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Relationship between our microbiome and personalized nutrition
Recently, it has been asked whether there are 'metabolic types' between humans that can benefit from a sort of personalized nutrition. One answer suggested that one discerning factor could be the human microbiome. It is known that host–microbial symbiotic states might respond differently to diet and drug intake, but whether this can be useful for personalized nutrition is less clear to me. I wonder:
does the microbiome affect food metabolism? (useful for personalized nutrition)
OR
is the food that we eat affecting the microbiome? (less useful for personalized nutrition)
I know the answer is probably both, but there are examples causally demonstrating one branch and excluding the other?

does the microbiome affect food metabolism?

Most definitely (and not surprisingly). The Arumugam paper [1] notes that

The drivers of [enterotype 1] seem to derive energy primarily from carbohydrates and proteins through fermentation, … because genes encoding enzymes involved in the degradation of these substrates (galactosidases, hexosaminidases, proteases) along with glycolysis and pentose phosphate pathways are enriched in this enterotype […]
Enterotype 2 … is enriched in Prevotella … and the co-occurring Desulfovibrio, which can act in synergy to degrade mucin glycoproteins present in the mucosal layer of the gut […]
Enterotype 3 is […] enriched in membrane transporters, mostly of sugars, indicating the efficient binding of mucin and its subsequent hydrolysis as well as uptake of the resulting simple sugars by these genera. […]
The enriched genera indicate that enterotypes use different routes to generate energy from fermentable substrates available in the colon, reminiscent of a potential specialization in ecological niches or guilds. In addition to the conversion of complex carbohydrates into absorbable substrates, the gut microbiota is also beneficial to the human host by producing vitamins. Although all the vitamin metabolism pathways are represented in all samples, enterotypes 1 and 2 were enriched in biosynthesis of different vitamins […]

[All emphasis mine.]

is the food that we eat affecting the microbiome?

Yes, just as certainly. I don’t have a publication handy but it should be obvious that our food influences our gut microbiome – in the extreme case, it can kill it (consider antibiotics side effects).
[1] Manimozhiyan Arumuga, Jeroen Raes & al., Enterotypes of the human gut microbiome, Nature 473, 174–180, May 2011.

Yes, the microbiome affects food metabolism and the diet affects the composition of the microbiome. +1 to Konrad for his response. This is an area of research in which I and colleagues are engaged. Frankly, it is easier to assess the changes to the microbiome based on diet rather than looking at the fecal material to determine (unused) metabolic energy or potential given a certain input (i.e, from a controlled diet).
Recently, we've fed humans a high number of servings of whole grains. The response is highly individualistic with some declines and others increases in Firmicutes, for example. Typically, Bacteroidetes numbers move opposite to Firmicutes, but not in all individuals. These observations are also seen by others in this growing field of research.
The "enterotypes" paper Konrad cites is beginning to see some resistance in the field in that the three enterotypes defined by those authors are not really so cleanly defined when one takes a closer look at more individuals. Time will tell how well one view or the other holds.


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How do plants intake minerals through their leaves?
How do plants intake the fertilizer when it is sprayed all over the leaf surface as a foliar feed?

A nice review by Wocjik (2004)

They absorb minerals through pores in the leaves known as stomata, this is some what similar to the way a medicine patch is absorbed on human skin except for the fact that the human skin has sweat pores instead of stomata.
Here is a animation of them opening and closing on a tomato plant provided by Wikipedia:
sources:

A nice review by Wocjik (2004) (from the comments)
http://www.wisegeek.com/what-is-foliar-feeding.htm
http://en.wikipedia.org/wiki/Foliar_feeding
http://cronodon.com/BioTech/Plant_Transport.html

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Resources for finding all drugs of a certain class
I may be embarking on a project involving a fairly extensive healthcare records data set, looking for the use of a particular type of drug (for example, "Proton Pump Inhibitors"). But these drugs are usually listed by their trade or generic names - is there a well maintained resource for looking up what drugs are members of a certain class (if class is indeed the right word)?

The WHO has their own methodology, the Anatomical Therapeutic Chemical (ATC, thank you commenter) classification system, for organizing such data (its impetus is comparing results between studies).
Also, if you have $900 sitting around, you can get a subscription for the United States Pharmacopeia.  I'm not sure if that can be spread across multiple subscriptions for an organization like the Red Book David mentions.

+1 for the links & mention. Does WHO publish any public data we can use? That could be interesting...

@DavidP.Hochman I think all of the WHO's data are public, but I don't know where it is published.

Comprehensive, up-to-date drug information including trade names and categories are available from Micromedex® (a division of Thomson Reuters) in the RED BOOK.
It's free to use anywhere (even on a mobile device) by anyone in your organization ... after you pay the subscription fee.  The fee for research is much less than the fee for commercial use.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Downloadable worldwide database of disease statistics?
I am looking for a downloadable database of disease statistics. I have emailed the good folks over at HealthMap, but they haven't gotten back to me yet.
As far as I can tell, their data relevant to my project is gathered from the World Health Organisation, ProMED Mail, GeoSentinel, Google News, Moreover, Baidu and SOSO.
I can scrape the data from each of these sites and aggregate it in the same way HealthMap has, but that is a large project in and of itself, and I only have a couple of months for this not-for-profit project.
Do you know of a downloadable worldwide database of disease statistics?

I assume the html spreadsheet produced by List View Only and Advanced Search on HealthMap is not granular enough?

I took a quick peek and HealthMap and their JavaScripts are publicly viewable.  As such, I believe cross site scripting would be quite feasible.  In other words, call their JavaScripts from a page you develop on your server to create a feed of the data you want.
In this way, minimal effort on your part could leverage their data scraping efforts.  If you're adding your own data then you're basically doing a Mashup.
That said, my concern with doing this is potentially violating their copyright.  I would email them saying if their database is not available then you wish to use cross site scripting to access this data for your project, and unless they let you know otherwise by (specific date) you will assume this is acceptable.
I'm not a lawyer, so use this advice at your own risk.  =)

Fortunately the Head of HealthMap got back to me yesterday, and we are currently in negotiations. However, it is good to have this fallback, so thanks. +1

Excellent news! - HealthMap are opening up a JSON API for us to use =D

In general it's always better to politely ask and wait for a reply. Cross-site scripting means you are using their bandwidth so you should only do that if you have permission.


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What data / tools exist for mapping of disease trends?
I was just looking at the Google Flu Trends map.  Google Insight could be used to gain similar information for other trends in disease keyword searches.
I started wondering how valid are keyword searches to represent the spread of diseases.  In some ways I think it could be a good representative, but in others I think it would be susceptible to influence by mass media.
Do maps of clinical data exist that could be compared to this Google data?  If so, where could I find some.  =)

You can use official sources such as hospital admissions, prescriptions for drugs fighting the disease you are tracking, sales of over-the-counter medicines.
CDC (cdc.gov/flu/weekly/, cdc.gov/outbreaknet/outbreaks.html, etc), WHO, EuroFlu Weekly Electronic Bulletin map official clinical data, Aurametrix uses these sources.
Several scientific studies have compared GFT, twitter, even facebook with official sources.  Johns Hopkins study (pubmed/22230244) used data from local hospitals in addition to CDC.
My sampling studies too showed that social trends are surprisingly good, despite all the noise, but provide good estimates only for highly populated areas.
You might also want to check Sickweather's algorithm, healthmap, usgs disease maps and industry databases providing coverage of pharmaceutical companies and product sales.

For myself, I've not been terribly impressed with the use of keyword searches and the like as methods of predicting influenza or other diseases. They are, when it comes down to it, somewhat glorified extensions of a syndromic surveillance system, just for "I feel sick" instead of "Honey, pop down to CVS and pick up some NyQuil?"
It's also apt to get you some odd results. I tried to use a "Google-style" analysis to match some rotavirus data to Google searches - I believe I was 7 entries down before I ever got to anything rotavirus related, and even that was "rotavirus", which doesn't suggest it would be useful as a symptom detector, but rather people Googling a disease their doctor said they had. The top results, some of which fit really well? A series of prom dress-related searches. In order for it to be useful, you'd have to extend Google's system.
But, as a thought experiment, if you'd like to match it to data, there's a number of potential data sources publicly available from the CDC. Morbidity and Mortality Weekly Report for example publishes weekly counts for a number of notifiable diseases.


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Automatic cropping of collimated digital X-ray images
Do you have any suggestions for a library which offers an algorithm to crop digital X-ray images automatically?
We receive full-size images (43x43cm) from a detector, independent of the collimator settings. If the collimator has been closed to 10x15cm, we need to crop this area. This should be done automatically, so that the user does not even see the full-size image because it contains a lot of information which is not needed.
Now we are looking for a good library which offers such an algorithm. This sounds like a simple task, but depending on the dose and the collimation, it can be pretty hard to detect the collimated area of the image. Therefore, we are looking for a professional solution rather than implementing it ourselves.
Any suggestions?

Why are you looking for libraries if you do not want to implement the software yourselves??? Are you rather looking for some premade software?

There is a software package ImageJ which can be used to what you are asking. Depending on your capability and the complexity of what you are doing you can either write a Macro in the program to crop images or you can extend the program in Java and write a custom plugin to do what you describe.
I used this program for years it is a very strong program.

Thanks for your comment, but... "we are looking for a professional solution rather than implementing it ourselves".

I think ImageJ is actually the best option. You can pay a freelance developer to write the macro for you: it does not seems a big task the way you describe it

I second the recommendation for ImageJ. It's not difficult to write a simple macro (or a developer to do so) to crop an image. The nice thing about ImageJ (and I would recommend using the updated Fiji software at http://fiji.sc ) is that it is open source and used heavily for many biological science needs. If it works for microscopy, it'll work for x-ray imaging.


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Human disease and associated phenotype database?
Does anyone know of any good databases that contain symptoms for diseases and other ailments in humans? I've tried working with UMLS, but thats been impossible to work with. I've also tried working with the disease ontology website (http://www.disease-ontology.org/), but that doesn't seem to be very...comprehensive...in terms of symptoms for the diseases they have.
I've tried looking at the the disease database (http://www.diseasesdatabase.com/), but they are reluctant to hand over the raw data, if I understand correctly.
Anyone have better ideas?

In what way is UMLS hard to work with? Can you elaborate?

Wouldn't ICD10 sufice if you index it properly?

Here is a list this might be of help http://www.nature.com/nrg/journal/v10/n1/fig_tab/nrg2483_T1.html

It seems to me like you're effectively wanting to make a decision matrix.
So... As said above, ICD and SNOMED CT going to have codes for your diseases and symptoms. I'd lean toward SNOMED CT due to the way it organises concepts. Essentially from broad to specific. That way users can enter very specific symptoms, and your matrix only needs to have symptoms as specific as is required.
For example you can say "vomitting" is a symptom of "alcohol poisoning" in your db. And if a user enters "projectile vomitting" the SNOMED structure recognises this as a type of vomitting.
However - Symptoms don't make the disease, and most diseases have a huge array of 'possible symptoms' (Which is why SNOMED CT doesn't have such relationships). So it's not an easy undertaking. Hence why those who've made such db's (as you've linked to) are reluctant to share their IP, at least without $$$.
If you're going to make your own, here's some tips.
Consider:

only diseases relevant to your use case - eg. Aged care doesn't require paediatric disorders;
exclude non-specific symptoms;
rank your symptoms by frequency - eg. 60% of pregnant women have morning sickness, where as 100% have an HCG > 10*

Hope this helps. And good luck.
edit- there is a similar thread on LinkedIn
*fabricated statistic :).


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Why do the brains of cocaine-users shrink faster than the brains of non-cocaine users?
http://news.sciencemag.org/sciencenow/2012/04/cocaine-may-age-the-brain.html?rss=1

Cocaine-dependent individuals showed a significantly greater-than-normal age-related decline in gray matter in prefrontal and temporal regions compared with healthy controls. By contrast, parts of the striatum appeared resistant to age-related volume decline in the cocaine-using group. Enlarged striatal volume has frequently been reported in stimulant-dependent individuals,5, 6 possibly reflecting a marker of reduced dopamine neurotransmission in this dopamine-rich brain region where drugs like cocaine work. Decline in striatal dopamine receptor density has been associated with normal age-related cognitive decline.7 The relative absence of age-related changes in the striatum of cocaine-dependent people may thus reflect another feature of an abnormal brain ageing process.

Could it be related to possible neurotoxicity, or to the long-term effects of dopamine receptor downregulation? Could the effects also be generalizable to those who take dopamine-based ADD medications?
A link to the Letter to the Editor appeared in Molecular Psychiatry to which the ScienceNow article refers:
Cocaine dependence: a fast-track for brain ageing?

Could it also not be related to non-cocaine lifestyle changes, such as diet?

The mechanism of action of cocaine is dependent on pre-existing dopamine production and secretion. Normally, secreted dopamine is cleared from the synapse via the dopamine transporter (DAT) located on presynaptic dopaminergic terminals. Cocaine inhibits
this reuptake of dopamine, increasing it's duration of action on post-synaptic dopamine receptors. Thus, cocaine's effect depends on neuronal dopamine production. Without intrinsic dopamine, cocaine would have no effect. This is actual not exactly true though because cocaine also inhibits serotonin and norepinepherine reuptake transporters as well but the same argument applies to those neurotransmitters as well.
The overall effect of cocaine on the nervous system is extremely complex as it prolongs the action of dopamine, serotonin and norepinephrine wherever those reuptake transporters are present. There is a particularly high density of DAT in the basal ganglia and nucleus accumbens. What these areas of the brain normally do is under intense study and debate. The accumbens may play a role in goal directed behavior and incentive salience, which is the attribution of value to various actions or objects in the environment. This is what naturally guides us to perform one action over another. The simplistic view is that cocaine "highjacks" this system such that cocaine itself acquires greater incentive salience than natural reinforcers such as food, sex, money etc.
Getting back to the original question regarding why cocaine causes brain atrophy. This appears to be a finding quoted from a paper by the original inquirer. It is not obvious to me what the mechanism of this atrophy would be. I suggest you look at the discussion section of the paper from which that abstract was quoted to see what the authors suggest. However, to my knowledge, such atrophy has not been widely discussed in the cocaine literature but I could be wrong.
For further information see Sulzer. 2011. How Addictive Drugs Disrupt Presynaptic Dopamine Neurotransmission.

To the poster talking about "brain shrinkage due to lack of fresh blood stimulation." This has no scientific basis.

Could you maybe add a reference to a good review article on the effects of cocaine to back up your answer?

Neuron. 2011 Feb 24;69(4):628-49. doi: 10.1016/j.neuron.2011.02.010.
How addictive drugs disrupt presynaptic dopamine neurotransmission.

Cocaine hits the brain with dopamine creating the desired high, which, the users seek. When used repeatedly, the brain begins to confuse it's own production with the user's introduction. Slowly, the brain begins to depend on the user's introduction and slows its own production to the point where it no longer produces it. This lack of production causes the part of the brain responsible for dopamine to shrink. It shrinks because it is tissue that is not being used and therefore doesn't get the proper blood flow to it and begins lose its health. Blood stimulation is lost, cell health is lost and size is thereby lost.
The brains of heavy cocaine users display little to no age-related brain shrinkage as compared to non-users because their brain has already shrunk to its limit. The shrink is due to lack of fresh blood stimulation. It is like a sponge that no longer is getting water and shrivels. After 2 days the sponge stops shrinking, it doesn't eventually shrink to a dust particle. It shrinks to its water-free size, the same way the cocaine user's brain shrinks to a blood-stimulation-free size. Age can't further shrink what's already maxed out in shrinkage.

Do you have any scientific sources to support your answer?

Nope.  "The loss of gray matter was most severe in prefrontal and temporal lobes, areas critical for executive function and memory."(ref)  Dopamine is produced in the substantia nigra and the ventral tegmental area.(ref)


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Why is 'Grudger' an evolutionary stable strategy?
I am currently reading 'The Selfish Gene' by Richard Dawkins, which I am sure many here have read. The topic are evolutionary stable strategies (ESS) regarding cooperation.
I apologise for the long question. If you are already familiar with the topic and Dawkins' model of Cheat, Sucker and Grudger: my question is, how can Grudger be an ESS if it could be invaded both by Suckers (because they have no disadvantage against Grudger) and Cheats (because a Cheat minority is unlikely to meet the same Grudger twice, turning Grudger into Sucker effectively)?
More detailed:
The model
Near the end of chapter 10 (p 185 in my version), Dawkins uses a model of birds who clean each other of parasites, therefore helping in survival (as cleaning themselves they cannot reach every spot of their body). He defines three different behaviours for the model:

Sucker - birds who indiscriminately help and clean other birds
Cheat - birds who let others help them but never do so themselves
Grudger - birds who help others and remember who they helped. If the same bird does not help them later (reciprocate), they will not help that bird again.

Claim: Cheat and Grudger are ESS
He claims that both Cheat and Grudger in themselves are ESS - that is, if all birds behave this way, none of the other behaviours can develop because they will be immediately penalised by lower chances of reproducing.
The part that makes sense: Suckers is not an ESS, Cheat is
Sucker is of course not an ESS. If all birds were Suckers, any Cheat that developed would have a huge reproductive advantage and Cheat genes would overtake the population.
Being an ESS makes sense for Cheat. If all birds cheat, nobody will ever be helping each other. A minority of Suckers would be spending all their time helping and not getting anything in return, Cheats have the advantage and Suckers die out again. Grudger would be unlikely to meet a Cheat who they helped before again, so they too will spend all their time helping and die out again.
The part that confuses: Grudger is an ESS?
But Dawkins also claims that Grudger is an ESS, and he seems very confident in that. Now I don't consider myself enough of a smartypants to claim that he's wrong, but I don't understand how Grudger can be an ESS. If all birds behave in this way, and for any reason some Sucker developed - the Sucker would have no disadvantage. All birds would still always be helping each other, so nothing would stop the Suckers from propagating equally well as the Grudgers, invading the gene pool. That's already the ESS broken, but even further, the presence of Suckers would mean that if Cheats came up, they would have a realistic chance of surviving - Grudgers would shun them after having helped once, but if the number of Suckers is large enough, Cheats will have an advantage.
Moreover, back to the initial setting of Grudgers only - if a Cheat developed, he would be unlikely to meet the same Grudger twice, receiving the benefit all the time but never paying the cost. He would have an advantage and spread Cheat genes.
The problem
I'm not familiar enough with how these kinds of models are calculated in order to state chances that Cheats will take over completely, but however I think of it Grudger does not seem to be an ESS to me.
Does anyone have an explanation why Dawkins is so sure that it is? Seeing as in nature we do see patterns like Sucker and Grudger all the time, I must be missing something important here.

great question. I hope one or all answers address group selection. Which I don't think was widely accepted at the time that the selfish gene was published.

@David It still isn’t widely accepted. There are some attempts to put it on a new footing but they certainly don’t represent the majority view of the evolutionary biology crowd.

It's not an evolutionary stable strategy from selection alone. For any positive integer n no matter how large, always defect is an evolutionary stable strategy because no mutants with any strategy in a population with the pure strategy of always defect will be selected for. However, in real life, if the prisonners dilemma is iterated 4,000,000 times, genetic drift will kick in leading to a mixed evolutionary stable strategy of complex strategies all of which are a type of grudger.

Unfortunately it is not necessary to invoke group selection to answer this question.  This is one of the reasons that Dawkins likes this discussion so much - he does not believe in group selection and so the discussion in SG does not invoke group selection.  ESSs are described in the book as the product of direct competition or interaction between genes.
ESSs in this case, can be described in terms of game theory.  In the famous Prisoner's Dilemma experiment, Grudger is similar to tit for tat, which 'won' the competition in the original Axelrod contest.
To see how this works you make a simple win/loss game matrix:
     G        NG
G    win 1    win 3
NG   lose 3   lose 1

if you are groomed you win 1, if you are groomed, but you don't have to groom - even better win 3 (say)
If you groom but are not groomed, lose 3
If neither of you are groomed, you both lose 1
one might argue the exact proportions, but the point is that getting some thing for nothing is better than reciprocating, and getting nothing for your efforts and time are a loss, because you could have been getting groomed by someone else. As you can see cheaters end up in the top row all the time.  grudgers end up along the diagonal, and once in a while in the lower left, Suckers get stuck in the lower left a lot whenever there is a cheater around.
now run this encounter over and over.  A behavior which scores negative the more times you run is not stable - they are going to disappear from the population, at least if this disadvantage is real
It has more than one stable outcomes in populations, a population that is full of Grudgers will all groom each other as before you know everyone, you assume they will reciprocate.  Everyone wins!
Any invading Cheaters will quickly be at a disadvantage, in that they will not be groomed more than N times where N is the number of grudgers in the community.  Note that there is an equilibrium here - the Cheaters may exist in a small number - when N is large enough for a cheater to get enough grooming to make a 'living'.
Suckers can also exist within a population of grudgers, but a population of Suckers where Cheaters show up are quickly sucked dry by the cheaters over several generations where you tally up 'points' and give more, healthier offspring to high scorers.  They are not ESS stable.
Cheaters are also stable - nobody ever wins, but they don't lose big either and any invading grudgers can't get groomed.

Thanks for the detailed answer :) After reading on, I found an explanation two chapters later, essentially what you said - Cheaters may exist in a small number and so may Suckers, but they would be decimated by the Cheaters again once both became significant. Dawkins admits this is not truly an ESS and instead offers what Axelrod called it, a 'collectively stable strategy'.

“… as the product of” is missing a few crucial words at the end. As an aside, your gibe at Dawkins’ opposition to group selection is really mis-placed. Last I looked his is still the majority position among evolutionary biologists, and this isn’t the right place for a detailed discussion of the subject, and your current formulation is putting Dawkins’ intelligence in question (“does not believe in”) and accuses him of using a sleazy argument (“[which is why] he likes this discussion so much”) which is quite inacceptable in polite conversation.

@Konrad Rudolph  yes, but EO Wilson et al's arguments (to cite one example) are serious ones.  Fortunately Science is not a democracy and alternative investigation is still allowed; There is still substantial reason for question and the best journal editorial boards still see this as a reasonable question to raise.

@Armatus this is an important point- it is essentially the reason one might find selfish genes.  Selfish Genes are the small proportion of 'cheaters' in the community of otherwise 'grudger' genes. It is the prediction of the existence of Selfish Genes, that proves that Genes are the medium of Genetic Selection that motivates Dawkins to write the book.  I personally think Dawkins is a man of great insight, but don't feel that means we must totally agree with the axiomatic assumption that DNA must be the only medium of selection in biology.

@shigeta I can’t personally comment on the validity of his arguments (but I will note that others who can have described them as “[revealing] a rather disturbing lack of familiarity with a huge body of scientific literature from the past few decades”, implying that their arguments are rather vacuous). But that’s not the point here. You didn’t raise a reasonable question, you used a questionable opportunity to accuse another scientist of intellectual dishonesty without a shred of evidence.

@shigeta You are using 'Selfish Gene' in a different sense than Dawkins explains, which has nothing to do with selfish (Cheat) behaviour. He also doesn't state DNA is the only medium of selection. But my question is answered and this is not the place for discussions like this. Thank you :)

@Armatus see http://en.wikipedia.org/wiki/The_Selfish_Gene#Genes_can_reproduce_at_the_expense_of_the_organism  Selfish genes are genes that reproduce at the expense of other genes in the same organism.  They are I think very much like Grudger - who takes reproductive advantage from other community members, the analogy I believe is made in the book because Dawkins wants to support his main point - why the prediction of the Selfish Gene and its subsequent discovery is so important to biology.  Maybe I should ask -why you think he discussed it in this book?

@shigeta It is very clear in his book that 'Selfish genes' are not a kind of genes. He explains how all genes are 'selfish' - please read the correct section of the Wikipedia article (http://en.wikipedia.org/wiki/The_Selfish_Gene#.22Selfish.22_genes). I personally find his choice of word an unlucky one because it asks for misunderstandings like this.

Not sure this is the case.  The Selfish Gene he gives as an example is a gene which does nothing for the organism or other genes.  See Triver's work on Selfish Genes. Triver's predicted their existence.  Some selfish genes literally freeload off of other genes.  Most other genes are cooperative.  I'll leave it at that for this question.

on Selfish Genes: "As Austin Burt and Robert Trivers show, these selfish genes are a universal feature of life with pervasive effects, including numerous counter-adaptations. Their spread has created a whole world of socio-genetic interactions within individuals, usually completely hidden from sight."  http://www.hup.harvard.edu/catalog.php?isbn=9780674027220

Yes, they may use the term "Selfish Gene" this way, but the conversation here was about Dawkins and as it seems, he uses the term differently (which is his good right). His theme is not that "selfish genes" exist, but that all genes are selfish, and nothing else - since all altruism/cooperation is merely a product of lower-level selfishness. I think I remember the "selfish gene" example you mentioned, but he used it only to illustrate that genes' interest does not have to be the organism's and he most definitely did not say that only this specifically was a selfish gene.

In an infinite, well mixed population with single pairwise encounters, Grudger is indeed not an ESS.  In fact, as you correctly note, in such a model the Grudger and Sucker strategies are indistiguishable, as the probability of anyone encountering the same individual twice is zero.
To make it possible for the Grudger strategy to survive against invasion by Cheaters, we must somehow extend the model to allow pairs of individuals to meet more than once.  Some ways to achieve this include:

Finite population size: if there are n individuals and they each participate on average in m encounters during their lifetime (or during the average time for which their memory persists), then each of them will encounter every other individual m / (n−1) times on average.
Viscous population: this is a general term for populations that are not well mixed.  For example, if individuals live on a spatially extensive landscape, have limited movement rates and interact only with nearby individuals, then two individuals that meet once have a higher probability of meeting again due to spatial proximity.
Iterated encounters: in these types of models, pairs of individuals are assumed to interact with each others some (fixed or random) number of times before parting and finding new partners to interact with.  In this way, repeat encounters can be included even in infinite, well mixed population models.  While this may be a reasonable approximation in some cases (e.g. for models of spousal cooperation in serially monogamous species), frankly the main reason for studying such models seems to be that they're mathematically simpler than finite or viscous populations.

Not entirely coincidentally, many of these mechanisms can also permit the survival of pure Sucker or altruist strategies against invasion by Cheaters through group and/or kin selection (or more general forms of assortment).
Ps. Even with these mechanisms, Grudger will never be a strict ESS anyway, since in any population consisting of only Grudgers and Suckers both have the same payoff.

BTW, if you have even a single cheater (which due to random mutations you usually will end up with), "Grudgers and Suckers both have the same payoff" becomes false.


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

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

Thank you.

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


text:
Is it possible to live without health problems sleeping one day and not the other?
Basically, I want to know if it would be humanely possible to sleep one day, skip the next, sleep, skip, sleep, skip, etc, with a 8 hour sleep time.
If you need any extra information, let me know.

What window of time are we talking about? 1 month, 1 year, lifelong?

It would be interesting to consider 6 years and lifelong.

You may be interested in Why do humans practice monophasic sleep cycles? biology.stackexchange.com/q/319/238

(too long to be a comment)
You may be interested in http://en.wikipedia.org/wiki/Phase_response_curve.
This graph shows how the body's circadian rhythm normally works: http://en.wikipedia.org/wiki/File:Body_Temp_Variation.png.  Body temperature decreases during the night (apparently due to more melatonin production.
I conjecture that the proposed schedule would interfere with the Circadian rhythm.  Melatonin is the hormone that regulates sleep--it causes drowsiness.  It is suppressed by blue light (because we get exposed to blue light in the daytime).
Aside from this, I am also very interested in the effects because I have personally wondered about the same question.  The thing I am worried about is significant immunosuppression.
A larger question might be--"Why is sleep necessary?"  Does it serve only to conserve food (which is very useful if you are living on subsistence) or does it serve a greater purpose? (whenever I have asked anyone about it, they always cite "regeneration" and some have cited the recycling of neurotransmitters.  Personally, I'm a little skeptical.)
One final study: there was a study by Dement on the effect of dream deprivation: he took several people and woke them up whenever they went into REM sleep.  Then, there was a period when the patients were not woken up.  He found that there was a "REM rebound"--that they would go into more REM sleep after they had been deprived of it.  This seems to indicate that dreaming, specifically, may serve a significant purpose.

I'm not aware of any study testing this hypothesis. I would surmise that adverse health effects are likely because the circadian clock operates on a 24-hour time frame, and because lack of sleep for ~40 hours every second day will alter hormone, cytokine and other measures to levels not normally seen in 8-hour sleep/16-hour wake cycle.

You may want to cite some paper showing that perturbation of sleeping results in significant perturbation of hormonal rhythms.

@nico Why don't you add an answer explaining that? And what about splitting 4hs each day?

@Peter Tamaroff: because I don't know any paper showing that (but I would be very interested in seeing one)!


text:
How can I normalize mRNA samples for sequencing?
Is there an easy, inexpensive, not too labor intensive way to normalise mRNA samples so that even though one loses information of gene expression levels, each of the transcripts in the transcriptome is equally represented in the sample for sequencing? This is to say, one has a uniform distribution of transcripts, so that the lowly-expressed transcripts still have a good chance of being sequenced.
I have seen a few papers mentioning protocols for mRNA normalization, but I can't tell if any of them are practical in real life wet lab situations.

I found the link to a commercial product by Evrogen here:
http://www.evrogen.com/technologies/normalization.shtml
They claim their method is compatible with nextgen sequencing platforms:

cDNA normalization using duplex-specific nuclease (DSN) is a highly
  efficient approach that can be applied for normalization of
  full-length-enriched cDNA (Zhulidov et al., 2004; Zhulidov et al.,
  2005). The resulting cDNA contains equalized abundance of different
  transcripts and can be used for construction of cDNA libraries and for
  direct sequencing, including high-throughput sequencing on the next
  generation sequencing platforms (Roche/454, ABI/SOLiD or
  Illumina/Solexa).

And the most up-to-date reference seems to be this Curr Protoc Mol Biol. paper by Bogdanova et al.:
http://www.ncbi.nlm.nih.gov/pubmed/20373503


text:
Does anyone have any TOPO directional cloning tips?
I'm just about to start working on a TOPO cloning after I couldn't get it to work with standard restriction/ligation. Does anyone have any tips for TOPO cloning?

Can you provide the protocol you actually used so that we can better identify what could have gone wrong? How old is the kit? Was it stored correctly? Which cells are you using for transformation?

Ah sorry I should clarify, I first tried the traditional approach to cloning by inserting restriction sites either side of my gene via PCR then double digesting the PCR product and target vector. Following double digestion I then attempted a ligation but I nor my colleagues could get any positive transformants. So I am moving to a different method of cloning using the TOPO kit and I am wondering if anyone has any pointers before I begin using it. It is the pET101/D-TOPO kit.

This may fall under the category of a discussion. I will say that you should make sure that you have the right polymerase if you're doing TA TOPO cloning.

And if you're troubleshooting, I would check the activity of your ligase. If your digestions are working then your doubly-digested PCR insert will ligate with each other. If not, you may have some issues with your restriction enzymes.

thanks @bobthejoe. I suppose you are correct it is more of a point of discussion, apologies for that. The original cloning underwent trouble shooting and the problem could could still not be solved.
This question can be closed.

I think the best way would be to include the details that you've mentioned into the question prompt. If we know what you've tried for troubleshooting, that would be the cherry on top! Essentially, everything that @leonardo asked and we'll go from there.

From what I read, @Ben seems to be saying that he is not looking to troubleshoot the original (traditional) method which failed and is only looking for tips on using the TOPO kit as a first-timer..

@gkadam - this is how I read the question as well. Ben may proceed either way (traditional or TOPO) but the PCR product is the problem with either approach as currently executed.

See this meta question on the closure of this question

I have lots of experience with the TOPO TA kit which is very similar to the kit your using. Here's a link to the TOPO Directional cloning product page which shows a schematic of the enzymatic ligation.
From your comments, you said you have doubly-digested the PCR product. This is likely your point of failure unless you are absolutely confident that your enzymes work at blunt ended DNA (which I can almost guarantee does not work). Restriction digestion of PCR products will only work if there are at least a few bases on either side of the recognition site so that the restriction enzyme is able to "grab on" to the DNA. What you are mixing instead, is blunt-ended PCR product DNA + cohesive-ended vector. This will not work under any circumstances as is.
There is a simple solution.
Add 3'-A overhangs to your PCR product directly. The back of the TOPO manual tells you how to do this as well as many other sources. Ligate this using your TOPO kit to produce a shuttle vector that you can then doubly digest your insert out and gel purify it. Then you may ligate this purified, digested DNA with your previously digested destination vector.
Note that in my hands and in others in our lab, topoisomerase is unstable and has a short half-life. It is especially sensitive to temperature changes (warming from -20°C to 4°C) which you wouldn't expect since it is designed to work at room temperature. The vector is not affected, but without a working topoisomerase, the ligation step does not occur and the DNA does not transform.
As an aside: If you plan on doing more cloning in the future and need to replace the kit, I would recommend getting the basic TOPO TA cloning kit, clone your PCR product (with 3'-A overhangs) into the vector, transform, pick white/light blue colonies for screening then cut out from the TOPO vector (the shuttle vector) for downstream applications. The fact that it is directionally cloned or not into the TOPO vector is of no consequence unless it also happens to be your destination vector.

You're welcome. :) I should mention that since you have the directional TOPO kit, you'll need a different ligation method that does work with either blunt DNA (eg, a blunt cut plasmid) or 3'-A overhangs (the original TA kit, pGEM-T, home made T-vector, etc). The addition of those extra bases in the directional kit will also hinder direct ligation.


text:
Does muscle growth trigger angiogenesis?
So heavier people generally have more blood than lighter people (this is why heavier people generally need to take higher doses of medication for the same effect of medication). They also have more blood to draw from. But this fails to differentiate between muscle mass and fat mass.
So here's my question: Is the net angiogenesis per gram of muscle more or less than the net angiogenesis per gram of fat?

Without having an exact proof, I'd definitely say yes. Muscles need more nutriments to function than fat, and if you look at the body builders you'll see that some those guys have thicker brachial veins than an average aorta.

See this article as to why your underlying assumption is incorrect.  Higher doses must be given due to the high fat solubility of some drugs as well as differences in liver and kidney size.

Oh wow - thanks for that information. Doesn't that mean that for those with high muscle mass (relative to fat mass), that the guidelines for how much drug they take might be inaccurate?

Specific doses are usually not calculated as several factors may dictate upgrading the dose, not only weight or fat content. Drug sensitivity can be caused by the speed at which the liver removes the drug from the blood or genetic factors that make the drug more effective or the severity of the condition for instance.  Weight is just one factor that will increase the dose, all other factors being equal.

Muscle is heavier than fat so actually it does. Muscle growth directly increases angiogenesis. Particularly the mechanism relies on hypoxia, any tissue with less than adequate blood supply secretes factors which result in angiogenesis. This is seen frequently when muscle is bulking as this increases the oxygen requirement but is also seen in heart muscle where subsequent to a heart attack tissue which isn't dead but mildly suffering caused new blood vessels to grow to supply this tissue (as the other ones are blocked which was the cause of the heart attack in most cases).


text:
Under what circumstances and why is terrific broth preferred to LB broth for E.coli growth?
Terrific Broth will result in a greater density of cells compared to LB but I have certainly seen it isn't as effective for the protein production of certain proteins compared to LB or defined media. I was curious what other limits and constraints exist with TB.
Migrated and derived from Quora http://www.quora.com/Under-what-circumstances-and-why-is-terrific-broth-preferred-to-LB-broth-for-E-coli-growth

I have used terrific broth to grow up transformed E. coli so they grow faster.  Often people will conduct a transformation, screen the cells, and grow them up in broth for plasmid extraction.  This growth would be for 12-16 hours.  Instead a person could use terrific broth to grow up the cells and it would take may 6-8 hours for adequate cell density for plasmid extraction.  If you are trying to express a protein then I would go with LB.
Also, I learned recently that terrific broth is also preferred over LB when needing to express proteins after transformation.


text:
Has anybody used Evrogen's DSN-normalization protocol for cDNA normalization?
I found the link to a commercial product by Evrogen to normalise cDNA samples for gene discovery projects here:
http://www.evrogen.com/technologies/normalization.shtml
The most up-to-date reference seems to be this Curr Protoc Mol Biol. paper by Bogdanova et al.:
http://www.ncbi.nlm.nih.gov/pubmed/20373503
They claim their method is compatible with nextgen sequencing platforms:

cDNA normalization using duplex-specific nuclease (DSN) is a highly
  efficient approach that can be applied for normalization of
  full-length-enriched cDNA (Zhulidov et al., 2004; Zhulidov et al.,
  2005). The resulting cDNA contains equalized abundance of different
  transcripts and can be used for construction of cDNA libraries and for
  direct sequencing, including high-throughput sequencing on the next
  generation sequencing platforms (Roche/454, ABI/SOLiD or
  Illumina/Solexa).

Has anybody successfully used it for next-gen gene discovery projects?

This seems to be more like a poll than a question.

Can I turn it into a poll in this website?

No, I meant more that poll-type questions can be closed as "not constructive".  You should probably reword it a bit to prevent this.


text:
How many agarose gel bands are typical for circularised DNA
I am aware that circular DNA can be both relaxed and super coiled. However when running an agarose gel of the circular plasmid along with singly digested plasmid with BamHI and HindIII, I see 1 band for the linearized plasmid (lanes 2-5) (as expected) but 5 bands for the circular plasmid (lanes 6 and 7).
What are these various conformations?

I don't have hands on it, but I will not be surprised if supercoiled DNA migrates at different distances according to some inner topological conformation (i.e., more or less coiled AND/OR more or less nicked). Similarly, this picture highlights >8 conformations. What is run in the gel is circularized phage DNA with some degree of knotting due to the circularization (phage DNA is otherwise linear).

Figure from: Arsuaga et al. 2005, PNAS 102 (26) 9165-9169 (free on PubMed Central)
Another theoretical possibility is that two or more plasmids of different sizes were grown in the same maxiprep because of some contamination. But in this case, you will spot the problem also in the digestion, so it does not seem to be your case.

Gianpaolo is correct that you are seeing the different conformations of circular DNA.
Growing plasmids up in bacteria produces 3 main forms: relaxed, coiled and super-coiled.

Relaxed tends to run a little higher than the expected size because it cannot travel as efficiently through the agarase;
Coiled migrates a little farther than the expected size because it is a little more compact and therefore migrates more easil;
Super-coiled, the most compact, migrates much farther than the expected size.

I would conclude from your picture the following:

That the HindIII cuts are efficient, and have linearized nearly all of your plasmid.
BamHI is cutting, but not as efficiently as HindIII for (presumably) the same amount of time. This should be digested longer if it's really important to digest with just BamHI, but for diagnostic purposes, it is fine. I say this because of the faint banding seen at ~4.5 and ~3.7 kb, which are likely your coiled and super-coiled plasmid DNA, respectively.
From your linear digests, the plasmid is 6 kb.
Looking at undigested control plasmid, your method of mini prep is not clean and looks to be contaminated, possibly by genomic DNA. Also, you see hints of streaking in the single digest lanes. Was this done using trizol?
I would expect the band at 10 kb to possibly be the relaxed form of the plasmid, with much of the plasmid DNA existing in a super-coiled conformation.

If these are important samples, I would consider purifying them using cleaner methods, for example using a column.

I think these answers have all missed the most likely explanation of the multiple bands in the uncut sample. I agree that you are likely to see supercoiled, linear and relaxed (open) circles in that order going up the gel. But then all of those higher forms are the same thing being repeated for dimers, trimers etc. formed by recombination between plasmid molecules. So, for example, I think the 10 kb band in the uncut lanes is a supercoiled dimer. I have a dim memory that you see more of this sort of thing if the DNA is prepared from a recA strain of E. coli.
update
Here is someone who I think would agree.


text:
What are the frequency ranges of most marine mammal vocalizations?
I am trying to determine a list of frequency ranges into which marine mammal vocalizations fall.
Ideally, I would like a list showing where the most popular marine mammal vocalizations fall, followed by the species name. That being said, I only really care about frequencies above 20 kHz, should they exist.
Example: (Numbers fabricated)

Orcas       : 30-40 kHz
Dolphins    : 100 kHz
Blue Whales : 60-88 kHz

etc.
Even if the list is 'quick and dirty', thats ok. The list will essentially point me to which species' songs/sounds I need to study.
Some additional context, this wikipedia link as well as this one have some nice sound files of many marine mammals' songs/sounds. I am trying to avoid having to download each one and analyze their spectral content. (I could, but would rather not).

Are you trying to find a list of frequency ranges, a range into which most vocalizations fall, or a list of marine mammals which vocalize above 20 kHz? It's three different (but similar) questions.

@Shep I edited.

Here there are spectrograms from Bottlenose dolphins (Tursiops truncatus), Killer whales (Orcinus orca) and False killer whales (Pseudorca crassidens).
Here there are spectrograms for Humpback whale (Megaptera novaeangliae) and from Sperm whales (Physeter catodon or Physeter marcocephalus)
Here there are spectrograms from Blue whale, Fin whale and Minke whale.
Some other google search for "spectrogram + your preferred cetaceans" should make your list. Enjoy.

Thank you. The majority seem to fall under ~20 KHz. Is this more or less true of marine mammals?

Dolphins can hear above 110 kHz, and produce vocalizations in this range.  Clicking has evolved in proposes and sperm whales and is predominantly above 100 kHz (to avoid being heard by killer whales). It's a bit subjective, of course: if you do a frequency decomposition of a click, it will always have some component with very high frequency.
That dolphins have evolved into such an niche highlights a problem with asking about "most" marine mammals, though: evolution often favors diversification between species, so you'd expect very different vocal ranges, to the point that many species have no overlap at all. (for the sake of illustration, ask yourself where most people live)

Thank you Shep I have edited the post for additional info/context.

Dwarf and Pygmy sperm whale clicks contain energy above 100 kHz, but sperm whales actually have lower frequency clicks with most energy below 20 kHz.

Baleen whale calls are typically low frequency (less than 5 kHz), with blue whales and fin whales producing the lowest frequency calls ranging from about 10 - 100 Hz, and some minke whale and humpback whale calls can extend up to 24 kHz.
Sperm whale echolocation clicks range from 500 Hz to 30 kHz.  Dolphin whistles typically range from 1 to 25 kHz, though some orca whistles are above 30 kHz.  Most dolphin echolocation clicks range from 5 to 130 kHz, while some dolphins, porpoise, and kogia species (dwarf and pygmy sperm whales) produce narrow-band high-frequency clicks in the 100 to 130 kHz range.
https://cetsound.noaa.gov/Assets/cetsound/documents/Roadmap/ONS_Roadmap_Final_AppendixA.pdf

Hi and welcome to Bio.SE. Thanks for posting. However, please provide support for your claims. Unsupported posts come across as opinions and are best reserved for comments. We have high expectations of good answers on this site to help avoid the spread of misinformation. Please consider revising your answer to provide some sort of support to attract more positive attention and to better (and more accurately) inform our future visitors. Thanks!

A quick reference point is dosits.org; their audio gallery has additional information on the species and references. This reference site was developed based on research (and much of it by researchers), so it is reasonably trustworthy and I suspect they update it periodically.
In general, above 20kHz is the realm of dolphins/porpoises. Echolocation clicks are short broadband clicks-- so they cover a very wide range of frequencies in a short little clicks.

All toothed whale echolocation clicks fall above 20 kHz (except sperm whales).
In addition to echolocation, porpoises and some of the small dolphin species also use ~130 kHz clicks for communication.
If you are interested in echolocation click frequencies, then this paper (which I co-authored) provides a detailed comparison and discussion of the frequency content of toothed whale clicks.
This paper also includes a table (Document S1. Table S1.) that summarizes biosonar click parameters of some 38 toothed whale species.
When acoustic recorders are placed directly on species like porpoises, frequencies above 200 kHz can be recorded, but it is only the energy below ~150 kHz that is likely to be relevant for echolocation, as this is about the upper hearing limit of porpoises and other small cetaceans (you can find an overview of audiograms and references on marine mammal hearing in this paper).
References
Sørensen, P. M., Wisniewska, D. M., Jensen, F. H., Johnson, M., Teilmann, J., & Madsen, P. T. (2018). Click communication in wild harbour porpoises (Phocoena phocoena). Scientific Reports, 8(1), 1-11.
Jensen, F. H., Johnson, M., Ladegaard, M., Wisniewska, D. M., & Madsen, P. T. (2018). Narrow acoustic field of view drives frequency scaling in toothed whale biosonar. Current Biology, 28(23), 3878-3885.
Southall, B. L., Finneran, J. J., Reichmuth, C., Nachtigall, P. E., Ketten, D. R., Bowles, A. E., ... & Tyack, P. L. (2019). Marine mammal noise exposure criteria: updated scientific recommendations for residual hearing effects. Aquatic Mammals, 45(2).

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


text:
Why do some trees have a life span, while some don't?
I have heard that there is no limit on the growth of trees, but then why do some trees, such as boxelders and poplars, tend to live shorter than redwoods, for example? Some advertisements for improved lombardy poplars state that their trees have an extended life span, up to 75 years? The trees with shorter life spans seem to weaken at a certain age, and then contract diseases more easily.

do clones count as part of the lifespan? If so, many trees have an infinite lifespan. (I'm not hunting for technicalities, I'm just guessing that most trees die as a result of macroscopic effects like rotting out, infections, etc)

No. clones, once established and detached from the parent plants, become essentially new plants, and have a whole life ahead of them.

The answer to (this question) may be relevant to you. I didn't see your question until now, and it is very similar to a recent question I answered!

The answer that @Luke gave seems to apply very well to this question.

The answer to this could be that there are many factors contributing to the length of the life of tree species.
Climate: You can see that trees that have a reputation of becoming really old live in environments that have low moisture levels and much sunlight over the course of the year.
For example, you can see that the most long-lived trees in America are located in California, where the temperatures are relatively high, while moisture levels are low. If you have one without the other trees don't tend to live that long. Cold climates make growth
harder for each individual, yet hot and moist climates tend to help trees grow easier, but also die easier. Think of the amazon. It is one of the richest forests in the world, yet the growth of bacteria and high competition in the areas of the equator make life a lot harder for the longest living and slowest growing species.
As you can see, the vast majority of the longest-living trees are located in California, or other regions of the same latitude!
http://en.wikipedia.org/wiki/List_of_oldest_trees
Other species and the life around it/Its Ecosystem: Individual trees tend to be less likely to be destroyed by a fire, as they are less likely to catch fire. At some instances, forest trees or dried-out grass can catch fire and pass it on to other individuals.
Microbes and bugs found in some parts of the world are known to their abilities to destroy trees!
Current size of the tree: Larger trees are generally less likely to die of causes like drought or damage to their trunks, as they have greatly extensive nets of roots and thick trunks and thus are able to, even partly, recover these incidences.
If a rockfall for example causes damage to one side of the tree, some of the brunches will probably die, but the rest of them, that have their own network to the roots, will probably survive.
This means that luck is involved and if the tree is lucky enough to avoid dying for a certain amount of time, regular fluctuations in the environment do not kill it as they would kill a younger, less robust tree.
Biology of tree species: Debate is held as to whether tree cells have telomeres working the same way as they do in animals. Research published in 2001 suggests that telomeres don't work the same way, as plants developed without telomeres after six generations continue living and growing without problems. But even if they do use telomeres, they may use them in a different way. This is an area where research is still being conducted, though, and you may find controversies in the bibliography!
For example in the paper "Analysis of telomere length and telomerase activity in tree species of various life-spans, and with age in the bristlecone pine Pinus longaeva"
Barry E. Flanary & Gunther Kletetschka which can be found in the rep
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CCgQFjAB&url=http%3A%2F%2Fwww.researchgate.net%2Fpublication%2F7709949_Analysis_of_telomere_length_and_telomerase_activity_in_tree_species_of_various_life-spans_and_with_age_in_the_bristlecone_pine_Pinus_longaeva%2Ffile%2F9c96052bcf0a51be49.pdf&ei=zzrCU9OcMIjV0QXmt4CwCQ&usg=AFQjCNH7853fvZ8yneznSfIQQPsxtIDQag&sig2=-PELK5RCQlAGTvQODoyZ2A&bvm=bv.70810081,d.d2k
we can see that sometimes, short lived trees have longer telomeres than long lived ones!
(Look in the second paragraph of the section "Results"). This means that actually, nobody really knows!! It may be the telomeres, it may be something else, it may be a combination of factors.
http://www.madsci.org/posts/archives/2002-04/1019349924.Bt.r.html
(notice that this post has links to pages that are no longer available).
Distillation and the most important point: The way that the tree is adapted to its environment determines its longevity in it. Planting an olive tree in the amazon is a great way of making sure it will not survive! Some trees are better at surviving in a certain climate (even if it is at your own garden) simply because they have evolved to live there.
That means that the trees probably don't have a defined lifetime in general, but the life expectancy is defined in each environment, depending on the circumstances!
This means that species we currently think of as short-lived can reach get really old:
http://www.ncbi.nlm.nih.gov/pubmed/11295506
What some companies may have done is   try to combine characteristics of individuals through selective breeding - and yes, it works for trees as well!- to match the climate and terrain characteristics found in the certain country or region! Or they may have selected for resistance against the most common pests in your area!
I hope I answered you question adequately!

Why do individual trees with no competition undergo a growth decline at a certain age, which lead to catching a disease, and the death of the tree? Some trees always do this. What is going on inside these trees?

Read the new section "Biology" in my answer!

Please change the !-. But looks pretty good.

Ya'll love explanation points!

Everything has a life span. When it comes to trees, there are significant variations between species (see here some examples).
Apart from the external factors, these variations seem to be related to telomeres length and telomerase activity [1]:

The results from this study support the hypothesis that both increased telomere length and telomerase activity may directly/indirectly contribute to the increased life-span and longevity evident in long-lived pine trees (2000-5000 year life-spans) compared to medium-lived (400-500 year life-span) and short-lived (100-200 year life-span) pine trees, as well as in P. longaeva with age.

Also, the lower metabolic rate of some trees increases life span [2]:

... the extremely high longevity of trees may be explained by the lower metabolism displayed by the stems. These results clearly reflect different energy allocation and energy expenditure rate strategies between leaves and stems, which may result in different senescence rates (and life spans) in these organs. They also suggest that, in contrast to animals, the ROL (rate of living ) theory of aging may apply to woody plants at the organ level, thereby opening a promising new line of research to guide future studies on plant senescence.

Leaf longevity is also correlated to shoot growth [3]:

These results suggest that leaf longevity is greater on shoots with low annual growth potential. Thus, a slow-growing tree at high elevation (low annual shoot growth potential) can have the same amount of foliage per shoot as a fast-growing tree at lower elevation.

References:

Flanary BE, Kletetschka G. Analysis of telomere length and telomerase activity in tree species of various life-spans, and with age in the bristlecone pine Pinus longaeva. Biogerontology. 2005;6(2):101-11. doi: 10.1007/s10522-005-3484-4. PubMed PMID: 16034678.
Issartel J, Coiffard C. Extreme longevity in trees: live slow, die old? Oecologia. 2011 Jan;165(1):1-5. doi: 10.1007/s00442-010-1807-x. PubMed PMID: 20963610.
Schoettle AW. The interaction between leaf longevity and shoot growth and foliar biomass per shoot in Pinus contorta at two elevations. Tree Physiol. 1990 Dec;7(1_2_3_4):209-214. PubMed PMID: 14972918.

On 'long-lived pine trees (2000-5000 year life-spans)', I haven't seen any evidence that there are trees older than about 4600 years old, but there are several trees of that age. I'm guessing there was an event at about that time that affected the trees. Those old specimens haven't been declining, so I think they might have a longer life span than people have thought. What are your thoughts on that?

Although most plants can potentially reproduce sexually, there are some plants that effectively always reproduce by shedding off branches which, when they fall in the right conditions, grow into new 'clones' of the same tree, which the exact genetic material. In these cases, it is advantageous for the tree to be able to survive as long as possible. Plants that reproduce sexually by the cross of two different individuals have a recombined genetic material in every generation, and the survival of that plant with that new genome is usually shorter.

why do you think that recombination of genetic material leads to shorter life span?

Because recombination is a mechanism to adapt to environmental changes. Then it is more important that nutrients, light and water are available for the "improved" next generation than for feeding yet unadapted elder individuals that might not survive long under new conditions.


text:
What is a coupled reaction and why do cells couple reactions?
I was wondering what exactly a coupled reaction is and why cells couple them.  I read the wikipedia article as well as several others, such as life.illinois.edu but I still don't get it.  Could someone explain it to me?

Think of this: would you rather take a can of fuel and burn it or take a can of fuel, put it in a car and let it burn (in a controlled way) in there?

It's pretty simple. A reaction occurs that releases energy (like ATP losing a phosphate to become ADP + Pi). If this is uncoupled, the energy will merely turn into heat. If it is coupled, then it can be used to fuel some other process. For instance, if you couple the ATP -> ADP reaction to a certain protein, the energy can be used to modify the shape of that protein.

A reaction where the the free energy of a thermodynamically favorable transformation, such as the hydrolysis of ATP, and a thermodynamically unfavorable one, are mechanistically joined  into a new reaction (or may be envisaged to be so joined) is known as a coupled reaction.
To put it another way, two or more reactions may be combined mechanistically such that a spontaneous reaction may be made 'drive' a non-spontaneous one,   and we may speak of the combined reaction as being 'coupled' (see, for example, Silby & Alberty (2001), quoted below). The combined reaction may be catalyzed by an enzyme, in which case the 'thermodynamic push' is provided by the coupling agent (such as ATP) and the 'kinetic push' is provided by the enzyme.
We need to take into account a very important point. As pointed out by Atkinson (1977),  the coupled reaction is a different reaction to the reaction we are trying to 'drive', with different overall stoichiometry and hence a different overall equilibrium constant (Atkinson, 1977, p52).
A coupled reaction does not "push a reaction past its equilibrium" (see Atkinson, 1977, p52). No enzyme, for example, can push any reaction past its position of equilibrium. This is forbidden by the second law. (If your favourite kinetic mechanism does not obey the second law there is, as Eddington put it, "no hope"). An enzyme (or enzymes) can however, cause a reaction to proceed further than it normally would by catalyzing a different reaction (or series of reactions).
Perhaps (in lysine biosynthesis from aspartate), nature requires the the (NADH-linked) reduction of a carboxylic acid to an aldehyde, a reaction normally considered  irreversible. And lets spell this one out: the equilibrium constant for a reaction such as the following:
        NADH + carboxylic acid = NAD+ + aldehyde        (1)
greatly favors aldehyde dehydrogenation so much so that the left-to-right transformation has never (to the best of my knowledge) been demonstrated (more on this below).
Lets first phosphorylate the carboxylic acid using ATP as coupling agent to give aspartyl-phosphate (aspartate kinase):
         aspartate + ATP = aspartate-4-phosphate + ADP        (2)
Now let's reduce the 'activated' acid (aspartate-4-phosphate) using NADPH as electron donor, where the equilibrium constant of the following reaction is  very much to the right  (aspartate semialdehyde dehydrogenase):
  aspartate-4-phosphate + NADPH + H+ ⇌ L-aspartate 4-semialdehyde + Pi + NADP+
So we have got our product (the aldehyde) from our 'starting material' (the carboxylic acid), but at the 'expense' (as we would see it) of  ATP hydrolysis.
We may think of the above reactions as being 'mechanistially coupled' by the formation of aspartyl-phosphate such that the overall equilibrium constant for the following reaction is much more favourable than that of Eqn (1)
  aspartate + ATP + NADPH + H+ ⇌ L-aspartate 4-semialdehyde + Pi + NADP+
Or, perhaps in more abstract terms, the coupled reaction may be represented as folows:
  carboxylic acid + ATP + NADPH + H+ ⇌  aldeyde + Pi + NADP+
The reduction of a carboxylic acid to an aldehyde has been given a thermodynamic 'push' by the coupling agent  (and a kinetic 'push' by the enzymes).
Before we move on to some specific examples let's consider three further points.
(i) What makes ATP a good coupling agent? To again quote Atkinson (1977, p48), a good coupling agent has two requirements: firstly, it must be thermodynamically unstable. That is, it must be "far from equilibrium in terms of some useful conversion" (Atkinson, 1977, p48). The hydrolysis of ATP nicely fills this criterion. Secondly, a good coupling agent must be kinetically stable. Again ATP 'fits the bill': solutions of ATP in water are stable (Atkinson, 1977, p48).
ATP (-39.7 kJ/mol), of course, is not the only useful coupling agent, or even the 'best' one. phosphoenol-pyruvate (-61.9 kJ/mol) , creatine-phosphate (-43.5 kJ/mol)  and acetyl-phosphate (-43.1 kJ/mol) are others. The figures in brackets refer to free energy of hydrolysis and are taken from Silby and Alberty (2001, p 282).
(ii) The coupled reaction need not involve direct hydrolysis of coupling agent. Any reaction in which ATP is converted to ADP has received a 'thermodynamic push equivalent to the free energy of hydrolysis of ATP' (Atkinson, 1977, p49). In essence, the concept of a coupled reaction is an abstraction, created by us for our convenience.
(iii) To state the obvious, a coupled reaction is exactly that: coupled.  The coupling may be 'chemical', as in many of the examples below, or may be conformational (as in ATP synthase), but there must be in some sense a mechanistic joining into a new (real) reaction. Two reactions occurring in isolation, even if one is ATP hydrolysis, are not coupled.
Specific Examples
An example of a coupled reaction is the  glyceraldehyde-3-phosphate dehydrogenase (EC 1.2.1.12; GAPDH) reaction [see here] .
 Glyceraldehyde-3-phosphate + NAD+ + Pi → 1,3-diPhosphoGlycerate + NADH + H+
We can think of this reaction in terms of two separate reactions which are coupled mechanistically by the enzyme. (i) The NAD+ linked oxidation of an aldehyde to a carboxylic acid (the aldehyde dehydrogenase reaction) and (ii) the phosphorylation of a carboxylic acid. (Like ATP, a phosphorylated carboxylic acid may be considered a 'high energy' compound, that is one where the equilibrium for hydrolysis lies very much to the left in reaction 2 below).
Reaction 1
 RCHO + NAD+ + H2O → RCOOH + NADH + H+
Reaction 2 (Pi is inorganic phosphate).
 RCOOH + Pi → RC(=O)(O-Pi) + H2O
As stated above, the NAD+-linked oxidation of an aldehyde (reaction 1) is practically irreversible. That is, at equilibrium it has proceeded almost totally to the right. As stated above, the position of equilibrium of reaction 2 lies very much to the left.
How can one 'drive' the formation of a phosphorylated carboxylic acid by coupling it to the (spontaneous) NAD+-linked oxidation of an aldehyde?
A simplified version of the GAPDH reaction is as follows (a more complete mechanism, supported by a lot of experimental evidence, may be found in Fersht (1999), which I quote below).
Step 1.  Formation on an enzyme-linked thiohemiacetal.
 E-SH + RCHO → E-S-C(R)(H)(OH)
A sulphydryl on the enzyme (part of a Cys residue) reacts with the aldehyde group on the substrate to give a thiohemiacetal.  (In the representation above, groups in brackets are all connected to a single (tetrahedral) carbon atom).
Step 2. The thiohemiacetal is oxidized by enzyme-bound NAD+ to a thiol-ester (the key step).
 E-S-C(R)(H)(OH) + NAD+ → E-S-C(=O)(R) + NADH + H+
This (enzyme-bound) thiol-ester is a 'high energy' intermediate wherein, it may be envisaged, the free energy of aldehyde oxidation has been 'trapped'.
The final step of the GAPDH reaction is now spontaneous (proceeds to the right).
Step 3. Attack on the thiol-ester by inorganic phosphate (Pi is inorganic phosphate)
E-S-C(=O)(R) + Pi → E-SH + R-C(=O)(O-Pi)
Thus, the free energy of NAD+-linked aldehyde oxidation has been 'sequestered' and used to 'drive' the thermodynamically unfavourable phosphorylation of a carboxylic acid, by coupling the two reactions via a ('high energy') thiol-ester: the coupled reaction is a different reaction.
The 'thermodynamic price' is that the GAPDH reaction (unlike NAD+-linked aldehyde oxidation) is freely reversible: the coupled reaction has a different overall equilibrium constant.
As stated above, this is a simplified version of the GAPDH reaction.  The (tetrameric) enzyme contains a tightly bound NAD+ for a start, and this needs to be taken account of.  A fuller account may be found in the following reference:

Fersht, Alan. (1999) Structure and Mechanism in Protein Science, pp 469 - 471, W.H. Freeman & Co.

For a fuller treatment of coupled biochemical reactions, see

Silbey, R.J. & Alberty, R.A. (2001) Physical Chemistry (3rd Edn) pp 281 - 283.
Atkinson, D. E. (1977) Cellular Energy Metabolism and Its Regulation.
Academic Press, New York

Pyruvate kinase (EC 2.7.1.40) [see here] is another great example of a coupled biochemical reaction.  In this case the reaction is almost irreversible in the direction of ATP synthesis!
The standard transformed free energy (ΔGo') for the hydrolysis of phosphoenol-pyruvate (PEP) to pyruvate and phosphate is ~ - 62 kJ/mol.  This represents an equilibrium constant of about 1010 in favour of hydrolysis! (see Walsh, quoted below, pp 229-230).
For comparison,  ΔGo' for ATP + H2O → ADP + Pi is about - 40 kJ/mol.
Thus the pyruvate kinase reaction may be viewed as a coupled biochemical reaction where the free energy of PEP hydrolysis is coupled to (almost irreversible) ATP synthesis.
Why does PEP have such a large negative ΔGo'? The enol form of pyruvate does not exist in appreciable quantites in aqueous solution at pH 7 (Pocker et al., 1969; Damitio et al., 1992).  PEP may be considered a 'trapped' form of a thermodynamically unstable enol which is released upon hydrolysis, thus 'pulling' the equilibrium to the right. (see Walsh, quoted below, p 230, for a more thorough explanation).
Personally, I have always considered the reaction catalyzed by PK to be pretty amazing.
Edit
In response to this question on the standard free energy of hydrolysis of phosphoenolpyruvate (PEP), I'll add the following.
The thermodynamically stable form of PEP in solution at 'physiological' pH is the enol form.  That is, the enol from predominates.
PEP hydrolysis may be formally divided  into two parts:
(i) the hydrolysis of the phosphate ester to give the enol form of pyruvate,
followed by (ii) tautomerization to the (thermodynamically stable)  keto form of pyruvate (Chiang et al., 1992).
Thus it is the enol form of PEP that predominates in aqueous solution at pH 7, but pyruvate exists predominately in the keto form under similar conditions.
In their in-depth study, Chiang and co-workers attribute 47% of
the free energy liberated by  the hydrolysis PEP to the ketonization of the enol form of pyruvate, and
conclude that "nearly half of the high energy content of this molecule resides in its masked  enol function" (And of course, they mean 'high energy' in the Lipmann ('squiggle') sense, that is PEP has a high standard free energy of hydrolysis).
We need to be careful with the following and acknowledge that the language is somewhat loose: we may
think of PEP as a molecule where the thermodynamically unstable form of pyruvate (the enol form)
is 'trapped' in a (thermodynamically stable) phosphate-ester linkage, which will be 'released' on hydrolysis. And to emphasize, the thermodynamically stable form of PEP is the enol form.
IMO, Chiang et al. (1992) is a very nice paper that rigorously backs up conclusions with strong experimental evidence, but it is surprising that they did not quote Walsh
 who (again, IMO) is the first to give the correct explanation?
References

Chiang,Y., Kresge, A. J. & Pruszynski, P. (1992) Keto-Enol Equilibria in the Pyruvic Acid System: Determination of the
Keto-Enol Equilibrium Constants of Pyruvic Acid and Pyruvate and the
Acidity Constant of Pyruvate Enol in Aqueous Solution  J. Am. Chem. Soc. 114, 3103-3107
Damitio, J.,  Smith , G.,  Meany , J. E.,  Pocker, Y. (1992).  A comparative study of the enolization of pyruvate and the reversible dehydration of pyruvate hydrate
J. Am. Chem. Soc.,  114, 3081–3087
Lipmann, F. (1941). Metabolic generation and utilization of phosphate bond energy.  Adv. Enzymol. 1, 99 - 162.
Pocker, Y., Meany, J. E., Nist, B. J., &  Zadorojny, C.  (1969) The Reversible Hydration of Pyruvic Acid. I. Equilibrium Studies.  J. Phys. Chem.
76, 2879 – 2882.
Walsh, C. (1979) Enzymatic Reaction Mechanisms.  W.H. Freeman & Co.

Oxidative Phosphorylation

Perhaps the most important coupled reaction is that which occurs in oxidative phosphorylation where the oxidation of  fuels via the respiratory redox chain is coupled to  the  'synthesis' of ATP.
I have 'steered clear' up to this point, as it is a very complex area and difficult to do justice to in a few lines.
In the chemiosmotic theory of oxidative phosphorylation (due primarily to Peter Mitchell)  electron transport via the respiratory chain to molecular oxygen creates a proton  gradient across the inner mitochondrial membrane by pumping protons outwards. This proton gradient, or protonmotive force, is used to 'drive' the following  reaction to the right:
ADP + Pi ⇌  ATP + H2O
This is commonly referred to as 'ATP synthesis' but, more correctly perhaps, it  maintains our coupling agent  "far from equilibrium in terms of some useful conversion" (Atkinson, 1977, p48), that is far from equilibrium in the hydrolysis of ATP.
Although all of oxidative phosphorylation may be considered a coupled reaction, all that will be (very briefly) looked at here is the reaction catalyzed by ATP synthase, which may be considered to catalyze the following coupled reaction.
 ADP + Pi + H+(Out) ⇌ ATP + H2O + H+(In)
This is an example of vectorial catalysis, but it is much more. The ATP synthetase has been described as a "splendid molecular machine" (Boyer, 1997b).

It is an example of sequential, cooperative catalysis between 3 active sites where the the release of products (ATP) at one site is dependent on binding of substrates (ADP and Pi ) at another.
It is an example of indirect conformational coupling where the proton gradient effects the release of of tightly bound ATP by eliciting sequential conformational changes in all active sites .
It is an example of a binding-change mechanism, where the proton gradient is responsible release of ATP from the enzyme, but plays no role in its synthesis.
Perhaps most dramatically,  it is an example of rotational catalysis, where the indirect rotation of a protein subunit brings about the sequential conformational  changes in the active sites.

Much of the mechanism of ATP synthetase is due to Boyer: this includes the prediction of rotational catalysis and the formulation (and defense) of the binding-change mechanism (see Boyer, 1997a,b). For some nice dynamic diagrams on the mechanism of action, see this SO answer.
Perhaps the most important considerations from the standpoint of the present discussion is the subtlety  of the coupling effect or 'mechanistic joining': it is brought about by a conformational change due to rotation of a protein subunit, and it is mediated though the dissociation of ATP from a subunit and not through its 'synthesis' from ADP and Pi at an active site.

[Aside] In a most famous experiment, rotary catalysis was 'physically' demonstrated by Kinoshita and  co-workers by attaching an actin filament to the rotating subunit of the enzyme and viewing under a fluorescent microscope (see here), which showed that rotation is anti-clockwise (viewing the enzyme from the 'membrane' side) when the enzyme is hydrolyzing ATP. A nice YouTube video, which seems to be base on the original Noji experiment, may be found here .
References

Abeles, R.H., Frey, P.A. & Jencks, W.P. (1992) Biochemistry.  Jones & Barlett, Publishers.
Boyer, P. D. (1997a) [Nobel Lecture] Energy, Life, and ATP (pdf available here)
Boyer, P. D. (1997b) The ATP Synthase. A splendid molecular machine Annu. Rev. Biochem.  66, 717–749
Mitchell, P. (1978) [Nobel Lecture] David Keilin's Respiratory Chain Concept and Its Chemiosmotic Consequences (pdf available here)
Walker, J. E. (1997) [Nobel Lecture] ATP Synthesis by Rotary Catalysis (pdf available  here)

A clear, comprehensive answer filled with examples. +1.

The answer was automatically converted to CW because you edited it more than 10 times. This is meant to discourage trivial edits to bump the question. I reverted CW in this case, as most edits were substantial.

In a coupled reaction energy required by 1 process is supplied by another process. For example: glucose + phosphate becomes glucose.6.phosphate. This is an endergonic reaction and the energy is supplied to this reaction by another reaction which has to be exergonic reaction i.e. ATP which can become ADP+energy.

Coupling process by which two or more chemical reactions depend on each other through energy once one is exothermic another is endothermic, one produce product or intermediate which is used by the another
Examples glycolysis and citric acid cycle , phosphorylation and dephosphorylation in steps of glycolysis and many other

Welcome to BiologySE! Please elaborate your answer a little bit (explain terms, format the text appropriately for reading, maybe some images?) and provide references for your claims and to give access for further reading sources to interested people.


text:
What are minerals (other than zinc) that the human body cannot store
It is known that zinc is an essential mineral that the body cannot store.
What are other minerals, especially metals, that the body cannot store?
(other than water-soluble vitamins such as vitamin B and C)
Sincere thanks.

Essential "minerals", i.e., metal cations are magnesium, zinc, iron, potassium, sodium, manganese, molybdenum, selenium, cobalt, copper and even calcium, as we lose a tiny amount of it through urine and sweat. They are all "stored" in some way, but only temporally, so some amount has to be taken up daily. It would show only weeks later, however, if you have a deficiency.
Wikipedia adds phosphorus and iodine but they are not metals.


text:
Do trees age on a microscopic level?
Most animals age via at least two mechinisms:

at a "macroscopic" level, basically wear and tear to the point where (on evolutionary time scales) it's more genetically advantageous to optimize for reproduction rather than longer lifespans.
at a microscopic level, e.g. shrinking of telomeres. This prevents cell division after a certain point (good to prevent cancer and other growths, bad for regeneration).

Do plants also age microscopically? If so, how are we able to clone (in the horticultural sense) plants?

Although I understand telomeres are fancy these days, I wouldn't really restrict aging at the microscopic level to their shrinkage. There are many more things going on, telomeres are surely one of the components of aging, but they are not the only one.

I don't mean to say telomeres are the only thing which causes aging on a cellular level, I just mean to say that something is happening. If you extract a single cell from an old animal, is should theoretically be distinguishable from a cell from a younger animal. Given that clones of plants are indistinguishable from plants grown from seeds, I'm wondering if such a distinction is possible in plants.

Hi. A quick google returned this review which implies that whilst plants have telomeres, their expression of telomerase is more wide-spread, and thus they have a greater regenerative potential. On a separate note, when cloning cells in the lab the biological clock needs resetting so that the 'old' donor cell loses its hallmarks of aging. This is done naturally for every germ cell created, and mostly involves epigenetic re-programming. Read this review, it's really interesting!

@Luke this smells like an answer to me...

@Shep I was only speculating about the plants really, and supplying additional (non-answer) info of interest. As has been pointed out, telomeres are only one aspect of cellular aging, and I am no expert on plant biology.

I’m not convinced by the distinction. Macroscopic aging doesn’t really make sense – do I age when I injure myself? Clearly not, since the body can repair itself. The loss of these repair functions is what constitutes aging. But that is once again at the microscopic level.

@Luke do you have a ref.  for the second review you mention? The Cell website is down.

@Poshpaws certainly: Rando, T. A., & Chang, H. Y. (2012). Aging, rejuvenation, and epigenetic reprogramming: resetting the aging clock. Cell, 148(1-2), 46-57. doi:10.1016/j.cell.2012.01.003

I've been doing some reading, and have come up with the following interesting information.
Telomeres
During cell division the DNA is replicated, but the mechanism is imperfect and in each round of cell division a small section is lost from the end of each chromosome. To compensate and protect the genetic information there are caps – regions of excess nucleotides – at the ends called telomeres (Silvestre, 2012).
Mammalian cells do not replenish their telomeres after cell division, giving them a replicative lifespan;  a maximum number of cell divisions before the telomeres run out. The cells then either enter a state of senescence and no longer divide, or initiate programmed cell death. However each cell has the genetic information for telomerase – the enzyme that can replenish the telomeres – but cannot use it. Only embryos and stem cells are able to express telomerase in mammalian cells - this protects against the build up of damage to DNA causing uncontrolled cell cycle progression. Activated telomerase is a core feature of many cancers (Campbell, 2012).
Plant Telomeres
You mention telomeres in your question, and it is an interesting question I had never considered. Plants have no germline preserved, so their progeny must bear all the defects of their particular parent cell, and that plant cells must therefore all have the capacity to regenerate their telomeres. I found a paper by Fajkus and colleagues that finds telomerase activity in plant cuttings grown in culture (Fajkus, 1998). Their hypothetical Plant Telomere-Length Regulating (PTLR) protein must arise in the early stages of the culture and last only a few cycles. Interestingly it seems that the efficiency of this process varies between different plant species. The authors note that their plant of choice – tobacco – is particularly proliferative and that other plants such as barley were harder to grow from cuttings, which may be down to a different way of regulating the telomerase (for instance it could only be activated occasionally at low amounts).
Do Plants Get Cancer?
It seems to me the next obvious question. One of the first papers I came across (published in 1916 by the Journal of Cancer Research!) talks of Crown Gall in plants and its relation to human cancer (Smith, 1916). Many websites cite galls as being the equivalent to cancer in plants, but it appears that the outgrowths (galls) that appear very tumour-like are in fact caused by bacteria encouraging their surrounding cells to proliferate. (See this question for more detail on galls).
I later found an abstract (I cannot access the full paper) from a paper published in Nature in 2010 called “Walls around tumours — why plants do not develop cancer” (Doonan, 2010). It appears that Plants can and do develop tumours, but they are less frequent and less lethal due to fundamental differences in development between plant and animal cells. Singh and colleagues found that in 2 plant species (Arabidopsis and rice) there were DNA damage repair pathways well conserved but with variation; there were several gene duplications in different DNA repair pathways (Singh, 2010).
Plants Do Not “Age” As We Do
Although I could find no conclusive evidence, it seems to me likely that plants may also have enhanced maintenance against other cellular stresses than DNA damage, such as build-ups of aberrant proteins. It therefore appears that in a protected environment some plants could live indefinitely. I say some, because others deliberately end their lives after reproduction. Traits such as longevity are inherently hard to be selected for, as the advantages come long after reproductive maturity and are therefore under much less selective pressure.
We see plants wither and die, but this is because they are constantly subject to environmental insult. Animals and insects may eat them, there may not be enough food or water, or sunlight, or the plant may become infected. All of which are at the macroscopic level. Due to completely different evolutionary constraints and pressures plants are highly resilient to cellar stresses, possibly due to differences in metabolic rate, and apparently have indefinite replicative potential.
Edit:
Although the more I think about it, the more it seems that most plant must have an ultimate lifespan, in that as they forever grow and expand their tissues would gradually harden and become less functional (I am mostly imagining bark plants here). Although as the layers of bark are pushed out the layers below take the place. In this way a tree could possibly live indefinitely by continuously remodelling it's layers.

Nice answer. See this question for more detail on galls. Also the Singh paper looked at Arabidosis (not a grass) and rice (a grass) :)

@RichardSmith - thanks for the correction and info - have updated my answer.

Even if outgrowth are caused by bacteria, that doesn’t make them less cancerous (plenty of human cancers are caused by viruses, but some also by bacteria). The criterion here is more likely lack of malignancy.

Very interesting answer Luke!


text:
Are mosquitoes repelled by high frequency sound?
I am totally confused whether ask this question to physics or biology stackexchange.
I downloaded a mobile application which claims to repel mosquitoes. This application basically produces sound from 16kHz to 22kHz (I doubt that it even produces more than 20kHz because we can't hear more than 20kHz naturally).
I totally doubt this application. Do mosquitoes go away in higher frequency of sound?

Try to ask one question per post. As is often the case with UPDATE titles, what follows should be its own question.

Have you heard of the proposed Bioacoustics Stack Exchange? It seems like you might be a valuable member of that community. Please consider committing to the page so we can get closer to making it to the Beta stage. Cheers!
https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680

After seeing your question, I decided to do a bit of research on the topic.

First Source: EurekAlert!

http://www.eurekalert.org/pub_releases/2007-04/jws-mrt041607.php

"Mosquito repellents that emit high-pitched sounds don't prevent
  bites"

Some key-points from the webpage:

A Cochrane Systematic Review of the use of electronic mosquito repellents (EMRs) failed to find any evidence that they work.

  To test these claims a team of Cochrane Researchers conducted a systematic review looking for trials conducted with EMRs. They located ten field trials that had been carried out in various parts of the world. None of these trials showed any evidence that EMRs work.

  All ten studies found that there was no difference in the number of mosquitoes found on the bare body parts of the human participants with or without an EMR

Second Source: Wikipedia

http://en.wikipedia.org/wiki/Insect_repellent

These electronic devices have been shown to have no effect as a mosquito repellent by studies done by the EPA and many universities.

Third Source: CBCnews

http://www.cbc.ca/news/story/2007/04/18/mosquito-repellent.html
Key points from the article:

"There was no evidence in the field studies to support any repelling effects of EMRs, hence >no evidence to support their promotion or use"

  -Ahmadali Enayati, researcher

This is a major point as well:

The study also said that in 12 of the 15 experiments, the landing rates of mosquitoes on subjects was in fact higher than in control groups.

The article also points out that female mosquitoes can't hear very well- Which supports the idea that high-frequency repellents are ineffective; Much more than you probably think. Why? Well, it's pretty simple:
Female Mosquitoes are the only Gender that Bite.

Overall, when you consider the countless studies and research put in to the effects of high-frequency sounds on mosquitoes, it's pretty obvious that:
No.High Frequency Sounds do NOT repel mosquitoes

All three sources reference the same study, and it's unfortunate that the details of the study haven't been made available for peer review.

Ok, so the results were published (http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD005434.pub2/full), but access to the article is not provided with the basic Wiley subscription package that (I assume) is available through most universities.

@DanielStandage http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD005434.pub2/abstract is the abstract where the relevant information is written: "All 10 studies found that there was no difference in the number of mosquitoes caught from the bare body parts of the human participants with or without an EMR".

The paper is now available without dealing with a pay-wall.
By the way, Wiley's website has this to say about the publication the paper was published in: "The Cochrane Library is a collection of databases that contain high-quality, independent evidence to inform healthcare decision making. Cochrane Reviews represent the highest level of evidence on which to base clinical treatment decisions. "

Ultrasound emitting devices are used to repel mosquitoes. We tested
  the repelling properties of a commercially available ultrasound device
  in a domestic setting in Gabon. Devices emitting three different block
  frequencies ranging from 3 to 11 kHz were tested in a paired,
  cross-over blinded and placebo controlled trial during eighteen nights
  in nine pairs of houses. A total of 7485 mosquitoes (10% Anopheles,
  62% Culex, 27% Mansonia and 1% Aedes) were caught, 23 per house per
  night. There was no significant difference in landing rate between the
  houses with ultrasound device and the houses with placebo for any
  species of mosquito. Thus the ultrasound device used was not effective
  against mosquitoes in this strictly controlled trial.

Sylla el-H K, Lell B, Kremsner PG. A blinded, controlled trial of an ultrasound device as mosquito repellent. Wiener Klinische Wochenschrift. 2000 May;112(10) 448-450. PubMed PMID: 10890136.

A bibliographic review about the use of electroacoustic devices with a
  supposed repellent action on the females of different species of
  hematophagous mosquitoes  is presented. 15 direct references and 2
  indirect ones are given, in which it is  concluded that these devices
  do not protect those who have them from the stings of mosquitoes. The
  names of 9 of the tested devices as well as of 16 of the main  species
  of mosquitoes present in the field tests are mentioned. These tests
  have  been carried out in very different ecological conditions from
  Alaska to Equatorial Africa. It is also stressed that the high
  intensity ultrasonic frequencies emitted by these devices produces a
  potentially harmful effect on man.

Rev Cubana Med Trop. 1998;50(2):89-92.
[Electronic repellents against mosquitoes: the propaganda and the reality].
[Article in Spanish]
Coro F(1), Suárez S.
Author information:
(1)Facultad de Biología, Universidad de La Habana, Ciudad de La Habana, Cuba.
PMID: 10349423  [PubMed - indexed for MEDLINE]

Answers are supposed to be written by yourself and not only consist of a citation.

@Chris I am not an expert in the field, what do I need to add to an abstract? I think it is self explanatory, doesn't it?