text:
If Evolution Is In Progress, Why Fight Extinction?
Natural selection is a central tenet of evolution. However, most biologists seem determined to prevent the extinction of the species that have been selected against. Why is this? Preservation of genetic diversity?
I thought evolution was supposed to create diversity not destroy it. What am I missing?

We're not trying to prevent extinction - species go extinct all the time. We're trying to prevent extinction caused by man. One of the big things that sets us apart from other species is how massively we manipulate the environment we live in. Some of those manipulations have a high destructive potential, and we do not understand ecosystems well enough to confidently say that destruction of species caused by us would go without lasting effects that we'd rather avoid.

@Armatus Couldn't the same argument be made for invasive species?

Yes, hence why they're trying to contain invasive species, or at least protect those species they're threatening. Same reason goes for containment of genetically engineered organisms as well.

@Armatus How does evolution pre-humans deal with the issue of invasive species? Aren't invasive species the "fittest" creatures that evolution through natural selection favours? Doesn't survival of the fittest imply an expense to the less fit aka non-invasive or native species? Why should humans interfere with invasive species? The fittest survive right? Genetic engineering would deserve its own question.

@PaulA.Clayton Doesn't natural selection assume that a local optimum (emerging species) is superior to a more global optimum (aka invasive species)? If it were only about preserving outdated ideas we would merely sequence their genes and let the endangered species die--that would be much cheaper in many cases. You mention "artificially increased mixing," but you ignore the fact that for much of early history the world is believed to have been a single continent, which means "mixing" back then was naturally easier than today and likely comparable to human induced mixing of the present.

Again, invasion may also happen in nature and we are not trying to prevent invasion itself. We are trying to prevent invasion caused (directly or indirectly) by humans, again because we cannot determine the effects it may possibly have on the invaded ecosystems and hence we try to avoid potential problems. The whole idea is that we want to prevent a nature that evolved based on human manipulations.

"Survival of the fittest" is not a central tenet. Scientists strongly prefer the term "natural selection".  Evolution is a very stochastic and opportunistic process, and much of it is not necessarily "progress" in the common sense. Are cows evolutionarily superior to elephants because we breed cows for food but slaughter elephants for their ivory? Or some island species that gets wiped out by a random meteor? Plenty more about it here: http://en.wikipedia.org/wiki/Survival_of_the_fittest

We are still a part of the evolution process though. I'll use the example of beavers creating damns that sometime irreversibly change local habitats. It's (cringe) a natural process to affect their environment as we do to our environment. My interpretation of the question is if a species is made extinct by us, WHY should we care? Money could be spent on preserving our own species instead.

@GoodGravy True, but as I said I think the relevant difference is the extent of manipulation, which is vast for humans. Aside from that, I think it boils down to fear of change.

First, a shorthand definition of Evolution is heritable change and not 'progress' (which is a rather loaded word). Also, evolution is not 'supposed' to do anything, and can lead to both an increase or a decrease in diversity, since (local) diversity is simply the net result of speciation rate and extinction rate (if we exclude colonization of new species from other areas). Therefore, I think the question is framed in the wrong way.
Second, there are many reasons why biologists might want to halt species extinctions, as hinted in the other comments and answers. Most obviously, conservation biologists want to prevent man-made extinctions which are due to how we have influenced/modified/destroyed the natural environments. I don't think conservation biologists in general are determined to halt all 'natural' extinction. However, most of the time it is really hard to pinpoint what would be a 'natural' extinction. Either way, the current rates of extinction, which have been estimated to lie 100-1000 times (IUCN, 2007) above background rates (some say it's closer to 10000 times higher), indicate that most extinctions are man-made.
The rationales people use for preserving biodiversity can however differ. Three distinct categories are:
1) For human survival and/or economy, e.g. through ecosystem services or resources we rely on.
2) For human welfare, e.g. recreation or esthetical reasons.
3) Ethical considerations, e.g. inherent value of species or to preserve the unique evolutionary history of the system.
Another way to structure these is to label 1) & 2) as instrumental values and 3) as inherent values. The instrumental values can then be subcategorized as services, goods/resources, information (e.g. genetic to be used in medical research), and esthetical/spiritual values.
Since the direct value of individual species are often (usually) uncertain (irrespectivly of the direct rationales used) the precautionary principle is often invoked to justify species conservation. Also, numerous examples exist of how aspects of biodiversity are related to human values (some recent examples are Garibaldi et al. 2013 and Gamfeldt et al. 2013), such as production or services, which can also be used to justify both conserving biodiversity or individual species. However, other aspects of biodiversity are functional diversity, which focus on preserving functional groups of species, or phylogenetic diversity, focusing on taxonomic coverage and uniqueness (evolutionary history), instead of 'overall' biodiversity (see e.g. Flynn et al, 2011 for a discussion of these concepts). Under these perspectives less focus is placed on individual species.

In the first paragraph you portray extinction due to invasive species as illegitimate. In the second paragraph you say there is nothing wrong with 'natural' extinction. It would seem that you are re-defining extinction to exclude extinction caused by invasive species, which is what humans are most like. Then you say that "current rates of extinction" are orders of magnitude larger than "background rates." It would seem that by background rates you mean "without invasive species." So instead of answering the question you have re-defined extinction to avoid the messy parts.

I think you have misunderstood some parts of my answer and I have tried to clarify my writing. The first paragraph is only dealing with (in my mind) the rather loaded statements on evolution ('progress' and what evolution is 'supposed' to do). Nothing about invasive species in implied. 'Background rates' is a standard concept referring to "normal" extinction rates pre-modern humans. Nowhere am I redefining extinction, or are implying that invasive species are unimportant or should be excluded (on islands they are one of the main reasons for extinction of native flora/fauna).

Evolution by natural selection requires heritable change but evolution is simply the change in the allele frequency of a population over time.

A change in allele frequency is inherited to the next generation, therefore it is heritable. So what is you point? For natural selection to lead to evolution the trait must be heritable, but that is another question. With genetic drift the allele frequency can also change. Either way, the result is a change in allele frequencies which is inherited to the next generation.

@fileunderwater I agree.  I misinterpreted what was being said on my first reading.

Evolution is simply a change in the allele frequency of a population over time.  It is not progressive nor does it have to create diversity.  Some of the mechanisms of evolution such as genetic drift and stabilizing selection tend to reduce the genetic diversity of populations.
Furthermore evolution and extinction are two independent processes.  Extinction is the complete loss of a unit of genetic diversity (e.g., a species) from the planet.  Evolution and extinction are linked because extinction eliminates a particular evolutionary history that cannot be recovered, but the two processes are affected by different factors within the environment.
Clarifying these definitions we can see that both evolution and extinction are value neutral from the perspective of the biosphere.
Humans tend to ascribe value to biodiversity based on aesthetics, ecosystem services, ethics, etc... and thus we may strive to preserve it for these reasons but this is unrelated to the biological function of evolution and extinction.

I agree with your last two paragraphs, but not the first two. Calling genetic drift a "mechanism of evolution" is inaccurate at best since no new genes are produced.
If evolutionary history cannot be recovered, as you say, then how have various traits "re-evolved" multiple times throughout history? It is only the "inferior" combinations of those traits that (hopefully) will never re-emerge. This is where I fundamentally disagree with evolution. Each creature is majestic in its complexity and to merely call it a "mistake" and "inferior" needing to go extinct for life to march forward is mad.

Genetic drift is a mechanism of evolution - that is a fact. Creation of new alleles and genes is another thing. Also, that traits "re-evole" is generally due to convergent evolution, where similar selective pressures or niche spaces can produce very similar evolutionary outcomes. However, the genetic basis for the reevolved (convergent) traits in different species are (in general) completely different. Therefore, it is not in any way a case of "recovering evolutionary history".

Good question.  Evolution will and does continue.  Mass extinctions have happened in the past and in fact we are the product and beneficiaries of that process; when niches open up from extinctions, other species just move in and take over, eventually they will adapt to take the place of those who have left.  Of course that's a useful perspective since it will happen.  A large number of animals and plants are endangered and while the impact overall can't be estimated since we have never counted all the animals and plants, much less microscopic species, an example of our dire straits can be gleaned from the fact that perhaps half of amphibians are endangered,
There are various arguments that there is lost knowledge - when these animals and plants we have never even cataloged disappear we will lose hundreds of millions of years of biological 'experience', of lost knowledge as well as an aesthetic/ethical argument that this is clearly wrong somehow; like a mass murder of animals and plants.
I think that most people who have never seen these animals and plants, understood how wonderful and awe-inspiring they are, how many odd abilities that evolution has gifted them.  It seems like a nearly universal experience that those who have seen this are pretty strongly in favor of efforts to save them.
But that's not the question at hand; really won't the ecosphere heal and eventually be okay?  Now that we have discovered life so far under the ocean and in the depths of the earth that even nuclear holocaust would probably not touch them.  The answer is yes.  The ecosphere and life will go on.  There are two other useful questions though:
1) will we go on with it? Mass extinctions are the result of changes in the environment - all living things in that environment will sink or swim as it were and humans should not exclude ourselves.  Will the future human race deal with loss of oxygen content, the loss of fresh water and the misery of population explosion?  If the environment just keeps getting worse, will we do well?  We're all assuming that we will figure out how to feed ourselves, find drinking water when both food and water are not really growing to meet our growing population, not to mention the desertification of arable land and the rise in temperature that will impact human geography and economics over the next 100 years or so.  If the environment were to stabilize at least we would not be standing on shifting ground. If you are familiar with Malthus' argument, when there is no food or land left to exploit nature will take its course with us - war, famine etc etc.  That is also a natural state, which we've managed to slowly eliminate.  We may be bringing it back in.
2) How long do we want to wait for the ecosystem to heal? After the mass extinctions of the past, hundreds of millions of years were needed for the species around to re-establish themselves as they are now.  Is that really a good trade off for a few decades of industrial-economic expansion?
Until then, the survivors are not necessarily the ones we'd prefer.
I volunteered at a survey of shellfish in the San Franscisco Bay.  At one time the shellfish here were so plentiful that the natives piled giant shellmounds the size of small hills from their regular diets.  Now because of fertilizer runoff and pollution these shellfish are nearly gone - we didn't see one the entire day looking around the survey area.  Instead they nesting shells were covered with a slimy bunch of sea squirts -  plant-like animals which can grow quickly enough to absorb the nutrients and robust enough to ignore the pollution and chemicals.  I'd probably rather have a bay scallops on my plate rather than a salad of seq squirts.  The Bay is swimmable, but is plenty slimy.
Got to sign off now, but that's the outline of an answer...

There are contradictions in this answer: First we "benefit" from the process of mass extinction, then we "loose knowledge." Some creatures benefit from the extinction of others. However the "loss of knowledge" argument seems hocus pocus since various traits have been shown to have evolved multiple times in different species. While I agree that organisms are majestic etc. I don't see how evolution provides any precedent for preserving diversity. Like you said; the extinction of one species provides room for a superior species to speciate. Human speciation would seem to be the ultimate good.

Your comment about nuclear holocaust is hilarious in its reference to morality for which evolution provides no basis. Your questioning human survival is even more comical since you previously said that humans are "too fit" and must be restrained from dominating other species. Your final joke about waiting for the ecosystem to heal is choice. Human speciation would "heal" the ecosystem, no? Wait! Humans aren't speciating! They are becoming inbreds! New question: how to reconcile speciation with inbreeding?

I can't find the word 'loose' in my writeup...?  Evolution doesn't preserve diversity - but people try to learn from it - if human values mean anything here, which I allow it might not.  Still, what goes away, never comes back.  Superiority is a different question - the superiority of one species over another is similar to questions of the value of diversity - it means nothing in absolute terms, overall, if we hold the mass extinction as fine, then we must also allow our own extinction or changes to our species as similarly valueless - our actions will change us, probably not for the better.

You could just as easily have said that "our actions will change us, probably for the better."

Not really.  Not all changes are improve human happiness or well being - global warming is like everyone moving south a few hundred miles or more, unless they own a house at low altitudes above sea level - then your whole country might disappear.  I see it more as a case of short sighted personal consumption trumping long term planning and rational thought.  Not human beings at their best in my opinion.  Using relativisitic values arguments are probably not going to change my reasoning in this matter.  Sorry.

You might want to try to understand the human tendencies that are at play here - you can look at "Tragedy of the Commons" and "cognitive bias and global warming" e.g. http://rd.springer.com/article/10.1007/s10584-006-9060-3#page-1  I don't think I'm alone in this perspective.

The "fight against global warming" has less chance of succeeding than the "war on drugs." both are fighting economics, which is supposedly the foundation of evolution. I would view an invasive species as "short sighted consumption" at the cost of long term planning, which is why I asked this questions.

That's true - Invasive species from human movements about the world have destroyed millions of acres of forest (pine beetle) and killed most of the grapes in Europe at one point or another.  We spend lots of money to fix those problems, not just give up and let fungus eat all our food and cause famines and the loss of productive forest.  The kind of diversity that is produced from environmental changes are not usually desirable to humans who evolved in the conditions previous to those changes.  Human misery will generally result, if that's worth anything.

Another thing here is that all this is an entirely theoretical argument.  Maybe you can post another question where you walk through a specific case as to what you mean by this theory.  Your question doesn't discuss its motives or what you feel this means should happen. It sort of sounds like 'don't worry be happy' about ecological catastrophe.

I deliberately seek to avoid a specific case, because such a case would constrain the topic to a narrow set of preconditions, which tend to obscure the preconceptions of those engaging in discussion. For example: your answer and comments have shown how it is actually humanism and not evolution that leads us to preserve endangered species. Every point you have made is about how extinction will affect us, not evolutionary progress, which we cannot hope to assist since by interfering with a system we disrupt causality. Please forgive my bluntness.

I do start my answer with a statement that its true that even if there were no people, the planet and life will get along somehow.  I make no bones about it.  Human beings will try to save their own bacon even if we have to evolve a more rational self to do it - that's natural too. Stack exchange is asking me to move this to chat - if you want to continue feel free to pull me into a chat room.

Simply put, evolution through natural selection is a process which occurs naturally. It will occur to any self-duplicating organism with: variations, hereditary traits and threats to propagation (e.g. all life forms we are familiar with). Evolutionary biologists study this, the same way astrophysicists study space, and studying black holes or life forms doesn't indicate anything other then knowing how it works.
Actually, considering that most people in a certain field take interest in it (because logic), it is to be expected that biologists as a whole would rather see life doesn't go extinct then it does - again saying nothing about whether extinctions have or have not happened in the past.

why the downvote?

I doesn't answer the question,


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Good poly-A filtering rules or tools
I am aligning a large number of ESTs. It seems poly-A tails show in many different ways. In addition to occurring at the very end, they can be flanked by the cloning sequence one one end, or have mismatches/errors. What is a good rule or available tools that will handle the usual cases?
A few examples of the non-trivial cases I found, with their Genbank Accs:
>EE409337
... AAAAAAAAAAAAAAAAAAAAAAAAAGGAAAAAAAAAAAAAAAAAAAAAAAAAAAACCTTGTC
>EE409340
... TTTCTACAAAAAAAAAAAAAAAAAAAAAAAAAAAAAACTTGTC
>EE409361
... TTGTTAAACTGAAAAAAAAAAAAAAAAAAAAAAAAAAAACCATGTCGGC
TTACTGAATTGAA
>EE420306
.... AAAAAAAGTTATGTTAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAGGGAAAAAAA
AAAAAAAAAAAAAAAAA

Cross-posted on SeqAnswers,Biostars.

Did the answer on Biostars not work for you? (If so, what is it that it doesn't do that you would like it to do?)

@dd3: trimest has an option for trimming the poly-A regions, but we have to specify the rules. I have already done the basic filtering, but what are the "good" rules? Is there something better than min-length and max-mismatches that will handle real sequences I have given examples of?

You could try the empirical approach. Take a random sample of N ESTs and calculate the distributions for min-length and max-mismatches. Use the distributions to pick appropriate cutoffs (some sort of statistics thing).

@dd3, that definitely makes sense and seems like a good idea. (although there's some judgement to be made for things like ...GAGAACTGGGCAAAA: where does the tail start?). Since EST processing is well established, shouldn't something like this already exist in the tools or the literature? How does everyone else do it?

I'm still a little unclear as to what you are trying to achieve that min length was failing (as you seem to be fine with trimming.  Are you wanting to trim from ACA... on 409340 and AAACTGA... on 409361 but don't want to set min-length less than 7?

@highBandWidth: that, I have no idea. I'm just getting into bioinformatics myself. sorry.

@AtlLED, I don't know what the right answer is. Min-length of 7 may be too high for some cases and low for others. Seems like max-mismatches should be high if there's a cloning palindrome at the end and low otherwise. Are there well-known settings everyone uses? Has anyone done empirical studies to see what the right conditions are?

@dd3: no, your ideas certainly help. I'm just curious as to what people have usually done.

Can you give the search criteria for the ESTs?  I have an idea for this I'd like to try.

@AtlLED, well for my purpose I am just using all the EST's for one organism from NCBI. You can just search EST's with an organism and download the results in FASTA, eg.,: http://www.ncbi.nlm.nih.gov/nucest?term=Brassica%20napus%5BOrganism%5D

Use dust and remove all low complexity sequences.. Or simply use a regex search to filter out poly-As

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Can PolyA tails be within Expressed Sequence Tags?
Can polyA tails occur within (rather than at the end) of a sequenced tag? Consider, for example the following two sequences from NCBI:
DY008075
>gi|119423037|gb|DY008075.1|DY008075 19ACACYS_UP_022_A11_29OCT2004_095 Brassica napus 19ACACYS Brassica napus cDNA 5', mRNA sequence
TGGTACGGTCAGATGCTTGCTAAAGGAGAAATAAATAGAGACATGGGTGATAGTATAAGCGGAAAGGGAA
TGATTCAGGGTGTTTCTGCAGTGGGAGCGTTTTACCAACTGCTTAGTCAGTCCAGCCTAAGTATATTGCA
TTCTGAAGAGAAGAAACCTGTGGCTCCGGTTGAATCATGTCCTATTTTGAAAACACTCTACAAGATACTC
ATCACAAGAGAACAATCAACACAAGCGATTCTGCAAGCATTAAGGGATGAAACACTGAATGACCCAAGAG
ACAGGATTGAGATTGCACAGAGCCATGCATTCTACAGGCCTTCCCTTCTAGATCAGCCTTGATTAGTCTG
TCATGGCTCATAATCCGAACTTCTAAGATCTTACTTGTGCAAACTGCAGATTCTGCTATGTTAAACATCA
TGTCTTAAAATTGATTGTTGTTCAGCCAAAAAAAAAAAAAAAAAAAAAAAAAAAAAACATGTC

or EE485195
>gi|126492146|gb|EE485195.1|EE485195 DHBN8DCT_UP_012_C05_25FEB2005_043 BRASSICA NAPUS SEEDS BNDH8DCT Brassica napus cDNA 5', mRNA sequence
GTTACAGCTGGTTGAGAACAGTGACAATTCCCGGTTGAGCAAAGAAATTGCAGACAAGAGCCACCAACTA
AGGCAAATGAGAGGAGAGGAACTTCAAGGACTTAACATAGAAGAGCTGCAACAGCTGGAAAAGGCCCTTG
AAGCTGGTTTGACGCGCGTGATTGAAACAAAGAGTGAGAAGATTATGAGTGAGATCAGTGACCTTCAAAG
AAAGGGAATGAAATTGATGGATGAGAACAAGCGGCTAAGGCAGCATGGAACACAACTAACAGAAGAGAAC
GAGCGACTAGGCAAGCAAATATATAATAATATGCATGAAAGATACGGTGGTGTTGAGTCGGAGAAGACCG
CCGTGTACGAGGAAGGGCAGTCGTCAGAGTCCATTACTAACGCCGGAAACTCCACCGGCGCTCCTGTTGA
CTCCGAGAGCTCCGATACCTCTCTTAGGCTCGGCTTACCGTATGGCGGTTAGAGATGGAACCATACAAAG
AAGTTCATGGAGTGAGGAGATGCTCTGTAGTAACAAGTGGCAATGTAGTAATTTCTCTTGTTTGATGTAA
GTTTTTGTCTGAGGAAGAGGTTTTCCTTTTATGTTCTCTTTGATATTATTATCTTTCTTCACTGCAAAAA
AAAAAAAAAAAAAAAAAAAAAAAACATGTC

It seems to me that both the polyA sequences at the end are some sort of tail rather than actual coding for poly lysines. If we BLAST either of the sequences, the polyA part doesn't align with any reliable nucleotide or protein (i.e., with the NCBI non-redundant databases). I can give more examples and show their best alignments to nr-Sequences but it will make the question too long.
Cross posted to SeqAnswers.

As you rightly put, these poly-A sequences are not a part of the gene. I haven't done EST analysis but I generally trim poly-A tails and filter out sequences with more than 7-10 contiguous As, for RNAseq

@WYSIWYG, but I thought they had to be at the very end. Why is there a CATGTC at the end after the polyA tail?

i tried BLASTing the second sequence against Brassica napus nucleotide collection. There is a match but only uptil 472nd residue of the query. The rest of the sequence (473-uptil the beginning of poly-A) didn't have any match in Brassica. (some gapped alignments with other non-plant genomes). Although the entry in NCBI says that the authors have removed the vector and adapter sequences, it seems that it is some kind of contaminating DNA sequence. Check their experimental procedures.

The CATGTC sequence at the end of the poly A tail is an artefact of the method used in constructing the original cDNA library.
According to https://www.ncbi.nlm.nih.gov/nucest/EE485195.1 this EST comes from a library constructed in the Clontech vector pDNR-LIB
The Clontech SMART cDNA cloning system manuals are linked to from here
and the general manual descibes the use of a primer for 1st strand synthesis:

CDS III/3' PCR Primer  5'-ATTCTAGAGGCCGAGGCGGCCGACATG-d(T)30N-1N-3'
(N = A, G, C, or T; N-1 = A, G, or C)

If you look carefully at the primer you will see that the oligo dT portion, designed to anneal to the poly-A tail of the mRNA is preceded by the sequence GACATG and a SfiI site that is used in some clever cloning strategy that I don't fully understand. What is clear however is that the use of this primer will put CATGTC immediately after the poly A in the cDNA:
           .....SfiI....
5'-ATTCTAGAGGCCGAGGCGGCCGACATGTTTTTTTTTTTTTTTTTTT...
   TAAGATCTCCGGCTCCGCCGGCTGTACAAAAAAAAAAAAAAAAAAA...5'

>>> turning bottom strand around -  5' ...AAAAAAACATGTC

Any idea about filtering diverse conditions on the poly-A tail? Follow up question : http://biology.stackexchange.com/q/9104/3922

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Why don't raisins lose water when in air?
It is common that we soak raisins in water, and they acquire water by endosmosis. That means that the cells are permeable to water, right? Then why don't they lose water when kept in air? Or kept in sugar without any water?
EDIT: Also, take the example of peeled potatoes. Put them in a hypertonic solution, and they lose water, but when kept there, in air, they don't. How come?

That means that the cells are permeable to water, right?

Correct.

Then why don't they lose water when kept in air?

They do, but it occurs very, very slowly. It might take a few months (or years in some areas), but if you leave raisins exposed to air they will eventually become harder until the water reaches equilibrium with the surrounding air.
This slow process is why there are tips on how to reconstitute raisins that are too hard to make them more moist and plump after getting a bad batch or finding old ones in your kitchen.

They already have!  Raisins are dried-out grapes, and according to a brief search are less than 20% water by weight but over 50% sugar by weight.  They've lost plenty of water already.  Your average grape is probably hypertonic to most solutions and thus will not readily lose more water.  Additionally, for water to be lost to air, it must be vaporized via evaporation, which is slow, inefficient from something as dry as raisins, and miniscule in effect.  Sun-dried raisins already went through that process.


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How suddenly does lactose-intolerance onset?
How quickly can the loss of lactose tolerance onset in an adult?
Such as being able to process lactose normally to having notice symptoms associated with the inability to process lactose.
I am not asking how long it takes to digest food, but rather how long it takes for lactose intolerance to become noticeable (hours, days, weeks, months, years).

Disclaimer: I am not medically qualified, and this answer must not be construed as being medical advice of any kind.
Primary adult hypolactasia is the most common cause of lactose intolerance. The majority of the world's population have this phenotype.
In these individuals, at weaning, there is a reduction in the level of the enzyme lactase, which is responsible for digesting lactose to galactose and glucose in the small intestine. Undigested lactose can create symptoms via osmotic effects (causing diarrhoea) and because it is metabolised by bacteria in the colon, producing gas and thus abdominal bloating.
About 35% of adults have a genetic variant in an region upstream of the lactase gene which results in the expression of lactase continuing into adult life. These individuals are lactose tolerant. This trait is most common in Northern Europe.
According to references cited in

Ingram, CJE et al. (2009) Lactose digestion and the evolutionary genetics of lactase persistence Hum Genet (2009) 124:579–591

(I have removed citations from the passage for clarity.)

"most lactase non-persistent individuals can tolerate small amounts of lactose (as in tea or coffee), and some can consume a lot without ill effects. Variation in the composition of the gut flora between individuals, as well as a psychosomatic component may account for some of the interindividual variation in symptoms."

The clear implication is that there is a lot of variation in the tolerance of lactose amongst those lacking the lactase persistence trait. Given the contribution of the gut flora to the symptoms these could presumably vary as a result of, for example, antibiotic treatment. Also I imagine that the effects of undigested lactose could be synergistic with some other gut disturbance.
Added in response to comment from the OP:
In someone with the (common) genotype that corresponds to 'no persistence of lactase' the possibility of showing symptoms will be present from a young age. Apparently there is a lot of variation in the severity of symptoms. If an adult suddenly exhibits symptoms then I am suggesting that this could be due to an interaction of non-persistence with some other gut disturbance - I imagine this could happen quite quickly. Alternatively I suppose that a change in diet could trigger symptoms.

So are you saying the question isn't answerable because of such a wide variance in symptoms? If so, could you say that? Perhaps you are saying that it varies wildly person to person? If so, could you say that? Because I can't accept this until you produce an section of answer directly related to my question.


text:
Mechanism of Muscle Growth
According to this video (sorry for the poor reference but it represents my level of understanding in physiology), muscle grow as a consequence of repairing micro-lesions.
How are these micro-lesions sensed in order to activate protein synthesis? What are the key molecules that trigger myosin synthesis and muscle growth?

It's not so much due to muscle damage, but due to certain proteins being released from the Z-disks of the sarcomeres which initiate certain signaling cascades involved in muscle proteins. Moreover, during exercise  there is a certain amount of metabolic stress which activates other pathways also involved in muscle protein synthesis. I suggest you read up on the STARS pathway (http://link.springer.com/article/10.1007/s00424-014-1475-5) and mTORC1 regulation.

During exercise muscles are put under stress which eventually causes micro tears in the muscle fibres.
These micro tears put pressure on the nerve endings which causes the pain.
The body will then repair the tears during rest and recovery using proteins and sufficient fuel. The muscle will then become slightly bigger and stronger.
Energy systems used to repair these lesions are the following
There are three different types of energy systems:

Phosphocreatine
Lactic Acid
-Aerobic
1.Phosphocreatine Energy System

The ATP-PC system lasts for 8-10 seconds.
During the ATP-PC system a phosphate breaks off of the ATP to form ADP and a lot of energy.
ADP will then bind with another free phosphate to form ATP.
The ATP-PC system is an anaerobic energy system as it dose not use oxygen.

Lactic Acid Energy System

Glucose is broken down sustain performance for a longer amount of time than the ATP-PC system.However this system does not use oxygen so is not suited for events over 90 seconds.
When the ATP-PC system starts to fade the process of anaerobic glycolysis begins.
Glycogen is stored in the liver and is broken down without the presence of oxygen.
This produces lactic acid which limits energy production.

Aerobic Energy system

The aerobic energy system is constantly being used in your body to supply the muscles with energy.
In sport the aerobic energy system is used for events that last anything over 90 seconds.
The aerobic system can be used constantly but only if there is a constant supply of glycogen and fatty acids.
The aerobic system uses oxygen, glucose and fatty acids to yield large amounts of ATP.
The system takes place within the mitochondria and produces two bi-products, carbon dioxide and water.

These are some generalizations, I beleive the aa which is responsible for protein synthesis is BCAA leucine.

Thank you. I am no so interested in "where does the energy allowing muscle work come from?" but I am interested in  "the key molecules that directly trigger the synthesis of new myosin proteins?" Sorry if my question was a bit unclear.

You summarized the three main energy systems (why?) and gave no explanation of the actual mechanism. This does not answer the question at all.


text:
Is there any definition of complexity about gene and protein according their function?
Sorry for such a question,if it is too naive.
Is there any definition of complexity about gene and protein according their function?If so,what is the relation between them?

Could you explain a bit more about what you are asking?  What do you mean by "definition of complexity according to their function?"

@Amory,like what the protein play

Proteins and genes usually are classified in superfamilies and families acording with its inner structure (mainly its domain organization). Domains are parts of the protein with its own 3D structure that usually have their own function and acts more or less in an independent manner.
However, this doesn't talk very much about their complexity. Myoglobin and hemoglobin, for instance, are very related proteins and thus are classified in the same family. However, hemoglobin forms tetramers, while myoglobin is a single molecule. It's not unheard that very close-related proteins may differ in their association with other proteins, polymeration pattern, addition of new domains, etc. Very similar poteins may have very different functions, i.e. catalyzing similar reaction in opposite directions or in very different pathways, or acting in different parts of the cell or the organism.
In biology, it is desirable for any classification to be based in evolutionary criteria, since not only it is a more neutral and unbiased way to classify biological things, but also provide information about the origin and structure of those. You could classify proteins by their structure, number of motifs, number of domains, number of different domains, size, function (in fact, there is a very useful and widely used classification for enzymes), etc; and you could classify the genes according to its number of exons, structure of its promoter/enhancer, policystronic or not, etc. However, this classification will usually prove itself to be inferior to an evolutionary classification.


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Identification of this Salamander
This salamander was found in a small forest pond somewhat near the Oregon coast. In the area are many rough skinned newts and a small number of another type of salamander that I still can't find the species of. I'm guessing it is either the salamander species or a rough skinned newt.

I found what it is, it's a torrent salamander.

It is a torrent salamander. Most likely this is the southern torrent salamander (Rhyacotriton variegatus)

I'm not convinced this is a Torrent salamander (Rhyacotriton variegatus)... I'll look into this a bit...


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What virus transforms full grown plants?
I read an article by a gardener describing how a virus had transmitted a negative trait to his plants. It rather shocked me, because I hadn't realized that a virus could transform an adult plant. I was aware of dipping arabadopsis flowers in agrobacterium tumefaciens, but the concept of non-reproductive structures being transformed seems fascinating. What kind of virus is capable of that?

You're asking for a specific virus?

@canadianer Any information will be appreciated. A category or specific type is what I had in mind.

These are just a couple of short examples, but Witch's broom structures in trees can sometimes be caused by viruses - see Wikipedia: Witch's broom (fungi is maybe the most common cause though). In rose species you also have the similar Rose rosette disease (also called witches’-broom of rose), which is caused by a virus. The same webpage from Missouri Botanical Garden also includes a list of other plant viruses that you might find interesting.
Plant viruses that infect non-reproductive structures are common though - a overview can be found here: The American Phytopathological Society: Introduction to Plant Viruses, the Invisible Foe. More indepth information can be found in Plant Pathology (Agrios, 2012) (see ch. 12: "Plant diseases caused by viruses").

Viruses can infect just about any living thing, so that it could infect a plant is no surprise.
Your article describes how a small virus-infected part of a plant had been cloned and consequently the entire cloned plant was infected, and it infected plants grown hydroponically in the same water. No surprise there either.
Plant viruses have been known for centuries. One of the earliest recorded descriptions of a virus-infected plant can be found in a poem written by the Japanese Empress Kōken (718–770), in which she describes a plant with yellowing leaves in summer. The plant (a Eupatorium) was described as "autumnal".
The top 10 plant viruses (in one paper) in molecular plant pathology were listed as:

(1) Tobacco mosaic virus, (2) Tomato spotted wilt virus, (3) Tomato yellow leaf curl virus, (4) Cucumber mosaic virus, (5) Potato virus Y, (6) Cauliflower mosaic virus, (7) African cassava mosaic virus, (8) Plum pox virus, (9) Brome mosaic virus and (10) Potato virus X, with honourable mentions for viruses just missing out on the Top 10, including Citrus tristeza virus, Barley yellow dwarf virus, Potato leafroll virus and Tomato bushy stunt virus.

Some plant virologists even care enough to argue about it.
One paper describes how a plant was improved by a viral infection:

In all cases, virus infection delayed the appearance of drought symptoms. Beet
  plants infected with CMV* also exhibited significantly improved tolerance to freezing. Metabolite profiling analysis showed an increase in several osmoprotectants and antioxidants in BMV**-infected rice and CMV-infected beet plants before and after drought stress.

*Cucumber mosaic virus
**Brome mosaic virus
Aetiology: The earliest recorded plant virus disease
Top 10 plant viruses in molecular plant pathology
The REAL Top 10 for Plant Viruses

Introduction to Plant Viruses, the Invisible Foe

Virus infection improves drought tolerance

I was killing my brain on the answer. This is it!


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For how long can a raven stay airborne (a week or more)?
I'm wondering for how long a raven can stay continuously airborne, if strained to do so? If it makes a difference, I'm mostly interested in the Common raven, Corvus corax. Are there for instance any information on long-distance dispersal (wind-blown individuals over sea?) that can be used to roughly estimate this? Information on other corvid species could also be interesting, as a rough proxy.
If you are wondering, my motivation for asking is the biblical story in Genesis 6–8 (the deluge of Noah). Here, Noah sends out a raven and a dove to look for land. From the story it appears as if the raven can stay airborne for a longer time than the dove, which returns to the ark to rest. Is there any realism in the claim that a raven can stay airborne for one or maybe even two weeks?
Some background from Genesis 8 (this translation):

After forty days, Noah opened the window he had made in the ark. He sent out the raven, and it departed. It went back and forth until the water had dried up from the land's surface. He then sent out the dove to see if the water had subsided from the land's surface. The dove could not find any place to rest its feet, and it returned to him, to the ark. There was still water over all the earth's surface. [Noah] stretched out his hand, and brought it to him in the ark. He waited another seven days, and once again sent the dove out from the ark. The dove returned to him toward evening, and there was a freshly-plucked olive leaf in its beak. Noah then knew that the water had subsided from the earth. He waited yet another seven days and sent out the dove [again]. This time it did not return to him any more.

So the raven couldn't find a place to land, and it flew around until it could do so. A week later, the dove still couldn't find a place to land, but a week later it could. Thus, either (a) the raven was flying around for more than a week (as much as two weeks) or (b) the raven could more readily land in a wet area than the dove. Can either of these be true?

This question appears to be off-topic because it is about a mythical story and not based any real observation or scientific speculation.

It is possible to edit the post to make a scientific question without religious/mythical connotations.

@WYSIWYG not sure if off-topic. Although the religious part is evident, I think the OP is asking whether such a raven could exists in reality (i.e. if biologically a raven could fly for such a long time), and the religious reference serves simply as background of why he/she is interested in the question. I think, anyway, the question can be improved by focusing on the scientific part- as you suggest.

Quite apart from using a mythical story to ask a scientific question, I don't see what makes you think that the raven was flying around all that time. For all you know, and as seems more likely, it drowned. Could you [edit] your question, remove the biblical references and just ask something specific about an animal's behavior?

@terdon, I could just ask "Can it be true that either a raven flies for more than a week straight or doesn't mind ground as wet as a dove minds?" but that is a very odd question absent the background. Note that my question as currently worded does ask something specific about an animal's behavior -- but does so with some background to indicate why I'm asking.

I am sure you can count it by checking how much energy a bird needs to fly, and how much it has in its energy storages. The equation will be possibly an integral, because the energy requirement of flight will depend on the weight, which will drop, just by rockets. Water may not be a problem, because afaik guano contains very few water.

Hmm I think the answer can be much more complicated, because birds can extract energy from atmospheric phenomenons.

Can't be very sure about ravens but the maximum recorded flight duration is of Common Swift — 10 months.
Alpine swifts also remain airborne for up to 6 months.
Pigeons can fly up to 1800km in a long flight. From this article (pubmed):

In the United States, the longest pigeon races involve flights of 1800
  km and, because substantial financial rewards accrue to the owner of
  the fastest pigeon, there is severe selection for those pigeons that
  home the fastest.

Wikipedia article on pigeons says that they can fly at 80km/h but I suspect because the other wikipedia page on flight speeds says that average flight speed of peregrine falcon is 65-90km/h. So assuming that average speed of pigeon is 60km/h it should be able to fly for 30h. According to this paper, the speed with minimum power consumption is 8-9m/s (~30km/h). At this speed they should be able to fly for 60 hours. In the same paper it is estimated that the maximum continuous power output is ~10.5 W; if a pigeon has 11g of stored fat (per 400g body weight — assumptions from the same paper), and given the calorific value of fat — 38kJ/g, it can fly upto 38 × 11 ÷ 10.5 = ~40h. This means that the best trained ones can perhaps manage to fly for 2.5 days straight.
Now ravens are heavier (~3 times heavier) but are more aerodynamic and can fly faster. However, I guess they cannot perhaps fly 7 days straight.

Ah, but is that an African or European pigeon?

@terdon I urge you to add that as an answer ;)

@terdon In principle (if we assume no speciation events after the Flood), it could be any Columba species or even any other similar bird for which יונה was used as the closest term :)

Who needs land? These birds spend 10 months of the year in flight

@theforestecologist thanks. This seems like a recent report. I'll update.

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


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Most suitable biodiversity index
I am conducting an investigation into the effect of two different grass management techniques (grazing vs. machine-mowing) upon floral biodiversity.
I have collected my data and now need to process it in a way that will yield meaningful and valid results. My data is in the form of 25 samples per area with %-abundance measured for each species in a 0.25m2 quadrat.
I am currently using a non-standard diversity quantification technique, called Disney's index (which I have been led to believe is named eponymously after R.H.L Disney, however I am unable to find any references describing this), in which we assign each species a weight based on percentage abundance, as follows:

We then use these weights to calculate the index as follows (i.e. by computing the sum of the weights of the species, over the number of species):

I want to know if this is the best possible diversity index I could use for this type of analysis, or whether there are others which I should be considering.
Thanks in advance!

It sounds like you are interested in beta diversity which is the change in taxa composition (i.e., alpha diversity) between plots.  There are a number of approaches to calculating beta diversity and the correct choice generally depends on the question(s) you are trying to answer.  The most common approaches are very well described in this paper:
Anderson, M. J. et al. 2011. Navigating the multiple meanings of Beta diversity: a roadmap for the practicing ecologist. Ecology Letters 14:19-28
P.S. I am not familiar with Disney's index so I cannot comment on its merits.
P.P.S. You may also be interested in this question.

I don't know anything about the "Disney index" but the equation you use looks like it's a version of Simpson's D, a very common biodiversity index.  If you're just estimating two different kinds of sites (your two management strategies) I would suggest a rarefaction method.  This can be estimated in either the vegan package in R, or EstimateS http://viceroy.eeb.uconn.edu/EstimateS/ by Robert Colwell.  Rarefaction takes into account the number of samples you have when calculating an estimate of the number of species you find.  You could also use straight forward species richness estimators like Chao1 and Chao2.  The best "diversity index" in my opinion is Hurlbert's PIE
Hope this helps.

You might want to look at Koleff's paper (open access @ JAE http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2656.2003.00710.x/abstract).
Given that you have quantitative data, you should look at the difference between presence/absence and quantitative measures. A Bry-Curtis measure or something to that effect would be way better than a Sorensen or Whittaker here, lest you lose information.

All the other answers are totally valid, and I agree with them. In your case I would not use Disney's index since you have reliable proportion for abundance and Disney's conventionally assign a number. I think this step might hide some of the information in the data.
In your case I would use a quantitative similarity coefficient.
You can find a lot more on similarity coefficient in this book Numerical Ecology along with other useful analysis like clustering.


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What Effect would Cannabinoids have on the Acute Porphyrias?
I should be clear in saying that this question is NOT intended for personal medical advice. Rather what I am looking for is journal articles and/or books that touch on this subject because I think it would be quite an intriguing topic to probe. I am unaware of any interaction between the endocannabinoid system and the formation of haem and porphyrins in general.

Do you have reason to suspect they would have an effect?

Sort of, I know they can interact with the P450 cytochromes and hence may bring on an acute attack.

A Web of Science search for endocannabinoid AND porphyria under Topic produces zero hits.

Yes, they can induce an acute attack.

Drugs metabolised by cytochrome P450 (CYP) such as analgesics may induce acute attacks in patients with hepatic porphyrias. In recent years, preclinical and clinical studies have suggested that cannabinoid pharmaceutical preparations may be potentially useful in the treatment of pain [1].

There is even a clinical case about acute intermittent porphyria in a marijuana user:

Mr. G is a 55 year old Caucasian male with a past medical history significant for acute intermittent porphyria (AIP), chronic back pain, renal insufficiency, hypertension, and nicotine dependence. The patient has presented to the hospital with multiple AIP exacerbations since diagnosed eleven year prior to the current case. [...] Urine drug screen was positive for cannabinoids, which he admitted to frequent marijuana use [2].

But an experimental study on mice failed to prove that:

Our findings indicate that CP-55,940 (a cannabinoid CB1 receptor agonist) and its metabolites do not behave as porphyrinogenic drugs and may potentially be safe for treating pain in patients with acute porphyrias [1].

References:

Fontanellas A, Manzanares J, García-Bravo M, Buzaleh AM, Méndez M, Oliva JM, Batlle A, Palomo T, Enríquez de Salamanca R. Effects of repeated administration with CP-55,940, a cannabinoid CB1 receptor agonist on the metabolism of the hepatic heme. Int. J. Biochem. Cell Biol. 2005 Aug;37(8):1620-5. doi: 10.1016/j.biocel.2005.02.010. PubMed PMID: 15896668.
Ware SK. Acute Intermittent Porphyria With Psychiatric Manifestations: A Case Report. Ment Health Clin. 2013;3(5):100. Available at: http://cpnp.org/resource/mhc/2013/11/acute-intermittent-porphyria-psychiatric-manifestations-case-report. Accessed July 27, 2014.


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Does the Enzyme Monoamine Oxidase, Isoenzyme A have an allosteric modulatory site?
Does the Enzyme Monoamine Oxidase, Isoenzyme A (MAO-A) have an allosteric modulatory site? I ask because I would like to know if it is possible, in theory at least, for a positive allosteric modulator of MAO-A to be developed.

I think an allosteric modulatory site has already been found, but it's not specific to Isoenzyme A, if that's what you were looking for.
See these papers:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1564771/
http://www.jbc.org/content/270/17/9856.full


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Where can I find an at least Semi-Comprehensive list of what biochemical reactions Acetyl-CoA participates in?
Acetyl-CoA has a number of biochemical roles in the body and I'm curious as to whether anybody knows where I can find at least a semi-comprehensive list (i.e. comprising all the major roles in the human body it serves) of the biochemical reactions in which acetyl-CoA partakes in the human body.

Have you tried wikipedia? All the major ones should be there.

I may be missing some fantastic resource, but my first thought is to send you to KEGG.  Is that crazy?  Maybe, but a simple search for Acetyl-CoA in humans can give you tons of useful information, including GO terms, enzymes, genes, and, yes, biochemical reactions; just use the KEGG Pathways tool and specify humans (hsa).  You can click on each individual pathway for more information, such as the cholinergic synapse.

Are these reactions solely those that occur in the human body?

@BrentonHorne Wow sorry, I TOTALLY missed that!  It's now updated to be homo sapiens only.

Metacyc is an excelent methabolic pathways database that includes all kind of organisms. Of course you can search for methabolic compound.

You should look at Lehninger's Principles of Biochemistry. Just search for Acetyl-coa in the index, and you will find it's roles in different aspects of the metabolism.


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Tree identification - Oregon
A bit west of Portland. It doesn't look native to me, and we didn't plant it. This is the first year it flowered, so I decided to see if I can get it identified. If it matters, the flowers are aromatic.

This is a Privet (Genus Ligustrum). It appears to be Ligustrum vulgare which is known as Common Privet, or sometimes European Privet.
It is a common woodland understorey shrub in Europe, often planted as garden hedging in urban areas as it is semi-deciduous and responds well to repeated pruning. You could never really call it a tree, it is a shrub species.
The white flowers as you say are quite fragrant and pleasant. They develop into shiny black/dark purple berries.

I would normally add some photos of my own, but yours are so good they show all the characteristic features very well.


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Streamside plant identification - Oregon
This is in the western cascades forest in Oregon. Leaves are at the ends of branches only, lives mostly in slightly muddy areas next to streams. Produces small black berries.

Posts (especially species ID posts) should have all photos copied directly into the post and not linked to if possible (i.e., as long as copyright issues allow). This way, we avoid the issue of having an ID question with non-working photo links in the future. Please copy the pics from your "More photos" link directly into your post. Thanks!

Yeah, I tried to do that, but it didn't work because they're too large. Is there a way I could get around that?

I'm not sure what you mean by too large? You mean that they're >2mb when you try to upload directly from your computer? If thats the case, you have to either crop/lower quality or post them somewhere else 1st (which, typically lowers their quality). I simply copied them from your other site and put them here.

It's a plant in the family Ribes, which includes currants.
If it stinks when you crush the leaves, it is probably Stink Currant, or Ribes bracteosum, a plant found in the Pacific Northwest.

Leaves are large, like maple leaves, sparsely hairy to smooth, with 5 to 7 lobes, stinky when crushed.  Flowers are numerous on mostly erect clusters; with white petals and brownish-purple to greenish-white calyces.  Berries are blue-black with a whitish bloom.

The leaf and berry are a good match. There are ~150 species, so it's a bit difficult.
It could also be Ribes acerifolium, or Maple-Leaved Currant.

Shrub with spreading branches but no bristles. Leaves maple-like, 1–3 in. across, with 5–7 rounded, finely toothed lobes. Hanging stem of 8–12 greenish flowers, each less than 1/3 in. across with tiny red petals and stamen filaments broad at base. Berry black, coated with bluish powder. Grows from mid elevations to treeline in Cascade and Olympic mountains.

I could not find a photograph that was not copyrighted. The flower color was pinkish to brownish.
It's not a perfect identification, but it's closer than 'in the ballpark'. If you google "Ribes western Cascades", you'll see what I mean. :)

Thanks, that gives me what I need. I looked through a fairly comprehensive identification guide of Pacific Northwest wildflowers (had a whole lot more than any book I've seen), and every native flower I've seen was in it except for this one for some reason.

@Tzacol - Because Murphy's Law... or it's not been identified yet. It does say brownish-purple though, so I woiuldn't rely too heavily on the color of the flower. :)


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A day in Beijing is like smoking Only one sixth of a cigarette
This is the title of this blog post followed by this other good post.
I'm particularly anti-tobacco-smoke, at the point of not always considering other pollution, and this article shows how this kind of domestic pollution (main domestic pollution is usually heating) is probably no insignificant in the global air pollution.
The weight of this pollution is also maybe increased since people tend to be nearer from potential smokers than from cars (e.g. near entrances).
I've not known the period of the past, without the smoke-free laws in buildings, but it seems in my country, that it has just moved the problem, possibly reinforced smokers reflex to smoke when outside
The author shows useful references, that all measure second-hand smoking in terms of PM2.5 which is the common indicator with PM10 for air pollution [car traffic,domestic heating,industry,coal combustion,construction,quarry,waste treatment].
The results are interesting showing the important rate of PM2.5 in second-hand smoke, it would even be very useful to indicate air pollution levels in terms of cigarette inhalation. 0.17 cigarette/day is quite more insightful than 150μm of PM2.5, at least to me.
But I'm still skeptic and think the effects of second-hand smoke are more important (second-hand smoke is smaller in size than 1μm, considering not only cigarette from manufacturers which include many brute carcinogens and poisons (arsenic, hydrogen cyanide,..), but other tobacco/or drug smoking that are different but considerably noxious too)) and this study is quite informative too, comparing diesel car exhaust to cigarette combustion.
I'm wondering:

is the pollution from cigarettes as volatile as the rest of air pollution?
is the concentration of second-hand cigarette global pollution not insignificant compared to the rest of pollution (in countries with high smoking rates)?
does it go in higher layers of the atmosphere, lower layers (more critical), or does it blend uniformly?
can air pollution mask (with PM2.5, and PM10 reduction filter) protect as well from it?

particles size in micrometer, from http://en.wikipedia.org/wiki/Particulates

edit: this http://ash.org/CAEPAProposal.pdf report is particularly interesting

ask on skeptics.stackexchange


text:
What are the characteristic structures of bacillus M. tuberculosis and what they cause?
I answered to this question:

In most forms of the disease, the bacillus M. tuberculosis spreads slowly and widely
  in the lungs, causing the formation of hard nodules (tubercles) in the
  respiratory tissues and form cavities in the lungs.

and got zero points.
What is the correct answer to the question?

Did you read the wikipedia article on this ?

It is not sufficient and very bad. Must be exact in the answer and answer exactly to the question. My answer was apparently too general.


text:
Why is the floral biodiversity of grazed grassland higher than that of mown grassland?
I have collected some data to compare the biodiversity of a field in which the plagioclimax is maintained by machine mowing with a field in which the plagioclimax is maintained by sheep grazing.
What I found was that there was a significant increase in floral biodiversity in the field which was managed by agricultural grazing when compared to the floral biodiversity of the machine-mown field.
I am trying to explain my findings, and I believe that it is due to the comparitively short amount of time that machine-mowing has been a grassland management technique, so there has been little time for natural selection to take place and for species to develop adaptations to machine-mowing (such as being low-lying, or extremely fast-growing). Whereas the field which is managed through sheep-grazing, contains multiple competing species which have adapted over time to grazing sheep, such as Cirsium arvense.
Moreover, the field which is managed by grazing has nutrients returned to it through defecation of the grazing animals, allowing for more favourable conditions for growth.
Is my explanation valid? Are there any other reasons why the floral biodiversity of a field managed by sheep grazing would be higher than one managed by machine-mowing?
Thanks in advance!

I think you may have covered the answer in your question... but here's my take;
The 'mowing' occurs at a distinct time-point and is highly destructive and uniform, so the selection pressure is very high and only highly competitive species that are fast to grow and reproduce will be successful.
As you point out, animals will defecate and naturally fertilize the land, thus favouring growth. Other favourable factors in an agricultural environment will be that the 'mowing' will be much less uniform; the animals may favour one plant over another - so a plant that is not eaten by the animals will continue to grow and reproduce, whereas in the mowing environment this plant would not succeed; this will allow various other species to succeed where they would not in the mown environment. Also, depending how many animals are in the area the height of the grass may be higher overall, so slower-growing plants could grow enough to reproduce.

Other possible reasons except your and Luke's:

Different agriculture techniques. I could imagine machine-mowed grassland could be processed by different chemicals (fertilizers, insecticides). I could imagine machine-mowed grassland could be sown with different grass that grows faster but dies when trampled with hoofs.
Most agriculture machinery works on fossil fuel i.e. emits CO₂ and other compounds.
You could also flip cause and effect. It could be that there're some reasons (dunno: soils, humidity, etc) why fields with lower biodiversity is more suitable for mowing.


text:
Do any birds beside the family Columbidae (or any reptile or mammal) feed their young "Crop Milk"
Birds from the family Columbidae (e.g., doves and pigeons) produce a fatty, milk-like substance in their crop.  The secretion is often referred to as "crop milk."  They feed crop milk to their young through regurgitation.  Does anyone know of another bird or reptile group (or even mammals) that has evolved such a mechanism; not regurgitation but secretion of a milk-like substance for feeding young?  Also, both male and female doves produce crop milk; are there cases where males of a mammal species produce milk?

Male galactorrhea exists in humans.

In mammals there are only two species (known, there may well be others) where males lactate. They are both species of bats and this paper discusses the evolutionary mechanisms that could underlie male lactation. I have ignored human cases because they are more of an unusual occurrence (often brought on by severe dietary stress) rather than an evolved mechanism.
Other non-mammals include Flamingo and Penguins. There is also a species of fish, called a discus fish, which produces a mucus from its skin which the offspring feed on (here). I would hypothesise that this evolved originally for different reasons (defence, scent communication, excretion...) but offspring "discovered" this was slightly nutritious so fed off it, those genetically predisposed to doing such things then had higher fitness and the trait spreads. Evolution of greater or more nutritious mucus production would be achieved because parents that produce more/better mucus would have more offspring that reach maturity.
The paper by Kunz & Hosken is a good discussion on current evidence and the potential for evolution of male lactation.
I hope that answers your question, happy reading!


text:
To diagnose osteomyelitis of vertebral column in chronic kidney failure
Assume you suspect amyloidosis because of the history of the patient: problem with vertebral column and "purulent" (serous, fibrous, or hemorrhagic) inflammation when patient very young.
Now, the patient has a chronic renal failure.
Is there any other method to diagnose the fracture of some bone than röntgen?
Assume you do not know where the fracture is exactly.

Osteomyelitis can be diagnosed with the following imaging techniques [1]:

first of all: radiography to view the anatomy of the bone
the sonography can be used to diagnose fluid collections, periosteal involvement. It is also the most useful procedure for kidney assessment [2].
CT is also useful to detect early osseous erosion, but is less sensitive when it comes to bone infection
MRI is the most sensitive and specific for osteomyelitis
Nuclear imaging can be used to identify multifocal osseous involvement.

References:

Carlos Pineda et al., Radiographic Imaging in Osteomyelitis: The Role of Plain Radiography, Computed Tomography, Ultrasonography, Magnetic Resonance Imaging, and Scintigraphy
American College of Radiology, Renal failure

Is there any techninques in Propedeutics to limit the area of the research. Assume you have no idea where the fracture is, not about side and how big fracture is.

You can look for the basic signs and symptoms of fracture http://www.webmd.com/a-to-z-guides/understanding-fractures-symptoms


text:
Could someone please identify this species?
I have come across these insects a lot more lately, as far as I can tell, they can sustain a hover state in flight. I'm actually quite interested to know what these are, seeing they look like a cross between a bumblebee and a common housefly...

For species ID questions, it is very useful to know where and when you saw the animal, and it can be useful to know details such as weather conditions. Could you provide some of these extra details?

Easily done, lower Blue Mountains, Bew South Wales in Australia, about 4pm AEST, overcast conditions...

Based on location, behaviour, and markings, I'd go with some sort of hoverfly (https://en.wikipedia.org/wiki/Hoverfly). I can't offer positive ID, but I would hazard a guess at https://en.wikipedia.org/wiki/Melangyna_viridiceps based on the all-black thorax and the fact that this species is relatively common.

New South Wales*

It's definitely a hoverfly (Syrphidae), but I don't you will get a certain identification to the species level based on that single photograph.

@bshane, in the few pics I've seen, Melangyna stands with the wings folded, while Eupeodes stands with the wings spread apart. But don't know if this is a useful taxonomic trait for that group.

Looks very similar to Eupeodes corollae (Syrphidae). But only a specialist in the group will tell you if its the same species, genus or family. And not with that low-resolution photograph (sometimes they need to take the genitals off for proper identification).

the photo was the best I could I at short notice... I'll see if I can update the photo at a later time.

Better talk to a specialist. Depending on the group, you can only know the species by capturing an individual. And sometimes, only knowing the place and the flower it's in, is enough for the identification.


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

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


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When writing about past research should I use the species name they employed or the modern version?
I am currently writing a literature review in which I am talking about the old research on the subject. When this research was carried out the species I'm talking about were classed under a different genus (specifically, it used to be called Vibrio fetus and is now called Campylobacter fetus). What is the correct approach for choosing when to use the older name and when to use the newer name? I see three options, although there may be more:

Always use the modern name.
Use the name used by the authors when discussing their work.
Largely use the modern name but make reference to the fact a different name was employed where it is appropriate to do so.

I'm tending towards option 3, but it's sometimes a bit unwieldy. Is there an accepted convention I should be following?

I would also use the modern nomenclature and introduce the old one in the introduction (and probably also in the abstract). I don't like the old nams sticking around, something that can regulary be seen for gene names. It is relatively complicated to search for literature, when you have to do this as well for half a dozen synonyms. Nomenclature exists for a reason.

3. is right thing to do. You can mention in the introduction that "Campylobacter fetus, which was previously known as Vibrio fetus [Ref] ........."
You should not use the old name anywhere again (also for the sake of consistency), once you have made it clear that the species was renamed, in the Introduction.
I don't think there is any written convention like that (As such usage of any obsoleted terms is to be avoided and the standard nomenclature as described by ICZN/ICBN etc should be used).

+1 Also note that it is common that older synonyms are given (sometimes many), e.g. in a parenthesis in the introduction or in methods (where the organism is described). In species determination literture or taxonomic papers clarification of synonyms are often done under a specific heading.

I've also seen cases like this written as "Campylobacter [Vibrio] fetus". Or just use the revised genus and ignore the old name.

There actually is a rule, called the 'Principle of Priority', which states that the nomenclature of a taxonomic group is based upon priority of publication hence option 2 in your question is the correct approach. In the principle III (Principle of Priority) section of the link above it is stated that

This principle states, in essence, that if a taxonomic group has been
  given two or more names, the correct name is the first name that meets
  the Code’s standards for publication.

But here the rule doesn't seem to apply....instead there is a piece of literature regarding the reclassification of gen. Vibrio to Campylobacter. In the paper "Neotype Strain for the Type Species,Campylobacter fetus (Smith and Taylor) Sebald and Vkon" (Veron & Chatelain, 1973) they state that:

A critical study of the present state of the classification of
  vibrio-like, curved, microaerophilic bacteria was made. The species
  originally described under the names Vibrio coli Doyle, V. jejuni
  Jones et al., V. sputorum PrCvot, and V. bubulus Florent are
  transferred to the genus Campylobacter Sebald and VCron
  1963. The authors suggest that the type species of this genus, C. fetus, be divided into two subspecies: C. fetus subsp. fetus (Smith
  and Taylor) comb. nov. (syn. V. fetus subsp. intestinalis Florent),
  which contains the neotype strain of the species, and C. fetus subsp.
  venerealis (Florent) comb. nov. The previously described subspecies V.
  fetus subsp. intermedius Elazhari is regarded as an infrasubspecific
  taxon with the name C. fetus subsp. venerealis biotype intermedius.
  CIP 5396 (=ATCC 27374=NCTC 10842) is proposed as the neotype strain of
  C. fetus subsp. fetus. This strain, then, is also the neotype strain
  of C. fetus (Smith and Taylor) Sebald and Vkron.

The highlighted words suggest how they have approached in naming the species...

While this link may answer the question, it is better to include the essential parts of the answer here and provide the link for reference.  Link-only answers can become invalid if the linked page changes.

@TheLastWord ..Thanks....Actually have joined just today..so a little low on these 'know-how's...

As I understand the question, this answer is not really relevant. The Q is talking about a reclassification of a species due to new phylogenetic information, so that it is moved to another genus. The Principle of Priority is mainly talking about what name that should take precedence, if there are several descriptions of the same species. In this case, the Vibrio genus is probably in use for another species (which should keep the genus name by 'Principle of Priority'), while Campylobacter fetus has been moved to another genus because of new information

@fileunderwater Ok....but the ambiguity normally arises due to placement of same species in different genus....for example-a species of oomycetes causing ' White rust' disease was named ' Albugo candida ' in 1751 & just after 2 years in 1753 it was named as ' Cystopus candidans ' & after that placed even in 'Acedium' & 'Uredo' genus...but the principle prevailed & the original name or basidionym is kept as " Albugo candida " and the rest were just designated by synonyms...there of course can be exceptions...but generally the essence & application of the rule is maintained...

I think you're confusing more than one thing here. Campylobacter fetus is the correct, current, internationally recognised name for the species. Like many species, it has been moved to a different genus than it was originally assigned to. The principle of priority applies when the same species has been identified by different researchers.

ya..got your point...I am modifying my answer...


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Why are particulate matter toxic to humans?
There are many studies on fine particles (PM2.5) and their fully negative effect on human health. There doesn't seem to have any positive aspect of inhaling particles, except very particular ones, but most often people smoke, and release all sort of unwanted and toxic PM2.5, same goes with for fuel combustion.
At a huge dose, we die within minutes, like in a gas chamber, at small dose below this hazardous health risk level, is it still dangerous to us? If yes, why aren't we equipped to fight them, I guess this smoke concentration and pollution level is very recent on human evolution scale, but at the lowest layer of life, bacteria may develop to break and eat toxic particles, does it happen it our blood? Is it hard to explain to a non-biologist like me?

Particulates can accumulate in the aveolae in the lungs. This leads to inflammation and tissue damage and scarring. This reduces the available surface area for gas transfer. Low level exposure over long periods is harmful. Asbestos workers are well known to get sick, but miners can get black lung or silicosis from inhaling mining dust, and farmers can get lung disease from inhaling dirt that gets blown up as dust. This damage usually isn't seen until they are in their 50s or 60s.

Interesting. For the 3 examples you gave, is it high level exposure? What level is it for someone using his bike everyday, with part of the itinerary inside traffic? thanks


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Why does the heart use lipids (and not glucose)?
Fetal hearts use glucose as their primary metabolic substrate.  Adult hearts use free fatty acids, which are less efficient (require more $O_2$ to synthesize the same amount of ATP); however, during cardiac failure, the heart can switch to glucose utilization.  Why doesn't it just use glucose all the time?

The heart uses lipid and glucose (although the fatty acids contribute a much greater fraction to cardiac energy production - you can experimentally cause damage to the cardiac myocytes if you decrease the ability of the heart to metabolize either glucose or fatty acid fuels

Lipids require more oxygen to burn, but also they are cheaper to store (since they have great calorific power than carbohydrates and they're hydrophobic, thus not requiring water for their storage). The body can store so much lipids that it becomes an almost everlasting energy source (A normal adult have enough energy stored as fat to allow basal metabolism for weeks to months), which cannot apply to glucose. If fat is not present, glucose would have vanished from the body long time ago. Glucose levels must be maintained at a certain level, because it's the main energy source for the brain (which cannot use lipids ). The brain can use ketone bodies (product of fat oxidation) as a last resort.
For all the previous reasons, the heart (and many other organs, like the liver) uses fat while possible. If possible just means when not starving to death and with sufficient oxygen supply. This second condition doesn't apply to heart failure. In this case, oxygen supply fails and the tissue switch to glucose just because they can use it without oxygen (glycolysis and lactic fermentation).

But...most tissues strongly prefer glucose under those conditions (not starving to death and with sufficient oxygen supply), even if you are fat, typically cited as being due to the increased oxidative stress of fatty acid metabolism; the question is why the heart prefers fatty acids instead, despite this.

The usual explanation is that glucose is potentially dangerous because there is always a chance glycolysis will run too fast and produce lactic acid.  While lactic acid buildup is no big deal for a skeletal muscle, lactic acid build up in the heart can affect the ion channels and hence the heart rhythm.
Fuels for the heart are fatty acids, ketone bodies, and lactic acid taken from the blood.  Evidently when the source of lactic acid is the blood, the heart does not take it up any faster than it can convert it to pyruvate (and then to AcCoA, etc.)
Since aerobic metabolism is so important for the heart, is has a high content of mitochondria.

Welcome. Could you add sources to your answer? As a scientific stack we appreciate, and factually demand answers to be backed up by references.

Why will glycolysis run too fast? Any reason?


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Why HIS tag is not detected in WB or dot blot?
I would like to know why the recombinant protein with his tag at c terminus is not being detected neither in western blot or dot blot.
I'm trying to validate protein expression of four proteins. Three of the four proteins have no assigned protein family or domain (PFAM). The size of the proteins is small:
Locus   Nucleotide length   Protein size    Membrane features   Cloned  WB  Dot blot    Dot blot urea   COG
HPNK_06205  360 120 signal peptide  yes no  no  -   -
HPNK_09829  129 43  signal peptide  yes low low -   -
HPNK_10446  756 252 transmembrane   yes no  no  -   COG1175 ABC-type sugar transport systems, permease components
HPNK_11461  264 88  signal peptide  yes yes yes -   -

Next steps:
-Discard possible his tag hidding by adding urea to dot blot.
-Revise annotation for the proteins. Since all are annotated as hypothetical proteins, maybe there is an alternative annotation that could lead to longer proteins and maybe more stable products.

Some troubleshootings can be found here, pointing to hidden his tag. https://www.researchgate.net/post/Why_am_I_not_able_to_detect_6_HIS_tag


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Do bacteria precipitate in static liquid culture media?
We performed 36h biofilm cultures and would like to know if this time is enough to planktonic bacteria to precipitate.
Since we observed biofilm formation one the surface of the microtiter plate. Were  biofilm bacteria derived from precipitation of suspended bacteria or rather replicated from some initial attached bacteria cells?
Specie: Haemophilus parasuis. A facultative anaerobe.

Maybe the question is irrelavant for the final outcome. The number of inoculated bacteria cells was so small that would not influence the numbers of biofilm bacterial cells observed, almost sure all were derived form initial attached cells.

You didn't specify the species, but I have left E. coli transformations (in 500µl of SOC) overnight due to rushing/forgetting to dispose of them after the transformation, and they were precipitated in the morning.

yup, e.coli for mini preps can precipitate pretty quickly (overnight growth in 3 mL culture). I notice clearing of media (sort of supernatant) after maybe 12-24hr. But other species might behave differently


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Downstream analysis after in vivo pathogen RNAseq
We performed RNA-Seq of in vivo bacterial samples and identified some key up- and down-regulated pathways.
We compared bacteria during infection with conventional agar plate.
Which could be the next steps to validate our findings? We are interested in antibiotic and vaccine developemnt.

You're going to need to be a lot more specific. To start with, when you say a pathway is up or down-regulated, what comparison are you making? Is there a treatment and you're comparing treated versus control? Are there  different populations and you're comparing to each other?

Updated. We compared bacteria during infection with conventional agar plate.

Okay, first, I would say to everyone planning a high-throughput experiment: Hypothesis first, then experiment. Otherwise you're setting up an expensive and time-consuming test that's not going to answer the questions you want answered.
In this case, the question your experiment is designed to answer is "What genes are crucial to growth in vivo that are not crucial to growth on a plate?", which is probably not the clearest model for vaccine/antibiotic design.
I guess you could say that a difference between the plate sample and the in vivo sample is the presence of a host, and therefore it's possible that upregulated pathways represent the bacteria's host adaptation, and maybe you can attack the bacteria by attacking its ability to colonize the host. A gene involved in immune evasion could make a good target.
(That's a very messy model, as there are tons of other differences going on, but since you've already run the experiment it's probably the best you've got.)
So then, use your data for a new round of hypothesis generation. Take your pathways and come up with a way that they might be allowing the bacteria to adapt to the host-- maybe a secretory pathway that could be interfering with the target immune system, or some membrane signalling molecules that get upregulated, or whatever.
Now you have a hypothesis, so design an experiment. For instance, take a key upregulated member of a pathway. The hypothesis is that it's crucial to growth in a host but not to growth in general. So, knock it down, either with chemical inhibitors or with genomic editing, and see if it's less effective at host colonization.
(Although host colonization effectiveness is pretty difficult to measure ethically if your target organism is humans. But you have some sort of proxy or model system to measure that, right?)

Thanks for your helpful answer @Transcriptase. We work with a pig model of infection, since is a swine pathogen.

Why do you think this is not the clearest model for vaccine/antibiotic design? Do you know better alternatives?

Okay, that does make experimental design much easier.

The reason I say it's not the clearest model, especially for antibiotic design, is that you're investigating the difference between bacteria in the host and bacteria on the plate. An antibiotic in particular probably isn't going to care about that-- it should kill in both situations, right?
And for a vaccine, there are so many differences between culture and in vivo that I'm not sure that you can attribute differences you see to immune evasion. Are there immune-compromised pig models? In vivo samples from those would be a much cleaner control for immune evasion.

Your comment contains some assertions that I agree or I had not think about it. Others are more objectionable. First, antibiotic resistance would be lower in vivo, due to reduced metabolic rate and that  common antibiotics rely on this assumption.

Pointing out that an immunocompromised model would be interesting makes me think why. Tell me if I am right. Immunocompromised models would make bacteria display a different transcriptome than with standard animal model since bacteria will only use certain genes related to immune evasion if animal has a working immune system. Right?

Right. The main thing is that you want your groups in an RNA-Seq experiment to focus as cleanly as possible on the difference you want to investigate. If you're interested in antibiotic resistance, use a resistant and a non-resistant strain. If you're interested in immune evasion, use samples in the presence and absence of an immune response. You expect many differences between cultured and in vivo samples-- you've already mentioned metabolism, antibiotic resistance, and immune evasion, and I'm sure there are lots more. So it's hard to relate any given gene expression change to a phenotype.

Sorry for the off topic but seems there is a mathematical method behind our RNA-Seq experimental designs with bacteria, host and antibiotics. We are using some kind of combinatorics and all these complex experimental variations may be as easier as we think.


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Mathematical modelling of omics data
I'm interested in modelling host-pathogen interactions using mathematics. I know there are good resources in Pubmed but seems I'm looking for a book or introductory reviews.
My background in maths is limited, knowing the basics about calculus and algebra, and more recently some machine learning.
The paper inspiring this question is this one:
Front Microbiol. 2015; 6: 235.
A review on computational systems biology of pathogen–host interactionsA review on computational systems biology of pathogen–host interactions

Why negative vote?

I'm a bit confused because your title and your question description don't seem to align perfectly (-omics data versus host-pathogen interactions). If you are interested in host-pathogen dynamics, in my opinion, the best general introductory text in this area is Keeling and Rohani Modeling infectious diseases and humans and animals.

The paper I posted in the question reflects what I'm trying to ask. I'm interested in studying host-pathogen interactions from an omics perspective.

As @Corvus said before me, the core of your post talks about mathematical modelling of host-pathogen interactions. The title talks about analyzing omics data. What are you really interested in? I will assume you are interested in modelling of host-pathogen interactions (as @Corvus did).
I agree with @Corvus (+1) that Modeling infectious diseases and humans and animals is a good book to understand host-pathogen dynamics.
If you feel a bit uneasy about mathematical modelling, I strongly recommend A guide to mathematical modelling in ecology and evolution.
Aside those recommendations, Evolutionary dynamics might interest you to understand evolution of viruses including evolution of virulence. Finally you might appreciate why we get sick although it is not heavy on math and a bit outdated.
In case you are interested, you will find on this post book recommendations for theoretical population genetics.


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Density of neurons/cells in the mouse brain
Could someone point out some relevant papers or resources (an online DB maybe?) describing the density of neurons (or, more in general, of cells) in different areas of the mouse brain?

The newest and most accurate method (far more accurate than older extrapolating/manual counting methods (Stereology) and yielding some surprising results) to estimate number/density of neurons/cells in brains is Isotropic Fractionator to my knowledge. Using this keyword you find some recent papers, comparing different brain areas (cerebral cortex, cerebellum,...) among rodents:

Combining our estimates of total cell number and percentage of NeuN-containing nuclei in each brain region, we find that adult rat cortex contains ∼80 million cells, 40% of which (∼30 million) are neurons. In comparison, rat cerebellum contains more than twice as many cells (∼170 million), >80% of which are neurons (Table 1, top). Therefore, the adult rat brain contains almost five times as many neurons in the cerebellum (∼140 million) than in the cerebral cortex. When all of the brain regions are taken into consideration, the cerebellum thus accounts for more than one-half of the cells and ∼70% of all of the neurons of the entire rat brain (Table 1, bottom). Overall, we estimate that of all of the cells in the adult rat brain, 60%, or 200.13 ± 21.17 million, are neurons. Glial cells, therefore, contrary to common belief, are not the most numerous cell type in the rat brain.

Isotropic Fractionator: A Simple, Rapid Method for the Quantification of Total Cell and Neuron Numbers in the Brain
Cellular scaling rules for rodent brains
The Human Brain in Numbers: A Linearly Scaled-up Primate Brain

This article seems to be at least part of what you're looking for (although I can only access the abstract at the moment). They report that:

In this study the density of neurons and synapses was measured in three different areas (8, 6, and 17) of the neocortex of the mouse. [...] The total average was 9.2 × 104 neurons/mm3 and 7.2 × 108 synapses/mm3.

It would only make sense for the neuron and synapse density of the different areas of the mouse brain to be reported in the full-text article.

If someone can manage to obtain the information, can you report it? I'll edit the answer afterwards.


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How many centrioles/basal bodies are there in multi-ciliated cells throughout the cell cycle?
I thought there were only two centrioles per cell, that convert to the basal body at some point during the cell cycle. I also thought there's one basal body per cilium, so I'm not clear on where the other basal bodies are coming from. I'd like to know the distribution of basal bodies and centrioles throughout the cell cycle in multi-ciliated organisms/cells.

check this review out..

There is a single basal body per cilium. During cell division the centrosome has two centrioles, however, during the differentiation of citiated cells, there is an amplification of basal bodies that nucleate from the centrioles.
In multiciliated cells the basal bodies arise from two pathways- 1. de-novo / deuterosomal / acentriolar pathway and 2. centriolar pathway.
In a work carried out by Al Jord et al (2014), the interplay of these two pathways had been studied in the brain ependymal cells. The study shows that post division, when the cell begins to differentiate, the daughter centriole serves as a site for creation of deuterosomes. During this stage deuterosome independent procentrioles also nucleate (the centriolar pathway) on both mother and daughter centrioles. However, the contribution to basal bodies is predominantly from the deuterosomes.

more than 90% of the centrioles were generated via deuterosomes and
  less than 10% directly from centrosomal centriole

Following figure explains the process nicely.

I am not really sure about multiciliated unicellular organisms. My guess is that they retain old basal bodies and new ones are created by a similar mechanism. Most ciliates can also undergo sexual reproduction.

It seems that there is one basal body per cilium in multiciliated cells. Centriole duplication (as far as I understand, a basal body is just a different name for a centriole that is attached to a cilium) is tightly coupled to the cell-cycle. There is always one pair of centrioles that are at the base of the primary cilium (of which there is exactly one in most cells).
But not in multiciliated cells. These cells are differentiated and can no longer divide, and their centriole duplication process is decoupled from the cell cycle. In fact, they aren't, strictly speaking, "duplicating", since many procentriolar bodies may form around one cylinder. Indeed, each cilium has its own basal body; thus a cell with hundreds of cilia has hundreds of basal bodies.

Ishikawa 2011 is a review that examines the structure of primary and motile cilia, and ciliogenesis. It does not spell out how the basal body gets there.
Anderson 1971 describes the formation of new cilia in monkey oviduct. They first remove the ovaries of these monkeys to prevent cells from differentiating (this apparently requires estrogen), then administer estrogen and look at EM images of the cells over the following 6 days. They describe at length the processes of basal body formation.
Dirksen 1991 is another review focusing specifically on basal body formation during ciliogenesis. From their introduction:

In order for the 200-300 cilia to form that the fully differentiated cell will need, production of that many centrioles is required first.
  The cell, after the last division, has usually retained a pair of
  centrioles. To what extent these mature centrioles are involved in the
  earlier stages of centriole formation, in which centriole precursor
  structures of varying sizes and shapes are generated and proceed to
  undergo transformational changes of great complexity, is largely
  unknown..

Sorokin 1968 is apparently a classic text which goes over EM images of ciliogenesis at various stages, and proposes a series of events describing what is happening. This is probably what you want, re: where are the other basal bodies coming from.
Bettencourt-Dias 2007 reviews the research on the formation of new basal bodies. This is another publication that answers your question very directly:

Many ciliated cells, such as those in vertebrate respiratory and
  reproductive tracts, can have 200–300 cilia per cell. This requires
  the generation of multiple centrioles during ciliogenesis. Here,
  centrioles are generated by two pathways, a centriolar and an
  acentriolar mechanism. In the first one, a parent centriole usually
  produces one daughter at a time; however, in certain cases several
  centrioles have been observed to develop simultaneously around one
  parent centriole, with the daughter centrioles being released into the
  cytoplasm to mature. The acentriolar pathway is the major pathway for
  basal body production. In this pathway, fibrous granules 124 that are
  70–100 nm in diameter first appear in the cytoplasm and subse quently
  move to the apical cytoplasm. Deuterosomes appear within the area.
  (...) Multiple procentrioles can grow out from deuterosomes, and
  mature daughter centrioles travel towards the apical region where they
  form ciliary basal bodies.

What about multi-ciliated protists?

@har-wradim I have no idea. The above is for mammals.


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Tracking of oxygen molecules in glucose oxidation
For this reaction, found in typical biochemistry textbook:
$C_6H_{12}O_6 + 6O_2 \to 6CO_2 + 6H_2O$
I am interested in where do the oxygen atoms of $6O_2$ go. I think they go to $6H_2O$, but this is not sufficient for balance. So Does oxygen atom from $6CO_2$ also get into the carbon dioxide. Experimentally these can be confirmed by iostope labeling experiments. Reference to any such experiments will be appreciated.
I am interested in this question because the central metabolism can be understood as a electron transfer process where glucose is donor and oxygen is acceptor. We need to calculate, effectively how many electrons glucose transfers to oxygen in case of full oxidation.

This reaction does not actually happen. This reaction denotes combustion, not respiration.

The reaction provided is correct...albeit it's just an empirical formula....& respiration can be theoretically called an example of controlled combustion....

I think this experiment (PDF file) will help you understand the basic concept about the fate of oxygen in aerobic respiration. Basically the result is:

The oxygen of respiratory carbon dioxide is in exchange equilibrium with body water.
Utilized molecular oxygen is converted to body water.

In respect to calculation of electrons donated to oxygen, just calculating how many NADH2 and how many FADH2 is reduced in how many steps during ETC will be able to answer your question.

Glucose catabolism is a multistep process involving a series of reactions. The reaction you gave is simply the overall, balanced equation; it doesn't actually happen like that in living cells. All diatomic oxygen is converted to water in the electron transport chain, but water is also consumed and produced throughout the preceding steps, which is why the equation doesn't balance that way.
Check out these images from Wikipedia and note all of the compounds entering and exiting the process.
Glycolysis
TCA Cycle
Mitochondrial Electron Transport Chain

I think it is high time for biochemistry books to change this misguiding summary of respiration.

@WYSIWYG I agree, or at the very least explain what it actually represents.

@WYSIWYG Can you please give some reference journal articles that calls for updating the current text and also offers a more realistic picture.

@DurgaDatta The equation is a gross oversimplification of a complex process perhaps only useful in introductory biology. That it was the cause of your misunderstanding illustrates his point. The images I linked to offer a more realistic picture.

@DurgaDatta. you can refer to Principles of Biochemistry - Lehninger


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Why does a coconut have exactly three "holes"?
Why do coconuts have exactly three "holes", as seen in this picture?

A theory says:
As coconut is a sibling of palm, somehow long time ago, three palms were in a same husk. Based on evolution theory, it's how the coconut was born in the world with three holes.
Reference:
"Why does a coconut have exactly three eyes?", Quora

I'm not exactly sure what your question is. Are you wanting someone to clarify or confirm this theory?

That's not evolutionary theory, that's mythology.

Is this a question?  If so, it desperately needs an edit.

Based on strictly on evolutionary theory: "because it can".

The three "holes" are the result of the 3 carpels in coconut flowers, and three carpels is typical of the family Arecaceae (Palms). The "holes" are actually germination pores, where one is usually functional and the other two are plugged. The new coconunt shoot will emerge from the functional, open, germination pore.
For further info and pictures, see this webpage or the paper Morphological and anatomical studies of the coconut (Smit 1970, link to pdf), which holds a wealth of information.

This must be truly the answer with the highest vote-to-text ratio ever! +1