm tracks database is derived from the storm data published by the National Hurricane Center (NHC). This web page provides a convenient user interface for casually browsing storm information, including location, category, and wind speed.
-- Traits --
TRY
TRY is a Plant Trait Database. More formally, it's a network of vegetation scientists headed by DIVERSITAS/IGBP, and the Max Planck Institute for Biogeochemistry, providing a global archive of curated plant traits.
BioTraits
This is an online resource for empirical data on how biological traits respond to environmental drivers such as temperature, light, and salinity.
-- Species --
GPDD
The CPB / NCEAS Global Population Dynamics Database largest collection of animal and plant population data in the world, and brings together nearly five thousand time series in one databa
Global Invasive Species Database
The GISD is a free, online searchable source of information about species that negatively impact biodiversity. It focuses on invasive alien species that threaten native biodiversity and covers all taxonomic groups from micro-organisms to animals and plants.
Movebank
Movebank is a free, online database of animal tracking data hosted by the Max Planck Institute for Ornithology. They help animal tracking researchers to manage, share, protect, analyze, and archive their data.
Global Plants
Global Plants is the world’s largest database of digitized plant specimens and a locus for international scientific research and collaboration.
COPEPOD
The Coastal & Oceanic Plankton Ecology, Production & Observation Database (COPEPOD) is an online database of plankton abundance, biomass, and composition data. COPEPOD's online zooplankton and phytoplankton data content ranges from long term ecosystem monitoring surveys to detailed process studies
COMPADRE & COMADRE
COMPADRE Plant Matrix Database and COMADRE Animal Matrix Database site. Contain matrix population models of hundreds of plant and animal species
Catalogue of Life
One of the most comprehensive and authoritative global index of species currently available. It consists of a single integrated species checklist and taxonomic hierarchy. The Catalogue holds essential information on the names, relationships and distributions of over 1.6 million species.
-- Forests --
FAO Forestry Database
The FAO Forestry Department maintains an array of online databases where information covering various aspects of forestry is stored for analysis and further dissemination.
FIA
U.S. forest Service's Forest Inventory and Analysis database contains continuous forest census data for the United States.
European Forest Institute Database
EFI is running a number of online databases with data and information on different aspects of European forests, forestry and forest research.
CTFS-ForestGEO
The Center for Tropical Forest Science - Forest Global Earth Observatory (CTFS-ForestGEO) is a global network of forest research plots and scientists dedicated to the study of tropical and temperate forest function and diversity
-- Other --
NutNet
The Nutrient Network (NutNet) is a grassroots research effort to address pervasive human impacts on ecosystems (via alteration of global nutrient budgets and changes in the abundance and identity of consumers) within a coordinated research network comprised of more than 40 grassland sites worldwide.

...Also see the Ecological Databases page on INNGE Wiki for more resources!!

Ex: Ecological Data Wiki:
The site is a source for finding ecological datasets and quickly figuring out the best ways to use them. Just think of it as the Wikipedia of ecology data.

You're quite welcome. Feel free to add more in the comments if you find any!

Wow, thanks! Wish I could upvote you three times. For Europe, the LEDA traitbase is used often: http://www.uni-oldenburg.de/en/biology/landeco/research/projects/leda/

For climate related data you can start from Realclimate pages on data repository. For ecological data I always found less global data, but a good starting point may be the Ecological Society of America Data Registry page. An overview of repositories can be found the the Simmons University Open Access Directory.

For species occurance data the Global Biodiversity Information Facility (http://www.gbif.org/) database should be an obvious choice. It contains both historical records from museums etc and information from more recent surveys and inventories. Note that the occurrence data can both come from standardized inventories and observational records from specialists and amateurs (Citizen science data).


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Indestructible Super Shrimp
How are shrimp and other animals able to not be crushed by the 1000x greater pressure at the bottom on the Mariana trench?
Wiki says the trench is home to "large living creatures such as a sole or flounder about 30 cm (1 ft) long, and shrimp"
I understand natural selection, but what features has evolution "selected" that enable soft flesh and bones to not be instantly crushed like our own skulls would be at that depth?

Should I ever have a band, I'll name it "Indestructible Super Shrimp".

Aquatic animals brethe the water around them and this equalizes their body pressure with that of the surrounding environment.
This is how you can still find say a piece of pottery or a watch from a shipwreck... They are filled with water and don't experience the pressure.
Such pressures do affect humans because we breathe air and so we can't adapt to pressures underwater and we need a shell that allows the ship environment to be tolerable for humans beyond a couple of hundred feet or so.
I think the change of pressure would also affect fish or other animals If they dropped in depth too quickly.


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High sequence similarity but start codon isn't methionine
I have noticed in a particular genome sequence of a prokaryote that various regions in a sequence share similarity which is high(>80%) with known proteins. However, the start is not a methionine. Is this a dysfunctional 'protein' sequence? Or are there alternative codons which translate those regions without a Met or fMet for that matter?
Technically, do all annotations of proteins have to start with a methionine?

Which prokaryote are you referring to? This could be important for answering this question.

There are alternative start codons to AUG used in prokaryotes: GUG and UUG. Those still match the initiation tRNA and encode N-formylmethionine. The rare start codons are matched by wobble pairing.

As far as I know it is a universal rule that the initializing sequence codes the amino acid Methionine (or, as you mentioned fMet in prokaryotes).
However, in very rare cases it is possible that Met is not coded by the expected sequence of AUG. This happens more often in mitochondria and prokaryotes, for example E. coli which uses GUG quite frequent.
For an overview check Wikipedia here. Papers to follow up are listed there.


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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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Why does sexual selection evolve beautiful features?
I have a very raw understanding of sexual selection:
Say a group of females of a certain species "like" some feature of a certain groups of males; by "like" I mean some behaviour that makes this group of females tend to mate with males having this feature, then the females are selecting their genes which make them feel appealed to males with the feature, and then this process becomes exponent since the group of females becomes bigger and forces the population of males to have this feauture, until an equilibrium is reached. I know this also happens with the roles interchanged.
My first question is, why do females tend to like males that have high amounts of these features, more than the average in the population?
My second question is, why do the end products of these selections are such beautiful features? Perhaps this may sound a little arrogant but I don't understand how an animal can appreciate this beauty, I suppose this is to make some sort of selection of healthy males.
Thanks

I think this may answer part of your question: http://en.wikipedia.org/wiki/Sexual_selection#Exponential_growth_in_female_preference

Hey! Welcome to Bio.SE :) This is certainly a good question. However, it requires a very broad explanation of how sexual selection works, so it seems unlikely that you will get a full answer that clears all of this up. It would probably be a good idea to read the Wikipedia article and see if that makes the issue more understandable to you. If you have any more specific question then, pleasea do ask here!

In regards to the "beautiful features" part, your Q2, Dan Dennett explains the issue well here: http://www.ted.com/talks/dan_dennett_cute_sexy_sweet_funny.html

I don't mean to be rude, but yes your second question is very arrogant and anthopocentric. Why would you think humans have a monopoly on beauty appreciation and emotion? The tails of peacocks just happen to coincide with human aesthetics, but a proboscis monkey's nose or elephan seal's blubber are just as beautiful to the right set of eyes.

I think I can expand on the answer by @boo2060.
The evolution of female mate choice depends on females achieving higher fitness by choosing certain males over others. At the broadest scale, there are two mechanisms by which this can occur, direct benefits, and indirect benefits.
Direct benefits
These are material things that (surprise) directly benefit the female. This might be the provision of food by the preferred male, access to a good territory or shelter that is under the control of the preferred male, protection by the preferred male, that sort of thing. Females will accordingly favour male traits that advertise potential direct benefits. These might include male size/condition/colouration, or even built structures like those of the bowerbirds. Basically, these traits show that the male knows how to look after himself, and by extension, he knows how to look after her (as males in good condition generally inhabit the best habitats and will offer the best protection and parenting).
Indirect benefits
These don't do much for the female, but they increase the genetic quality (and thus potential fitness) of her offspring. This is a much more complicated area of mate choice, and can be split into a bunch of (non-exclusive) hypotheses (below). And of course, attractive males may well offer both direct and indirect benefits.
Sensory bias: Males may, by chance, possess a trait that holds intrinsic appeal for a female. The best explanation might be that it mimics the colour or shape of a food source (e.g. fruit) that the animal eats, and thus the animal has pre-evolved preference for that colour or shape (e.g. red patches). From that point, males with more of that trait, whatever it is, will tend to be more attractive, for no rational reason. This hypothesis is sound, but is currently lacking good empirical evidence.
Fisherian sexy sons: This can in fact lead on from an initial sensory bias. Females may choose males that they find 'sexy', because their offspring will also be sexy, and thus be successfull in reproduction. This can lead to 'runaway' selection for sexier and sexier sons, at considerable survival cost for males. In this case, natural selection and sexual selection work in opposing directions.
Indicator mechanisms: This is the handicap principle or 'good genes' principle. If a structure is costly to produce or maintain, or increases the risk of predation, and yet the male possessing it is still alive, he must have good genes to have withstood such a handicap. It may also advertise that the male is not infested with parasites. The extravagant plumes of birds may be largely explained by this one, but also sexy sons and sensory bias.
Genetic compatibility: Individuals seek partners that are genetically compatible. A certain proportion of the fitness of the offspring depends on the specific combination of genes (i.e. it's not additive), and individuals that can signal or detect signals in such a way that they can choose compatible partners will have an evolutionary advantage. The best example is scent (e.g. preference for dissimilar MHC immune genes - see the human t-shirt experiment).
These mechanisms are well known in theory, but not always well-supported by evidence (yet). This is probably the best reference.

Of course 'beautiful' is a subjective, human concept. But we probably appreciate a lot of 'beautiful' things (like a male bird of paradise) for the same reasons as other species. We like shiny things, colourful things, delicate things. These also happen to be the best indicators of health, and are most likely to exploit existing sensory biases. Fascinating topic.

Hello @atrichornis, thanks for your answer. As you can see in my question I have a "Fisherian" view of sexual selection, this seemed a little arbitrary, as almost any feature could be seen as "selectable", and with your explanation of sensory bias I get a better understanding of why beautiful features end up being selected.

Yep, the current consensus is that for the evolution of a sexual signal (e.g. ornamentation) to occur in the first place, it should exploit sensory biases, AND/OR be costly for the male to maintain and so serve as an indicator of health. Mathematical theory suggests that either one can be enough, provided that there is some mechanism (i.e. cost) that prevents low-quality males from 'cheating' by pretending to be healthy. If males can cheat, the system breaks down, because females can no longer use it as a basis for choosing, and males possessing this trait no longer have an advantage.

Nice highlighting of indicator mechanisms.  That seems to be the best match with the "beauty" term used in the question.

I'm not completely certain about the vocabulary used in this context so let me know if you wish clarification
There are a few hypothesis why females care about the sexual features of males, the two most prominent are:

The sexy son hypothesis states that a sexually attractive male will have sexually attractive offspring which, in turn, is also more likely to mate. This way a female choses to maximize the chance to pass on it's genes to next generations.
The good genes hypothesis says that males who can afford to develop features that do not benefit their survival but are only for the purpose of sexual selection are healthy, strong and fit. If not, they would not spend resources on sexual attractiveness.

But why are all these features beautiful? Well, the purpose here is that they are beautiful, in terms of attractive, to the recipient of the message: the potential partner. We as humans may find these features also beautiful, as is most likely the case with the colourful feathers of the peafowl. But what about the antlers of deer? Beautiful, dangerous? This is subjective for us ..

Have you got any sources?

I was rather thinking of how many attractive features convey a sense of fertility and lack of genetic abberations.

I thought I had my books at hand before I wrote the answer but in the end I didn't find them .. so apart from my experience and a quick verification on the Internet the sources are still to add.

I'm not aware of a study quantifying features that are considered being subdue to sexual selection. I think that rather the potency of one feature communicates fertility, health etc - I'm not an expert on evolution though .. your thought is interesting.


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Relation between goose bumps and temperature
As we all know, cold weather will cause us to have goose bumps. I honestly don't know why (1), because our skin contracts?
Apart from that something quite contradicting happened this morning. I was taking a hot shower and it was so hot that I suddenly felt that I had goose bumps. Not because it was cold, but because it was so hot. How can this happen? Because of a sudden change in temperature the skin goes haywire? Or aren't goose bumps related to temperature in a way, but is a sort of safety reflex?

Oh dang I highly suspect that Ca++ ions are binding troponin on actin filaments and blocking the action of tropomyosin thereby exposing cross-bridge binding sites and promoting the hydrolysis of ATP to an inorganic phosphate and a diphosphate.

Goose Bumps (a.k.a. - Goose Pimples) are caused by the Arrector Pili muscles in your skin:

Their purpose is to increase the distance from epidermis to the top of the follicle, and increase the area between follicles. This has the effect of increasing the amount of air trapped between the hair and surface of the skin. In other mammals the end-result is an increase in the insulatory properties of their fur, meaning they will stay warmer or cooler depending on their current needs.
Another function in our mammalian cousins is to simply appear larger, and thus more of a threat to any predators or dangerous animals. Much like the shoulder and lower back hair on this dog:

Thermoregulation in humans has evolved since our furrier ancestors; we sweat to cool off, and shiver to keep warm. We also use tools and weapons, can create fire, and have other ways to communicate our lethal capabilities.
Goose Bumps are the human body utilizing old instinctual reflexes in the proper situations, but we lack the thick mattes of hair our ancestors had for the reflex to have any significant effect. They're a fun Easter-egg, a leftover that doesn't do us any harm and are an easy way to tell if someone is cold or scared - which might be useful under the proper circumstances.

Great answer! Will wait for a day or two before accepting. Give other peeps a chance as well. :)


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What is the efficacy of Pertussis booster vaccine among different age groups?
The Murray Microbiology book says that it is prefentially 10 years, similarly Estonian and Finnish health associations.
However, my professor says that it can be 5-7 years.
I started to think if the age is affecting here to the result.
When should you take booster vaccination of Pertussis if you are
a) 25 years old,
b) 50 years old,
c) 70 years old, and
d) 90 years old?
My professor says that there is no significant studies about the efficacy of Pertussis booster vaccination among different age groups.
Is this true?

No, it is not true, see references 1 and 2 for this purpose. From these articles which followed up booster vaccinations for pertussis it seems that there is at least some protection 5 and 8 years after the boost.
There is another study, which says that 10 years are relatively safe to assume, as the reduction in antibody levels over time estimated from the 5 year study would still allow protective levels of antibodies. See reference 3 for details.
One of the problems to make statements about the duration of the protection is the lack of data. Additionally there was a change in the vaccine from whole cell (which is pretty immungenic, but has higher number unwanted side effects) against a acellular vaccine. This change happened in the 90s, so there are no longterm data available. See reference four for more details.
The common recommendation at the moment for adults is to repeat the booster vaccination every 10 years (together with tetanus and diphteria) and for people which have close contact to unvaccinated persons every 5 years to prevent infections (see reference 4).
References:

Immunity to pertussis 5 years after booster immunization during
adolescence.
Immune responses to pertussis antigens eight years after booster
immunization with acellular vaccines in adults.
How long can we expect pertussis protection to last after the
adolescent booster dose of tetanus-diphtheria-pertussis (Tdap)
vaccines?
Acellular pertussis vaccine use in risk groups (adolescents,
pregnant women, newborns and health care workers): A review of
evidences and recommendations


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ChIP-seq and the output of SPP
I have been processing some ChIP-seq data with the R package spp. I looked through the literature (ENCODE uses it) and it seemed that spp is indicated as a good program to use.  I have found and adapted the two tutorials I found for using spp (first and second), and read the original paper. I have also e-mailed Prof. Karchencko and posted on the bioconductor listserv - all with no response. My question is about the MSER and the predicted sequencing depth - additional output of spp. So what I think the MSER is, is the score value above which a peak is authoritatively determined? When I look at peaks above this score value they are very well defined. Also, is the predicted sequencing depth is a prediction of the number of additional "tags" necessary so that the MSER and the FDR value coincide? It is hard to find decent information about this program.  Any advice or additional information is greatly appreciated!
TIA

does the inline spp documentation(> ??spp) explain it any better?

I found the answer in this paper, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191340/

especially this figure,http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191340/figure/F3/

There are no inline spp docs.

if you type in ??spp at the R prompt you'll get the docs. They're not expansive, but they explain the different parts of the library.

If you've found the answer, perhaps you might consider posting it as a full solution in the answers section so that others with the same difficulty can see it?

I found the answer to this question and some more interesting details that people who stumble upon this might also need. First look at this paper, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191340/ and especially this figure, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191340/figure/F3/. The MSER is a ratio of the fraction of discovered peaks to the fraction of the sampled reads to recapitulate them, so if you are able to return all of the peaks with a small sample of reads then you have excellent coverage. Now even though you have great and well defined peaks you need another sample to confirm that they are indeed significant, and you can do this with the IDR, see this website - https://sites.google.com/site/anshulkundaje/projects/idr. The IDR is laid out pretty well in the supplemental material for this ENCODE paper, http://www.nature.com/nature/journal/v489/n7414/full/nature11245.html. Beautiful!!


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Is there a standard definition for plant "maturity"?
Is there a species-agnostic metric for identifying plant maturity?
There seems to be plenty of literature defining life-history stages for specific crops, but it is not clear if there is a generic definition.
In the context of crops, I would like to be able to identify the stage at which plants are no longer exhibiting juvenile traits.

Exactly what types of traits are you looking for? First onset of flowering seems to me to be an obvious choice, since sexual maturity is the definition of being an adult. Do you find this insufficient, and if so, why? It is generally easier to use "positive" definitions (presence of traits) than "negative" ones (e.g. lack of juvenile traits).

Also, I realize that some plants only reproduce clonally, but this should be less of a problem(?) in crop plants.


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Do individual (free) nucleotides base-pair with other free nucleotides?
I had a student ask me about this and my google-fu let me down. He asked if individual nucleotides (not in a nucleic acid) base-pair with their complementary nucleotides, essentially forming many dinucleotides. I would think this would occur, but have no evidence one way or the other. If it does, how does this impact the usage of nucleotides in nucleic acid synthesis? I'd assume they have to be broken apart first...

The base-pairing in solution only provides 2-3 hydrogen bonds, which the nucleotides could also form with water itself. There are no stacking interactions between bases in water like in a DNA helix. So I strongly doubt that the nucleotides would form a significant amount of dimers in water.
I found a paper confirming my assumption:

Short nucleotide fragments such as mono- and dinucleotides are
generally unable to form stable hydrogen-bonded base pairs or duplexes
in water.
Minimal nucleotide duplex formation in water through enclathration in self-assembled hosts.

An easy way to confirm this would be to observe the proton NMR spectra of free nucleotides. Base-pairing in nucleic acids shows characteristic signals in the imino proton region (around 10-15 ppm), which are not visible in unpaired nucleobases due to chemical exchange.

In a DNA strand, there are additional energetic advantages of the hydrophobic bases being internalized to the core the DNA double strand and the polar phosphate backbone being more uniformly exposed to solvent.
Thermodynamically, the formation of the two individual molecules of base monomers forming a pair the solvent will still be exposed to the hydrophobic bases. So such a single base pair would be driven by the energy of the two or three hydrogen bonds in the base pair formed.
This is why you will not see such a complex forming in water; the hydrogen bonds with water are at least as strong as the hydrogen bonds with the bases. But such base pairings can in other circumstances be made to form.
If there are no exchangeable protons for hydrogen bonding in the solvent itself, there will be an energetic advantage to the complex.  If there are no exchangeable protons (as with DMSO or carbon tetrachloride) such complexes can be detected by NMR.  Even in cases with single hydrogen bondable protons on the solvent, these bimolecular complexes are observed.


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How compatible are mammalian digestive systems?
I'm interested in what kinds of nutrients mammals extract from food and would like to know how similar are the outputs of these systems.
For example, if it is possible to successfully replace one mammal's digestive system with another mammal's one (all the connections are correct). Would the recipient survive or experience some form of malnutrition resulting in death?

There would be a powerful immune reaction. they try to use pig valves in human hears, and those are just cartilege. AFAIK no trans specis grafts have been done.

I think this would depend entirely on the diet of the host and donor mammal.
Assuming they are of similar size and diet, I don't see any reason why this wouldn't work. The gut tends to absorb more or less everything in the food.
If the diet of the two mammals differed significantly, I could see some problems with eating the correct foods. Herbivores with the significantly shorter carnivore gut would have trouble killing and eating things without carnivore teeth/claws/what have you, and the plants would not provide enough nutrition on their own. Rabbits, for instance, have a two-pass digestive system, so in order to use a rabbit gut the mammal would have to eat their own feces regularly. (Rabbits have digestive bacteria in their colon, but grass has to travel to the colon and then back 'upstream' to the absorptive part of the gut. So this is achieved by going around again.)